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UlrichWernery Oskar-Ruger Kaaden

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,,Dedicated to thefond memoy of Lt. Gen. Hamoodah Bin Ali, from Central Veterinay Research Laboratoy/ Priv.-Doz. Dr. Dr. habil. Ulrich Werney"

UIrich We rnery Oskar-Ruger Kaaden

Infectious Diseases in Camelids
2nd, revised and enlarged edition
With 179 figures and 62 tables

Boston . Copenhagen * Edinburgh . London Melbourne Oxford .Tokyo

Blackwell Science Berlin Vienna 2002 -

Blackwell Wissenschafts-Verlag GmbH Kurfiirstendamm 57,10707 Berlin Firmiangasse 7,1130 Vienna Blackwell Science Ltd Osney Mead, Oxford, OX2 OEL, UK 25 John Street, London WClN 2BL, UK 23 Ainslie Place, Edinburgh EH3 6AJ, UK Munksgaard International Publishers Ltd 35 Nsrre Ssgade 1016 Copenhagen K, Denmark Blackwell Science, Inc. Commerce Place, 350 Main Street Malden, Massachusetts 02148 5018, USA

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With contributions by: Jorg Kinne Central Veterinary Research Laboratory Dubai, United Arab Emirates

Editors' addresses: Ulrich Wemery, Dr. Dr. med. vet. habil. Central Veterinary Research Laboratory P.O. Box 597, Dubai, United Arab Emirates
Oskar-Riiger Kaaden, Prof. Dr. med. vet. Institute for Medical Microbiology Infectious & Epidemic Diseases Munich University Veterinarstr. 13,80539 Munich, Germany

Set Bornstein National Veterinary Institute Uppsala, Sweden Whilst every effort has been made to ensure the accuracy of the contents at the time of going to press, neither the Authors nor the Publishers give any guarantee whatsoever as to the accuracy of the information contained herein and accept no liability whatsoever in respect of any loss, damage, injury or expense arising from any such error or omission in the contents of this work. Registered names, trade names and descriptions etc. mentioned in this book are not exempt from the laws regulating the protection of trade marks. Such names cannot be used by anyone without specific acknowledgement. This work is subject to copyright. All rights are reserved, whether the whole or part of the material is concerned, specifically those rights of translation, reprinting, re-use of illustrations, recitation, broadcasting, reproduction on microfilms or in other ways, and storage in data banks. Duplication of this publication or parts thereof is only permitted under the provisions of the German Copyright Law of September 9,1965, in its version of June 24, 1985, and a copyright fee must always be paid. Violations fall under the prosecution act of the German Copyright Law.

Proofreading and translation assistance: John H. Buzanoski, MD, MPH Front cover: His Highness General Sheikh Mohammed Bin Rashid A Maktoum, Defense Minister of the 1 United Arab Emirates, with his best racing camels
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Wernery, Ulrich: Infectiousdiseases in camelids / Ulrich Wernery ; Oskar-Rueger Kaaden. [Transl. John H. Buzanoski]. - 2., rev. and enl. ed. - Berlin ; Vienna [u. a.] : Blackwell Wiss.-Verl., 2002
ISBN 3-8263-3304-7
1st edition: 0 1995 Blackwell Wissenschafts-verlag, Berlin 2nd edition: 0 2002 Blackwell WissenschaftsVerlag, Berlin Vienna e-mail: verlag@blackwis.de Internet: http://www.blackwell.de

Set by: Type-Design GmbH, Berlin Printed and Bound by: Grafisches Centrum CLlnO Printed on chlorine-free bleached paper.

ISBN 3-8263-3304-7 Printed in Germany

Foreword

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The first edition of Infectious Diseases o f Camelids was a sigruficant contribution to the scientific literature of camel medicine. Clinicians, scientists,pathologists and camel owners all over the world used the book. The information was current, reflecting the extensive experience obtained at the Central Veterinary Research Laboratory (CVRL) and from world literature. The CVRL is one of the premier diagnostic laboratories in the world, with the staff devoting their efforts towards the diagnosis of disease in camels, horses and falcons in the Middle East. The CVRL has a professional staff of microbiologists,pathologists, molecular biologists and parasitologists working together to further the scientific knowledge necessary for the proper husbandry of camels. The authors are pre-eminently qualified to write on this subject, having devoted much time, effort and expertise to studying camel infectious and parasitic diseases. The second edition continues the excellence of the first edition and adds significantly more information. The etiology of heretofore-questionablediagnoses has been clarified. More specific diagnostic procedures have been studied for sensitivityand specificity in camels. Two new contributing authors have been invited to expand the areas of diagnostic pathology (Dr. J. Kinne) and parasitology (Dr. s. Bornstein). Publications dealing with the details of camel pathology are few and with this edition a valuable service has been rendered to diagnosticians and camel owners all over the world. The husbandry of camels will be improved as a result of more basic knowledge about diseases and disease processes in camels.

An important addition is the new chapter on parasites. Information on many of these parasitic diseases is now in concise, usable form. It is significant that superbly skilled scientists have been given an opportunity to investigate and conduct research on camel diseases in the United Arab Emirates. His Highness General Sheikh Mohammed Bin Rashid A Maktoum deserves the thanks of 1 camel owners all over the world for having the foresight to establish the Central Veterinary Research Laboratory. Following more than a decade of investigation and collection of data on camelid diseases, the CVRL accumulated the expertise and knowledge to publish this book. His Highness' continued support of ongoing investigations on camel health is a reflection of his intense interest and support of the athletic camel. Camel owners, trainers, veterinarians and scientists from many disciplines are deeply.appreciativeof His Highness' benevolence. The second edition has been completely updated, particularlyin the areas of pathology, parasitology and mycology. The book is divided into bacterial, viral, fungal and parasitic diseases, with each chapter containing information on etiology, epidemiology, clinical signs, pathology, diagnosis, treatment and prevention. Treatment and control has been given special emphasis in this second edition. Congratulations to the authors for their dedication and willingness to share their experiences with colleagues around the world.

Murray E. Fowler, DVM Professor Emeritus, Zoological Medicine University of California, Davis, USA

After working for a short period of time with dromedaries in Somalia some years ago, I now have the privilege of dedicating much of my time to this animal species in an optimal environment. The Central Veterinary Research Laboratory in Dubai was founded in 1985 and one of the major tasks of this institute was research on infectious diseases of camelids. Before 1970, very little was known about infectious diseases of camels. However, during the last two decades there has been a tremendous increase in the number of scientific papers in the world literature. It is now known that infectious diseases cause 50"/0 of fatalities in New World camelids and 65% in Old World camelids. Pneumonia, peritonitis and diseases of the intestinal tract are the main ailments in NWC, whereas infectious diseases of the alimentary tract are the main causes of fatalities in OWC. Most species of the camel family are domesticated and are used as beasts of burden, as "ships of the desert", and provide man with high quality fiber, meat and milk. OWC can produce a considerable

volume of milk with excellent nutritional value in areas of the world where the traditional milk animals, the cow, the sheep and the goat, have difficulty surviving, not to speak of producing milk. It is therefore inconceivablethat such a favorable animal species is so seldom used as a farm animal. Many people still believe that the camel is of low economic value and is synonymous with underdevelopment. Only recently has the camel family been considered to aid man in many different respects. Understanding and utilizing this special gft could lead to the development of camel farms in famine areas and a reduction in human starvation. This book is written as a gesture of appreciation from four European camel researchersfor all that this animal family has meant to us. Autumn 2001
U. Wernery, Dubai 0.-R. Kaaden, Munich J. Kinne, Dubai S. Bornstein, Uppsala

Acknowledgements
nil,.’

The authors are deeply indebted to His Highness General Sheikh Mohammed Bin Rashid A1 Maktoum, Minister of Defense of the United Arab Emirates, whose generosity helped realize the publication of the second edition of this book. Sincere thanks are given to the owners of the Bin Hamoodah Group of Companies for their generous contribution to financing the publication of the second edition of this book and their interest in safeguarding camel breeding and racing traditions in the UAE. The authors gratefully acknowledge the cooperation, help and advice from Dr. Ali Ridha, the Administrative Director of the Central Veterinary Research Laboratory. Dr. Ridha has taken a keen and critical interest in all of the authors’ scientific work and has been our mentor during many years in a new culture. Very special efforts have been contributed by the CVR Laboratory staff in Dubai: Dr. J. Sasse, Mrs. R. Wernery, Mr. 0.Mathai, Mrs. R. Zachariah, Mrs. S. Joseph, Mrs. S. Korah, Mrs. L. George, Mr. Y. Abubakr, Mr. A. K. Nizarudeen, Mr. F. Joseph, Mr. A. Ali, Mr. Y. Ali, Mr. A. Siddique and Mr. N. Muthuvattil without whose help we could never have completed this work. With great enthusiasm and invaluable assistance, they helped to introduce new laboratory techniques and cared for our experimental animals. We warmly thank the veterinarians and nutritionist who work for the ruling family of Dubai, Dr.A. M. Billah, Dr. J. Akbar, Dr. A. U1-Haq, Dr. G. Munawar, Dr.M. Ali, Dr. A. Ali, Dr. H. Tesfamariam and Mr. J. Wensvoort, for their support. Their contributions and submission of specimens have

made it possible for this laboratory to discover new facts regarding camel diseases. The authors are particularly grateful to Mrs. S. Robinson, Mr. R. Babu and Mr. N. Chaudhry for their care and patience in typing the manuscript and to Mr. D. Wernery who introduced me to the world of computers and who had the painstaking job of typing most of the tables. Many thanks go to the staff of the Camel Reproduction Laboratory in Nakhlee, Dr. J. A. Skidmore and Mr. M. Billah, for their support and to Dr. B. N. Kumar, who works for the Bin Hamoodah Group of Companies. Many other people supported and helped us with this project, but we owe a particular debt of gratitude to Dr. E. Zabegina from Moscow and Dr. Zhao Xing-Xu from China, who introduced us to many excellent camel scientists in the former Soviet Union and China. We are also extremely grateful to Prof. M. E. Fowler from the USA, Prof. R. Gothe and Prof. M. Rommel from Germany for their valuable contributions. Finally, I must thank my family, especially my wife Renate, for her invaluable assistance and advice as well as for her understanding of my absence from many social events. Last, but not least, the authors are particularly thankful to the publisher, especially to Dr. A. Miiller from Blackwell Wissenschafts-Verlag for his continuing support and the excellent design of the second edition of this book. U. Wernery 0.-R. Kaaden J. Kinne S. Bornstein

. .. 246 Candidiasis ..1. . 272 Classification of Protozoa ..2. ...6.7 Bovine Virus Diarrhea .2... . 126 Integument . 1.3 2.7 1. 97 Urogenital System .. Nervous System .. ... .3.7.. . Generalsurvey .2. 217 2. .. 254 Mucormycosis .... ..2....2 Botulism ..... ... Acknowledgements .. 32 . 1.. 124 Urinary Retention in Young Dromedaries . ..7..........1.7 Leptospirosis .... 212 2.. ..... .. ...5..1. ... 195 Neonatal Diarrhea .. ... 13 .... ....8 Rift Valley Fever ....... . ..1 . .1..5 2....1 2..... . .... .. .. .......... ..6 Vesicular Stomatitis .2 2 2-1 2. . ....... 1........... ... ....... 134 Staphylococcusaureus dermatitis . ... .. 1.... ..2..... 1.. ... ... . .............4.9 Rinderpest . ....... 36 .... .. 157 Viral Diseases .... .... ...2..... ...2 1...4 Endotoxicosis (Endotoxemia) 1.. 134 Pseudotuberculosis (Caseous Lymphadenitis) .... ... ...... ...... . Fungal Diseases 1...1.2.2 1....1. 138 Dermatophilosis . 267 16 ..... .... 1. . 155 Tetanus .. ........ ... . . ..9 Rhodococcus equi in New World Camelids .1.... . .. 111 Anaerobic Infections .. .. ..... . 1.. ..4.... ... . 161 Viral Infections Causing Disease . 168 Rabies .1..2 2....7 2... 237 Mycotic Dermatitis ...3 Digestive System ... ... ... .. ....... .. . . .4 2....5... 91 Pneumonia .. 223 2.... 109 Brucellosis . . . 35 . ... 5.......... 91 Tuberculosis .... . ........1 1. . ...... . 1 1 Bacterial Diseases .. ...... ..2. 19 21 21 31 33 36 49 54 55 59 65 73 73 78 83 11 .2 1........... Paratuberculosis (Johne's Disease) .... .....Foreword ... .. .... ...8 22 . ..3 Aspergillosis . 214 2.....3 Anthrax .4 Respiratory System .. 155 Listeriosis .1 1.. . 1... .2 14 ..... ....1 1. ..2 African Horse Sickness ....... ... .2. .. 198 Equine Herpesvirus .5 Pasteurellosis . 187 Papillomatosis ...1 Protozoal Infections . ... . 209 2. .... . .. ... ... XIII Introduction .....1.. .. . ..5.. ....8 Rickettsial Diseases ..... . 1.2 1.1 1... ..1.. 257 Vaccination Programs .. 230 2. ...... ... Colibacillosis ..... . .. . ......4 Retrovirus Infection .. ... ...... 1........ .6 2... . 249 Coccidioidomycosis ........ .... . . ..168 Borna Disease .... 34 .... ... .. 224 2. . ...1 1... .4....6 Camel Plague . 209 2. ..5 Foot-and-mouth Disease . 116 Chlamydiosis .... .. 1.. .... 272 . ... .. .... . ...... Salmonellosis . .. . .......109 Infections of the Uterus .1... 141 Udder .... .. .3 1. .2.4.....3 Bluetongue . . 176 Contagious Ecthyma . . . ..... ......1....3.. ... ... ...1....2.......... ....2.. 256 Miscellaneous Fungal Infections .... ... 174 Camelpox . .... 149 Nonpathogenic Viral Infections ... 1..1 Respiratory Viruses .1....2.. .. 149 Infectious Mastitis .. .. .10 Unusual Arboviruses .. . ..1. 192 Influenza . ..... ..... . 240 4 5 51 .. 33 .. 219 2.....1.. ........ . V VI1 IX Preface . 261 Parasitic Diseases . ..1.5 1.. 228 2.... .. 234 3 31 . .. .... ... 206 Abbreviations .

. . .1 Classification of Cestodes . .8 Oxyuridosis (Pinworm Infection) . . . . Giardiosis . . . . .1 5. . . . . . .11 5. .3 Schistosomatidae .2. Besnoitiosis . . . 5.2 5. . . . . .3. . . . . . . . . 5. . . . . .6.5. . . . . . . . . . . . . .7. . .3 Cestodes of the Intestine .4. . 5. . . . . . . . . . . .2. . .2 Index Infection with Hirudinea (Leeches) . . . . . . . . . . . .5 5. . . . .1. . .11 Onchocercidosis . . . . . . . . . . .6 5. . .5 56 . .3. .1. . .6. . . 5. . . . .10 Gongylonemosis Parabronemosis Thelaziosis . . . . . .2. . . 5. 354 356 357 358 360 360 361 363 366 369 370 370 370 374 376 378 378 378 378 385 385 5. . .2 5. . 5. . Coccidiosis .2. . . . . . . . . . .5. . . .6 5.1 5.4 5. . .8 5. . .4. Ceratopogonidae Infestation (Midges) . . . . . Toxoplasmosis . . . 5. . .3. . . .3 Dictyocaulosis (Lungworm Infection) Parelaphostrongylosis (Meningeal Worm Infection) Angiostrongylosis . . .7. . . . . . . . . .2. 5. . . . . . . Neosporosis . . .5. . . . .6 5.3 5. . . . . . . 5. .2 5. 5. . . .2. . . . . . . . . Tick-borne Diseases: Babesiosis. . . .3. . . .6.1 Classification of Trematodes . . . . .4. . . . . . . . Balantidiosis . . . . .2 Paramphistomatidae Rumen Flukes . . . . . . . . . . . . . . . . . . . Theileriosis . . . . . . . . . . . . . . Infection with Nematodes. .2. 5. Tick Control . .13 5. . . .7.7 Strongyloidosis . . . Classification of Arachnea . . .1. .2. . . . . . . . . . . . . . . Infestations with Ectoparasites . . . . . . . . . . . . . Demodectic Mange . . . . .2. . . 5. . . . . . . . .6 Bunostomosis (Hookworm Infection) . . . . . . . . . . . . .12 Treatment of Nematode Infections . . . .9 Trichuriosis (Whipworm Infection) Capillariosis . .2. .2. .2. . .5. . . . 386 . . . . . . . . . Infestation with Siphonapterida (Fleas) . .2 5. . . . .9 5. . .1.6.3. . . . . .1 Trematodes of the Liver .2. . Infections with Molineidae . . . . . . .3. . . . . . . . . . . . . . . Chorioptic Mange . . . .1 Cestode Larvae in Internal Organs . .3 5.2. . .8 5. . . .12 5. . . . . . . . . . . .3. . Ticks Found on Camelids . . . . . . 5.7 5. . . . . . . . . .1.2. .1 5.1. Classification of Insects . 5.2 5. .7. .1. Trichostrongylidosis (Gastrointestinal Worm Infection) . Infestation with Flies . . . . . . . . . . . . .2. . . . . . . .7. . . . .3. .5 Oesophagostomosis and Chabertiosis (Nodular Worm Infection) . . . . .2. Tabanidae Infestation (Horse Flies) .1. . . . . . . 5. . Linguatula serrata Infection (Tongue Worm) . . . .XI1 Table of Contents 5. . . . . 5. . . . . . . . . . . . . . . . . Insects Found on Camelids . . . . . .2. . 5. . . .3.4.5 5. . Infection with Cestodes (Tapeworms) .3.2 Tapeworm Infection . . . . . Sarcocystiosis . . . . . .2. . . . 389 . . . . . . . .7 5. . . . . .4 5. . . . . .1. . 273 282 283 284 286 287 295 296 298 299 302 303 312 312 313 320 322 322 323 324 329 330 331 331 331 333 333 341 341 342 347 348 348 353 5. . . . Tritrichomonosis . . . . . . . . . . . . . .3 Infection with Trematodes (Flukes) . .3. . . Cryptosporidiosis . . Psoroptic Mange . 5. . Infestations with Metastigmata (Ticks) . . . . . . . .7. Classification of Nematodes .2. . . .1 5. .1. . Hammondiosis . .4. . . . Sarcoptic Mange . 54 . . . . . . . .5 5. . . . .4 5. .5. . 5. . . . . 386 Infection with Leeches . .3. . . .2. .4 5.6. . . .2 Cestode Larvae Found in Muscles . . . .1 5. .1. . . .2 Trypanosomosis . .10 5. . . . . Tick Paralysis . . . . . . .3 5. . .1.3 5. Infestation with Lice .2. .2 Trematode Infections . . . 386 Classification of Hirudinea . . .2. . 5. . .

Abbreviations AGID CFT CVRL ELISA ELM1 FAT NWC OWC UAE SNT Agar gel immunodiffusion test Complement fixation test Central Veterinary Research Laboratory Enzyme-linked immunosorbent assay Electron microscopy Fluorescent antibody test New World camelids Old World camelids United Arab Emirates Serum neutralizing antibody test .

Introduction .

r T. To the Bedouin of the Arabian Peninsula and North and East Africa. vital for survival in a most inhospitable environment. Wilson (1998). approximately 1000 New World camelid veterinary references were published. for example. Higgins (1986). fiber and fuel. the vicufia and guanaco remain wild species.. Until recently. Israel. scientific interest in camels and the majority of research projects involving camels have been concentrated in countries actively involved with the care and maintenance of the camel as a domesticated animal. 1992. and the edition of a camel journal (Journal of Camel Practice and Research. Further international meetings and conferences took place in 1996 in Eilat. Gauly (1997). A frequent opinion encountered in those countries not involved with camel husbandry is that the camel is an anachronism.Introduction 3 Camelids have served the needs of people for thousands of years and have provided them with food. 1986). Doose (1990). In South America. Tibary and Anouassi (1997). Fowler (1998). Beil (1999). the most suitable domestic mammal for uses in climatic extremes (Yagil. Gahlot). K. (1999). Wernery. There was obviously an urgent need for a comprehensive compilation and evaluation of the published literature for all those involved with camels. and in 1999 in South and North America and in Morocco. Saltin and Roose (1994). Prior to 1987. Wilson. The camelid family has become the focus of increasing study in the last few years. In many parts of the world they have also served as beasts of burden. Proceedings are available from most of these conferences. 1985.. Yagil (1985). editor D . 1999). In many countries camelids have now adapted to contained management. and still is in some parts. while the llama and the alpaca are domesticated.It is therefore not surprising that many publications on camels appear in journals that are difficult to obtain or in lesser-known languages. Bactrian camels inhabit the high deserts of Asia where they survive -40°C temperatures. Wernery et al. in 1997 in AlAin. Mukasa-Mugerwa (1981). an animal of the past and without a future (Wilson. due to its physiological attributes. the dromedary was. They secured trade and communication throughout wide arid and semiarid expanses. 1992). For hundreds of years they have carried goods along the Old Silk Route to China. This has become apparent not only through the increase in scientific publications by. Griindel (1988). Faye (1997). . This is especially true as the camel is. the camel should play a more important role than is currently the case in a world where food and energy reserves are dwindling (El-Gayoum. Wilson (1984). A few wild Bactrians still roam the steppes of the Gobi desert in Mongolia and China. United Arab Emirates. Additional bibliographies about the camel can be found under Farid (1981). As an important source of milk. and Wilson et al.Wernery and Kaaden (1995). in February 1992 (Allen et al. but also through the increase in joint research projects between European universities and institutions in and countries. and in the last few years there has been a renaissance in both Old and New World camelids. They have adapted well to high altitude survival. Manfield and Tinson (1996). This growing general interest in camelids also became evident when 300 camel experts from 30 countries took part in the First International Camel Conference in Dubai. (1990). 1992). An impoctant step in this direction was the publication of the bibliography Sur le dromadaire et le chameau by Saint-Martin et al. During the period from 1987 to 1996 one thousand four hundred new references appeared in the world literature (Wernery et al. 1989. Bitter (1986). meat and wool as well as transportation and labor. and Gahlot (2000). (1990). UAE. in which approximately 5500 pre-1990 publications regarding camels are catalogued by author and subject matter. 1984). George.

Firstly. There were two main reasons for this belief. (c) Guanaco. They populated South America where the different types are known today as llama (Lama g l u m . they died out in some of these regions. E.Camelus ferus. the two-humped wild camel . North and East Africa and eastern Asia (Koehler. USA) (a) Llama. (d) VicuAa . guanaco (Lamaguanicoe . After some time. the ancestors of the humpless NWC migrated south over the newly formed isthmus between the half continents of North and South America (Sielmann. When the OWC migrated eastwards after crossing the Bering Strait. M. The tylopods originated in North America 50-60 million years ago (Tertiary period) at which time they branched into eight different families (Zeuner. 1988). KoehlerRollefson.wild) and alpaca (Lama pacos .4 Introduction For a long time it has been incorrectly assumed that one and two-humped camels derive from a sole wild species. Today’s OWC evolved from these early camels. the latest osteological investigations on post-cranial skeletons of dromedaries (Camelus dromedarius) and Bactrian camels (Camelus buctrianus) have shown that they are in fact derived from two different species (Peters.e. vicufia (Lama vicugna . 1997). Fowler. i. 1).domesticated). the ancestors of the OWC migrated to northeast Asia across the isthmus today known as the Bering Strait.wild). Then. They were most widely spread during the Pleistocene era (endingtwo million years ago) when they reached as far as Eastern Europe. the crossbreeds between dromedaries and Bactrians are fertile. However. The Figure 1 The four different South American camelids (courtesy of Prof. both the one and two-humped camels pass through a two-hump embryonic stage.domesticated) (Fig. branching out westwards. They were at that time the size of hares. Six of the eight families died out in the middle Miocene. 1981. five million years ago. 1982). Secondly. 1963). (b) Alpaca.

1998) Class Order Suborder Suborder Mammalia Artiodactyla Suiformes Tylopoda Old World New World 5 Hippopotamuses.803 < 100 in zoos 0 100 161. Torres. antelooe.000 > 2.000 2. In North America.400 Vicuiias 23.000 Alpacas 2.Introduction Table 1 Classification of camelids and other artiodactylids (Fowler.Bactrian camel Lama glama .000 < 5.000 12.020. an achievement of high Indian culture.alpaca Lama guanicoe . swine.000 > 5.vicuAa V: vicugna mensalis (Peruvian) V: vicugna vicugna (Argentinean) Cattle.000 ? 20.000 years ago. giraffe. bison Suborder Ruminantia OWC and NWC belong to the Camelidae (camel-like)family under the suborder TyZopoda (Table 1). the last being the genus Camelops.000 5. sheep. Of the OWC.000 900. goats. In South America today. wild population of camels in China and Mongo- Table 2 Estimated population o f South American camelids (Carpio.guanaco Vicugna vicugna .343 < 100 in zoos < 100 in zoos 145. which was most probably hunted into extinction by the indigenous Indians. mostly in zoos 397 572.000 28. the two remaining species domesticated today are the one-humped camel or dromedary (Camelusdromedarius).llama Lama pacos .000 > 6.344.000 300.000 Guanacos 550.498 In lSlS registry in zoos* Total Grand Total * ISIS = International Species Inventory System .000 3. deer.000 > 110.000 < 1.683.000 343 3.dromedary camel Camelus bactrianus . water buffalo.000 98.000 years and were among the first recorded domesticated animals. and the two-humped camel (Camelus buctrianus). peccaries Camelids Camelus dromedarius . between 7 and 8 million small camels have been counted (Peru.with the exception of a small.761.000 85.142 0 > 10 > 9.500 303 3.000 1. 1991.500.000 A few in zoos < 2. all camel species died out 10.210 7. 1992) Country Argentina Bolivia Chile Peru Austra I ia Canada Europe United States Llamas 75. Bolivia) (Table 2). Lla- mas and alpacas have been domesticated there for 7.

The Bactrian camels fulfill a similar role in Mongolia. . Arabia and the Near East is mainly one of transportation of goods and man. until today it has been impossible to establish whether the remaining populations of Bactrian camels in these regions are feral or genuinely wild camels. China) and (b) a wild Bactrian camel (Camelus bactrianus ferus) with a newborn calf (courtesy of J. TransCaspian. 3 and Table 3. The extent of the OWC habitat and worldwide population is shown in Fig. b (a) The Bactrian camel. Zhao XingXu. However. UK) lia (Fig. Hare. The Wild Camel Protection Foundation. Western Siberia. rutting male (courtesy of Dr. The dromedary’s role in North and East Africa. Iran and Afghanistan. School Farm Benenden Kent TN174EN. 2b). Asia Minor.6 Introduction Figure 2a.

600.000 270.000.000 1. 1990.000 580.000 120.000 5.000.Introduction Table 3 Old World camel population (Higgins.000 Grand Total * Independent states of the Soviet Union Figure 3 Distribution of C.000 18.255.000 610.000 6.256.000 7.Bhattacharya.000 173.000 250.150. 1986.999. Wilson et al.000 230.000 210.000 5. dromedarius and C.000 6.000 200.000 10.000 Total 12.000 1.000 6.000 60..000 780.000 800. 1988.000 12.000 135.000 4.000 410.000 173.000 446.000 90.000 6.000 120.000 600.000 1 1.000 880.000 1 4. 1997) Africa Algeria Chad Djibouti Egypt Ethiopia Kenya Libya Mali Mauritania Morocco Niger Nigeria Senegal Somalia Sudan Tunisia Upper Volta Western Sahara Camel Population Asia Afghanistan India Iran Iraq Israel Jordan Kuwait Mongolia Oman Pakistan Qatar Saudi Arabia Syria Turkey United Arab Emirates Yemen IPS* China Australia Canarv Islands Total 18.000 2.000 27. bactrianus .000 7 Camel Population 150.Wernery.000 92.

However. The average wool clip is 3. the Bactrian camel produces superior wool to the dromedary (Anonymous. However. Of the OWC. milk. The Bactrian camel was named after the Bactria region of South-WestAsia (Allen et al. in strict taxonomic terms. 4).. It has been shown that camel hides are very strong with a tensile strength five times greater than hides. Differences between camelids and ruminants are shown in Table 4 (Wernery et al. but also for meat. However. 1992). This is one of the reasons why scientists have been involved in cross- Figure 4 The forestomach system of Tylopoda (Fig. soft leather Figure 5 Crossbreed (male. Camel wool is one of the world's most expensive natural animal fibers. there is an increasing demand for NWC fiber since it is known that the vicufia produces the finest wool of all animals. hides and wool. 1995). Camel leather is now being crafted into fine fashion garments..It produces only 200 grams of wool per year.10 kg for females. Their three forestomachs are called compartments wallets. thus ruminating. Wool is an important dromedary by-product in many camel-producing countries. It is similar to cashmere in both fiber diameter and texture. Camels are used not only as draught and riding animals. the protein content is comparable with beef. The Bedouins produce carpets and tents from camel wool. Camels regurgitate and re-chew their food. 1999). Male Bactrians can produce 10-16 kg of the magnificent fiber. The interest in its fiber has saved this magnificent animal from extinction. 10 months old) between a guanaco (mother) and a dromedary (father) .8 Introduction OWC have adapted marvelously to life in either hot or cold environments and NWC to life in high altitudes. but unfortunately there is very little interest in the camel wool industry. Sophisticated mechanisms have evolved that guarantee survival of this unique animal family under extreme conditions. handbags and purses.28 kg for males and 2. Comparative technical information shows that the fat content of camel meat is considerably less than that of beef. The word dromedary is derived from the Greek and means "running". they are not recognized as belonging to the Ruminantia.

re-chewing and re-swallowing stomach .Introduction Table 4 Differences between camelids and ruminants Camelids Evolutionary pathways diverged 40 million years ago Blood red blood cells elliptical and small (6. resistant t o bloat compartment 1 has a stratified squamous epithelium 2 glandular sacs in C1. sheep and goats Infectious diseases minimally susceptible t o tuberculosis bovine brucellosis is rare mild susceptibility t o foot-and-mouth disease rare clinical disease with other bovine and ovine viral diseases Ruminants Evolutionary pathways diverged 40 million years ago Blood red blood cells round and larger (10 p) predominant white blood cell is lymphocyte Foot has hooves and sole second and third phalanges are nearly vertical Digestive System same (parallel evolution) -/ 9 stomach . act as "reserve water tanks" Reproduction induced ovulator no estrous cycle follicular wave cycle copulation in prone position placenta diffusa epidermal membrane surrounding fetus cartilaginous projection on tip of penis ejaculation prolonged Urinary kidney smooth and elliptical suburethral diverticulum in female at external urethral orifice dorsal urethral recess Parasites unique lice and coccidia share some gastrointestinal nematodes with cattle.3 compartments.4 susceptible t o bloat . with regurgitation. papillated epithelium no glandular sacs Reproduction spontaneous ovulation estrous cycle no follicular wave cycle copulation in standing position placenta cotyledonary no epidermal membrane on fetus no cartilaginous projection on tip o f penis ejaculation short and intense Urinary kidney smooth or lobed no suburethral diverticulum dorsal urethral recess in some species Parasites unique lice and coccidia share gastrointestinal nematodes infectious diseases highly susceptible t o tuberculosis.5 p) predominant white blood cell is neutrophi1 Foot has toenails and soft pad second and third phalanges are horizontal Digestive System foregut fermenter. bovine brucellosis and foot-and-mouth disease .

at ince of Oman. The first suc. no skeletal remains or rock paintings ologists are still trying to locate the fabled of camels in the Sahara mountains support city of Ubar (Shisr) that was supposedly this theory. tion began at that time. Archaeever.000 caravans brought incense from Oman and to 20. Exactly when the wild camel tle is known about the dromedary’s ances.000 years ago during extremely cold Yemen to the Mediterranean. which made temperatures coupled with drought.was domesticated 4.as the wild dromedary population died toric sites in Kazakhstan and Mongolia. the southernmost provonly found once in South West Asia. This city was the center of Figure 6 Routes of the incense trade . but it t .became domesticated is uncertain. is believed to have begun on the Arabian ry the ”giant” camel. lit.out 1000 BC. How. wherean camels’ ancestors discovered at pre-his.mains were found at Sihi. is known zoologically as Peninsula (Wensvoort. It was written in These camels are presumed to have existed the Bible that around 1100 BC the Median in a wild state during the last ice age in Bedouin tribes used dromedaries to occuNorth Africa and in the Negev Desert.the beginning of the Holocene era. Bones excaCamelus thomasi (named after the French vated at trading settlements in Jericho. Camelus thomasi is Shar-I-Sokhta and Umm A1 Nar (near the now considered a possible ancestor of the city of Abu Dhabi) prove that domesticadomestic one-humped camel (Peters. dromedary and a female guanaco (Fig. a village in ed Arab Emirates (UAE) between a male Yemen.both countries indescribably rich. 1998). and were dated at 7000 BC. Evidence of wild camels was situated in Dhofar. 1991). 5). In 1000 BC large dromedary where they probably died out some 12. The recessful hybrid was produced in the Unit. It is widely believed that the dromedary Although there is evidence of the Bactri.500 years ago. paleontologist Thomas). py Palestine.10 Introduction breeding NWC with OWC. An ancestor of the dromedary camel.

25% in the Northem Territory. and 25% in western Queensland and northern South Australia. which nowadays number approximately 200. With the advent of Christianity the incense trade began to decline. there was renewed interest in camels. the camels were abandoned and it is believed that as a result of being eaten by lions and bushmen. An estimated 10. they disappeared in southern Africa in the late 1960s (Massmann. it was not introduced into Tunisia and the Atlas countries before Hellenistic times. These feral camels are scattered throughout the arid interior of Australia with an estimated 50% in Western Australia. oxen were eradicated by rinderpest and footand-mouth disease.000-12. the country with the highest proportion of dromedaries per person. Camel breeding may have increased because of the lucrative incense trade. South America and the Caribbean. which have hot climates. Lorenz Hagenbeck shipped 2. When trade began with Arabia. 1991). Dromedarieswere also used in the United States after the Mexican war of the 1840s. 6). and thirdly. camel races were held at Berlin’s famous horse race course Hoppegarten in . 1995).Several races were held in Sydney in August 1998 (with the support of the UAE) in preparation for the Olympic Games in 2000. In 1906. In the late 1960s. after motorized transport became popular. dromedary numbers increased in Africa. In August 1997. and Arabia Felix reverted to the deserted Empty Quarter. but also into Australia and southern Africa. The caravanserai reached its zenith during the reign of the Nabateen. on mail express routes across the newly acquired arid regions. when motor vehicles began operating in the central areas of Australia.000 camels imported into Australia between 1860 and 1907 were used as draught and riding animals by people pioneering the dry interior (Viswanathan. from where the camel caravans made their way through Marib. In the semi- arid deserts of Australia they established free-ranging herds. Medina and Petra towards Gaza and the Mediterranean.000 animals. as in Australia. the English police force then took possession of all remaining camels in Namibia. only the Bedouins continued to utilize the dromedary. It is presumed that between 1500-2000 BC. Most of the camels were released in the mid-l920s. In Europe. because they are highly suited to the Australian desert climate. Dromedaries were not only introduced into countries with temperate climates such as Europe. These heavily laden “ships of the desert” took about 50-70 days to cross the deadly stretch of land between Marib and Petra. After the Versailles Peace Treaty (1919). around 1890. only dromedaries could survive in the Namibian and Kalahari deserts. the “ship of the desert” spread north and westwards. However. After the caravans vanished. but they were later eradicated. mainly Namibia. However. The other incense routes through the great Arabian deserts towards Gerrha on the Arabian Gulf could only be traversed with the help of the camel (Fig. horses were severely decimated by the devastating African horse sickness virus. 1981). Terracotta finds from Petra are richly decorated with dromedaries. Beyond Somalia. and by 1970.Introduction 11 the incense trade. Australia had two camel tourist businesses with camel races being held around Australia (Anonymous.000 Sudanese camels to the small outpost of Swakopmund in Namibia. camel societieshave emerged during the last two decades and animals have been used to attract tourists. dromedaries spread into Africa from the Arabian Peninsula via the Horn of Africa. They were used by the German Schutztruppe in Namibia until the end of World War I for three reasons. Dromedaries were also brought into southern Africa. Firstly. secondly. The camels introduced into Australia were almost exclusively dromedaries.

1969). Until now. not only with scientists. 1998). Its milk. the dromedary has again fourth generation is infertile. However. Since the 1980s. The confusion is compounded be. The future of the dromedary species is assured despite the competition of modem transport and other domesticated animals. or racing (Wilson.old) between a Bactrian male and a female groups. 7). Turkey.by naming them after the tribes who rear them. this cause of the crossbreeding of Bactrian and was not the first camel race in Europe. 2 years gions. Scientists have recently intensified their study of the dromedary and are debating whether there are different dromedary "breeds". or whether they are riding or transport camels. dromedaries in Russia. skin and meat are all utilized and. by their color. As the second generation place in Cologne-Weidenpesch in 1969 of these crossbreeds (Tulu) are generally weak and susceptible to diseases and the with Moroccan camels (Leue. and it offers no threat to domesticated animals or any endangered wildlife. Afghanisas was then claimed. additionally. physical characteristics or their use for milk. This categorizationhas given rise to the classification of dromedaries under 48 "breeds" in 9 regions and sub-re. for riding and transport. the dromedary has been classified in the following ways . The first races took tan and Syria.12 introduction Figure 7 Geographical distribution of dromedary breeds (after Wilson. the breeders become popular. it has become a tourist attraction.000 spectators.Figure 8 Crossbreed (Tulu) (female. 1998) front of 60. 8). under 3 main groups and 8 sub.dromedary . have to start all over again to achieve a but also in the countries where it is used good crossbreed (Fig. geographical background (Fig. meat.

Phoenicians. the tribe with the quickest and most nimble dromedaries had the most chance of surviving.000 10. described disputes that still occurred until some 30 years ago. Only through its indispensable patience and perseverance did it enable survival in the perpetual sands. Sumerians. the dromedary raises many questions which are not easily explained. in his book Arabian Sands. such as weddings or births. Over this period.000 200.000 6.Introduction 13 In its great genetic diversity.000 Figure 9 One of the authors examines a valuable female asil dromedary . In an effort to find new grazing areas. In its perseverance. the desert played a big part in the evolution of the dromedary as the only domesticated animal to survive in such extreme conditions. In the Arabian Desert. intelligence and beauty. but it is also used as transport over thousands of kilometers.The tribes could only survive in the desert thanks to the dromedary. Obviously. not only were the dromedaries vital during tribal conflicts.121. which the Bedouins call Ata Allah (God‘s Gift).000 1. meat and wool. the Bedouins and their dromedary herds wandered through the great Arabian deserts and lived undisturbed throughout the successive reigns of the Pharaohs. it was the Bedouin who managed to breed the precious Arabian horse. This sometimes resulted in feuds and skirmishes. The quickest dromedaries were selected to run over short courses. Assyrians. is comparable with the Table 5 Dromedary population on the Arabian Peninsula Kuwait Oman Qatar Saudi Arabia United Arab Emirates Yemen Total 5. the Arabian dromedary. However. Not only the ”ship of the desert’s” ability to survive in the hottest climates. bred over hundreds of years in one of the hottest climates on earth. Thousands of years before the Pyramids were built. Greeks. but the Bedouins also used them for racing during social occasions.000 120. Sir Wilfred Thesiger. it was often necessary for the Bedouin tribes to cross enemy territory. Romans and Turks. but its natural resistance to such deadly animal diseases as rinderpest and African horse sicknes makes it indispensable to its owner.000 780. Not only does the dromedary produce milk. the Saluki dog and the dromedary.

It indirectly aids in cooling the body as the accumulation of fat leaves the subcutis of the body fat free. 8. However. allowing easy dissipation of heat. water will be present in the stomach. 13. water rapidly enters the bloodstream after drinking. Dehydrated camels can "store" sugar in their blood in order not t o lose water through the urine (sugar is highly hygroscopic). Goats kept in an open yard with no shade are unable t o survive more than 3 days without water.3 liters of fecal water. Salt is also well handled by the camel kidneys. Camels lose 1. blood sugar rose as high as 1300 mg% without the appearance of glucose in urine. Thermoregulation in the camel is greatly affected by the availability of drinking water. 4. Bedouin goats kept 4 days without water die of hemolysis after replenishing a 40% water loss in 8 minutes. a network of small blood vessels supplying the brain and eyes. 9. This is one of the primary ways of combating water deprivation in the desert. and as long as the camel continues t o eat. it can lose one third of i t s body weight in water without suffering any ill effects. These high concentrations of electrolytes are also found in the saliva and intestines and play an important role in the camel's utilization of alimentary water. 12. . After 4 hours water is apparently equilibrated throughout most o f the body. 3. A dehydrated camel is able t o continue lactation. In a trial. The camel adapts i t s body temperature t o the outside temperature. They are induced ovulators with a relatively short mating period. but camels can survive 20 t o 30 days without drinking water. Their gestation period is 13 months. Barki sheep also die after 3 days of dehydration. Camel kidneys have long loops of Henle. The water vapor from the exhaled air stays in the long nose and cools the carotid rete. 11. Camels withstand more than 3 weeks without drinking water and s ti l l continue t o eat normally. because their stomachs still contain relatively large quantities of fluid. preventing it from sweating. By then. 2. A t the end of the experiment the appetite declined. Camel can excrete urine with a salt concentration almost twice that o f seawater. The hump is an accumulation of fat for the time when energy is needed. A rise in body temperature saves a camel a lot of water that would otherwise be used t o dissipate the heat load. 5. A dehydrated camel reacts t o changes in external temperature. High blood temperature would do permanent damage t o the brain and retina cells of the eyes. 7. In a trial. Camels mate in crouched position. The camel has a great dehydration tolerance. an enormous diuresis followed and blood glucose returned t o normal. Camels can drink seawater without showing any side effects. a camel was dehydrated for 51 days and was only fed on dry grass.14 Introduction Table 6 The main physiological particulars of dromedaries 1. No other animal has such a rapid entry of water into the blood. and urine production is greatly decreased in the dehydrated camel. alimentary tract water is i t s body's sole source of water because this water is continuously absorbed from the intestines. 10. the camel's body temperature is low: 34. Camel erythrocytes are extremely resistant t o hypotonicity. As soon as drinking water was made available. Cattle lose 20-40 liters of fluid a day via their feces.0"C. Camels hold 75% of their weight in fluids. 14. Compartment 1 contains high concentrations of sodium and bicarbonate and low concentrations of chloride and potassium. In a dehydrated camel. In the morning when the desert is cold. In the late afternoon the body temperature can reach 42°C. A 600 kg camel can replenish its entire water deficit of 200 liters in 3 minutes. In camels. camels are able t o cool the brain and eyes through extraction of water from exhaled air. the camel had lost 37% of i t s body weight.

J. References Allen. Proc. In the cooler months between September and May. in recent years.000 racing camels are kept in the UAE. the dromedary competes at distances between 3 and 10 kilometers. Beil. The majority of the literature encompasses the one-humped Camelus dromedarius as the available literature on the two-humped Camelus bactrianus is unfortunately very difficult to obtain. long-legged. camel racing has gone through a fundamental change. Snow and J. Camel Cod. Bhattacharya.1992. A. In the 30 years since the oil boom began. PO Box 8760. A dromedary can cover the 10 km course in 17 to 18 minutes (Wernery.F.Eine gewichtete Literaturstudie. Australia:1 4 . 1992). Brochure of the Central Australian Camel Industry Association. in conjunction with various research institutes abroad. Both the camelids’resistance to a number of pathogenic microor- 15 ganisms. where oil has brought nomadism to a virtual standstill (Wilson. more than 100. will also be presented. Mayhew. viral and fungal diseases as well as pathology and parasitology in the camelids as completely as possible. may have been decisive in the dearth of publications on infectious diseases of camelids. What was earlier seen as playful competition and a pleasant pastime between the Bedouin has become a scientifically founded racing discipline following the oil boom of the 1960s. A. it has become an agile. it is hoped that more comprehensive data will soon become accessible. This is especially true of viral diseases. (Newmarket) Ltd.Wade 1992. I. New scientific findings of NWC are also included.5 million (Wilson et al.. The camel population has decreased in only a few countries. As the exchange of scientific research with countries where the Bactrian camel lives is now improving. competitions are held on 20 racetracks throughout the Emirates. 1999. Anonymous.R.000 racing dromedaries (including breeding animals) in the UAE. Higgins.3 million (Table 3). In addition to a compilation of the known literature. the Bedouin are extremely careful to keep the bloodlines pure. Published by R. The second edition of this book will attempt to close this gap by surveying and compiling the published literature regarding bacterial. Thesis. There is no other dromedary that compares with the Arabian. Ministry of Agriculture and Water De- . an opposite trend has been observed in the UAE where the dromedary is experiencing a renaissance resulting in a revival of the old Bedouin tradition of camel racing. Alice Springs. Camel production research i northern Saudi Arabia: a monon graph.N. 1964) (Table 6). 1986. 1984).J. 1st int. 1987). In the last few years.H. 1988. Hannover. although bacterial ailments play a larger role. Margan. Due to a number of specific anatomical and physiological characteristics.. Publications. results of the authors’ personal research conducted since 1987 on a camel population of 30. Based on the age of the animal. Through breeding.introduction Arabian horse. However. the worldwide camel population has risen from 17. 9). Christiane. and W. 1981). fast. Reproduktion beim weiblichen Kame1 (Camelus dromedariusund Camelus bactrianus). The central Australian camel industry. brown racing dromedary with fine limbs and a long head (Fig. 1995. D. the dmmedary can survive and perform tasks in the extreme climate of the desert that can be utilized by man (Schmidt-Nielsen. 1990) to 18. Based on this development. slender.. such as Libya and the Gulf States.Although no studbooks exist. as extensively examined by scientists in the Institute for Horticulture and Animal Hygiene in Goettingen (El-Gayown. and the previous lack of interest in the camel family in general. A further advantage is the low susceptibility of the camelids to disease (Fazil and Hofmann. W. Feb 24.

Camels. Koehler-Rollefson. Dubai Natural History Group 6: 6. Desert animals: physSouth American Camelids. Namib und Meer 9: 31-54. 1991. Das Dromedar: Herkunft.813126. Thesis. Anouassi. Kamels (Camelus dromedarius). ing and Publishing Co. Thesis. Bailliere Tindall. Dromedare.Mukasa-Mugerwa. und Krankheiten des Kamels. . Dromedare in Arabien. aus veterinarphysiologischer. Peters. lung in friihgeschichtlicher Zeit. H. Viswanathan. Tierarztl. U. Dubai Natural Somalia. 1997. mas. Vergleichende Untersuchunbesonderer Beriicksichtigung der Mektion gen zur Bedeutung der alternativen Komplemit Trypanosoma evansi (Steel 1885). and R. 1986. SAU/OO8/SAU. Tieriirztl. G. 1982. H. Ed. 1981. M. and Florez. 1986. Funktionen und MorphoILCA Monogr.A.F. Sielmann. Tinson. La dromadaire et le chameau. Eine Litera. Gauly.Torres. Wschr. 1990. die Rennpferde ropa 1969 auf der Pferderennbahn in Koln Arabiens. M. IUCN/CSE.16 Introduction partment of Agricultural Research. M. possible ancestor of the one-humped camel? Farid. El-Gayoum. Tome 2: Index. Scand.und Vertiebsgesellschaft mbH. 1988. 1990. 1987. J. 1997. 33501 Libourne.W. M. History Group 6: 5. and A. Tierurztl. Dtsch.genetischer and Wernery. 1997. Medicine and surgery of Schmidt-Nielsen. Ames.E. Miinchen. Umschau 4 7 801. Roose. Fowler. of Mammalian Biology 63: 372-376.F. Zur Domestikation des Kamels. Int. 1893. Guide de l'devage du droand M. The racing camel Fazil. von Kamelen (Camelus dromedarius) unter Margan. 8. 1998. Camelids Bibliography. Lima. Gruendel.Acta Physiol. 1988.Tibary. Gland. Sanofi Sant6 Nutrition Animale. J. South AmerHiggins. Richard. Ute. Monchengladbach.A.Massmann. Hannover. Perssons Tryckeri AB. T. Gahlot. India. Hannover. M.R. mentaktivierung bei Rindern und Kamelen. Arbus. Saint-Martin. D. 1992. Thesis. Hungerford Vade Bitter. a Gottingen 22.. PatholGeorge. Bibliographie sur le madaire. zerland. Sahara ogy and ArtificialBreeding. 1998. Doose. The T. M. 1991. 1997. Koehler. Carpio. Domegen Kamels (Camelus dromedarius). 2nd edition. S. Haltung and Zucht w n Neuweltkameliden 78 (18): 500-502. Selected topics on camelids. Labiomechanischer Sicht. Haltung (Camelusdromedarius). Abu Dhabi Print6: 47. lis Verlags.Peters. 1981. Koeping 150 (617). tierarztl. ics).A. Thesis. France: 115-116. Camelidos socio-economia An. Neuweltkamele. M. 1992. Camelus thomasi Pomel. B. Hannover. 1. 1986. Parey Buch.K. Iowa State Uniiological problems of heat and water. NaturaThe Camelid Publishers. ijberleben. South American Camelids: an turiibersicht. A.G. J.Wernery. ACSAD-AS 15. don Press. Thesis. A. 1969. 5: 4-119.: A produc. 1997. The Gazelle. Geo Spezial. logie des Verdauungssystems des einhockri. G. h u e .. J. 1981. H. stikationsgeschichte und KrankheitsbehandHannover.E. Tome Ballastiere . Clarenversity Press. Anatomy. Abu Dhabi. Kumla/Chister 9: 389-402. 1994. gy in camelidae. More about camels. The Thesis. Camels. Novoa. International Livestock Center for Africa. Erstmaliges Kamelrennen in Eu. Nitcheman.. Kamele in Siidwestdina (Camelids and Andean socio-economafrika. and R. 1964. Bikaner. M. action plan for their conservation. The camel (Camtion de Rumiantes Menores: Alpacas. Physiology. The introduction of Wensvoort. Cedex. U. nism of resistance to camel diseases.Working paper 24. 1981. Gazelle. elus dromedarius): A bibliographical review. I. Peru.K. The camel in health and disican Camelid Specialist Group. U. Richard Faye. 1992. 2000. C. Saltin. Mina. Gottingen 33. Untersuchungen zur Resistenz Mecum Series for Domestic Animals. J. Study on the mechaPraxis 25: 559-565. Anette. Sankhla Printers. L. Weltreich der Tiere. 5 (1): 34-36. camel nutrition and the camel into Africa with special referenceto racing camels.A. and A. 1996. Das Blut des einhockrigen UAE. 1981. Ursula.J. Re rumen: 3-16. Hofmann. Oxford. Switease. G. UTFN/ Manefield. 1991. E.Praxis Wernerssons Grafiska AB. Theriogenoloverlag Berlin. A compendium.

Skidmore. Hutchinson.T. The Tropical Agriculturalist. 4 (2). 1997. 1995. Binns. R.T. Berlin.A. Fowler and R. R. Camel Prac. An analytical and annotated bibliography.. Color Atlas of Camelid Hematology. 4 (2). J. The one-humped camel. Lond. Blackwell Wissenschafts-Verlag. . Wilson. Zeuner. 1989. J. London. Basel. 1984. Wilson. U. Hare. Evolutionary history and differences between camelids and ruminants. 1999. R. Status and distribution of wild Bactrian camels (Camelus bactrianus ferus) in China. M. F.Introduction Wemery. Billah. Longman. 1985. Yagil. 107110. Infectious Diseases of Camelids. R. Camels. Allen.N. U. and Res.R. Springer Verlag. B 266. London. The Desert Camel.E. Camel Prac. R. The United Nations Sudano-Sahelian Office (UNSO). Kaaden.The camel. Blackwell Wissenschafts-Verlag. Wemery. Technical paper series 3. Wernery. 649-656. MacMillan: 106. Wilson.. Proc. 1998. Short and W.V. 17 Further reading Fowler.T. and Res. Wilson. Verlag Karger. Hybridizing Old and New World camelids: Camelus dromedarius x Lama guanicoe. 1963. Berlin. Astier Araya and Azeb Melaku. Hare.T. London and New York. 99-105. M.N. Ecophysiology of the camelidae and desert ruminants. R. 1990. The lost camels of Tartary.E. SOC. M. 1998.E. 1997. M.-R.. J. R. Little Brown and Company.and 0. 1999. A history of domesticated animals. J. I.

Bacterial Diseases .

chauvoei. Clostridial organisms are commonly present in soils and the intestinal tract of animals. and mucosal lesions. 1995. errors in nutrition Intoxication complex . This new development is summarized in Table 7. 1992). Most of the pathogenic species produce one or more exotoxins of varying potency. type A-F.335.1 General Survey 1. perfringens possesses a capsule in animal tissue and is non-motile. mensis. Madagascar wild strains 217. These methods have also allowed the division of the epidemic anaerobic complex into three groups: .parenteral C. Contaminated soil can contain up to 105 CZostridiurn perfringens spores per gram of soil (Seifert. anaerobic wounds . C novyi. Modern methods of infectious agent identification utilizing gas chromatography allow an exact determination of the etiological agent.enterotoxemia complex. septicum. anaerobic. type A-F. C. The spores bulge the mother cell. The vegetative organism is capable of forming spores that are able to survive long periods of time in the soil. type A-F. The ubiquitous character of clostridial bacteria makes eradication of clostridiosis virtually impossible and necessitates control by prophylaxis. C. C histolyti. endospore-producing rods. Clostridia are oxidase-negative and catalase-negative and the anaerobic requirements vary among the species.gas edema complex. haemolyticum.1 Anaerobic Infections Clostridial diseases are a constant threat to livestock in many parts of the world. C. Fowler. C. lack of food. Mexico wild strains (809 and others) C.per 0s .per 0s . C.intoxication complex. Clostridia are all potent producers of exotoxins upon which their pathogenicity depends. C. periods of drought. C.enteral Errors in husbandry. overcrowding Gas edema complex . botulinum. sordellii. perfringens. type A-F C. Gram-positive. tetani Errors in husbandry. . Clostridial diseases are caused by bacteria of the genus Clostridiurn. C. perfringens.1. difficile Intoxication complex .per 0s C. overgrazing. and cause disease only in special circumstances. . . C. overcrowding 735. mineral deficiency. chicahard lignin-containingfeed. sordellii. Epidemiology and Clinical Signs :Bi The older classical etiological classification of anaerobic infections that ascribes particular clinical signs to a specific clostridial agent can no longer be considered valid. P-deficiency. Table 7 Etiologic differentiation of the most important clostridial infections and intoxications in domestic animals modified after Seifert (1992) Enterotoxemia complex . including man.1. type A-C. perfringens. Clostridium bacteria are large. Changes in intestinal permeability.parenteral deep. skin cum. Both W C and OWC may suffer from some of the clostridial diseases (Wernery and Kaaden. overcrowding. 1998).

it is possible that these disorders were falsely diagnosed in the past due to the prevailing incomplete. The other two diseases of the gas edema complex. The pro. 1992): . novyi type A X . C. B and C. begin. facthrax caused by Bacillus anthracis. . soyl . 1956. is also found in the intestines of North and East Africa. C. malignant edema. change of ning with subcutaneous swellings on the pasture. Recent publications regarding gas edema in camels are not known. transportation. gas edema. haemolyticum. 805 Mexico). The disease in lamoids is caused by C.C. perfringens has little disease-prebut these reports are contradictory. perfringens type A-F and wild strains (217 Madagascar). C. septicum have all been isolated from camelids. but there is one report of natural infection in a female llama that died suddenly. C. septicum with two types of syndromes: the typical wound infection and edema and the acute systemic disease. sordellii. novyi (Anonymous. C.C. been reported as possibly occurring in 1988). novyi. chauvoei. C. most C. Blackleg has been produced experimentally in alpacas. C. chauvoei and C. per- are seldom isolated from camelids. Enterotoxemia caused by the exception of Cross (1919). chauvoei infections in dromedaries have frequently type A (Bisping and Amtsberg. Hutyra et al. and weighing of shoulders that lead to the animal's death animals. of C. chauvoei. Malignant edema is an economicallyimportant disease in alpacas in Peru and has also been associated with rattlesnake bites in llamas in Colorado (Moro Sommo. . as well as in Chad healthy animals so that cultural evidence and India (Gatt Rutter and Mack. which may kill animals instantly. septicum. however. The causative agent was C. infectious necrotizing hepatitis dellii and C. traditional analytical methods used. Acute and subacute enterotoxemia as within 2 to 3 days.As most of the available literature is outdated. (1946) reported that camels were not susceptible to well as hemorrhagic enteritis due to C. The type of swelling should allow the differentiation between gas edema and anthrax. climatic influences. spiroforme can cause the enterotoxemia complex. chicamensis.22 Bacterial Diseases Diseases caused by clostridia are often difficult to identify in the tropics due to indigenous ecological influences. C. wild strains that have been exactingly characterized (335 and 735 Madagascar. 1998). perfringens. making diagnosis a challenge. According to Seifert (1992). 1998). Cross (1919) was able to elicit the disorder experimentally in three dromedaries through intramuscular injection of C. histolyticum. perfringens is found all over the world (1947) believes that many previous authors and is also found in all types of domestic have confused black-quarter with true an. Gas Edema Complex The causative agents of the gas edema complex. C.tors predisposing to disease include digression of both disorders is similar. have not been reported in Camelidae. Current techniques have identified the following causative agents of the gas edema complex (Seifert. which according to Seifert (1992) include the following diseases: - black-quarter (blackleg). With dictive value. Curasson C. perfringens types A.animals. bacillary hemoglobinuria and infectious necrotizing hepatitis. It is believed that OWC and NWC are more resistant to blackleg infections than bovines. Fowler. bacillary hemoglobinuria. perfringens as well as C.etary errors.C. 1963). Enterotoxemia Cornplex Al types of C.

Fowler (1998) has reported enterotoxemia due to C. 1986). types A. In another incident.seizures Affected animals died within one hour after the onset of clinical signs. predisposing etiological factors were proven to be responsible for the outbreaks.hydropericardium with fibrinous exudate. salmonella paved the way for the outbreak of C.subpleural (Fig. The animals developed intractable diarrhea and died after 4 days. For all three age groups of dromedaries. (1992b) and Wernery and Kaaden (1995). (1966)) Ipatenko (1974). 71% of the dromedaries were found to have an acute Typanosoma evansi infection. In those animals autopsied.petechiae in the mucosa of the third compartment (Fig.muscle tremor .petechiae in the pharyngeal mucosa. 12). perfringens enterotoxemia: subpleural hemorrhages . (1991). 11)and the stomach.and may have been the predisposing factor for the peracute C. perfringens types A. . since nutritional errors and environmental influences had been excluded.General Survev 23 fringens.aggression . . (1986). C and D in NWC.petechiae in the thoracic musculature. perfringens type A in racing dromedaries. Extensive studies of C. .dark kidneys.ataxia . The camels affected exhibited the following clinical signs: . They included .Seifert et al. Chauhan et al. . even more severe pathological changes were Figure 10 C. C and D have been described in camels by Moebuu et al. perfringens outbreak in this group. Wernery et al. Peracute and acute enterotoxemia in breeding and racing dromedaries as well as severe myocardial degeneration and “pulpy kidney” in dromedary calves are known to occur. perfringens type A outbreaks in racing dromedaries in the UAE have been performed by Wernery et al.petechiae in the cerebellum and brainstem. Trypanosomosis is known to be able to cause immune suppression in domesticated animals (Losos. with adherence of the capsule to the parenchyma (Fig. 10) and subepicardial petechiae. The pathological changes found in autopsied animals were mild.perspiration . . (1992).hyperexcitability . (1985) and Gameel et al. In a herd of 90 breeding animals. .

cow milk.daries are the heart and kidneys. (1992b) have reported severe myofa. Wernery crushed barley. honey and alfal. At autopsy. percompetition. terotoxemia. large amounts of undigest. The target organs for C. fringens type A toxins in young dromedromedaries are fed large amounts of un. The stress of hydropericardium with fibrinous exudate racing is also certain to play an important and ecchymotic changes in compartment 3 role in the development of peracute enand the stomach. found in their abomasum.24 Bacterial Diseases Figure 11 C. Most likely due to ignorance. 13 and 14) are These included severe hemorrhagic colitis.et al.cardial degeneration (Figs. 15 and 16) and Figure 12 C. A further important etiological factor in The dromedary calf exhibits distinctive the outbreak of enterotoxemia in racing features when affected by the enterotoxdromedaries is a nutritional error prior to emia complex. ed milk or barley (Figs. perfringens enterotoxemia: kidney capsule adherent to parenchyma . perfringens enterotoxemia: petechial hemorrhages in Compartment 3 found in the same organs as listed above.

Degeneration. 18). the sand where the breeding camels had been kept for years was heavily contaminated with vegetative cells and spores from clostridia. 17) in 4-6-week-old dromedary calves. Autopsy findings in dromedary calves revealed. perfringens enterotoxemia: undigested barley in the gastric system of a racing dromedary . the young calves begin to take nourishment other than milk.General Survev Figure 13 C. Examination of soil samples from these herds found up to 104 C. A predisposing factor for this disorder appears to be weaning. Although the paddocks were cleaned daily. perfringens enterotoxemia: undigested milk in the gastric system of a racing dromedary 25 ”pulpy kidney” (Fig. calcification and necrosis of the myocardium in 3 to 5-week-old cam9 calves in Saudi Arabia that died due to 1 C. in- creasing amounts of sand in the developing compartments (Fig. perfringens type D enterotoxemia have also been described by El-Sanousi and Gameel (1993). perfringens vegetative cells per gram of soil. Between 4 and 6 weeks of age. in addition to curdled milk and small amounts of roughage. This situation represents a continuous risk Figure 14 C.

26 Bacterial Diseases Figure 15 C. perfringens enterotoxemia in a young dromedary: hyaline degeneration of heart muscle Figure 17 C. perfringens enterotoxemia in a young dromedary: "pulpy kidney " . perfringens enterotoxemia in a young dromedary: severe myocardial degeneration Figure 16 C.

phosphorus. (1987) Examined by the J.8-2. Dromedary milk samples were obtained and analyzed using the same method. iron and phosphorus.083 0.1.A. receives its passive protection against dis- Table 8 Magnesium.2 83 Magnesium Phosphorus Ca Icium Iron **Reference values g/kg 0. Knowledge of this epidemiological connection has increasingly led dromedary owners to relocate their breeding herds more often or to replace the contaminated sand with fresh sand.5-1 1.9 10.0 9.7 neonatal diarrhea).2 3. Comloquoy. An additional important aspect in the development of clostridiosis in Cumelidue is the amount of serum immunoglobulin in the young animals (see also 2.82 1. so that the calf. fringens enterotoxemia in a young dromedary: sand in the compartments 27 of infection for the maturing young dromedaries.5 80-1 30 Herd 1 22 samples 1.2-6. so it was assumed that the dromedary calves ingested the sand more out of curiosity than due to an as yet undetected nutritional deficiency. blood samples were taken and examined for the minerals calcium.8 10.7 10.32 ~ * ** *** Normal values are for adult dromedaries (Samples were examined in a Dimension Autoanalyzer. To investigate the reasons for the young dromedaries ingesting sand.3 89 Herd 2 26 samples 2.95 1. The results are summarized in Table 8. Dubai Aluminum Plant . as in the foal. magnesium.5 9.64 Milk ***5 samples 0. Dupont) Whabi et al.078 0. Cumelidue have an epitheliochorial placenta.General Survey Figure 18 C per. Mineral licks were also placed in all the dromedary enclosures. The tests revealed no evidence of a deficiency of these minerals. calcium and iron values in sera of dromedary calves and milk from breeding dromedaries from herds where sand eating occurs Sera *Reference values mgldL 1.

should be taken from freshly (less than 4 hours) dead animals. 1963. The pathological changes in alpacas are very similar to the lesions seen in OWC with petechiae in different organs. Fluorescent antibody (FA) technique is also routinely used for disease with C. Type C and D enterotoxemias are more common in lamoids than they are in OWC.5-6. In suspected enterotoxemia. 1980-1981. 1981.. The globulin fraction is naturally low at birth. 19). septicum. three different C. perfringens from organs of dead dromedaries is performed on Sahidi-Furgeson-Perfringens (SFP)agar and Zeissler agar under anaerobic conditions with the gas generating kit. It also has the advantage that the fluid can be diluted and a titer estimated. perfringens outbreaks in the UAE. novyi and C. the globulin level declines after the seventh day and reaches the lowest level between the 20th and 30th day post partum. 20). The highest losses due to C.2 mg/mL). The intestinal contents are removed immediately post mortem and deep frozen. Cultivation of C. Specimens. C. perJrrngenstype A is a very serious disease in alpaca crias in South America and it is named “MaZ de AZpucas” (Rath. Even after ingestion of colostrum. The animal mortality rates vary between 10 and 70% and even on carefully managed farms may approach 50%. 1990. sterile filtered and tested for pathogenicity in mice. He determined that the globulin content of NWC serum is very low at birth (< 5. as clostridia are rapid postmortem invaders. perfringens hyperimmune serum is very rewarding. perfringens enterotoxemia occul during this time. Ramirez et al. 1950. The next day the material is thawed. increased following ingestion of colostrum to 5. Huaman et al. Ramirez and Huaman. Fowler (1998) made similar observations in NWC. 1990.. C.. perfringens type A strainswere identified using chromatography (Heitefuss et al. Treatment and Control Treatment of sick dromedaries with a bovine C. Toxins are very labile and therefore small intestinal contents should be frozen as soon as possible until processed.This procedure can be repeat- . the more toxin is present in the gut (Fig. One milliliter of the sterile intestinal contents is injected intravenously into the tail vein of laboratory mice. In the presence of clostridial toxin. sordellii. the endogenous antibody production is not sufficient to produce a protective immunoglobulin level within the first month of life. the mice expire within 2 to 8 hours. Fowler. The laboratory diagnosis of ”clostridial enterotoxemia”is made by identirylng clostridial toxins in the duodenum of recently expired animals.28 Bacterial Diseases ease through the intestinal reabsorption of immunoglobulinsfrom the colostrum after birth. hyperemia. Moro Sommo. The colorimetric tetrazolium cleavage test (MTT) has widely replaced the mouse lethal test and is regularly used for the detection of clostridial toxins from intestinal fluids. Heitefuss. The disease o c c u ~ s crias between 8 in and 35 days of age with sudden death or a short disease period during which the crias are recumbent. including intestinal fluid. C. Although the newborn calf is immunocompetent at birth. showing nervous system disorders.Ellis et al. excess serosanguinous pericardial fluid and lesions in the intestinal tract.. These strains are now included in a local vaccine to protect dromedaries from clostridiosis.2 mg/mL within 45 days yet reached its lowest level 3 to 4 weeks post partum. 1996). exhibiting seizures and the characteristic opisthotonus. The higher the titer. 1991).the presence of large numbers of Gram-positive rods from mucosal scrapings from the small intestine of fresh dead animals is presumptive evidence of clostridial enterotoxemia (Fig. chauvoei. 1983a and b. In C. Many valuable racing camels were saved by the intravenous application of 1OOmL of antiserum.

The vaccine should be Goettingen. since neonates rived strains give optimal protection.ti toxoid vachs should be added to the feed.before parturition and a booster administion of this important disease. as it is known that locally deadministered to the dam. vaccine prevented further cases of C. This are unable to produce enough antibodies. pefrinThe dam should be vaccinated 2 months gens enterotoxemia in adult dromedaries Figure 20 C. In endangered herds. Isolation and identification of clostridial feeding and general husbandry practices should be optimal. For camels in the UAE.General Survev Figure19 MlT results on vero cells indicating toxin in the intestinal fluids of dromedaries with clostridial enterotoxemia 29 ed without any side effects. plied Biotechnology of the Tropics (IBT) in sheep and llamas. perfringens: increased number of Grampositive rods in a mucosal scraping from the small intestine of a dromedary with clostridial enterotoxemia . Toxoid vaccines are commonly used to cine was produced at the Institute for Apprevent enterotoxemia outbreaks in cattle. sanitation. For the preven. tered 1 month prior to delivery. strains are necessary to confirm the diagnochlortetracyclines at a rate of 25 mg/kg feed sis and to develop a specific clostridialvaccine.

directed against a locally specific C. Neg. 1 :64 1 :32 1 :64 1:32 1:128 1 :32 1:16 1 :64 1 :32 I :64 6 1 :64 1:16 1 :64 1 :32 1 :64 1:32 1:16 1 :64 1 :64 1:32 12 1 :32 1:16 1 :64 1 :32 1 :64 1 :32 1:16 1 :64 1 :32 1 :64 24 1 :64 1:16 1 :64 1 :32 1 :64 1:32 1:16 1 :64 1 :32 1 :64 After colostrum ingestion 1 2 3 4 5 6 7 8 9 10 1:32 1:16 1 :64 1 :32 1 :64 1 :32 1 :32 1:16 1:16 1 :32 1 :32 1:16 1:32 1 :32 1 :64 1:16 1:16 1 :8 1:16 1 :32 1:16 1:16 1:16 1 :32 1 :32 1:16 1 :8 1 :8 1 :8 1 :4 1 :8 1 :4 1 :4 1 :4 1 :2 1 :4 1 :8 1 :2 1: 2 1: 2 . Neg. Neg. perfringens enterotoxemia: local reaction following subcutaneous vaccination with a Montanide adjuvant cell toxoid vaccine Table 9 Development of antibodies. perfringens (type A) toxoid vaccine in dromedary calves and their mothers before and after tw o consecutive maternal protective vaccinations Dromedary cows Prior t o vaccination Neg. 1 :2 1 :2 1 :4 Prior to colostrum ingestion Neg. Neg. Neg. Neg. Weeks after vaccination 2 1 2 3 4 5 6 7 8 9 10 Dromedary calves 1 :2 1 :4 1 :2 1 :4 1 :2 Neg. Neg. Neg. Neg. examined with the HIT.30 Bacterial Diseases Figure 21 C.

1991). 1992). botulinum are destroyed at 100°C for 15 minutes. 1991) was used to detect the production of antibodies in dromedaries following vaccination with the clostridia toxoid vaccine (Seifert.1. botulinum is usually found in the soil and mud. These results show that dams that were vaccinated twice with the clostridia toxoid vaccine prior to delivery developed a much higher antibody titer. a devastating outbreak of botulism occurred on two feedlots in Queensland. 30% of the vaccinated dromedaries developed local allergic swellings (Fig. 1991). Chicken scraps in the feed caused the outbreak. 1. whereas at least the toxins C1 and D can only be produced in the presence of bacteriophages (Westphal. By introducing phages. an aluminum hydroxide vaccine has been used that is well tolerated both intramuscularly and subcutaneously. Eight types and subtypes of C. the animals attempt to cover this deficit by ingesting phosphoruscontaining substances of animal origin. The results are shown in Table 9. 21) (Seifertet al. It is believed that camelids are susceptible to C. If there is a lack of minerals in their pasture grass. Wernery and Haydn-Evans (1992) have reported cases of botulism in seagulls. botulinum (Fowler. 1992)produced in Goettingen in the bioreactor. After subcutaneous application of the Montanide adjuvant cell toxoid vaccine.. In 1990. Death is caused by circulatory failure and respiratory paralysis. Their distribution is shown in Table 10. botulinum strain into a toxigenic strain. it is possible to transform a nontoxigenic C. 40. Camels appear to be particularly sensitive to oil-based vaccines. Eight different neurotoxins are produced by this Epidemiology Botulism is a classical epidemic of arid and semi-arid pastureland in the tropics and is distinguished by a characteristic paralysis. Etiology and Clinical Signs C. botulinum have been identified serologically by their toxin pattern.2 Botulism CZostridium botulinum is responsible for botulism in man and animals. Australia where over 5500 bulls died (Jones. The spores are resistant to heat and are only killed at 121°C for 15 minutes while the toxins of C. Today it is known that the bacterial cell alone is only capable of producing toxin C2. only a few clinical cases have been described in OWC (Wernery and Kaaden. Devastating losses due to botulism have also been observed in waterfowl.000 waterfowl died of botulism in the marshes west of Hamburg (Westphal. However. where the organisms can survive for many years. strict anaerobe and even small traces of oxygen will inhibit growth. a neutral type of C. In 1983.. botulinurn toxins are synthesized intracellularly in the last stage of the logarithmic growth phase and are first released through lysis of the bacterial cell. 1991). 1995). The hemolysis inhibition test (HIT) (Schaper. for example. botulinum is a straight Gram-positive rod which produces subterminal spores at a pH near or above neutrality. botulinum strain is infected with a C1- . ducks. Since then. C. botulinum and its bacteriophages is a decisive criterion in understanding botulism. 1992) and reduced losses in young animals. Cadavers serve as the source of the intoxication. 1998). The toxin is absorbed from the intestinal tract and is transported via the bloodstream to the peripheral nerve cells resulting in flaccid paralysis. The maternal protection that the young dromedaries then received by ingesting the colostrum of the vaccinated mothers lasted at least six months. herons and flamingos in the UAE. The disease is found primarily in cattle and is associated with a lack of phosphorus in the soil (Seifert. 1992). The knowledge of the relationship between C. If.General Survey 31 (Seifert et al. The C.

Europe Australia. wounds Meat and meat products Lucilia larvae. botulinum and its specific bacteriophages. between the different types and strains of C. the mouse test is not very sensitive when large animals like camels are tested. plants. Ukraine Central and Eastern USA. 1988) Type Toxin Distribution Western USA. clinical signs and identification of toxin in serum of moribund or recently dead animals or feed. Northern and Central Europe North and South America. former USSR Argentina Source of Intoxication Feed. meat. horse. botulinum strain with a phage of the closely related C. as the concentrationof toxin in the serum . and collapsed and died within a few hours. novyi and to convert the strain into a C.32 Bacterial Diseases Table 10 Types of Clostridium botulinum toxin and their distribution (Bisping and Amtsberg. horse. Europe South Africa. complex variety of new combinations are possible. It is also possible to isolate C. Reports of botulism in camels are rare. South Africa. Australia. Provost et al. the animals are superbly cared for.It is even possible to infect a phageless neutral type C. Canada. Additionally. 1991). Infection with a D-Tox phage transforms the same neutral strain into a type D strain (conversion). One milliliter of serum from diseased animals is inoculated intraperitoneally into mice. USA. waterfowl Waterfowl Cattle. a confusing. Denmark. cattle. cadavers Cadavers Fish and fish products Liver pdte. waterfowl. mink Cattle Man Man - Tox phage. The conventional differentiation between the types can no longer be upheld. South Africa. In general. fish Susceptibility Man. Upon inspection of the herd of 150 animals. It was presumed that the well water was contaminated by a cadaver. Unfortunately. 45 were already dead and 40 severely ill. mud Spoiled food. (1975) reported a catastrophic outbreak of type C botulism in dromedaries in Chad. If toxin is present. the strain will then produce the C1 toxin and will also become a type C strain. Diagnosis tli Botulism is often difficult to diagnose.A presumptive diagnosis is based on history. which was the source of the toxin. botulinum in suspect foodstuffs. mink Man. developed hindquarter paresis. former USSR Northern Europe. The danger of a botulism outbreak in racing dromedaries in the UAE is slight. Alaska. fish. the feed is well balanced without animal additives. novyi strain (Westphal.All together. The sick animals had difficulty in standing. the camels are watered from deep wells and lick stones and mineral additives are readily available. the characteristic ”wasp waist” appearance in the mice will be seen within a few hours to 3 days. former USSR. Japan Scotland.

the sensitivity does not exceed that of the mouse bioassay. by septicemia and sudden death. cation the colonies give the appearance of Vaccines are commercially available.the presence of oxygen at temperatures ing camelids suffering from botulism.lating bacterium. which can affect camelids (Davis et al. some. The antiserum is given intravenously. 1981. non-motile.3 Anthrax discharged from the body in the final stages of the disease and sporulate in and Bacillus anthracis causes anthrax in man and on the ground at temperatures of 2032°C animals.Camelids should be vaccinated in endangered areas. septicemic disease.General Survey 33 or ruminal fluid is generally so low that toxin cannot be detected. As the type of C. even though for years by buried cadavers. horse. 1998). Fowler. Pigs are not immune to anthrax. complement fixation test and ELISA. anthracis is an aerobic sporupensive. The toxicity of feed samples may be determined by test feeding the sample to specifically immunized laboratory animals or sheep. In orto diseased OWC and 3 mL to NWC intra. for example. botulinum responsible for the disease in animals is generally not known until some time has relapsed.nary solid media and no hemolysis is protion. though they are generally afflicted with a subacute or chronic course of the disease following a primary lesion in the pharynx. Spores develop only in ment. Other methods for detection of botuh u m toxin include immunodiffusion. Soil can be contaminated single uniform antigenic type. This is the case. . 1992).boo-stick form. elephant and mink. cylindrical rod. good nursing is essential when treat. which then there are differences between local specific strains. The diagnosis then relies on the history and clinical signs. The initial vac. which can presumed that 5 mL should also be given be demonstrated by special stains. apart from the administration of hyperimmune serum specific to the toxin type involved. but may save very valuable cam. which is a Gram-posielids. It is ex.Epidemiology and Clinical Signs i b Ancination should be followed by a second thrax is a peracute disease characterized 5 weeks later and annually thereafter. B. Treatment and Prevention specific treatment for diseased animals sufferingfrom botulism. correction of phosphorus deficiency duced on blood agar. Anthrax occurs throughout the world and is especially a problem where high concentrationsof animals occur. Under natural conditions.1. Throughout the world there is a (Seifert. The treatment may be repeated in short chains forming a so-called bamwithin 24 hours. 1988). and black-quarter. Wernery and Kaaden. Masses of vegetative bacilli are 1. 1995. the a i nmals most frequently affected are the cow. sheep. Birds (with the exception of the ostrich) and reptiles have a low susceptibility and are seldom affected (Bisping and Amtsberg. it is possible to mix antisera before administration. anthracis grows on ordiPrevention of botulism includes: vaccina. animal markets and salt licks. Cattle and horses are treated with tive. Anthrax is an acute. except for the CFT. In addition to this treat. above 12°C. reindeer. buffalo. Under low magnifiand removal of the source of intoxication.gan smears the bacilli lie either singly or venously.. but these tests are not commercially available and. goat. at watering holes.Etiology IK B.a Medusa-like head or a woman’s curly times as a combined vaccine for botulism hair. Inside 5mL of each type of antiserum and it is the host it forms a capsule. The anthrax endospores can survive for years in the soil.

anthracis infection of an animal. peracute. flooding or drought. excreting dark. The dromedaries affected exhibited difficult breathing. the base of the neck and the groin region. or via an airborne route. Inhaled contaminated dust can also lead to pulmonary anthrax. The disease ceased when town water was supplied. Similar cases of sudden death due to anthrax have been described by Curasson (1947) and Gatt Rutter and Mack (1963). and apoplectic forms. A leaflet was prepared on anthrax in dromedaries by the Syrian German Technical Cooperation. along with trypanosomosis and mange. The infection normally occurs via the alimentary tract due to ingestion of contaminated feed or pond water (Boue. The agent can enter the human host cutaneously. foamy blood from the body orifices (Fig. Anthrax is one of the most important zoonoses of the tropical regions and always occurs through a B. Mustafa (1987) believes that. anthrax is one of the most loss-inducing diseases in dromedaries. anthracis carried by nasal bots (CqhaIopina titillator) can enter the body through injured mucous membranes. enterally. Anthrax is greatly feared by nomadic camel breeders. Figure 22 Unclotted blood protrudes from the nose of a dromedary with anthrax More than 10 dromedaries died from anthrax infection. They have given the disease many different names and are aware of its dangers. Fazil (1977) believes that anthrax is the most frequent bacterial disease of camels in Kenya with acute. Punskii and Zheglova (1958) reported an outbreak of cutaneous anthrax in 37Asians who came in contact with meat from a dromedary that had been infected with the disease. Barakat et al. 1997). Barakat et al. 22). especially when the grazing animals bite off the pasture grass at ground level during periods of food scarcity. 9 apoplectically. in which the clinical signs and the pathological lesions are described (Tabbaa. (1976) are of the opinion that an outbreak of anthrax in . 1962). such as heavy rainfall. the remaining animals treated with antibiotics and the herd vaccinated. (1976) reported an anthrax outbreak in Egypt during which 123 dromedaries died within 4 days. Curasson (1947) has postulated that Tabanidue can induce cutaneous anthrax in dromedaries and that B.34 Bacterial Diseases serve as sources of infection. An acute or peracute form of anthrax can be found in dromedaries that leads to sudden death without any previous clinical signs. Epidemics of anthrax tend to occur in association with marked climatic or ecological changes.A camel herd of 100 dromedaries from the steppe of Syria contracted the disease after drinking from a pond which was temporarily flooded with rainwater. Before death camels became recumbent. trembling and pronounced swelling of the throat.

. anthrax vaccines should be carefully used in camelids and the dose adjusted to the weight of the animal. A single inoculation provides effective immunity for 9 months. the thermo-precipitation of Ascoli can be applied. 1998). avirulent. white mice are the animals of choice.10% hot caustic soda solution. Some dromedaries develop painful swellings on the throat and neck. Darkred. The clinical signs of anthrax in dromedaries are similar to those in the cow (Gatt Rutter and Mack. . The following disinfectant solutions can be used: . 1997) of the carcass with oozing of bloodstained fluid from nose. spore vaccine developed by Steme. bloat and severe cardiovascular and pulmonary disturbances. 1963): fever up to 42"C. if anthrax is suspected one should avoid a necropsy to exclude contamination of the soil with spores. Prevention and Control To prevent sporulation of B. unthrucis in laboratory animals. An enlarged pulpy spleen. They should be incinerated with the contaminated bedding. Pasteur developed the first effective B. unthrucis. It was replaced by the live. A small quantity of blood is sufficient for the diagnosis.calcium hypochloride with 5% active chlorine. They are subcutaneously infected and will die within 2 to 4 days. including penicillin and tetracyclines. B. equipment must be properly disinfected. administration of procaine penicillin and 50 mL of anthrax antiserum per dromedary over 5 days. anthrucis is susceptible to many antibiotics.. Bloody discharge may exude from all body orifices and lamoids may die after 1 to 3 days (Fowler. . After contact. Pathology The principal lesions in septicemic anthrax in animals are hemorrhages. anthracis is easily cultured from blood and tissues. carcasses should not be opened. Sudden death without any signs may occur as well as subcutaneous swellings on various parts of the body. A half sheep dose is recommended for NWC weaners (Fowler. This vaccine has been used worldwide with great economic value to the livestock industry and to wildlife. In advanced autolysis. For the cultivation of B. edema and necrosis. In dromedaries. 1987).General Survev 35 a dromedary herd was due to migrating birds. 1998). when no anthrax bacilli are demonstrable.2%glutaraldehyde. 1996). However. since bacteria-induced anthrax has been reported in young llamas (Cartwright et al. However. diarrhea. A gelatinous edema develops at the injection site. There is no rigor mortis and the blood fails to clod. The outbreak was controlled by strict hygienic measures. mouth and anus. there is evidence of rapid post mortem decomposition (Tabbaa.4% formaldehyde solution. has also been described in camelids (Manefield and Tinson. . A smear or a culture as well as a fluorescent antibody test (FAT) will confirm the diagnosis. extravasation of tar-like blood from the body orifices. petechiae and ecchymoses are observed throughout the carcass. Splenomegaly with black tarry pulp. whch is the most characteristic feature at necropsy in ruminants. generalized congestion and lung edema were also observed by Boue (1962) and Richard (1975). Diagnosis B. colic. but annual booster vaccinations are recommended. . In NWC the clinical signs described for anthrax resemble those seen in OWC. OWC should be given the dose of cattle and NWC should receive the dose that is recommended for sheep. Anthrax can be a serious danger to camelids and it is therefore recommended to vaccinate Cumelidue in endangered areas. unthrucis vaccine.7% hydrogen peroxide. poorly clotted blood.

with severe consedotoxemia or endotoxin shock. They are decline of rumen pH. but the result of it.animals and more in a herd can fall sick. Due to the vascular endothelial not the toxic factor. 1.Core Region: acts as the link between the of the first clinical signs. the liver.They are chemically very stable and boilria constituting the normal flora of the gas.4 Endotoxicosis (Endotoxemia) . when amounts of endotoxins are regularly prothe compartments’flora is destroyed by the duced in the gastrointestinal tract. ”hemorrhagic disease” (HD). Widespread vascular endothelial minal Gram-negativebacteria are destroyed and subsequent tissue damage can be exin large quantities. It is believed that Endotoxins are lipopolysaccha. This is especial.has been called ”hemorrhagicdiathesis” or ing practice has gained huge momentum. which are found in the outer cell outbreaks of this disease. . Cases have been diagnosed at all times of “hemorrhagic diathesis” or ”hemorrhagic the year.high fiber to a high carbohydrate and proins are composed of three parts: tein diet. which 80% are between 2 and 4 years old Intensive investigations over the last or even younger.Lipid A buried in the cell wall.of training sessions ahead of the new race leased during periods of rapid growth or season and a change of diet from a more death of organisms.vidual camels. but also groups of up to 10 tery surrounding a disease of racing cam.1. endotox. els known as “ B u d u s cereus intoxication”. the WBC counts inner (lipid A) and outer (0) regions. acidosis often manifest clinical signs of en.merous years a disease has been rife among ries is the feeding of highly digestible diets racing dromedaries in the UAE that due to to a desert animal.enzymes present in abdominal fluids. However. Clinical Signs and Pathology The cause of lactic acidosis in dromeda. during the summer months’ high temperatures and high humidity.ing does not destroy them.into the circulation and are detoxified in ets leads to inappetence and lactic acidosis. Structurally.The endo. whose forestomachs are its clinical and pathological presentation adapted to poor-quality feed. because ru. since huge quantities of damage. Three to 4 days after the onset . is characterized by a dramatic decrease in . if hepatic efficiency is Ruminants and Cumelidue with acute lactic reduced or the amount of toxins is too large. Small ly true for ruminants and Cumelidue. The new feed. The disease affects indidecade now seem to have solved the mys. The disease since camel races on the Arabian Peninsula occurs primarily in racing dromedaries.36 Bacterial Diseases Endotoxins are extremely toxic and may be lethal at a concentration of 10-9 g/mL.0 Region: gives antigenicspecificityand the total number of leukocytes(WBC). The large number of Gram-negative bacte. but also the start wall of Gram-negative bacteria and are re. 1995).as high as 41”C. it mediThe initial stage (24-48 h) of the disease ates most of the toxic effects of endotoxin.Lactic acid is apparently pected. and dullness. Impairment of rumen absorbed through the intestinal mucosa fermentationcaused by highly digestibledi.fever is highly variable between bacterial spe.d a r coagulation (DIC). depression cies.quences. increases (Table 11). The toxins are trointestinal tract provides a potential pool also not significantly altered by acids or of endotoxinfor the animal. inappetence. of have become extremely competitive. toxin of alimentary origin is not the cause of lactic acidosis syndrome.not only the extreme climate aggravates rides. but the highest incidence occurs disease” (Wernery and Kaaden. endotoxin activates the clotting endotoxins have been detected in cell-free cascade and causes disseminated intravasruminal fluid of acidotic animals.toxemia is produced.

GOT) Lactatedehydrogenase (LDH) Glucose Blood Urea Nitrogen (BUN) IU/L mg/dL mg/dL 44 25 2.6 3.1 10.5-12.8 12.2 250-400 17.2 82.9 298 594 0 0 9.4 10.0 93 24.4 48.3 4.3 142 81 11.5 8.4 27 1 320 236 93 70 62 116 182 12.9 i 13 590 142 120 104 83 97 110 350 48 21 490 1812 86 75 119 675 92 195 257 730 99 60 421 1557 106 44 401 1210 107 146 Hemoglobin Platelets Creatine Kinase (CK) Glutamateoxalacetatetransaminase (AST.6 X X X X X X X Reference Values** 6.1 9.0 7.2 12.0 82 13 5 2 86 12 X 3 t o 4 days 19.6 77 20 3 XI 031~ 2.0 372 438 0 1 0 8.9 8.0 0 0 8.1 201 362 0 0 8.6k1.6 1.2 50.0 Creatinine (Crea) Fibrinogen Prothrombin time (PT) Partial thromboplastine time (PIT) mg/dL mg% Sec Sec x Differential count due t o toxic changes not possible ** Wernery et al.0-13.8 18.0 350-450 40-1 20 % % % % % X I OVL g/d L XI 031~ IU/L IU/L 60-1 20 400-775 390 70 21 2.7 298 20.8 291 612 0 0 White Blood Cells Neutrophils Lymphocytes Monocytes Eosinophils Basophils Erythrocytes 7.6 60.3 80 78 16 6 24.0 9.0 98 28.6 46.1 9.9 47.0 72 27.2 53.8 17.4 3-2 1 0-2. (1999) .4 60.6 66 27 X X 2.0 4.9 65 28 6 8 1 50-60 30-45 23 6 6 1 2-8 0-6 0-2 70 12 0 0 0 7.4 11.0 11.3 26.2 305 18.8 54.Table 11 Blood parameters and serum enzymes of 10 dromedaries with endotoxicosis (blood was taken 1 t o 2 days and 3 t o 4 days after the onset of the disease) 1to 2 days Parameters Units 0.2 102 22.3 70.5 1.6 10.1 168 46 12.6 172 21.0 62.3 201 17.2 2.0-1 5.5 180 19.8 106 26.0 23 65 220 70-1 10 46 19 2.5 2.0 9.9 12.

1996). Mucous membranes are often injected.or bilateral enlargement of the body lymph nodes (Fig. The development of nervous signs is a feature of terminal cases. complete atonia of compartment 1. 23). Affected dromedaries die between the 3rd and 7 h day. Only very few camels develop diarrhea (Manefield and Tinson. Two or 3 days before t death. It is unknown in other camel-rearing countries. The disease is the most serious ailment in racing camels and has been reported from all countries of the Arabian Peninsula where camel racing is performed.38 Bacterial Diseases Figure 23 Swollen and hemorrhagic inguinal lymph node Some animals develop a cough and swelling of the throat accompanied by a marked uni. the animalsbecome recumbent. lacrimation and hypersalivation. Figure 24 Tracheal ulcers caused by endotoxemia . Additionally. Some dromedaries develop central nervous system disturbances. Rectal examination of affected dromedaries reveals normally formed balls of stool that are covered in fresh or tar-like blood. abdominal pain and regurgitation have been observed.

.intestinal tract. 24).renal pelvis (mostly petechiae. primarily in the ascending colon (the intestines are frequently filled with fresh or tar-like blood. Figure 26 Hemorrhage in the abomasum caused by endotoxemia .General Survev Figure 25 Subendocardial hemorrhage caused by endotoxemia 39 Over a 15-year span more than 200 racing dromedaries that died of endotoxicosis were autopsied. 25).pharynx and trachea (some dromedaries develop ulcerations in the trachea) (Fig. Fig. 29). During necropsy the most striking changes are severe hemorrhages and bleeding into organs and the intestinal tract. 26 and 27). 28). . Figs. Ecchymotic hemorrhages of varying severity are seen in the following organs: . Fig. some with blood clots attached to the ulcers. .abomasum (ulcers are always found on the top of the folds of the fundus.epicardium and subendocardium (Fig. .

some with attached blood clots caused by endotoxemia Figure 28a. b Ecchymosis in the ascending colon and small intestine caused by endotoxemia .40 Bacterial Diseases Figure 27 Ulcers in the abomasum.

33). including the spleen and tonsils. Severe hemorrhages are also observed in the abomasum. hemorrhagic often with necrotic centers (Fig. Pronounced necroses are regularly seen in the epithelium of the convoluted and straight renal tubules. Smears from the ruminal fluid of necropsied racing dromedaries show a Grampositive bacterial flora (Fig. 31). Hemor- rhages. but extensive studies including animal experiments yield no indication of viral diseases. In Figure 30 Enlarged. intestinal tract and the subepicardial as well as subendocardial layers of the heart. 32) and there are no protozoa in the fluid of C1. 30).General Survev Figure 29 Petechiae in the renal pelvis caused by endotoxemia 41 All lymph nodes are enlarged. All of the animals exhibit ruminal acidosis. The lungs are congested and exhibit subpleural and interstitial hemorrhages (Fig. Histopathological examination demonstrates an intermediate to severe loss of lymphocytes in the lymphatic tissues. hemorrhagic prescapular lymph nodes with necrotic centers caused by endotoxemia . the pH values are between 4 and 6. necroses and karyorrhexis are primarily seen in the follicular centers and are very prominent in the Peyer’s patches and in the mesenteric lymph nodes (Fig. The changes point to viral involvement.

the Bowman’s space is dilated and filled with protein material.42 Bacterial Diseases Figure 31 Interstitial hemorrhages in the lung caused by endotoxemia Figure 32 Gram-positive bacterial flora of compartment 1 of a camel with endotoxemia (left) and Gram-negative flora of a healthy camel (right) numerous glomeruli. The livers of the animals autopsied exhibit a pan- . segmental necrosis of capillary loops is observed (fibrinoid necrosis). Some of the glomerular capillaries contain microthrombi (shock bodies). The Bowman’s capsule is often thickened due to deposits of PAS-positive material (Fig. PAS-positive cylinders block the lumen of some distal tubuli showing tubulonephrosis. In dromedaries which survive longer. 34).

The agranulocytosis induced by the lipopolysaccharides produces severe immunosuppression in diseased camels.General Survev Figure 33 Necrosis and karyorrhexis in follicular centers of a mesenteric lymph node of a racing camel with endotoxemia 43 Figure 34 Dilated Bowman's space of a dromedary kidney: note the thickened Bowman's capsule due t o deposits of PASpositive material lobular fatty degeneration as well as necrobiosis in centrolobular areas (Fig. kidneys and contents of the compartment 1 are negative for cumarine and its derivatives as well as organophosphates. 35). which is demonstrated in lymph nodes. most probably due to the toxin-induced destruction of follicles in the lymphoid tissues and the destruction of the circulating white blood cells. which are often not identifiable due to their toxic changes. tonsils. It also has a direct toxic effect on the circulating leukocytes. predispos- .The endotoxins have also a direct impact on the leukopoietic system causing aplasia and destruction. no inflammatory response is observed in any organs. Chemical analysis of the livers. Hyperemia is regularly seen in the brain and both a perivascular and a meningeal edema may be observed. spleens and other lymphoid tissues. Strikingly.

.Leukopenia generally persists for 1to 2 days and is reversed with an overshooting reaction (Tables 1 and 12)after the third day. Masses of different bacteria are regularly isolated from all organs: E . Walz..0 x lO3/L of WBC.These changes include pyknotic nuclei. 1960. Wernery and Kaaden.44 Bacterial Diseases Figure 35 Severe panlobular fatty liver degeneration with necrobiosis in centrolobular areas of a racing camel with endotoxemia ing them to secondary bacteriemias. because very early diagnosis and treatment is the key to recovery. A sharp rise in serum enzymes is observed in the final stages of the disease. The disease was also reproduced by intravenous infusion of cell-free toxin of a toxic B. Staphylococcus spp. It is now known that the systemic effects of endotoxicosis can be experimentally demonstrated by the intravenous injection of purified toxin of many Gram-negative bacteria (Krogh. 1994. cereus strain (Wernery et al. Nagaraja and Bartley. some of the values are greater than 20 times the normal level. 1995). Proteus spp. indicating internal organ damage. Pseudomonas aeruginosa.. it is not possible to perform a differential count due to toxic changes in the white blood cells (Fig. Bacillus cereus was formerly made responsible for this disease because toxic strains had been isolated from organs and feed of camels that had died from endotoxicosis. Anthrax bacilli are never identified.5 but . Clinical Pathology Changes in total and differential leukocyte counts are typical of endotoxemia. Wernery. Camels develop a forestomach atony and forestomach acidosis. coli. Creatinine and blood urea nitrogen (BUN) are always greatly elevated. Staphylococcus aureus. indicating renal damage that is also seen histologically. 1979. producing further local toxins. Huber et al. Klebsiella pneumoniae. Nothelfer and Wernery. 1992a. 1995. and Streptococcus spp. 1979). There is a dramatic drop of leukocytes due to a decrease in neutrophils and lymphocytes (see Table 11). 1993. vacuolation of the cytoplasm and false staining. As can be seen in Tablell. 36a) (Wernery et al. Normal forestomach fluid pH in camelids is higher than 6. 1999).. These facultative and opportunistic microorganisms multiply rapidly in all pre-damaged organs. 1 In many severe cases with less than 1. A correct hematological result is essential. The lowest WBC count is usually recorded on the day of presentation and is pathognomonic for this ailment. A rise towards a normal count occurs as the disease progresses.

8 112 680 1083 70 58 4.General Survey Table 12 Blood parameters and serum enzymes of a dromedary that survived endotoxemia Parameters Units Reference Values* 6. smooth stratified squamous epithelium in camelids.1 301 324 60-1 20 400-775 70-1 10 3-2 1 0-2.3 11.5 251 882 0 7.8 78 16 5 1 0 8.1 13.0 12.9 61 32 4 3 0 7.5-12.1 210 232 660 78 34 2..2 250-400 196 338 46 13 1.6 39 1 Wernery et al. Furthermore. The camel cannot detoxify the cell-free endotoxins produced in the forestomachs due to their extreme stability and due to the pre-damaged liver. This anatomical aspect makes them very vulnerable to endotoxemia. Consistent gross lesions in all dromedaries are hemorrhages in different organs and severe bleeding into the intestines.4 84 10 4 2 11 25 9.2 10. not only do bacterial endotoxins accumulate.0 350-450 40-1 20 Days 1 45 2 1. especially in the colon (see Fig. the fluid is soursmelling and yellow and always contains undigested pieces of barley. as these are lined with non-papillated. 28a).1 103 475 819 44 51 3.3 12.2 193 721 0 8. It is also known that camels in general have a very rapid entry of fluids into the bloodstream.0-1 5. which is always observed with endotoxicosis in racing camels.2 92 7 1 6 22. These changes have also been described in acidotic NWC (Cebra et al.1 483 140 White Blood Cells xlO3/L Neutrophils % Lymphocytes % Monocytes Yo Eosinophils % Basoph i Is % Erythrocytes x 1OYL Hemoglobin g/d L Platelets x 1031~ Creatine Kinase (CK) IU/L Glutarnateoxalacetatetransaminase (AST. (1999) through compartments 1and 2. The colon of camels has an extremely effective absorbing capability. which explains why bleeding in this part of the intestine is very intensive. The intestinal motility ceases due to lactic acidosis.5 140 112 0 0 7. Diarrhea is seldom observed in camelid endo- most HD cases were presented with pH between 4 and 6 .2 176 67 0 1 9.6 12.6 370 160 379 108 22 1.7 92 380 790 38 23 3.6 11.5 84 10 5 3 5.5 50-60 30-45 2-8 0-6 0-2.0-13.0 7. Protozoa are not detected during microscopic examination of gastric fluid and Gram-stains of the fluid reveal a population of predominantly Gram-positive bacteria. 1996). GOT) IU / L Lactatedehydrogenase (LDH) lU/L Glucose rng/dL Blood Urea Nitrogen (BUN) mg/dL Creatinine (Crea) mg/dL Fibrinoqen mq% * 1. Furthermore. but metabolic toxins also are produced as a result of impaired metabolism in the compartments caused by ruminal and intestinal impaction. It is also believed that huge quantities of toxins are already absorbed .o a2 12 4 2 20.

Lipopolysaccharidestrigger disseminated intravascular coagulation (DIC). most probably due to the special structure of the cells in the rectum. Partial thromboplastin time (PTT) and prothrombin time (PT) are prolonged (Table11). which absorb most of the fluid accumulated in the rectal feces.0 x 1OYL leukocytes with two unidentifiable WBCs with severe vacuolated cytoplasm and pycnotic nuclei Figure 36b The pathogenesis of camelid endotoxemia toxicosis. Both findings are often observed in dromedaries suffering from endotoxemia. but may also clog the glomeruli of the kidneys. the presence of soluble fibrin and fibrinogen degradation products and severe deficiencyof coagulationfactorswhich inhibit thrombin activity. fibrin polymerization and platelet aggregation. whereas the tar-like blood in the colon (melena) is fermented oozed blood from the small intestines. Fibrin not only further elevates blood viscosity. DIC is characterized by a decrease in fibrinogen content. Fresh or tar-like blood may be passed through the rectum depending on where the intestinal bleeding occurs. Tarlike blood in the abomasum is caused by the coagulation of oozed blood caused by gastric acid effects.46 Bacterial Diseases Figure 36a Endotoxicosis of a racing camel with 1. Most blood samples of the early stages of the disease possess very .DIC is a most serious consequence of endotoxemia.

The application of thiabendazole as an antifungal agent had no affect on the outcome of the disease. foul-smelling diarrhea is also always present. The effects of the decrease of coagulation factors are often visible when a blood sample is drawn from the jugular vein of affected camels. were able to isolate Aspergillus fumigatus from nearly every organ of autopsied camels. despite the best treatment.General Survev 47 little serum after centrifugation. However. Binding of endotoxins and their removal from the system 2. The mycotoxic disease exhibits a course similar to endotoxemi? with agranulocytosis and intestinal hemorrhages. The authors added that it was not possible to determine whether these findings were due to a secondary infection with the fungi or were the primary cause of HD. who have intensively studied hemorrhagic diathesis in dromedaries. Broad spectrum antimicrobial administration . camel owners nowadays inform practitioners when the first signs of disease are observed. A second group of researchers from the neighboring emirate of Abu Dhabi.0x 103/L are curable. The lack of organ mycosis in the autopsied camels is a strong indication that the hemorrhagic diathesis is not caused by mycotoxins. These clinical signs were reproduced in five young dromedaries by feeding them hay that was highly contaminated with fungi.. 34). the greater are the chances of survival. in which ruminal acidosis was artificially induced by feeding a high carbohydrate diet. Endotoxemia is a very severe and complex ailment and extremely difficult to treat. The supernatant above the blood clot is composed mainly of fibrin. the puncture hole continues to bleed. 1990). The therapy for endotoxemia should include these main treatments: 1. Not every acidotic camel develops an endotoxicosis. which is indicated by the elevated levels of BUN and creatinine. as well as detecting aflatoxin in some sera (EL-Khouly et al. Camel owners wonder that some animals develop endotoxemia and some do not. The pathogenesis of endotoxemia in camels is summarized in Fig. A connection between mycotoxins and hemorrhagic diathesis has long been known (Blood and Radostits. but a gray. With early treatment. Treatment and Control Therapeutic success of endotoxemia of camels depends primarily on early diagnosis and treatment. After the needle is withdrawn from the vein. Administration of antacids to reverse the lactic acidosis 3. yearly losses due to mycotoxins are seen in the rainy season (Gareis and Wernery. protein deposits are seen in the glomeruli (see Fig. Further evidence of this situation is the low platelet count in all camels with the disorder. Since so much knowledge has been accumulated over the last decade on this disease. (Wernery and Wensvoort. A field trial with 2 camels. although they receive the same feed. Gareis and Wernery. 1992). It is not clear which mechanism ultimately triggers the disease. Supportive therapy to increase the detoxifying capacity of the liver 7. Prevention of the development of gastric ulcers 6. Fluid therapy 4. so that fungal contamination of the fodder can usually be ruled out. even cases with WBC counts of less than 1. The earlier the diagnosis is made. On histology. Control of inflammatory response 5. 1994). 1992. Racing dromedaries in the UAE are given fodder of superb quality. 1992) did not yield clinical signs similar to endotoxicosis. 36b. fatalities can be expected. The prognosis is poor once the condition has reached an advanced stage. This leads to renal failure. In breeding herds of dromedaries where animal management occasionally does not meet the standards seen in racing dromedary herds.

purified endotoxin-specific IgG and. dates. Great quantities of fluids are lost by internal bleeding due to the impairment of capillary wall integrity. infusion of 601/ camel of a 1.5 mg/kg polymyxin B sulfate. The recommended dose in horses is 1 to 2 mL/kg body weight (Gaffin. a portion of endotoxin. may reduce the cell-free endotoxin by adsorption. It is still common practice in the UAE to feed racing camels with cow milk. Correction of the circulatingfluid deficits is an important procedure to save camels from endotoxic death. It is available from Veterinary Dynamics as Hypermune-J@ from Immvac.48 Bacterial Diseases 8. but should be tried in camels suffering from endotoxemia due to its known endotoxinbinding capacity.v. diluted in up to 5 liters of saline and given by slow i. to correct acidosis. in the presence of complement. which always follows the endotoxin shock.v. but it is toxic for camels. This product has already been used in camels suffering from endotoxemia. Furthermore.3% sodium bicarbonate solution in saline with dextrose. The content of one 60 mg vial provides a single dose for an animal of 200 kg body weight. In horses a dose of 250 mg to 1 g/kg every 12 hours is recommended. . Compartment 1 should be emptied and washed out with a siphon and the compartment ingesta replaced by ingesta from healthy ruminants such as sheep and goats. If carbohydrate overload occurs. To avoid endotoxicosis. Columand bia. ketoprofen or flunixin should be used to block the formation of inflammatory mediators. In severe cases of ruminal lactic acidosis and endotoxemia involving very valuable camels. A more stringent laxative may be used in severe impaction with magnesium sulfate at a dose of 500 to 1000 g per animal. It has been demonstrated in a number of studies in equines that the administration of an antiserum directed against the core region of the endotoxin reduces mortality. MO 65201 as Endoserum@. analgesic. In addition to this therapy. the product is also bactericidal against many Gram-negative microorganisms. In endotoxemia. The suggested dose rate in equinesis 6000 W/kg or 2. Prevention of cerebral corticonecrosis (CCN). at a dose of 5 l/camel in the very early stages of the illness followed by an i. excessive barley and fresh alfalfa. Activation of the coagulation system 9. 1987). at a dose of 500 g daily (for a 400 kg racing camel). Finadyne has been shown to be efficient in horses since it possesses an anti-endotoxic. This drug is toxic in horses with severe side effects of renal damage. a rumenotomy should be considered. It is believed that charcoal also administered through a gastric tube. anti-inflammatory and anti-pyretic effect.A better balance between high energetic diet and roughage has to be achieved. infusion. Phenylbutazone. special attention is to be paid to feeding. Ideally. oxygen-free radicals lead to tissue damage and inflammation. Polymyxin B is an antimicrobial drug with a good affinity for lipid.v. the treatment with these sera should start in peracute cases. Stegantox 60@(ScheringPlough Animal Health) is a freeze-dried. antacids should be administered twice daily through a gastric tube including 500 g/camel of magnesium hydroxide dissolved in warm water. Dimethyl sulfoxide (DMSO) should be given as a 10 to 20% solution with isotonic fluids or water through gastric tube. a rigorous fluid replacement therapy should immediately take place. a laxative such as liquid paraffin should be given by gastric tube to reduce the gastrointestinal transit time and to avoid any impaction and bacterial proliferation and endotoxin absorption. Non-steroidal anti-inflammatory drugs are very important in the control of the inflammatory response. A 5% sodium bicarbonate solution should be given i. This treatment has to be repeated daily for several days.

1996). It has been shown that even modest grain feeding can cause severe acidosis with fatal consequences (Cebra et al. To help prevention of polioencephalomalacia thiamine hydrochloride at a dose of 2. I? haemolytica has analogous capsular types. and in combination with the mutant Re-17 bacterin it seems to protect against other endotoxin-mediated diseases. .1. Pasteurella sp.5 Pasteurellosis Pasteurella species have a worldwide distribution with a wide host spectrum. was isolated from a slight exudation of the left external ear. except one from Fowler and Gillespie (1985) of a llama with osteitis of the ear. honey. Because of the role the liver plays in the storage. dates. excessive uncrushed barley and alfalfa should be carefully considered as well as the prophylactic administration of probiotics. or i. 1985). non-sporing and facultative anaerobes. the second in Southeast Asia. Most pasteurella organisms are commensals on mucous membranes of the upper respiratory and intestinal tracts of animals. Pasteurellae grow best on media enriched with serum or blood. 1. They are nonmode. the first one being the cause of HS in Africa.. which are identified by numbers. It is not known if camelids harbor their own Pasteurella species. because of its detoxifying capability. In endotoxemia. multiple vitamins (including K) and liver stimulants should be administered. training of very young racing camels should be avoided in order to reduce stress. vaccine against E. OWC seem to be less susceptible to pasteurella than ruminants (Awad et al. has also been tried against endotoxicosis in camelids. The vaccine enhances both the T.v. activation and synthesis of many vitamins and. Gramnegative rods or coccobacilli. 1976b) and few scientists have observed hemorrhagic septicemia (HS) caused by I? multocida in dromedaries (Hassan and Mustafa.and B-lymphocytes. This drug prevents the secretion of gastric acid through blocking the H+ and K+ ATPase. research should be directed into the prevention and prophylaxis of endotoxemia. Etiology The Pasteurella are small. The mechanism of disease production by Pasteurella is not fully understood. the substituted benzimidazole. Furthermore. They are oxidase-positive and catalase-positive. antisera to endotoxins and paramunity inducer like Baypamun@. D and F. Pasteurella multocida has been isolated from the respiratory tract of healthy NWC and no reports exist that pasteurella causes disease in NWC (Fowler. 1998). A I? multocida serotype is identified by its serotype followed by its somatic type. C. hepatic function is also compromised. Somatic types (lipopolysaccharides) have also been identified and given numbers.5 to 10 mg/kg should be given i.The practices of feeding cow milk. Types or serotypes of I? multocida have been identified based on differences in capsular substances (polysaccharides). should be orally given at a dose of 0. Consumption coagulopathy may be stopped by the administration of heparin. For example: I? multocida E: 978 or B: 925. but it is known that endotoxins are particularly important in septicemic cases such as HS. B. Endovac-Bov@. but this treatment has not been tried in camelids. Since much is now known about the pathogenesis of this devastating disease. Hundreds of valuable racing camels have succumbed to endotoxemia on the Arabian Peninsula.7 mg/ kg body weight. These polysaccharides have been designated A.General Survev 49 For the prevention of gastric ulcers. Some scientists believe that camelids are not susceptible to bovine Pasteurella species.m. coli a mastitis. omeprazole.. Its efficacy has not been proven in camelids.

According to Higgins (1986). use of Asian buffaloes for plowing at the beginning of the rainy season). (1986) reported that HS in camels is a highly contagious disease caused by l? multocidu. The disease spreads through contact and contaminated feed and water. However. . Russia. Chauhan et al. haemolytica. The form of stress varies but often appears to be linked with overexertion and fatigue such as caused by working (e. 1981. serotypeA (2) and Pasteurella (Munnheimiu) haemolytica (A1 and A2). caused by P. at night. . bovine herpes virus 1. . 1963) and not susceptible to bovine pasteurellosis. Schwartz and Dioli (1992) suggest that the acute form is identical with HS. 1919. various authors believe the camel to be generally very resistant to HS (Leese. Different authors have documented Pusteurellu infections in camels. multocidu outbreaks in camels have been reported in various African countries. pheasants and quails. type A 2.Schwartz . Leese (1927) isolated Pusteurellu-like organisms from exudates of 2 camels in India that exhibited acute pleurisy. According to the WHO/FAO/ OIE (1961).hemorrhagic septicemia (HS) in cattle and buffalo caused by Pusteurella (P. a septicemic disease of chickensand waterfowl. The belief is that once an index case occurs (in a stressed animal) . trekking (hence the belief that ”change in pasture” is a cause). pericarditis and peritonitis. and although they are responsible for a few primary diseases. Mustafa. seasonally in Mauritania and is suspected to exist in Chad and the Sahara. i.g. mucosal disease virus. bovine respiratory syncytial virus). congestion of mucous membranes.e. Fazil and Hofmann. nasal discharge. 1987) has led to uncertainty in defining this disease in camels. transportation in mechanical vehicles with associated fear and prolonged muscle tension.”fowl cholera”. India and Iran (Table 13). Viruses occur along with the Pusteurellue in transit fever pneumonias (e. there are discrepancies regarding the clinical presentation and the pathogenesis to a distinct species of Pusteurella.g. allowing it to pass to other less stressed individuals. The latter is differentiated by diarrhea that is frequently mixed with blood. or closely confined in a truck.) multocidu. HS occurs in Bactrians in the former Soviet Union. personal communication) differentiate the following diseases: . Seifert (1992).pasteurellosis in cattle (shipping fever) accompanied by bronchopneumonia. 1918. Clinical signs are associated with fever.50 Bacterial Diseases Epidemiology and Clinical Signs Pusteurellu species can be found associated with numerous animal diseases. parainfluenza 3. swelling of throat and neck. as well as Smith (1994. in dromedaries from Algeria.l? unutipestifer infection in ducks. caused by l? muItocidu. Sudan and Somalia. especially if the group is housed in a crowded corral e. geese. dyspnea. multocidu.g.the organism undergoes a tempo- rary increase in virulence. Cross. However. The nomenclature of diseases caused by pasteurella organisms is non-uniform and confusing. peracute and an abdominal form. Gatt Rutter and Mack. and pneumonia. Mistaking outbreaks of Pusteurella with other diseases presenting similar clinical signs such as anthrax and salmonellosis (Donatien and Boue. l? multocidu exhibits three different clinical courses in camels: acute. in HS of cattle and buffalo and in transit fever (shipping fever) of cattle. lacrimation. P. . serotype B (1)and E. 1944. their main role is as the causative agents of secondary disease. Stress is thought to be of great importance in the initiation of pasteurellosis in large animals.pasteurellosis in sheep and goats (enzootic pneumonia) caused by P. De Alwis (1992). Blood and Radostits (1990).

Momin et al. generalized myositis and diarrhea as well as exudative pericarditis and peritonitis (Donatien. multocida. 37). Different authors have reported on the clinical course following experimental infection of dromedaries with cultures of Pasfeurella. Awad et al. serotype B. was isolated by Hassan and Mustafa (1985) from the organs and bone marrow of Sudanese dromedaries that died during an HS outbreak. The authors were able to prove that this strain causes HS in cattle calves. They are found on mucous membranes (mainly in the upper respiratory tract) assuming pathogenicity when the host's resistance is lowered due to a disturbance of the host-parasite balance as in mange. Cross (1919) also inoculated two dromedaries with a bovine "HS culture" and observed no systemic disease other than minor local swelling. 1994. different authors have described other clinical presentations.General Survev 51 and Dioli (1992) have characterized HS as being associated with pyrexia (up to 40°C). Donatien and Larrieu (1922) observed pneumonia. trypanosomosis or heat stress (Higgins. Pasteurella are also symbionts in camels. Two out of the four camels developed an increase in body temperature to 39. type 1. None of these reports provide any information regarding the isolation or identification of the causative agent. type E: 978). However. cervical edema with acute respiratory problems and sudden death. The mandibular and cervical lymph nodes are swollen and. The dromedaries infected by this route all recovered after 5 days. personal communication). A further symptom of this disease is the occurrence of chocolate colored urine. a slight rise in white blood cell count (WBC) .2"C. Furthermore 5 mL of the same strains containing 106 CFU/mL were given intratracheally into four healthy 8-month-old camels (Fig. in nearly all cases. 1986). fever. 1921). since the clinical signs and lesions described resemble anthrax. No laboratory confirmation has been performed on any of these cases and it is believed that the disease could have been confused with anthrax. All of the isolates were pathogenic for mice and rabbits. Fayed (1973) isolated 6 P. The morbidity is low. (1976a and b) reported happetence. multocida strains from 100 nasal swabs of healthy dromedaries in Egypt. unpublished) two I multocida strains (type ? B: 925. the disease was not reproduced in dromedaries. The ani1 mals developed high fever. (1987)reported an outbreak of pasteurellosis in India in which 1 out of 14 dromedaries died. which are both highly virulent in cattle and buffalo (Smith. Pasfeurella multocida. However. a hemorrhagic enteritis occurs with tar-like feces. hypersalivation. Outbreaks of HS are mainly seen in the rainy season and in areas that are regularly flooded. These camels developed no signs of illness. but not from the blood. In a small field trial (Wernery et al. but a bacterin vaccine used for cattle and sheep controlled the outbreak in the camels. 1994. As in other animals. Bipolar organisms were seen in blood smears that resembled P. but the mortality can reach 80% (Schwartz and Dioli. were sprayed into the nostrils (5mL of nutrient broth containing 106CFU/mL) of two healthy 9-month-old camels. 1992). anorexia and extremely painful swellings on the neck. In addition to the septicemic form of Pasteurella infections. rapid pulse and respiration in dromedaries following intramuscular and nasal application of P. two dromedaries that were infected intranasally with these strains recovered following a brief period of illness.Richard (1975) believes that abortions occur more frequently in conjunction with Pasfeurella infections. The application of a bouillon culture to rabbits led to their death within 24 hours. The disease occurs primarily in adult camels but can be seen in all age groups. Pasfeurella was re-isolated from the saliva. multocida. tachycardia and tachypnea.

However. loss of appetite and severe nasal discharge. P. multocida. Diseases with sim- ilar clinical pictures such as anthrax. A diagnosis can only be 1 . (1997) (see under chapter 1. Tesfaye (1996) and Bekele (1999) reported a respiratory disease that has caused 29. Necropsied dromedaries revealed hydrothorax.2 Pneumonia). type I (Table 13).6% morbidity and 6. D. this is the first recent report that dromedaries can suffer from pasteurellosis. the authors have not had evidence of or encountered one case of HS among 30. The sera were obtained from healthy dromedaries. A comprehensive scientific study is necessary to clarify the disease complex “Pasteurellosis in camelids”. E and P. Serological studies by various authors have identified the presence of antibodies to P. It was not clear from the authors’ report whether this outbreak had any connection with the one reported by Yigezu et al. haemolytica was isolated from the lungs. 1996). depression. After 3 days the body temperature and the WBC had reached normal values.000 racing dromedaries during a period of 15 years. It is unlikely that pasteurellosis is an important disease in OWC (Manefield and Tinson.Early treatment with oxytetracyclinesresulted in the recovery of many diseased camels. multocida and P. emphysema. haemolytica. hydropericardium and fibrinous pericarditis. salmonellosis and endotoxemia mentioned above would be less likely to be confused with pasteurellosis.4% mortality in the Somalian region of Ethiopia. The authors believe that a morbillivirus may have been the initiator of this outbreak.52 Bacterial Diseases Figure 37 5 mL containing 1O6 CFU/mL of t? multocida type E is injected into the trachea of an 8month-old dromedary and one out of the two also showed a slight mucopurulent nasal discharge from which no P. As previously mentioned. thoracic fluid and whole blood from diseased and dead animals that showed fever.3. B. pneumonia. serotypes A. this may be due to the excellent management and the superb feed given to dromedary herds in the UAE. goats and cattle in the Emirates and dromedaries live in close association with the smaller ruminants. multocida was isolated. Although Pasteurella infections (P. and no nasal discharge was detected. The aforementioned demonstrates that most of the reports about pasteurellosis in camels are confusing and often contradictory. further proof that many dromedaries are host to the organism without any ill effects. haemolytica) are widespread among sheep.

Dahl Momin et al. S salmonellosis ? Mortality 50% Fever. A. b 1973 Author Kane Kane Leese Ramachandran et al. 80% positive: t? multocida A. an outbreak may be controlled by the early administration of sulfonamides. B. Treatment and Control I The acute nature of pasteurellosis limits the efficacy t of antimicrobial therapy of sick animals. pathology and the isolation of Pusteurellu organisms from blood. E. 65% positive: t? multocida. R multocida Serology: 427 sera. Oinakhbaev Sotnikov Disease/lsolate t? multocida E antibodies Swelling in the neck region Septicemia. Serotyping should be done in reference laboratories. Specimens of the bone marrow in cases that have been dead for some time should be submitted. penicillin or oxytetracyclines to healthy camelids that only show a febrile reaction. Perreau and Maurice Perreau Awad et al. Fayed Hassan and Mustafa Donatien Donatien and Larrieu Delpy Goret Ono Richard Burgemeister et al. myositis. Maurice et al. E No reaction in 52 sera ? multocida t Iran 1936 1969 1943 1975 1975 1965 1973 Ethiopia Tunisia Russia made on the epidemiology. Specific identification of the organism as to species and serotype is essential to establish if Pusteurellu bacteria unique to camelids exist. Intraperitoneal inoculation of mice is sometimes necessary to recover Pusteurellue from clinical samples that contain large numbers of other bacteria. There has also been considerable success in Asia by the immunization of buffaloes with alum-precipitated or oil-adjuvant vaccines. fever. However. diarrhea Pasteurella isolated Hemorrhagic enteritis Serology: 161 sera. clinical signs. (1987). Vaccination with bacterin and alum (Alum potassium sulfate) Pusteurellu vaccines to control outbreaks of HS in dromedaries was reported by Hassan and Mustafa (1985) and Momin et al. Large-scale vaccinations of cattle and sheep against pasteurellosis are practiced in Asia and Africa and dromedaries are also vaccinated against HS in the Emirates. D and t? haemolytica /? multocida I (experimental infection) Chad Egypt Inappetence. HS Sudan French North Africa 1985 1921 1922 H confused with anthrax. spleen.General Survey Table 13 Occurrence of Pasteurella infections in camels in various countries 53 Country Mauritania India Year 1985 1987 1927 1968 1987 1987 1967 1968 1971 1976a. B. hypersalivation t? multocida from healthy dromedaries f? multocida B. kidney and lymph nodes. D. pneumonia. inappetence. liver. .

Vietnam. non-sporing and capsulated. soft and may sup. India. The pneumonic plague is an Mauritania and Libya where outbreaks of airborne infection and droplets may allow plague involving men and dromedaries aerosol infection between humans. Africa and Russia. alum precipitated vaccine and the combination of the two vaccines. multocidu antigen seroconverted and protected mice against challenge with P. Fedorov (1960) considthird. Etiology N Y pestis is a short.6 Camel Plague (Curasson. Y. occurring singly or in pairs when directly stained from tissue or exudate. 11 Epidemiology and Clinical Signs The camel's role in the epidemiology of plague has been known for hundreds of years 1. Great care must be taken during necropsy of an animal that might be infected with plague. the bacilli tend to form chains. One such and can therefore pose a health hazard to outbreak in Russia affected numerous peohumans in endemic areas. 1959).breaks of plague in camels in Mongolia. described by role in the transmission to humans (Sot. The recent out. cutting Europe's population by one breaks in camels. various plague outbreaks in man were due Cats are also susceptible to rabbit Y. Dissemination via the Plague as a zoonosis has played a role in blood stream may lead to pneumonia and the past. India. Indonesia.54 Bacterial Diseases Mohamed and Rahamtalla (1998) used an indirect hemagglutination (IHAT) and a mouse protection test (MPT) to assess the antibody response in dromedaries vaccinated with HS type B plain bacterin. heavy rain and flooding. In fluid culture.important role as anthropozoonoses as viet Union. not only in Russia.Sacquepee and Garcin (1913) as occurnikov. mu2tocidu type B. no challenge experiments were performed in vaccinated and unvaccinated dromedaries. This have been recently reported by Alonso form of plague is fatal. ring among dromedaries of French North . 1973). (1980). purate (buboes).1. grows on nutrient. In smears from tissues stained with methylene blue.(1936) and Pollitzer (1954) have reviewed duced pandemics which killed millions of past reports of camel plague and deterpeople. break in humans in Zambia was linked to China. Yersiniu ported to occur in OWC and both Bactri. It is said that the "Black Death mined that many scientists are skeptical killed 40 million Europeans before 1400 about the earlier reports of plague outAC. The last bacteria reach the regional lymph nodes. oval coc. The authors could show that sera from camels vaccinated with vaccines containing type B P. the camel meat (Kowalevsky. Plague has been re. and well as zooanthroponoses.Plague outbreaks among Bactrian camels vade higher grounds. in the former So.pestis was isolated from buboes in dromans and dromedaries play an important edaries.curred in 1926 (Strogov. 1912). Iran. 1960). Fedorov. pestis is Gram-negative. blood and McConkey agars. pestis is mainly have been known in Russia since 1911 and transmitted by fleas from tolerant rodents. the bacilli show characteristicbipolar staining. non-motile. causing rats to in. Y. In previous centuries. Iraq. Y pestis . even up to the in some parts of North and South America present. but also in meningitis. Nowadays plague is still endemic in ered that Yersiniu pestis infections play an many countries of Africa. Bubonic plague.Wu et al. There are two ple following the consumption of infected forms of plague. reported outbreak of plague in Russia ocwhich become inflamed. In bubonic plague. Sotnikov (1973) reported outwhere natural foci exist. pestis to contact with Bactrian camels. cobacillus with rounded ends.(1971) and Christie et al. Yersiniu pestis pro. 1947. However.

1998). Direct or indirect infection of man or a i nmal is possible from these reservoirs via contact with infected urine or ingestion of urine-contaminated food or water. should be administered for at least 5 days. which are of significanceto animals and humans: . Algeria and Mauritania.All of the pathogenic leptospirae are included under this designation. based on human cases.Spirochaetaceae: Serpulina (Brachyspira) Treponema Borrelia . Y pestis was isolated from . often for several months. Streptomycin and tetracyclines in combination are effective and. The authors also proved that the flea is the main vector of disease transmission among camels. Streams and ponds can be the source of infection as well as aerosols of urine in cowsheds and milk from infected cows. Sotnikov (1973) used a freeze-dried anti-plaguevaccine for the immunization of camels. Due to a varying antigenic structure. Fowler. Within the genus Leptospirae.The incubation time in camels is 1to 6 days followed by death within 20 days. Alonso (1971) and Klein et al.7 Leptospirosis occurs worldwide and there are reports of leptospirosis in OWC as well as NWC (Wernery and Kaaden. mainly to protect armed forces operating in countries where plaque occurs naturally and where Y. their immunity lasted for 6 months. Leptospires are present in tubules of mammalian kidneys and are ex- . chronic renal involvement serves as a reservoir for the organism (Bisping and Amtsberg. In addition to a cutaneous manifestation. but also caused abscesses disseminated over the entire body. The order Spirochaetales includes the families Spirochaetaceae and Leptospiraceae with the following genera. All domesticated animals. 1960). According to Seifert (1992). rodents in particular. cats and rabbits and their fleas. creted in urine. 1. 1959 and 1967). only the species L. can be expected. Leptospirescan be demonstrated in urine. from inappetence to more severe clinical signs. 1988). Before necropsy of a plague-suspected camel is carried out. interrogans is of medical importance. Ticks of the genus Hyalomrna and Ornithodoros are also able to transmit the disease mechanically (Fedorov. Leptospires grow in special media like Stuart or Korthof broths. 1995.Leptospiraceae: Lep tospira Leptospira are spirochetal organisms divided into serotypes based on their antigenic structure. interrogans consists of 19 serogroups and approximately 180 serotypes (serovars). A broad spectrum of manifestations. Martynchenko (1967). body fluids and tissues by dark field microscopy and fluorescent antibody technique (FAT).General Survey 55 Africa. wild game. In some animals. pestis may be used in biological warfare. septicemic and pulmonary forms also occur in the camel (Lobanov. as well as man are susceptible to infection.I Leptospirosis . (1975) described the clinical presentation of camel plague in dromedaries in Turkmenistan. Epidemiology * Leptospira are found ubiquitously around the world. Treatment and Control Prevention involves eliminating contact with infected rodents. Man. these lesions as well as from pleural effusions. the entire carcass should be sprayed with insecticides to destroy any ectoparasites. rodents and dogs serve as the most important epidemiological reservoirs in intensive cattle husbandry in the tropics. A genetically modified vaccine against bubonic plaque has recently been developed in Britain. L. not only affected the lymph nodes.

Wilson (1984) also observed hema- turia in dromedaries without finding a cause.56 Bacterial Diseases Figure 38 Dromedary suffering from hematuria: calcification of the renal papilla living in close contact with his animals. but rarely in breeding stock. Intensive microbiological examination and serum biochemistry (cre- Figure 39 Histological preparation (HE stain) of a kidney from a dromedary with hematuria: spotlike paratubular calcification with hemorrhage . The clinical presentation of leptospirosis in OWC has not yet been described and there is some doubt as to whether the camel is even susceptible to the disease. Rafyi and Maghami (1959) as well as Higgins (1986)suspected that hematuria may occasionally be caused by Leptospiru. can also be affected. Wilson (1984) and Higgins (1986) considered leptospirosis as being insignificant in OWC. Serological examinations of and cultural isolation of Leptospirae from 50 dromedaries with hematuria were negative. 1990). Hematuria has mainly been observed in the Emirates among racing dromedaries. Bloodied urine occurs in both genders of racing camels in the UAE. but is not associated with leptospiral infection (Wernery and Wernery.

but in general the studies of leptospirosis in lamoids are not clearly defined. This test. one animal with hematuria was euthanized and the urinary organs examined. vaccination with the appropriate strain is only recommended in endemic areas. Some strains produce hemoglobinuria (red water). vitulina. Serology titers of over 1:lOO using the microscope agglutination test are considered positive. dark-field examination of urine and FA technique of smears or cryostat sections from organs as well as cultivation and laboratory animal inoculation are used for diagnosis. Leptospirosis has been described in alpacas (Ludena and Vargus. kazachstanica I. Here the leptospires persist for long periods.000 dromedaries over a period of 15 years. Also. Treatment Clinically ill camelids can be treated successfully with 25 mg/kg body weight of dihydrostreptomycin administered intramuscularly for 5 days..These studies originated in various African countries. which uses live leptospires as antigen. The authors are of the opinion that subclinical leptospirosis in dromedariesis a worldwide phenomena and therefore may pose a health risk for man. It has been surmised that these deposits result from the higher mineral content of the feed given to the racing dromedaries. I1 and L. Mongolia and the UAE. but since leptospirosis is of less importance in Camelidae. Russia.6% of racing dromedaries. Diagnosis In suspected leptospirosis serology. examination of the urine did not disclose an increased precipitation of crystals or casts. This would explain why hematuria has rarely been known to occur in breeding stock. No clinical signs of disease were described. India. However.They localize and proliferate in parenchymatous organs after hematogenous spread. Wernery and Wernery (1990) found serological reactions to Leptospira in 2. 1982) and in a 3-month-old guanaco at the Detroit Zoological Park (Hodgin et al. Gross lesions include icterus of the mucous membranes and of the fat. Further studies should clarify possible connections in the etiology of the hematuria. Krepkogorskaya (1956) is the only author to have isolated Leptospira from camel organs. Breeding animals are given a less well-balanced diet. is highly sensitive and serovar-specific. The authors have not observed clinical leptospirosis in any of 30. Maronpot and Barsoum (1972) found leptospiral antibodies in 34% of the dromedaries examined in Egypt. and in histology there may be interstitial and tubular nephritis. All other studies report agglutinating antibodies specific for different leptospiral serovars (Table 14). During intensive research of hematuria in dromedaries. Iran.General Survev 57 atinine and urea) yielded no indication of renal infection or renal insufficiency as the cause of the hematuria. A wide range of bacterin vaccines are available for farm animals. consisting mostly of hay. Leptospires gain entry into the organism through mucous membranes or damaged skin.5% of breeding stock and 5. Since it is difficult to interpret a disease from a single sample. This revealed massive calcification of the distal renal tubules surrounded by hemorrhages (Figs. The etiology of this disseminated renal calcification has not as yet been elucidated. . the organisms propagate in the lumen of the proximal convoluted tubules. The following species were identified: L. leptospires may only be isolated during the short acute stage of the disease. 38 and 39) as well as focal glomerulonephritis. It is believed that clinical signs and pathology changes are similar to those in other species. Afghanistan. 1984). In the kidneys. sera from acute and convalescent cases should be collected. The affected dromedaries exhibited no signs of kidney-related pain or systemic disease.

butembo L. autumnalis L. L. bataviae L. kazachstanica II L. butembo L. 48. Shigidi Moch et al.0 16.0 51. vitulina (serologically and in culture) Zoo camels 2. grippotyphosa L. 0.4 Serotypes L. L. pyrogenes L.0 1976 Hatem Ahmed 9. icterohaemorrhagiae L.6 4. javanica L. Sebek Sebek et al. tarassovi L.0 1989 Russia 1956 Gallo et al.4 - icterohaemorrhagiae canicola grippotyphosa ballum Tunisia 1975 Burgemeister et al. pyrogenes L. L. Wernery and Wernery Afzal and Sakkir Breeding dromedaries Racing dromedaries L.0 15. butembo L. kazachstanica I L. prevalence and serotypes Country Afghanistan Year 1972 1974 1978 1974 1975 Author Sebek et al.0 - canicola icterohaemorrhagiae ballum pomona L.1 Mongolia UAE 1974 1988 1990 1994 Sebek Sosa et al.8 0. Prevalence % 0. wolfei L. L. pyrogenes L.2 Iran Somalia 1959 1960 Rafyi and Maghami Farina and Sobrero 20.58 Bacterial Diseases Table 14 Leptospirosis in camels. grippotyphosa Sudan Ethiopia L. L. pomona L.2 1982 1986 India 1986 Arush Hayles Mathur et al. interrogans . icterohaemorrhagiae L. Krepkogorskaya 0. tarassovi L.5 5. borincana L. L. L. autumnalis L. Egypt 1964 1972 Brownlow and Dedeaux Maronpot and Barsoum 34.

1990) mention that camel may suffer from cowdriosis.I Rickettsia1 Diseases .General Survey 59 1. With the exception of Coxiella burnetii. The authors are of the opinion that dromedaries do not play any role in the epidemiological cycle of classical epidemic typhus. 1992). multiply by binary fission. A systemic classification of Rickettsiae important to veterinary medicine is presented in Table 15 and their diseases in Table 16. rickettsii.4. 1995). 1987. Table 15 Taxonomic classification of Rickettsiae (modified from Bisping and Amtsberg. Reiss-Gutfreund . have their own metabolism and are sensitive to some antibiotics. Seifert. 1997). R.who isolated R. but they stain well with Romanowsky stain or Giemsa stain. They possess both DNA and RNA. However. since mammals can only be infected with the help of insect intermediates. who did not succeed in re-isolating R. A few authors (Beer.but there are no reports that the disease occurs in OWC (Wernery and Kaaden. there have been no reports of disease or losses in the camel due to this group of organisms. Etiology 'It Rickettsiae are often erroneously called large viruses.They may be cultured in tissue cultures or embryonated chicken eggs. Anonymous. prowazekii from ticks (Hyalomma rufipes) on dromedaries in Ethiopia. Rickettsiosis has been described in NWC (Barlough et al. (1971). Most of the Rickettsiae require living cells for their multiplication. This observation was confirmed by Ormsbee et al. Anaplasma and Cowdria. C. Kornienko-Koneva Rickettsia prowazekii. Rickettsiae are rods and coccobacilli.. 1988) and their vectors Classification Order 1: Family 1: Tribe 1: Genera: Vector Rickettsiales Rickettsiaceae Rickettsiae Rickettsia Rochalimaea Coxiella Ehrlichieae Ehrlichia Cowdria Neorickettsia Wohlbachieae Wohlbachia Rickettsiella Bartonellaceae Bartonella Grahamella Anaplasmataceae Anaplasma Paranaplasma Aegyp tia nella Haemobartonella Eperythrozoon Chlamydiales Chlamydiaceae Chlamydia Chlamydophila Tick Louse Flea Mite lxodidae Heteroptera Tick Tribe 2: Genera: Tribe 3: Genera: Family 2: Genera: Family 3: Genera: Tick Horsefly Mosquito Louse Flea see 1. Infections with Anaplasma in dromedaries appear to be subclinical. Reports from Somalia (Monteverde.3 Order 2: Family: Genus 1: Genus 2: (1955). Epidemiology and Clinical Signs QFever.Although various authors have identified antibodies to Coxiella burnetii. conorii. R. R. found no clinical signs of disease in the animals. but there was no original case report traced by the authors. They stain poorly with basic aniline dyes. tick fever. Rickettsiae are typical causative agents of vector epidemics. 1939 and 1960) regarding cases of Anaplasma marginale in healthy dromedaries support this observation. which are used in Gram stain. non-motile and aerobic. Legel. petechial fever. Heartwater and anaplasmosis can cause great losses in cattle and small ruminants in the tropics (Blowey and Weaver. prowazekii from the blood of young dromedaries that had been artificially infected.8 Rickettsiae are tiny obligate intracellular Gram-negative bacteria. burnetii can be transmitted either by ticks or by inhaling contaminated dust. 1991. they are true bacteria. mooseri. 1937. They are important parasites of arthropods and replicate in the gut cells.

splenic hyperplasia.60 Bacterial Diseases Table 16 Rickettsiae of veterinary importance and their diseases Family Genus Coxiella Species burnetii Cell parasitism in cell vacuoles of the reticulohistiocytic system G ranuIocytes Disease Q-Fever Ehrlichia (Cytoecetes) Rickettsiaceae Ehrlichia Cowdria equi phagocytophila canis rnononuclear cells rurninantiurn cytoplasm of the vascular endotheliurn marginale Ehrlichiosis Heartwater Anaplasrna Anaplasrnata. a zooanthroponosis. C.. The role of rodents and domesticated animals as hosts or reservoirs for infection in man has long been established. Eperytkrozoon-like organisms resembling Eperythrozoon suis have frequently been diagnosed in these immunodeficient llamas. 1990. 1979) have indicated the danger of rickettsial disease in humans due to close contact with dromedaries. moderate diffuse non-suppurative interstitial pneumonia. Different authors have identified antibodies to various rickettsial species in the camel. Semrad. During necropsy. There is an indication that this Rick- . marginale in 10. necrotizing enteritis. 1968. The greatest danger is most likely from the consumption of raw camel milk. The dromedary is no exception. Mathur and Bhargava. A summary appears in Table 17. the two-humped camel may be susceptible to natural infection of A. (1984) found antibodies to A. Ristic (1977) and Ajayi et al. from weaning to several years old. have been found to have apparent immunodeficiency disorders. burnetii is the organism responsible for Q-fever. severe fibrinous polyserositis involving the thoracic and abdominal organs. Affected llamas usually die or are euthanized because of the grave prognosis. However. Eperythrozoonosis has frequently been identified in young llamas (McLaughlin et al. widespread vascular thrombosis and anemic infarcts in the liver are observed. Such llamas have a history of weight loss and stunted growth and develop acute or recurrent infectious conditions. In these cases. marginale. Ristic and Kreier (1974). 1994).7% (3/28) Nigerian camel sera using 3 different serological tests. Juvenile llamas.Aegyptianella ceae Haernobafionella centrale 0vis pullorurn felis marginal (in erythrocytes) central (in erythrocytes) Anaplasmosis marqinal in erythrocytes Aegyptianellosis on erythrocytes (in folds) on erythrocytes on erythrocytes on ervthrocvtes Hemobartonellosis Eperythrozoonosis wenyoni Eperythrozoon ovis suis (1955) was successful in transmitting Anaplasma-contaminatedcamel blood to cattle. Numerous authors (for example Maurice and Gidel. infections with uncommon pathogens or opportunistic microorganisms are often detected.

Author Blanc et al. Imam and Labib Maurice et al.7 12.6 4. Giroud et al.9 20. Mathur and Bhargava Addo Harrag Abbas et al.7 1. conorii Anaplasrna Somalia Nigeria Sudan 4. Karrar et al. Gosh et al.8 17.6 6.6 Experimental Experimental 26.06 0. Bares Maurice and Gidel Pathak and Tanwani Choudhury et al.0 11.8 11.0 (direct) R.2-12.8 11.9 12. Rafyi and Maghani Veeraghavan and Sukumaran Kalra and Taneja Elyan and Dawood Brown El-Nasri lmamov Maurice et al. Maurice et al.o 40.7 Cowdria ruminantiurn .9 23.8 13.5 3.0 R. Sabban et al.7-7. Reiss-Gutfreund Imam and Labib Maurice et al. Burgemeister et al.8 5. Karrar Year 1948 1954 1954 1954 1954 1955 1956 1962 1964 1967 1968 1968 1968 1969 1971 1972 1974 1975 1976 1978 1979 1980 1986 1987 1988 1989 1955 1963 1967 1968 1970 1971 1963 1967 1970 1968 1978 1967 1937 1939 1960 1974 1977 1981 1984 1963 1968 Country Morocco Chad Iran India India Egypt Kenya Sudan Kazakhstan Chad Egypt Chad Central Africa India India Sudan India Tunisia India Egypt India Nigeria Tunisia Sudan Tunisia Tunisia Ethiopia Egypt Chad Chad Mongolia Egypt Egypt Chad Mongolia Chad Egypt Chad Somalia Prevalence 22. prowazekii Ticks 44.0 14.0 4. Bares Reiss-Gutf reund Ormsbee et al.8 3.0 13. rickettsii R.3 15.2 2. mooseri R. Harbi and Awad E l Karim Kulshreshtha et al.4 (direct) 10.6 Experimental 1.0 0. Monteverde Anonymous Anonymous Ristic and Kreier Ristic Anonymous Ajayi et al. Reiss-Gutfreund Bares Schmatz et al.8-26. Djegham Gallo et al.1 1.General Survev Table 17 Literature survey reqardinq rickettsia1 antibodies in OWC Species 61 C burnetii . Schmatz et al.

monocytosis and eosinophilia. but after treatment with oxytetracyclinesrecovered fully. (1997) reported the identification of an Ehrlichiu in a llama suffering from granulocyhc ehrlichiosis.40) (Wernery et al. Cytoplasmatic inclusion bodies of Ehrlichiu were detected in neutrophils.The same Ehrlichiu was also found in llama-associated lxudes pucifus ticks collected from the same llama farm. The llama showed a mild lymphopenia. Barlough et al. Figure 41 Eosinophilic inclusion bodies in the cytoplasm of a neutrophil of a guanaco with rickettsiosis (Giemsa stain) .. Epeythruzoon-like parasites are attached to the surface of red blood cells of the affected llamas and are often found in clusters. The llama became recumbent. This Ehrlichia strain was sequenced showing close relationship to members of Ehrlichiu phagu- cytuphilu. Clinical signs were non-specific and included lethargy. slight ataxia and anorexia.62 Bacterial Diseases Figure 40 Eperythrozoonosis in a young llama suffering from immunodeficiency disorder (Giemsa stain) ettsiu is responsible for the anemia which often accompanies this ailment. usually towards the edge of the cell (Fig. 1999). and the diagnosis ”granulocytic ehrlichiosis” was made.

Indirect FA test on serum for antibody Giemsa-stained blood or bufFy coat smears. ELISA or microagglutination). Paired serum samples for serology (CFT. 41). Indirect FA test on serum for antibody FA or Giemsa-stained blood smears. canis but cells or inclusions present in granulocytes. especially neutrophils Equine ehrlichiosis (Ehrlichia equi) Potomac horse fever (Ehrlichia risticii) Purplish-staining agent in monocytes. Machiavello or Leishman stains as well as FA staining are used for both blood and tissue smears.. Rickettsiae do not grow on agars and it is therefore necessary to cultivate them in embryonated hen’s eggs or tissue culture. Antibody rise 2-3 weeks post infection Appearance of agent in Giemsa-stained smears Small purple-red cocci (0. burnetii in 66% of Egyptian dromedaries with the competitive enzyme immunoassay (CEIA). .0 pm diameter in monocytes or lymphocytes As for E.. Soliman et al. microagglutination or ELISA. Giemsa. Inclusions similar t o other Ehrlichia spp. 1999) (Fig. The laboratory diagnosis of important rickettsial diseases is summarized in Table 18. Similar in appearance t o Chlamydia psittaci when stained with the Giemsa stain Canine ehrlichiosis (Ehrlichia canis) Giemsa-stained blood smears. best at about the 15th day post infection. This guanaco was also lethargic and anorexic and revealed a monocytosis and eosinophilia. 1994) Disease Q fever (Coxiella burnetii) Laboratory diagnosis FIuorescent anti body (FA) or Giemsa-stained smears from ruminant placentas. Romanowsky. Demonstration of Rickettsiae by animal inoculation is also advisable. Furthermore. Penicillin and streptomycin should be added to the test sample to suppress contaminants. Some embryos might die 6 days after infection and the remainder should be examined after 12 days. As Rickettsiae are poorly stained by Gram. Inclusions can be seen 48 hours after onset of disease. especially when few bacteria are expected in the sample.General Survey 63 Cytoplasmatic inclusion bodies were also observed in neutrophils of a guanaco in the UAE (Wernery et al. The animal of choice is the guinea pig.5 pm diameter) or inclusions (morulae) up t o 4. (1992) detected antibodies to C. unclotted blood and affected tissue including brain (Heartwater) should be dispatched to the laboratory. a serological diagnosis can be made for some rickettsial diseases like Q-fever on paired serum samples using the CFT. Table 18 Laboratory diagnosis o f important rickettsial diseases (after Quinn et al. Giminez. ELISA or indirect FA for antibodies in serum Purple-staining cells (0.2-4 pm) or short rods within cells. Diagnosis For the laboratory diagnosis of rickettsiosis.

Eperythrozoon. Up t o 50% of red cells may be parasitized Great variety of violet-reddish forms: oval. Serology: CFT Deep purple. With acridine orange staining. Largest species in the genus Reddish-violet-purple cocci in RBCs or WBCs Porcine eperythrozoonosis (Eperythrozoon suis) Camelid rickettsiosis (Anaplasma. and also larger inclusions in erythrocytes Avian aegyptianellosis (Aegyptianella pullorurn) Feline infectious anemia Giemsa or FA-stained (Haemobartonella felis) blood or tissue smears. Serology: indirect FA or CFT Giemsa.2-0.3-0. acridine orange and FA staining of blood smears.2-0. A few ring-forms occasionally seen Pale purple organisms in disc. there is bright orange fluorescence Giemsa or FA-stained blood smears.2 pm diameter) organisms on erythrocytes. acridine orange blood smears. Inoculation of susceptible birds by parenteral routes or skin scarification with infected blood Salmon poisoning (Neorickettsia helminthoeca) Anaplasmosis (Anaplasma marginale) Reddish-violet pleomorphic forms (0.5 pm) or short bacillary forms in cytoplasm of vascular endothelial cells of capillaries in the brain Purplish morulae in cytoplasm of macrophages with individual cocci (0. Rod-forms are most common at the margin of the erythrocytes Bluish-violet cocci or ring-forms (up t o 2. basophils and monocytes Purple-staining cocci (0. Inoculation of mice or susceptible cattle Clinical signs and the finding of fluke eggs (Nanophyetus salmincola) in feces. CFT and card agglutination Giemsa-stained blood smears. small coccoid or rod-shaped (0.or ring-forms (0.0 pm in neutrophils.3-3.O pm diameter).5 pm diameter) on erythrocytes.9 pm diameter).4pm) scattered within the cells FA or Giemsa-stained smears from brain tissue (cerebral cortex).7-3.4 pm diameter) within erythrocytes and near the periphery. round and ring (0. eosinophils. Ehrlichia) . Serology: indirect FA.5-1 . Check Giemsa-stained smears daily for 1 week as the presence of the agent on red cells is inconsistent Ovine eperythrozoonosis (Eperythrozoon ovis) Giemsa-stained blood smears. Demonstration of the agent in lymph node aspirates Giemsa.64 Bacterial Diseases Table 18 (cont.) Disease Tick-borne fever (Ehrlichia phagocytophila) Heartwater (Cowdria ruminantium) Laboratory diagnosis FA or Giemsa-stained blood smears Appearance of agent in Giemsa-stained smears Purplish inclusions varying from 0.

Anonymous. Onyali. B. USA) . Rhodococcus equi is primarily an equine pathogen. Oluigbo and S. Figure 42 Rhodococcus equi abscess in a llama liver (courtesy of Prof. 1987. E. E. of Vet. Dept. A R.. A?. 1. . equi was isolated (Fig. since it is known that camel ticks spread many diseases. S. 1980. Long-term medication of feed is sometimes necessary to eliminate carrier animals as in an A.The authors described multiple caseous abscesses in the lungs. BY.I Rhodococcusequi . Elev. Ajayi.M. Elissalde and Renshaw.l'etude de la peste en Mauritanie. Alonso. F. Ministry of Livestock. III. 1960. 1981. Notes on animal diseases. Notes on animal diseases. 4 (6): 463-468. 1995). Epiz.B. Afzal. marginale infection. J.O.0.9 in New World Camelids Corynebucteriae are small pleomorphic Grampositive rods or cocci. Vet. Yassin and A. Anonymous. equi-associated necrotizing lymphadenitis in a llama was also reported (Hong and Donahue. Agric. 1975. Med. 1971.General Survev 65 Treatment and Control i ' Tetracyclines and chloramphenicol are the drugs of choice. For acute cases they should be administered for 2 weeks. 1980). Fowler.E. Forestry and Range. Vet. sci. Serological evidence of exposure to Anaplasma marginale in Nigerian onehumped camels. Elzubir. Somali Democratic Republic. Annual report of the Veterinary Laboratory.. Vet. 1994. 1939. and M. A?. but seems to play an important role in NWC (Leite et al. 40 (3): 231-233. M. Ajayi. 136 (5):519-521. Kisimayo. M. 1. Sakkir. A P ~ cFor. Piroplasmosis and anaplasmosis of animals other than cattle and trypanosomiasis. Anonymous. liver and spleen of llamas from North and South America from which A. United Arab Emirates.T. Contribution . III Piroplasmosis and anaplasmosis of animals other than cattle. 25 (3): 147-152. Rev. P. References Abbas.A. Addo. 1984. and trypanosomiasisof domesticated animals. Survey for certain zoonotic diseases in camels in the Sudan. J. 42). Rec. some of which are extremely dangerous to other livestock and humans. 114 (19): 478. Survey of antibodies against various infectious disease agents in racing camels in Abu Dhabi.M. Prevention is enhanced by controlling ectoparasites. J. 13 (3): 787-792. A serological survey for evidence of Q fever in camels in Nigeria. For. off. Rev. Pays hop.T. J. E.. T. Services. int.A. Thesis (Doctorat de medicine) Paris 6 59. They are pyogenic bacteria causing a variety of suppurative conditions in many animal species.

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L. Pays trop.2000 (in press. Higgins. Field and D. Yamini.A. C. lSt Camel Conf. 1987. Ofiint. 8. FAO. Kopcha. 7 145-146. 76 (4):253-254. U. an "all purpose" animal. Der praktische Tierarzt 11: 974-987. Shommein. S. McGrane. Eds: W. Om.a review. J. Food and Agriculture Organisation of the United Nations. Bailli&re. J. E. sci. G.72 Bacterial Diseases duction in Somalia by Hjort a Omaes. C.F. A. 1946. R. W. Wemery. V 1985.J. Snow and J. Davies. 1985. ..J. and A. Almaty. Cockrill. vet. and S.O. Richter. 1998. bacteria and fungi. Refai. A. H. Newmarket. Silveira. Publications. A. Allen. 1990. Bomstein. Diseases of camels in the Sudan. Gaiger and Davies Veterinary pathology and bacteriology. camels in Egypt.M.. Sudan. 2001. 1999. D. tech. G.R. Wernery. C. A note on the diseases of camels in Saudi Arabia. 1998. Thesis. Vet. Anderson and F. The geographical distribution of animal viral diseases. Epiz..Tindall and Cox. J. Viral infections in camels . Guleed. J. A. Leese. M.J. Australian Vet. and Res. Camel Practice and Research 2 (1): 1-12. Kazakhstan.H. Pilot study of the health of Somali camel herds. Greiner. Krankheiten bei Ruminantia und Tylopoda im Miinchener Tierpark Hellabrunn.J. Wemery. 1983. Br. f Book: 189-206. Heller. 1985. I. Academic Press.A. Le dromadaire et son 6levage. Camel Prac. Sci. Beitrag zum Spektrum der . 29 (2):228-232. Proc. Wernery. Rahamtalla. R. Two diseases of young camels.M. WHO. A.. D. Faculty Vet.G. Tierpark Hellabrunn. Agroeconomics of Camelid Farming. Camel Forum working paper. Rm. Mineral deficiency: a predisposing factor for septicemia in dromedary calves. 1995. Wilson. Haemorrhagic septicaemia (Pasteurella multocida) in camels: Immunity status. Vet. 31d ed.H. 1987.A.. Maisons Alfort. Manuel des maladies du dromadaire. H. 1984. Odend'Hal. Richard. Higgins.Peyre de Fabregues and D. Mogadishu and Uppsala: SOMAC/SIAS 23. Zoo and Wildlife Med. Infectious diseases of the camel.). 99.S. 1994. 6 (2):481. U K 59-64.R.9. J. serological and bacteriological studies. J. IEMVT. Abraham and U. Streptococcal peritonitis in a young dromedary camel. New aspects on infectious diseases in camelids. 1986. Epidemiologische Aspekte bedeutender Kamelkrankheiten in ausgewahlten Gebieten Kenias.-12. 8. Ramosvara.J. Eldisougi. U. and W. M. Wade: R. 1982. M. Dolan. Mayhew. A. Juansalles and B.R. Sci. 6 (1): 87-91. Projet de d6veloppement de l'6levage dans le Niger centre-est. viruses. Patterson. and A. Schwartz. D.S. Uppsala: 496-502. The Camelid. New York p. Roettcher. Mkd. J. Bacterial and mycotic diseases of int. Elm. J. I. Scandinavian Institute of African Studies. Watson. Animal Health Year Book. Osman. 2nd lnternational Camelid Conference. I. London. M. 4: 1-7. J. Kinne. Richard. Hoste. University of Khartoum. 1992. Rome. M. 141: 529-547. Actinomycotic splenitis and intestinal volvulus in an Alpaca (Lama-Pacos). 1909. Trop. Ali.

Ethiopia (Pegram and Tareke. (1998) examined 27 fecal samples from diarrheic dromedary calves aged between 1and 10 weeks raised in 9 herds in the Moroccan Sahara. 1995) and the UAE (Wernery. Faye (1997) reported 68. coli. S.5% (4/42) diarrheic camel calves from Sudan (Mohamed et al. (1995)reported a case of ear tip necrosis. 1944). weight loss and death within a few weeks (Fazil and Hofmann. 1943).3% deaths in young dromedaries in Niger caused by a mixture of enteric pathogens: Salmonella. rota. Yassien. induced in part by the global animal and food trade. 1996)as well as from 9. rotavirus. Berrada et al.. septicemia and abortion.2. In camels. The highest incidence of salmonellosiswas during the month of October. 1977). saint-Paul are the most important serovars in camels. The dried-off ear parts could easily be re- . several scientists have reported severe Salmonella enteritis in association with E. Nothelfer et al. Salmonellosis in livestock is caused by the infection with both host-specific and non-host-specific Salmonella serovars. The author believes that S. leading to losses of up to 20% in some parts of the country. 1992). Some Salmonella strains can cause an unusually wide range of clinical syndromes including ischemic necrosis of the tips of the ears. USA (Bruner and Moran. 5 different Salmonella strains were isolated. 1918). Salmonellae were also isolated from 8 healthy dromedary calves and from 1 diseased calf from the UAE (Nation et al. Osman. 1949) and more recently from Somalia (Cheyne et al. S. Salih et al. acute and chronic enteritis. 1985. typhimurium. tail or limbs. who examined 106 diarrheic camel calves cultured Salmonellae from 14 (13%)of them. 1984. coli and Eimeria cameli.and coronaviruses. Eimeria cameli.Egypt (Refai et al. typhi was the most prominent strain. The disease is characterized by one or more of 3 major syndromes: septicemia. Chronic salmonellosis is characterized by diarrhea. In recent investigations of camel calf deaths.. The disease manifests itself in hemorrhagic diarrhea with dehydration and death. With the exception of S. 1998). 1981). coronavirus and E. Epidemiology and Clinical Signs merous authors have reported salmonellosis and Salmonella infections in camels in different parts of the world. 1981). Salmonella infections occur worldwide in all animals and are the focus of intensive scientific study. S. Palestine (Olitzki and Ellenbogen. Salmonella can cause enteritis. Infections occur due to ingestion of feed or water contaminated with Salmonella as well as by direct contact with the contaminated excreta of carriers.1 Salmonellosis The incidence of salmonellosis in humans has increased in recent years and animals have been incriminated as the principal reservoir. Etiology :!$I The genus Salmonella comprises a single species that has been divided into more than 2000 serotypes (serovars). kentucky and S. A widespread distribution of known serotypes has occurred. Reports of Salmonella infections have appeared from Sudan (Curasson.. a l Sall monellae are motile with peritrichous flagella.. (1998 a and b).A literature summary appears in Table 19. French North Africa (Donatien and Boue. whose members are Gram-negative coccobacilli. gallinarumpullorum.8% of the diseased calves. From 14. Pegram and Tareke (1981) reported that salmonellosis in Ethiopia is the most important disease in young dromedaries. enteritidis.1. The genus Salmonella is classified in the family Enterobacteriaceae.

Salih et al. El-Monla Sayed Pegram and Tareke Elias E l Nawawi et al. 43). Mohamed et al. Ramadan and Sadek Ambwani and Jaktar Cheyne et al. as well as from . This is evidence that endotoxin damages the endothelium of blood vessels leading to a localized disseminated intravascular coagulation that causes terminal ischemia. They found that 3% of healthy dromedaries showing no sign of diarrhea were Salmonella carriers. Yassien Selim Pegram Wernery Anderson et al. compared to 17% of dromedaries with enteritis. Andreani et al. Nation et al.. Selim (1990) compared two groups of dromedaries in Egypt. Salmonellae have been isolated from the feces of healthy camels in India (Malik et al. 1992). Refai et al. Faye Berrada et al. 1973) and in the UAE (Wernery.74 Bacterial Diseases Table 19 Summary of literature regarding salmonellosis and Salmonella infections in camelids Author Kowa levsky Curasson Olitzki Olitzki and Ellenbogen Donatien and Boue Year 1912 1918 1942 1943 1944 Country Russia Sudan Palestine Palestine French North Africa Number of serotypes not typed not typed 1 1 not typed Disease enteritis enteritis none enteritis abortion enteritis septicemia enteritis enteritis none none none none none none none none enteritis None None None septicemia enteritis None None None None enteritis None septicemia diarrhea diarrhea septicemia diarrhea diarrhea diarrhea Sandiford Bruner and Moran Floyd Zaki Farrag and El-Afify Hamada et al. 1944 1949 1955 1956 1956 1963 1963 1967 1971 1973 1977 1978 1978 1979 1981 1982 1982 1984 1985 1990 1992 1992 1995 1996 1997 1998 1998a 1998b 1998 Egypt USA Egypt Egypt Egypt Egypt Egypt India Egypt India Somalia Somalia Egypt Egypt Ethiopia Egypt Egypt Egypt Egypt Egypt Ethiopia UAE USA UAE Niger Morocco Sudan Sudan 1 2 3 1 1 2 7 6 8 5 1 1 7 5 2 5 11 5 6 28 llama 3 4 5 1 4 moved by hand leaving a clear and slightly bleeding surface (Fig. Ambwani and Jaktar. 1967. Kame1 and Lotfi Malik et al.

They isolated Salmonella species from 3. over-stocking. . Wemery et al. type A outbreak among racing dromedaries in the UAE. However. 1984.1% of the animals examined (S. different Salmonella serotypes were isolated in various countries. which presumably served as harbingers of the deadly C. surgery and medication (Blood and Radostits. 1963. saint-paul (6 x). cerro were the predisposing factors for the loss of several dromedaries. They identified Salmonellae in all of the organs of the dead animals. Yassien. S. slightly bleeding surface is visible the lymph nodes and intestines of slaughtered dromedaries in Egypt (Zaki.. typhimurium (15 x). Wemery and Makarem (1996)identified a large number of identical Salmonella serotypes in the stool of people afflicted with salmonellosis and in the fecal samples of dromedaries. either of the individual animal or of the breed of animals. 1991). Sinkovics (1972) observed an increased C. In Egypt. l. eastborne (1x). Disease resistance is due to a combination of a genetically determined insensitivity towards certain pathogenic microorganisms (Mayr. the age. Kame1 and Lotfi (1963) examined intestinal lymph nodes and fecal samples from 915 slaughtered dromedaries for the presence of Salmonella. the infective dose and stressors play an important role in outbreaks of salmonellosis in older animals. In the UAE. immunological status.. perfringens activity in the small intestine of piglets when they were infected with enteropathogenic E. coli infections in piglets appear to play a role similar to that of Salmonellae as described above. a clean. S. S.Digestive System 75 Figure 43 After removal of the dried-off tip of the ear. 1985). 1990). 1956. reading (3x). s. (1991) reported a Clostridium perfringens. This variation in pathogenicity is a consequence of individual resistance. perfringens enterotoxemia. malnutrition. Ramadan and Sadek (1971) and El-Nawawi et al. Refai et al. Food poisoning due to dromedary meat has been reported by Sandiford et al. saint-paul and S. Preventive measures must also take into account that inadequate treatment can lead to unapparent subclinical cases or carriers that may then persist in the stock. the Salmonella spp. Enteropathogenic E. enteritidis (1x). Sudan and Somalia where meat from dromedaries is consumed. El-Nawawi et a . 1982. stamina and condition of the animal. (1982). These chronic carriers are not only a threat for the remaining animals. Salmonellosis has increased in importance as a zoonosis in the last few years. The authors believe that their study proved that the dromedary is an important reservoir for Salmonellae and could therefore represent a health hazard for man. coli. S. birth. Hamada et al. bovis-morbifcaus (1x)). isolated from diseased and healthy camels were identical. Additionally. As seen in Table 20. Sandiford (1944). S. This is especially true in several African countries such as Egypt. The authors indicated that a concurrent infection with S. dublin (2 x). but also present a human health hazard through contact with contaminated animal products. (1943). It is generally accepted that this disease can be promoted by transportation.

5. 5. senftenberg. 5. heidelberg. 5. 5. 5. goettingen. meleagridis. 5.76 Bacterial Diseases 37 38 to 69 5. newlands. amsterdam. johannisburg J . 5. 5. chailey. 5. newbrunswik. 5. brazzaville. 5. shubra. havana. 5. 5. newport. 5. agona. oranienburg. nchanga. kottbus. 5. 5. sandiego. 5. livingstone. brandenburg. lokstedt. infantis. 5. ’ 5. Uganda. Santiago. tshiongwe 5. 5. 5. ’ UAE 5. 5. hindmarsh. 5. 5. thompson. 5. mbandaka. israel. 5. tarshyne.

Death occurs within 48 hours.) Chronic enteritis is a common form in adult camelids. 4 4 . but infection via the mucous membranes of the conjunctivae or upper respiratory tract as well as through the skin occurs. ears and tails. pulmonary congestion and hemorrhages of the mucous membranes. The animal revealed hydropericardium. coccidiosis or candidiasis exist. The feces have a putrid odor and contain mucus and sometimes blood. . Prevention and Control for Salmonellae is the intestinal tract of warm-blooded and cold-blooded animals and the majority of infected animals become subclinical excretors.plasmids. . A severe hemorrhagic enteritis may develop (Fig. The second case was a premature llama infected with S.Digestive System 1 Special toxins of Salmonellae are responsible for the systemic and enteric forms of salmonellosis. meninges. selective procedures are used for the isolation of Salmonella from specimens that contain a mixed flora.lipopolysaccharides(LPS).endotoxins. causing septicemia. There is persistent diarrhea. It is therefore important that every ef- Figure 44 Hemorrhagic enteritis caused by S. (1995) reported septicemic salmonellosis in a llama caused by S. pleuritis and peritonitis. The organisms also frequently localize in the gallbladder and mesenteric lymph nodes. From the lamina propria of the intestines. Salmonella septicemia is a usual syndrome in newborns with outbreaks occurring for up to 6 months. typhimurium.cytotoxin. cholerasuis. Serotypingis based on the 0 (somatic)and H (flagellar)antigens.enterotoxins. . Colonies characteristic for Salmonellae can be easily serotyped. pregnant uterus and distal aspects of limbs. emaciation and poor response to treatment. The bacteria penetrate into the lamina propria and production of cytotoxins and enterotoxins contribute to gut damage causing enteritis. The llama had been in contact with pigs. Transmission of Salmonella is usually by the fecal-oral route. . typhimurium in a young dromedary . The disease was characterized by fibrinopurulent pericarditis. 77 The usual route of infection is oral. During septicemia. . These virulence factors include: . Salmonellae have simple nutrient requirements and growth in vitro is therefore possible on many different media. hydrothorax. Acute enteritis is the common form in camel calves and in adult camelids when predisposing factors like clostridiosis. and survivors intermittently shed the bacteria in the feces. Salmonellae may be transported into the vascular system. This illness is acute with fever and depression. Salmonellae may localize in the brain. At necropsy there are petechiae in all organs and often pneumonia. Anderson et al. However. A factor predisposing to Salmonella septicemia seems to be mineral deficiency. with intermittent fever.

These vaccines should be used in problem herds and should be administered twice before parturition in order to provide protection against salmonellosis for the newborns. may be of benefit since it is diseases of great economic magnitude. Carrier animals should be identified.1..the following diseases to E.4) (1981).2.2 Colibacillosis cies in the dams and their offspring. but the drug of choice should be based upon culture and sensitivity. 5. Treated camels must be re-examined several times before there can be confidence that they are not carriers. avirulent vaccines are now available.78 Bacterial Diseases fort be undertaken to prevent introduction of carrier animals into a herd. Certain procedures should be followed in a Salmonella outbreak on a camel farm: 1. such as While Escherichia coli is the cause of various ketoprofen. which should be administered either intramuscularly or subcutaneously at a dosage of 5 to 8 mL depending on the weight of the animal.pecially in young animals. ic resistant strains of Salmonellae. However. This includes oral or parenteral rehydration. All persons should be aware of the health hazards of working with infected camels. coli: nellosis is controversial because it may cre. It is also very important to avoid factors that lead to mineral deficien. (1994). The autogenous vaccines are killed vaccines. Supportive therapy and good nursing are important especially in camel calves with enteritis.1. Wernery and should be followed.colisepdrugs generally recommended for particemia in piglets less than 1week old.colisepticemia in bovine calves less than should be administered parenterally.colibacillosis (white scours) in bovine ate a carrier state in camelids and antibiotcalves less than 1week old. . amoxycillin and trimethoprim-sulfonafter weaning. esknown that many camel calves subsequent. In these tutes a large part of the normal commencases. it also constily also suffer from endotoxic shock. correction of electrolyte imbalances and stabilization of the acid-base equilibrium. Quinn et al. Movement of animals around the farm should be restricted. The drug . enteral use in salmonellosis are ampicil.neonatal diarrhea (colibacillosis).. 2. of the gastrointestinal flora. Kaaden (1995) and Fowler (1998) ascribed Antimicrobial drug treatment of salmo. Antimicrobial . It should also be ensured that feed supplies are free of Salmonellae. Some commercial live. The colostral immunity will last approximately 6 to 8 weeks. amide combinations. BaytriP is also a very effective drug.joint ill in bovine calves surviving a colruminates can create severe disturbances isepticemia. Treatment must start immediately and should be continued daily for up to 6 days. The use of vaccines should be considered. 4. Feed and water supplies must be protected from fecal contamination (beware of pigeons and rodents). It is of no use to vaccinate newborn camelids because their immune system is still immature. 3. oral treatment of an animal species that . autogenous Salmonella vaccines (see chapter 4) are of greater value because they include the Salmonella strains involved in the outbreak. the treatment protocol described sally aerobic intestinal flora. Willinger under the heading Endotoxicosis (1. Camelid calves in problem herds whose dams have not been vaccinated should receive up to 50 mL of the herdspecific vaccine orally for 14 days. Nonsteroidal anti-inflammatory drugs.colibacillosis in piglets about 2 weeks lin. isolated and treated vigorously. since 1week old.

tia syndrome) in sows.intestines of all mammals and is excreted ment. of which there may be more than one in an E.mortality can reach 100%. are frequently associated with SalEtiology Escherichia coli is a straight monella. coli strains possess a variety of virulence factors upon which their path.Schwartz and Dioli (1992) reported a morbidity of 30%in neonatal dromedary calves eases. coli possess different antigens (K = natal lambs. E. 1998). . can cause henisms: 1. coli in water and food samples is taken as evidence of Colibacillosis and colisepticemia have been fecal contamination. coli is a natural inhabitant of some parts of the piratory tracts. heatarrhea. Attaching and effacing E. Different serotypes can cause differEnteric infection caused by E.and Gram-negative motile rod that belongs like rotaviruses as well as Cryptosporidia infecSalmonella to the Enterobacteriaceae family.wound infections and healing impair. 1988). code for several virulence factors includ. coli infections in young animals are Kaaden. coli enterotoxemia in weaned pigs. which can be used to . microvilli .septicemia. .verotoxin. in feces. A plasmid. coli can be ent clinical signs. Some strains. 1995. of elabo(ewes). Clostridia. Fowler. . coli infections in dromedary calves 4. labile and heat-stable enterotoxins and 3. capsular polysaccharides. which cause teria operating through different mecha. "watery m o u t h in neona. a-and p-heproduce enterotoxins.mastitis in cattle and other animals . tions.The authors believe that the unsanitary conditions in the breeding herds along with drome in children. reported in OWC and NWC (Wernery and E.strains produce enterotoxins. These factors include neonatal colibacillosis.dysentery in rabbits. . coli cell. F = fimbrial). ing antibiotic resistance. . 5. . corona. and of possessing plasmid-encoded virulence factors. fimbrial adhesions K88.colibacillosis and colisepticemia in neoE. may elids 2 to 4 weeks old.molysins. H = flatal lambs. Enterotoxigenic E. A considerable economic loss to terocytes and produce virulence factors the camel industry results from colibacillo. coli (EIEC)invade en. coli (EHEC)cause in East Africa. coli (ETEC)with their molysis (Bisping and Amtsberg. in calves. - E.Digestive System 79 All five pathogens share the general properties of demonstrating specific interactions with the intestinal mucosa. especially pathogenic ones.rating various toxins. mostly due to errors in husbandry and.enteritis with dehydration.serotype strains. Pasteurella.Epidemiology and Clinical Signs E. Enteroinvasive E. 2. Enterotoxigenic E. Enteropathogenic E.diarrhea and pyometra in dogs. Without immediate veterihemorrhagic colitis and have been asso.MMA-complex (metritis-mastitis-agalac. ciated with the hemolytic-uremic syn. coli (AEEC) produce verotoxins and destroy the have been described by various authors. These losses can reach 40%. The presence of E. and release endotoxins when dying.colibacillosis and colisepticemia in cam. . protein adhesions. but can cause di. K99 and others Pathogenic E.these strains cause the majority of ogenicity depends. Enterohemorrhagic E. coli due to at least 5 different varieties of bac.they produce enteric dis. coli-granulomatosis in fowl. coli (EPEC) do not endotoxin.they are responsible for colisepticemia sis or colisepticemia in young camelids. 0 = cell wall or somatic.capsular. gellar.nary intervention.inflammation of the urogenital and res.

coli serotype 083 from the fecal samples of the afflicted animals. coli. Death occurs within a few days. Some dromedaries developed CNS signs. 2 as EPEC and 1as VT2 pathotypes. The authors isolated E. Severe losses have occurred in certain breeding herds. (1998) who examined 42 one to 3-month-old dromedary calves in Sudan found 40% (12/42) infected with pathogenic E. anorexia and dehydration. only in animals between 2 and 4 weeks old. (1997 and 1998 a) isolated 69 (66%) E.. The camels showed severe swelling of the abdomen and a distention of the abdominal cavity. The affected animals develop a yellowish watery diarrhea. ears and forehead. coli was isolated from intestinal contents and from the abdominal fluid. The hemolytic E. Mohamed et al. fever. Chauhan et al. The hind legs and tail are covered with dried feces (Fig. coli infections in dromedary calves occur regularly every year in certain breeding herds in the UAE. Salih et al. which was filled with 100 to 150 liters of fluid. general malaise and anorexia. Colibacillosis develops mainly in undernourished crias. The incidence of the disease was more than 50% and the mortality rate approached 90%. coli (K88. coli infections in newborn dromedaries with severe diarrhea. A rare case of E. throat. coli dysentery appears to be associated with the initial con- sumption of solid food and sand. Hemolytic E. The calves suffer from dysentery abdominal pain. Neonatal colisepticemia is a serious disease in NWC in the USA followed by Figure 45 Colibacillosis in a 3-weekold dromedary calf with yellowish diarrhea . 1998). E. F41) out of 106 diarrheic camel calves with different adhesion factors. of which 5 were identified as EIEC. coli enterotoxemia due to a hemolytic E. Clinical signs have not as yet been seen in neonates. coli are isolated from the gastrointestinal tract and most of the organs. coli. serotype 0139 reportedly occurred in dromedaries in Bahrain (Ibrahim et al. coli infections in young NWC are an important ailment. Sporadic cases were observed in adult breeding camels at different camel centers.80 Bacterial Diseases contaminated water and inadequate feeding of colostrum cause the disease. Strauss (1991) and Fowler (1998) have remarked that E. 45) and the eyes are sunken deep in their orbital cavities due to the resulting dehydration. Rombol (1942) also described E. There was also edema of eyelids. (1986) reported colibacillosis in two dromedary calves presented with diarrhea. As in cases of clostridial enterotoxemia in young dromedaries. the E.

Method- Figure 46 Extreme pallor in a young dromedary with colisepticemia . In severe cases of colisepticemia. Haenichen and Wiesner (1995) also described colisepticemia in alpacas with severe meningitis. petechiae in the serous membranes and edema of the meninges are observed. Salmonellae and Coccidia. Young dromedaries develop a fever of between 40°C and 41°C. mesenteric lymph nodes and pieces of different organs. Death follows within 2 to 3 days. fever and yellowish diarrhea (Chauhan et al. coZi has no special nutritional requirements and grows on many different agars. The affected animals suffer from profuse diarrhea.. The disease occurs in calves up to 6 months of age. On autopsy. In camelids. Pathology Lit Colibacillosis and colisepticemia in camelids produce anorexia. there is an extreme pallor of the entire cadaver (Fig. At necropsy there is congestion of the small intestine with catarrhal enteritis. Specimens for bacteriology should consist of sections of intestinal tract. E. selective media are generally employed to differentiate them from other Enterobacteriaceae.46). Individual serotypes are found more frequently in certain species and in certain disease conditions. Colisepticemia often develops in animals suffering from enteric colibacillosis. abdominal distention and debility. mastitis and abscess formation.47). especially in compartment 1 (Fig. The contents of the gastrointestinal tract are gray colored with a pungent foul odor. coronavirus. In colisepticemia. a generalized congestion. but may also occur without any evidence of enteric involvement. weakness. 1985). However. In both enteric colibacillosis and colisepticemia lesions are non-specific. regularly varying amounts of sand in the compartments. weight loss. a fibrin exudate covers the abdominal organs (Fig. 48). coZi strains has just begun (Jin. 1987). The clinical characteristics of colibacillosis are similar to those manifested in infections caused by rotavirus. Al tissue saml ples should be collected asepticallysoon after death. The diagnosis therefore depends on microbiological examinations. the gut contents are gray to yellowish and the mesenteric lymph nodes are edematous. inflammation of the intestinal mucosa and. Camelids that are affected by enteric colibacillosis are dehydrated and their hindquarters and tails are soiled with feces caused by diarrhea. serotyping of cultured E.Digestive System 81 metritis.

It is also recommended to restrict milk intake. Colostrum banks should be established for emergency cases. initial ingestion of colostrum should occur within the first hours of life to maximize the absorption of immunoglobulins. coli dysentery ological procedures about the agglutination for the identification of various E. Oral or parenteral electrolytes must be administered to restore fluid balance because death usually results from dehydration. However. Figure 48 Colisepticemia in a young dromedary with fibrin exudate covering the internal organs . coli isolates possess multiple resistance to antibiotics. Before antibiotic therapy. Camelids with diarrhea caused by E . resistance testing should be performed on the E.82 Bacterial Diseases Figure47 Sand in compartment 1 in a young dromedary with E. but it should be kept in mind that many E. Colisepticemia must be treated with injectible antimicrobials like BaytriP. coli strain causing the outbreak. coli should follow the same regimen of treatment as mentioned under the chapter salmonellosis. coli antigens are provided by the commercial companies which produce the antisera. Treatment and Control .

Ovdienko et al. Fassi-Fehri (1987) and Buchnev et al. Mycobacterium avium spp. The incubation period is generally 18 to 24 months. M . Paratuberculosis is also seen in dromedaries. losses in young animals were greatly reduced. Due to intensive animal keeping. 1995) and in NWC (Appleby and Head. 1996). The authors believe that older camels may recover from the disease. paratuberculosis is excreted in the feces of infected animals and so can then be ingested with contaminated food or water. paratuberculosis. coli. 1956.2. 1957). The disease has also been diagnosed in Bactrian camels from Mongolia suffering from severe diarrhea (Guake et al. aerobic and oxidative bacterium which Epidemiology and Clinical Signs M. For this reason. Strogov (1957) and Buchnev et al. debilitation and eventually death.. goats. Etiology Mycobacterium avium spp. farmed deer and other domestic and wild ruminants. contagious enteritis and affects cattle.Digestive System trimethoprim/sulfonamide. sheep. 1995). avium spp. The disease can be diagnosed by the demonstration of the bacteria and by serological and allergic tests. maternal vaccination with herd-specific E. The disease produces a chronic. considerable losses can arise due to E . Belknap et al. (1987). In order to reduce losses among young dromedaries.3 Paratuberculosis (Johne’s Disease) This disease is characterized by persistent and progressive diarrhea.3 and 1. 1957). weight loss. (1985).. Strauss (1991) applied a protective maternal vaccination (Colivac@) twice to all pregnant camels about 8 and then 4 weeks prior to the calculated date of parturition. Schwarte. 83 1. does not take up dyes of the Gram stain because the cell wall is rich in lipids and mycolic acid. Ridge et al. M. paratuberculosis presents a serious economic problem. Not all infected animals become clinical cases. paratuberculosis enters the lymphatics through the tonsils and the intestinal mucosa. paratuberculosis is acid-fast and the best stain is ZiehlNeelsen. coli vaccines should be administered annually or oral vaccinations in young camelids should be tried. as reported by Ivanov and Skalinskii (1957).kanamycin or colistin (Manefield and Tinson. non-sporing. paratuberculosis is a non-motile. paratuberculosis is also able to cross the placenta to the fetus. Peyer’s patches take up the microorganisms from the intestinal lumen and transport them through the intestinal mucosa. A cell-mediated immune response appears to be involved in the pathogenesis of this disease. Following oral infection. The annual incidence of infection in Bactrian camels in Turkmenistan between 1946 and 1952 was between 0. but they remain excretors of M. avium spp. After that. (1987) reported that paratuberculosis is more prevalent in young Bactrians between weaning and 4 years of age. It has also been reported to occur in OWC (Wernery and Kaaden. avium spp. M . Paratuberculosis is one of the most important and widespread diseases of the Bactrian camel in the former Soviet bloc. In tropical areas with intensive dairy farming. avium spp. The bacteria spread to the intestinal mucosa or mesenteric lymph nodes where they can cause chronic inflammation. 1964) and has been known in Turkmenistan since 1949 (Strogov. Paratuberculosis occurs worldwide. avium spp. 1994. but is less prevalent than in Bactri- . paratuberculosis is shed in feces and the organisms are found within macrophages of the intestinal mucosa and adjacent lymph nodes. 1954.5% (Strogov. for example in animal parks and zoos.. Recovery of adult infected camels takes place slowly over a period of 6 months.

(1964). although additionally inflammation of the liver. Some lamoids develop weakness and weight loss as well as terminal diarrhea over a 3-month period and other llamas lose weight and become debilitated without developing any diarrhea. (1994) and Ridge et al.7g/dL. Amand (1974) described severe intestinal thickening and enlargement of the regional mesocolic lymph nodes. In NWC. spleen and lymph nodes has also been reported. weakness and emaciation. (1994) stated that dromedaries can contract paratuberculosis from cattle. Chauhan et al. mucoid. Death follows after 6 to 10 days in these cases. (1995). (1991) and in NWC by Belknap et al. cecum and colon. Of 105 dromedaries in India. Paratuberculosis was also found in one female dromedary in an American zoo (Amand. Radwan et al. Infected a i nmals die within 4 to 6 weeks after the initial occurrence of diarrhea. (1991) were the first to identify the disease in Saudi Arabia. with some animals developing severe diarrhea. the clinical signs of paratuberculosis vary.The dromedary was weak and emaciated and passed blood streaked. Histologically the lesions are characterized by a marked accumulation of macrophages in the mucosal layer that were laden with acid-fast bacilli (Fig.5 g/dL).. Gameel et al. Six- Figure 49 Acid-fast rods in macrophages of intestinal mucosa of a dromedary suffering from pa ratuberculosis . Pathology 1111 Pathological lesions of paratuberculosis were described in Bactrians by Strogov (1957). All clinically affected lamoids develop hypoproteinemia. The camel showed a marked hypoproteinemia (total protein: 2. However. Lesions have been observed in the ileum. normal is 5. 1995). Clumps of acidfast rods were detected in fecal samples. which may be used as a diagnostic tool as in sheep (Scott et al.7-7. in dromedaries by Amand (1974) and Radwan et al. 49). These dromedaries suffered from intractable diarrhea and acid-fast bacilli were identified in one animal upon biopsy of the rectal epithelium. loose stools. intradermal tests with Johnin and tuberculin were negative. At necropsy. Russian authors are of the opinion that paratuberculosis causes more pathological changes in Bactrian camels than in cattle.8%). (1986) found only four that had paratuberculosis (3. All four dromedaries had a positive skin test following the intradermal application of "Johnin". 1974).84 Bacterial Diseases an camels due to the conditions in which the dromedaries are kept. Ivanov and Skalinskii (1975) and Guake et al.

However. In another investigation. Seifert. from which M .Digestive System 85 ty cases of paratuberculosis were found among three dromedary herds consisting of 3000 animals. The lesions of paratuberculosis in lamoids are similar to those seen in OWC. Paratuberculosiscan be diagnosed by culture and allergic and serological tests. Histological sections of the lymph nodes contain numerous colonies of acid-fast staining bacteria. no acid-fast bacilli were isolated from the fecal samples taken from 600 reactive animals. In spite of antibiotic treatment. avium spp. Dependable serologicalresults in the detection of paratuberculosis have been obtained with the complement fixation test (Khon. Bacteriological culturing of feces is the most sensitive and specific test for M. examinationof feces will detect only about 25% of subclinical excretors. the animals died 1 to 4 months after the development of the initial clinical signs. paratuberculosis. The intestinal lymph nodes were greatly enlarged. but it can require up to 16 weeks to obtain the results. In some animals the jejunum. the intradermal injection of avian tuberculin produced a reaction in 40% of the Bactrian camels tested. cecal and colonic walls was seen upon autopsy. Acid-fast bacilli were found in the feces. avium spp. Intradermal testing with avian tuberculin or "Johnin" produced from M. The animals are emaciated. In Russia. However. the ileocecaljunction and the proximal large intestines are thickened and there are sometimes granulomatous lesions in liver. (1975) were able to detect an- Figure 50 Prominent Peyer's patch of a dromedary with paratuberculosis . no changes typical of paratuberculosis were identified at post mortem despite a strong test reaction in 7 Bactrian camels (Khon. A massive thickening of the ileal. paratuberculosis organisms. avium spp. 1983a). 1992). The dromedaries were between 2 and 4 years old and suffered from severe weight loss and chronic intermittent diarrhea. intestinesand the lymph nodes. paratuberculosis yields unsatisfactory results (Higgins. 50) and the mesenteric lymph nodes are edematous and enlarged. Biopsy specimens of intestinal mucosa and fecal smears stained by the ZN-stain usually yield characteristic clumps of M . Burgemeister et al. paratuberculosis is isolated. 1986). The animals did not develop fever. avium spp. 1983a and b. the Peyer's patches are prominent in the intestine (Fig. lung and lymphatics of the peritoneal serosa.

Radwan et al. The available vaccines are prepared from either a live or heat-killed strain of M. confirming the diagnosis. Five cases were diagnosed between 1987and 1993. The slants of Herrold’s medium are incubated at 37°C and examined for growth. Treatment and Control < No satisfactory treatment of paratuberculosis is known. Benzalkonium chloride (Zephiran) is used to decontaminate specimens and Herrold’s egg yolk medium with mycobactin is often used as culture medium. Feldmann et al. 5. Appropriate sanitary measures should be applied to prevent contamination of food. In many countries. 51). M. The animals suffered from intractable diarrhea. but they are of value when entire herds are screened. Complement-fixing antibodies (titers between 1:64 and 1:256) were found in the infected animals. camelid calves should be removed from their dams at birth and reared in a paratuberculosis-free environment. avium spp. Serological tests include CFT. 2. serological tests for paratuberculosison individual animals are often inconclusive. AGID and ELISA. 3. avium spp. Acid-fast bacilli were found in all five fecal samples (Fig. Control requires good sanitation and management. purutu- Figure 51 Acid-fast bacilli (ZiehCNeelsen stain) in a stool sample of a dromedary with paratuberculosis . Newly purchased camels should be examined for paratuberculosis. Nothing is known about their specificity and sensitivity in camelids. Vaccination should be considered.2%) dromedaries in 1 Tunisia. 4. Clinically suspected camels should be isolated until the disease is confirmed. sheep and goats. water and soil. All of the animals died in spite of antibiotic treatment within one year. However. (1991) suggested methods of eradicating the disease in dromedaries. They include the following recommendations: 1. All infected camels should be slaughtered and carcasses properly disposed. paratuberculosis can be differentiated from other mycobacteria by its mycobactin-dependence in culture. vaccines are used in cattle. Where possible. Sporadic cases of paratuberculosis have also been seen among racing dromedaries in the UAE. avium spp.86 Bacterial Diseases tibodies to M. and ponds and ditches should be fenced off. paratuberculosis in the sera of 1 of 52 (21. (1981) were also able to diagnose the disease serologically in Kenya. once a week for up to 16 weeks.

Shulaw.. H. Moran. and P. A case of suspected Johne’s disease in a llama (L. JAVMA206 (1):75-76. Johnson. Ellis.W. 1995. JAVMA 204: 1805-1808. K.V. Bruner.A. Path. Untersuchungen uber Vorkommen von Parasitosen.M. G. 6 (2): 487-495. Comp. Anderson. Proc. 1949.C. ovini. Leyk and R.B. bakteriellen und viralen Mektions- . However.R. 1994. Sci. Bisping.Z. L. Pisa 31: 65-72. R. Med. Burgemeister.W. Jaktar. and G. E. J. Accidental self-inoculation can result in severe reaction with synovitis and tendonitis. Prosperi. M. glama). Sansyzbaev. 1973.1998. W. Paratuberculosis. Verlag Paul Parey. Tulepbaev and A. Thompson and W. S.A.N. and O. Belknap. Salmonella infections of camel in Bikaner..P. Ann. E.R. Camels that have been vaccinated may develop severe granulomas of several centimeters in diameter at the inoculation site (Fig. 1974. 1954.L. caprini e dromedari delle Repubblita Democratica Somala. Ambwani. Fikri.B. camels with these local reactions have shown a detectable serological response.E. tech.: 150-153. 1990. Berlin and Hamburg. Cheyne. D.J.P.W. Vet. Salim. Idigane sulla presenza di porta- tori. G. Fac. 1975. Infectious diseases of camels 8 in the USSR. but does not eliminate infection. W. Univ. whereas camels without skin reactions were negative in the CFT (Cheyne. 52) causing camel owners to dislike this vaccine. Al Ah.B. D. El Mjyad. Goessler. N. nary Medicine. Int. 1998. Buchnev.. S. Radostits. Salmonella infections of domestic animals.R. Indian Vet. 1988. R.C. Andreani. Amtsberg. Touti and A.H. and A. Mycobacterium paratuberculosis infection in two llamas. 1995). di salmonelle trabovini.M.Digestive System Figure 52 Severe abscess formation 4 months after vaccination against paratuberculosis in a dromedary (ringworm lesions are also seen. J. Arush and A. Septicemicsalmonellosis in two llamas. Fac. Kennedy. Amer. Zoo Vet.. Epiz.W. J. 64: 52-53.sci. W. References Amand. L. 1978. Anderson. D.May 2-3.E. Gengouni. Salmonella infection in newborn dromedaries in Moroccan Sahara. 39 (1):53-63. Blood. Getzy. Berrada. UAE.. 7*h London: BailliPre Tindall. M. courtesy of Dr. Ann. Vaccination can be effective in reducing disease incidence. Head. Qatar) 87 berculosis and both vaccines seem to possess the same efficacy. Mycobacterium paratuberculosis in a dromedary camel. of Agric. Repenning and G.. Meeting on Camel Production and Future Perspectives. Veteried. 0 int. V. E. Colour atlas for the diagnosis of bacterial pathogens in animals. Strathe. Leipold. In general young animals less than one month of age are vaccinated. 1987. and K. Proc. R. Rev. Appleby. D. Cornell Vet. 50 (1):100-102. Ass.

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O. 1950. Hussein. and Impr. A. 1999. N.. Salmonella in slaughtered camels.M. A. S. Infectious Diseases of Camelids. Tobruk. U. Diop. Sc. Elm. Workshop on the young camel. Vet. nauchno-issled. 42.A.I.T. Wemery. Wernery. Ass.. Yassien..H.1990. M. Alma Ata 5: 29. Comparative study on salmonella serovars isolated from humans and camels in the United Arab Emirates.N.G. 1999.V. A. Salmonellosis in camel in Egypt. U.J.O. 257-343. hung.. Sinkovics. Dec. Kaaden. M. Workshop on the young camel. 1996.K. 1975. The incidence of salmonella infections in camels. Trud. Strogov. University Khartoum. and M. Diarrh6es du chamelon en Mauritanie: Rksultats d'enqu@teau cnerv. Quarzazate. Workshop on the young camel. Sci. 148 (5): 445-450. eksp. Publ. J. The incidence of bacterial infection in young camels with reference to Escherichia coli.M. Kane. 10-13.. Morocco. M and S. Paratuberculosis in camels. 77. Fac. 44 (2): 147-152. Workshop on the young camel.Escherichia cob. 40. Acta vet. Proc. Dia.Taleb. Pal'gov.L. Morocco. Bornstein.Inst. Faculty Vet. Int.A. In: H. Y. Nayel. Thesis. Zaied. 31 (2):75-79. Zaki. 20: 120-131. Hlth. Morocco. O. Sudan Vet. 1985. M.. Assoc. Berlin. Billah. H. Ali. 22 (21): 133-139. Mohamed. Wemery. 24-26 Oct. A. 1999. Int. and E. 1990. M. Predisposing factors in enterotoxemias of camels (Camelus dromedarius) caused by Clostridium perfringens type A. 41. 1-3 in Stuttgart. Pays trop. G. Me'd.. Strauss. Abuobeida and Y. Vet.. Colisepticemia in a camel calf. 24-26 Oct. Quantitative changes of clostridia in the intestine of early-weaned pigs diseased in Coli-enterotoxemia. Diallo. Fadlalla. Bornstein. 24-26. 23. Salih. 1991. Younan and R. The prevalence of salmonella infections in camels (Camelus dromedarius) in the United Arab Emirates. Saad. Donnees sur la pathologie du chamelon en Mauritanie. Morocco. 1956. R. 1991. Inst. Tagungsbericht: 80-83. Seifert. . Younan.S.M. Wilson and A. ve't. 7 t h con$ on meat industry. Ahmed 0. Rev. A case of neonatal camel colibacillosis. Libya. U. Blackwell Wissenschafts-Verlag.. G. Makarem. Br. Cairo University. H.A. S.90 Bacterial Diseases Selim. M. Wemery. Med.A. 24-26 Oct. and A. Sudan. and B. 1993. Isolation of salmonellae from camels in Sudan. 1999.-R. Abdelrahman. 1981. No title.. 1999.F. Quarzazate. Int. Camel Newsletter 12 (9): 55-59. C.M. 24-26 Oct. 1957. Egypt. Nov. Willinger. Schliesser: Handbuch der bakteriellen Infektionen bei Tieren. Arbeitstagung der Zootierarzte im deutschsprachigen Raum. Aetiological and epidemiological factors associated with camel calf diarrhoea. M. Thesis.E. A. Khartoum. Inter Con6 on Camel Prod.. 1995. M. Oct. Quarzazate. Algabara.. Workshop on the young camel. Int. U. 1992.A.C.M. Trudy vses. Quarzazate. IIXWardeh. Feinstein. A. and 0.A. Further reading Abubakr.S. Morocco. Blobel und Tr. of Vet. 1972.H. Vet. M. Diop and El Hacen 0. Quarzazate. Erkrankungen junger Neuweltkamele im Tierpark Berlin-Friedrichsfelde 11. Jena: VEB Gustav Fischer 3: pp. Int.

poor hygiene and inadequate management (Shah and Khan.3. it is not known if these agents are responsible for the disease. leukemia. dogs.occurs in many animal species including man. except in tuberculosis. The lesions are granulomas known as tubercles. soil and water. 1. Both have been isolated from OWC and NWC. non-motile and non-sporulating.1 Tuberculosis Tuberculosis is a chronic contagious disease caused by mycobacteria. 1990). 1987) as well as underlying debilitating conditions (Wemery and Kaaden. . tuberculosis and M .. paratuberculosis (see chapter 1. pigs. bovis has recently been isolated in 2 llamas in south Wales and the strain is identical with isolates causing TB in cattle. avium spp. canaries. However. tuberculosis did not occur in nomadic camels but in those belonging to . which affects many vertebrate animals and particularly manifests itself in lungs and lymph nodes. conservation agencies and veterinarians responsible for the health status of animals in zoos. tuberculosis affects humans.3) which causes bovine farcy. 1974). the atypical mycobacteria being grouped by Runyon..2.3). Badgers are considered to be a wildlife reservoir for TB and this increase in TB has been observed in cattle-keeping areas where badgers are common. horses. non-human primates. chronic skin infections and vitamin E/selenium deficiencies. Some of them may infect animals. bovis .) of the family Mycobacteriaceaeare acid-fast rods of various lengths. colibacillosis.3 Respiratory System riiiiiiu IIWI In general. bovis. M . Gatt Rutter and Mack (1963) reported that in Egypt. Many strains have become resistant to medication. The genus Mycobacterium contains multiple species (about 50) with different pathogenicity. it is usually initiated by predisposing factors such as a sudden change in weather. camels do not suffer from respiratory disease. The most important mycobacterial species causing disease in livestock are: . The atypical mycobacteria are widespread in pastures. .5. Pneumonia has been observed in association with endotoxicosis.M . it has caused more deaths in humans than all the wars together. . 1971. The two most important members of the genus Mycobacterium are M . The widespread outbreaks of M . One is the introduction of an infected animal into a non-infected herd (Bush et al. animal parks and private herds. Epidemiology and Clinical Signs A severe increase in tuberculosis (TB) has recently been observed in cattle in Britain. 1. However. 1935-1936. tuberculosis are of considerable concern to public health officials. There are different modes of spread of tuberculosis between camelid herds. when it occurs. Manefield and Tinson. and psittacines and has also been isolated from camelids (Elmossalamiet al.several serovars of the M . deer and badgers. farcinogenes (Nocardia farcinica? See chapter Dermatophilosis. The lesions differ greatly according to the animal species infected and the species of mycobacteria involved. 1995. Mustafa. These facts must be kept in mind when pneumonia is diagnosed in camelids. Etiology The genus Mycobacterium (M. wild birds. Tuberculosis in humans still remains one of the major global reportable diseases.1.M . avium complex occur in poultry. enterotoxemia. M . Osman.M . A number of bacterial specieshave been found in camels with respiratory disease. 1996).

Hayles Chauhan et al. Donchenko et al. Kibasov and Donchenko Donchenko and Donchenko Richard Arush Kennedy and Bush Chamoiseau et al. Mycobacterium bovis = Bovinus) Country Egypt India India India Sudan Egypt Egypt Egypt Germany Somalia Egypt Somalia Circus camel Russia Somalia Circus camel Russia Russia Russia India Egypt Egypt Russia Russia Russia Egypt Russia Russia Russia Russia Russia Ethiopia Somalia USA Mauritania USA Somalia India Mauritania Pakistan USA UAE USA Year 1888 1905 1908 1910 1910 1912 1917a. Humanus Atypica I Bovinus. Bush et al.92 Bacterial Diseases Table 21 Summary of literature regarding tuberculosis in OWC (Mycobacterium tuberculosis = Humanus. Casati Panebianco Abramov Angrisani Dekker and Van Der Schaaf Abramov Abramov Abramov Damodaran and Ramakrishnan Abd El-Aziz Elmossalami et al. Humanus Bovinus. Donchenko et al. Type Bovinus Bovinus Bovinus. Humanus Bovinus. Wernery and Kaaden Bush et al. b 1917 1918 1928 1942 1953 1957 1957 1962 1962 1962 1963 1964a 1964b 1969 1970 1971 1971 1972 1972 1974 1975a 1975b 1975c 1976 1978 1979 1982 1983 1985 1986 1986 1986 1989 1993 1977 (llamas) 1995 1990 (Bactrian) Author Littlewood Lingard Leese Leese Archibald Mason Mason Cross Mason Andree Pellegrin i El-Afifi et al. Humanus Bovinus. Fedchenko Akhundov et al. Fedchenko Osman Donchenko et al. Humanus Bovinus Bovinus Humanus Bovinus Bovinus. Diatchenko Rana et al. Thoen et al. Humanus Bovinus Bovinus Bovinus Bovinus .

Osman. The disease occurs more frequently when camels are kept in close quarters with other camels or in close contact with cattle. 1974). Other than unheated camel milk.7% 16. 1981). kansasii. M . Tuberculin tests were performed in these herds whereby 9. substantial economic losses can occur. Donchenko et al. 1971. Leese. venereal and cutaneous routes that may occur in cattle have not been described in camelids. kansasii M. (1975b) isolated M . There are only a few reports on tuberculosis in NWC. also plays an important role among nomadic people where milk and milk products are consumed raw (Seifert. The mode of transmission of tuberculosis is unknown in camelids. paratuberculosis have been isolated from NWC as well as some atypical mycobacteria (M. 2. Aerogenic transmissionby inhalation of the organisms in contaminated droplets from infected animals. 1962). of which 85 (93.. bovis (typus Bovinus) and atypical mycobacteria (Table 22) have been isolated from dromedaries (Elmossalami et al. 1974. Dekker and van der Schaaf. aquae M. where tuberculosis has received little attention. Donchenko et al. smeamatis 33. tuberculosis. Most of the publications regarding tuberculosis originate from these countries (Table 21).1% were reactive.7% 16. Table 22 Atypical mycobacteria isolated from dromedaries in Egypt M. especially in cattle..4%)belonged to typus Bovinus and 6. avium and M . 1957. avium spp. Tuberculosis.The 4 major mycobacteria. tuberculosis (typus Humanus). congenital. M.As can be seen in Table 21. 1971. It is believed that camelids suffering from pulmonary tuberculosis infect healthy animals via aerosols. 1888) and in India (Lingard. 1992). In cattle it is mainly horizontal. Castagnino Rosso et al. Cambre et al... Natural and experimental infections of tuberculosis have also been reported in NWC (Moro Sommo.7% Osman (1974) examined 120 lymph nodes that had been collected from slaughtered camels in 3 abattoirs in Egypt showing macroscopic lesions of tuberculosis. Tuberculosis is rare among camels kept under nomadic conditions. In 91 camel lymph nodes tubercle bacilli were found. 1975a and c). M . Alimentary transmission by ingestion of food contaminated with infected feces. bovis.This is also true for camel milk. In tropical animal husbandry there are two different routes of infection with tuberculosis: 1..7% 16. There were several occasions in North America where cervids and llamas were kept together. for example in Russia and Egypt (Mason. Kogramanov et al. tuberculosis to Bactrian camels. 1905. bovis strains from 46 pooled milk samples from 712 lactating camel cows in Russia. Tuberculosis is a disease that had already been diagnosed around the turn of the century in dromedaries in Egypt (Littlewood. 1957. The primary lesion is in the lung. fortuitum M. circus and zoo camels with active disease also present a danger to man (Panebianco. urine or milk.3% 16. The primary lesion is in the intestinal lymph nodes. Although many of the cervids developed tuberculosis. aquae var. It is believed that llamas are not particularly susceptible to tuberculosis. (1971) found that the Ixodes tick Hyalomma asiaticum can transmit M . 1908). M . In tropical developing countries. M. M . as a zoonosis. either directly or on dust particles. The alimentary.ResDiratorv Svstem 93 farmers who kept them in close contact with cattle.6% to typus Hu- manus. microti). Elmossalami et al. only two llamas in two herds . but it is presumed similar to that in cattle. ureolyticum M. 1917 a and b and 1918.

2% incidence rate. 53).94 Bacterial Diseases ~ contracted the disease developing diffuse granulomas. bovis was isolated. show animals. Bovine tuberculosis was described by Barlow et al. Mycobacterium tuberculosis and M . M. pack animals for trekking. 1977). Intradermal tuberculin testing. The authors showed that the M . UK) . bovis was cultured from eight llamas during a 5-year period at the Veterinary Service Laboratory in America (Thoen et al. and for guarding sheep. 1995). The literature contains reports of dromedary camels with positive responses to intradermal tuberculin testing that range from 1. Tuberculosis infections have been reported in llamas in South America and most infections occur when camelids live in close contact with other infected livestock or infected humans. Tuberculin testing in Bactrians in the USA resulted in a number of false positive reactions. bovis were seen in 10 to 20% of Australian dromedaries whereby no indicative lesions were found after the animals were slaughtered (Schillinger. (1999) in a small llama herd near the border of England and Wales. which is the classical diagnostic test. A. None of the tests available can diagnose tuberculosis with certainty. bovis isolate from the llama was the same type as that of isolates from cattle and badgers of this area. The bronchomediastinal lymph nodes were enlarged and also showed caseous foci (Fig. Barlow. avium and M . but only 68% of the camels with tuberculosis had positive tuberculin reactions (Abramov.9% reactors in India (Chauhan et al. 1978). A female llama that was in poor condition was necropsied and numerous caseous lesions were observed from which M. Several papers report non-specific skin reactions in OWC and NWC. These included pleura. Diagnosis 1 The diagnosis of camelid tuberculosis in living animals faces many difficulties. In a study of 874 Bactrian camels in Russia. 1986) to 37%in Kenya (Paling et al. lungs and pericardial sac. often gives nonspecific reactions in camelids. M . Positive tuberculin test results with M. bovis infections were diagnosed in guanacos in zoos and private herds in Germany (Haenichen and Wiesner. there were 107 cases of tuberculosis resulting in a 12. Llamas are being kept in increasing numbers in Europe as pets... although the lymphocyte stimulation test was also positive (Kennedy and Bush. Figure 53 Caseous foci in bronchomediastinal lymph nodes in a llama (courtesy of Dr. 1988). 1963).. At necropsy no tubercles were observed and no mycobacteria isolated.

because many camels showed positive skin reactions. who also unsuccessfully used the caudal tail fold for tuberculin testing in Bactrians.. However. Mycobacteria are slow-growing organisms that usually appear on culture media within 2 to 6 weeks. such as lymphocyte transformation and ELISA tests. trachea and many regional lymph nodes. For the isolation. In a small experiment. A program to control tuberculosis in camelids based only on intradermal tuberculin tests will face severe deficiencies. The tuberculin testing with old mammalian and avian tuberculin (MOT. He suggests that the base of the pinna may be the most suitable location for tuberculin testing. A definitive diagnosis of tuberculosis requires the culturing and specification of the organism. AOT. USA (Bush et al. but they still remain inadequate for the clinical application of this disease. have also not been very reliable in undomesticated mammals because of false-negative and false-positive reactions. bovis was diagnosed in 2 of 19 Bactrian camels in a herd of the National Zoological Park in Washington. liver. The common antigens shared with Nocardia and Corynebacteriae further negatively affected the specificity of these tests. 1990). M . the infected tissue is minced and decontaminated by treatment with alkali or acid. Tuberculosis caused by M . the axillary site was determined to be a sensitive site for the allergic tuberculin test. pancreas. the author injected avian and mammalian tuberculin intradermally into different sites in 12 llamas. This is also true for tuberculosis testing in camelids. it is recommended that several tests be used to aid in the diagnosis of tuberculosis in camelids (Fowler. The Mexican study concluded that the axillary site was sensitive in lamoids. . but the response was more diffuse and more difficult to interpret than the cervical area. It is obvious that OWC and NWC are susceptible to tuberculosis but this disease is very difficult to diagnose on clinical grounds. skin. but no clinical disease or indication of infection was discovered on post mortem examination. Simmons (1989) believes that one of the reasons for the non-specific reactions in llamas is that the skin of the neck of the llama is very tluck and resilient. Bush et al. 1998). One of the main reasons for false-positive or false-negative reactions is not the structural compounds of the camelids skin but the presence of atypical mycobacterial antigens that are common in camelids. which makes an accurate measurement very difficult. These camels were euthanized and disseminated pyogranulomatous lesions were observed in various organs. spleen. Several years later two Bactrians developed marked leucocytosis that persisted for 3 months despite broad-spectrum antibiotic therapy. bovis was isolated from these lesions. Cultural methods are as reliable as animal inoculation methods. A cervical tuberculin test using MOT. BPPD and APPD had been performed before euthanization with negative results. The ante mortem diagnosis of tuberculosis in lamoids also presents a challenge. In other experiments in North and South America. (1990). proved that 12 Bactrian camels showing a positive intradermal test possessed antibodies to atypical mycobacteria when tested with the ELISA and the fused rocket i m munoelectrophoresis. AOT) as well as with avian purified protein derivative (APPD) and bovine purified protein derivative (BPPD) were discontinued in this herd. Different agars like Loewenstein-Jensenor Ogawa media are used and some mycobacteria require enriched media for successful culturing. Other than the intradermal test. mesentery.Respiratory System 95 1987). The Bactrians were tuberculinized into the caudal tail fold and the cervical area. Considerable efforts have been undertaken in the development of serological tests for the diagnosis of tuberculosis. the ante mortem tests. including lung.

pleura and liver. bronchial and mediastinal lymph nodes. (1971) and Osman (1974).4mg/kg of pelleted feed. on Egyptian dromedaries especially. which was given ad libitum to Bactrian camels (Bush et al. and bovine tuberculosis has been eradicated due to large-scale campaigns. Similar changes in the organs of dromedaries have been described in India by Leese (1918). 1917. exhibiting severe leukopenia and thrombocytopenia. Tuberculosis in dromedaries is rare in the Emirates.96 Bacterial Diseases The studies by Mason (1912.5% phenol. Histopathological lesions are pyogranulomas with dense centers containing caseous remnants of neutrophils surrounded by epitheloid macrophages with few giant cells.000 dromedaries has been seen within a 15-year observation period. Differentiation of the tubercle bacilli was not performed. Miliary nodes on the surface of the lung and deep in the tissue have been observed. Only one case of pulmonary tuberculosis (Fig. Treatment and Control I tries tuberculosis is a reportable disease. several camels died.. However. most probably due to an overdose. The lesions primarily observed in the lymph nodes and lungs revealed a productive and proliferative response of fibrous tissue and few Langhan’s giant cells. The organs most frequently affected in the dromedary are the lungs. Application of the Ziehl-Neelsen staining technique to these sections reveals few acid-fast bacilli. Permission was sometimes granted to treat valuable zoo camelids with isoniazid at a dose of 2. kidney and spleen can also be affected. 1990). in Somalia by Pellegrini (1942) and in Egypt by Elmossalami et al. On infected properties. Figure 54 Pulmonary tuberculosis in a dromedary . 1918). 2% Lysol and 2. Tubercle bacilli have been isolated from these lesions that cause typical tuberculous lesions in the guinea pig and rabbit. Positive animals must be slaughtered. The trachea. The disseminated form of tuberculosis is rarely observed and the alimentary form has not yet been reported in camelids. 54) among 30. A program to control tuberculosis in camelids based on intradermal tuberculin tests is not possible. have provided information on pathological changes found in the disease. surfaces and utensils are disinfected with 3% formalin.

The bacteria are inhaled into the lungs in large numbers where they multiply after they have overwhelmed defense mechanisms. The authors described seven different forms of pneumonia (Table 23). chronic) Dromedary 50 (abattoir) Farrag et al. subacute. Nocardia farcinica?) Pseudotuberculosis Histoplasma caosulatum Nocardia asteroides Aspergillus and C. One useful method is to class@ according to the appearance or etiology of a particular pneumonia. Semushkin Buchnev et al 1994 1993 1983 India USA India endemic endemic 1968 . fungus or aspiration. Al Darraji and Wajid (1990) identified bacteria in 56% of the lungs of 220 slaughtered dromedaries in Iraq. Pneumonia can be caused by direct infection with viruses. Epidemiology. which has been done for pneumonias in camelids (Table 23). pyogenes Hem. as well as by toxins arriving hematogenously or by inhalation. C l i ni cal Signs a n d Pathol- ogy Various authors have reported changes in the inspected lungs of slaughtered dromedaries. transport. a sudden alteration in the normal nasal bacterial flora with a dramatic increase in one or more species is the trigger for a lung infection. (1990) examined 204 slaughtered dromedaries in Libya and found pathoanatomical changes in the lungs due to hydatid cysts and pneumonia in half of them. uiridans 20 5. mixing and overcrowding are also often considered predisposing factors.Respiratory System 97 1. 1953 . Abdel Rahim et al. Bhatia et al.Also a viral respiratory infection may act as precursor to bacterial pneumonia. There are several systems for classifying the various types of pneumonia.2 Pneumonia The most common respiratory disease is pneumonia. Table 23 Types oi ineumonia in camelids (except tuberculosis) Type of pneumonia Microorganisms isolated Streptothrix cameli (Actinomyces farcinicus.Mongolia 1987 Russia Catarrhal (Acute. In many pneumonias. enteritidis 2 Coliforms 16 Alcaligenes 22 faecalis Actinomyces pyogenes 2 Animal Cases species Dromedary 2 Authors Mason Leese Year Country 1919 Egypt 1927 Sudan Egypt Granulomatous Dromedary Llama Dromedary Bactrian Bactrian 2 1 1 Chandel and Kher Ching-Dong Chaw et al. Strepto12 cocci 16 Diphtheroids Str. Handling. bacteria. pyogenes Diplococcus Didococcus % 20 C. which is defined as an inflammation of the lungs.3.

Aerococcus viridans Klebsiella ozaenae Edwardsiella Y O Animal species Dromedary (abattoir) Dromedarv Cases 79 1 1 Authors Moallin and Zessin Abdurahman Vitovec and Vladic Bergin and Torenbeck Wernery et al. equi Spp. Ps.98 Bacterial Diseases Table 23 (cont. 1993 Pakistan 6 5 Dromedary 6 Al Darraji and Wajid Arora and KaIra Al Darraji and Waiid Al Darraji and Wajid Al Darraji and Wajid Al Darraji and Waiid Abdurahman 1990 1973 Iraq India Klebsiella pneumoniae Dromedary 2 Dromedary 6 Dromedary 83 Chronic nonsw wra t iv e Interstitial Lymphoid Chronic Droliferative Fibrosis (Si Iicosis) like MaediNisna 1990 India 1990 1990 India India Dromedary 6 Dromedary 7 Dromedary 11 (abattoir) 1990 India 1987 Somalia . pneumoniae St.. aeruoinosa Hem.Ethiopia Dromedary 20 (abattoir) Elmossalami and Ghawi 198 Unspecified (mixture of different types) Corynebacterium Staphylococcus Streptococcus E coli . Pseudomonas Proteus Klebsiella Bacillus Suppurative 21 30 12 5 Dromedary 63 8 (abattoir) 11 Rana et al. with puruleni bronchitis Necrotic Dromedary 15 (abattoir) Dromedary 4 1 Dromedary Epizootic 1991 Australia 1997 UAE Hemorrhagic 1997 . equi St. epidermidis Micrococcus roseus Micrococcus luteus Str. 1970 . aureus Micrococcus sp. Yiaezu et al.. Streptococci Staphylococcus Burkholderia pseudomallei it r . pyogenes Str.) Type of pneumonia Abscess Microorganisms isolated Staphylococcussp. Year Country 1990 Somalia 1987 1983 Somalia India Somalia Gautam et al.

It is therefore surprising that reports of respiratory diseases in the camel are rather rare. sweating and depression. Buchnev et al. Cough- . The correlation between the pathological findings and the organisms isolated is seen in Table 24. the same authors identified 9 different bacterial species of acute and chronic pneumonia. (1953) diagnosed a large number of cases of pneumonia in slaughtered dromedaries in Cairo. this disease was also known in Mongolia and was called "black lung" or "contagious cough. 2 to 3 months pass before they are slaughtered. Dromedaries that are slaughtered in Cairo must first endure long periods without food on the trek to the slaughterhouse. pathoanatomical changes in the lungs of the camel appear to occur frequently.. According to Semushkin (1968). As a rule.. Farrag et al. Etiologically. Staphylococcus and other bacteria in the pathoanatomically altered lungs in 6 (3%)of 200 slaughtered Somali dromedaries. Moallin and Zessin (1990) isolated Staphylococcus spp. Only a few scientists Table 24 Comparison between the bacterial flora and the pathological findings of 100 dromedary lungs Microorganisms Staphylococcus Corynebacteriurn Klebsiella Pseudomonas Staphylococcus Streptococcus Klebsiella Corynebacterium Escherichia Staphylococcus BaciIIus Proteus Bacillus Proteus Mycobacterium FrePathological quenw findinqs 7 8 2 5 6 7 2 5 3 6 2 4 1 3 2 Congestion Congestion Congestion Congestion Hepatization Hepatization Hepatization Hepatization Hepatization Bronchitis Bronchitis Pneumonicosis Pneumonicosis Hydatid cyst Tubercle nodule have reported cases of bacterial pneumonia or bronchopneumonia. Abdurahman (1987) found Pseudomonas spp. high fever and general illness. (1987) reported a septic pneumonia that they called "contagious cough". coli. In the histological examination of 50 lungs with pathoanatomical changes. One hundred dromedary lungs from Lahore and Faisalabad abattoirs were examined histologically and bacteriologcally. Upon arrival they are kept in dirty and unkempt stalls. the pulmonary changes arose from a pyogenic bronchitis that tended to spread into the pulmonary parenchyma. enlargement of lymph nodes. The disease was widespread but was not mentioned before 1920 (Amanzhulov et al. These stressful conditions presumably lead to the increased incidence of pneumonia among these dromedaries. and Ghawi (1978) isolated St. Such lowered resistance aggravated the illness. It is believed that starvation. heavy work and prolonged and exhausting journeys were responsible for this respiratory disease. Oinakhbaev (1965). Judging from slaughterhouse reports from various countries. It manifested itself as an acute catarrhal inflammation of mucous membranes of the upper respiratory tract and lungs. E. The causative agent was an encapsulated diplococcus that was fatal for guinea pigs. Once the disease became clinically evident. The authors believed that predisposing factors led to the disease development in these cases. described a cough outbreak when 5000 camels were moved from Mongolia into Kazakhstan. Pseudomonas aeruginosa and Citrobacterfreundii from the lungs of Somali dromedaries that were infiltrated with abscesses. Diplococci. the disease lasted for 1 to 2 months with fever. aureus and Klebsiella pneumoniae from pneumonic camel lungs in Egypt. 1929).Respiratory System 99 Vitovec and Vladik (1983) found lung abscesses in 15 slaughtered Somali dromedaries from which they isolated hemolytic Streptococci..

The animals exhibited a protracted course of the illness. has been described by Thedford and Johnson (1989). pyogenes from dromedaries (Thabet. Actinomyces lumue may also produce pneumonia with abscessation. loss of appetite. coli is the most common bacteria. Kame1 (1939) reported pneumococcal pneumonia in Egyptian dromedaries and Agab et al. equi from a sick dromedary during an epizootic outbreak in Ethiopia. viriduns.. 1993). The disease was highly contagious with high morbidity and low mortality. and a P-hemolytic Streptococcus also from dromedaries (Pal and Chandel. 1988. lacrimation. a septicemia caused by Str. Mahmoud et al. The authors failed to report the causative agent. The morbidity reached 30%.. zooepidemicus was also isolated from a septic peritonitis of a male Australian dromedary (Heller et al. (1997) who cultured Str. It had died from suffocation due to necrotic material completely blocking its nasal passages and frontal sinuses. zooepidemicus. (1970) described a pulmonary abscess in a 10-year-old dromedary encompassingnearly the entire right lung. Stress is often a predisposing factor in the disease. 1965). (1993) isolated a pathogenic Bacillus couguluns from a camel lung with pneumonia. pneumoniue and Str. but they have also been isolated from the lungs of clinically healthy camelids (Shigidi.A hemolytic Pneumococcus has been isolated from Bactrian camel lungs in the Gobi Desert (Oinakhbaev. Different authors have reported individual cases of pneumonia in the dromedary. dyspnea and purulent nasal discharge. "Alpaca fever".100 Bacterial Diseases ing became steadily worse with prolonged attacks and difficult breathing (Kuznetsov. during which time they were unfit for work thereby causing economic losses. Microscopically. 1973. Voikulesku. Ibrahim et al.. Streptococcal infections are also common in NWC. edema of the throat and supraorbital fossa. septicemic animals often develop pneumonia. The predominant clinical signs were fever. 1998) and several bacterial agents are involved. Upon necropsy the lungs revealed hemorrhages and thickened interlobular septae. (1998) cultured Str. Pneumonia is especially common in NWC neonates (Fowler. Gautam et al. It is assumed that donkeys were responsible for this outbreak. Arora and Kalra (1973) described cases of chronic bronchopneumonia in Indian dromedaries. 1994). This is the first report of the isolation of bacteria that causes equine strangles. 1998). 1993).. Klebsiellu pneumoniue and hemolytic Diplococci were isolated from the lungs of two dromedaries that died of bronchopneumonia. Of great importance is the report by Yigezu et al. equi spp. Str.Diatchenko (1989) compiled a summary of the literature of the different bacterial and viral respiratory diseases in the dromedary. E. cough. yet only a few camels died. Various streptococcal species have been isolated from NWC abscesses and septicemic enterococcus infections in adult llamas have also occurred (Burkhardt et al. 1963). As in other animal species (also in NWC calves). A llama which was euthanized due to severe dyspnea and cyanosis revealed necrotic pneumonia from which Nocurdiu usteroides was isolated. (1987) described lung silicosis in dromedaries in Somalia. zooepidemicus serotype 2 from the nasal cavities of a dromedary. The authors reported that the disease occurred only during the colder months and affected almost exclusively adult animals. In Bahrain. Str. 1989). Streptococcus species seem to play an important role in lung infections and other ailments. the lung contained multiple small scattered pyo- . Leese (1927) attributed some isolated cases of respiratory disease to pulmonary abscesses. Pathoanatomical changes in the lung of a young Sudanese dromedary with pseudoactinomycosis similar to tuberculosis were described by Mason (1919) and Hansen et al. Rana et al. 1962. Str.

1997). Six dromedaries died of this disease in two different outbreaks in Queensland. other Mycoplasma species have been cultivated from the respiratory tracts of healthy dromedaries. Walker (1921) was not able to elicit this pulmonary disease through the subcutaneous application of "virulent lymph. The significance of these results is unclear since the causative agent was not isolated. the authors urge great care in the treatment of dromedaries with pneumonia. Severe necrotic pneumonia was observed in all of the dead animals. though they have not provided any supporting scientific proof. spleen. The Australian authors are of the opinion that dromedaries living in damp climates appear especially susceptible to this disease. It is believed that the prolonged antibiotic administration that was given to this llama increased the likelihood of infection by the opportunistic Nocardia bacteria. Australia. This group includes Vedernikoff (1902) and Kowalevsky (1912) who supposedly have often observed respiratory CBPP among Bactrian camels in Kazakhstan. Gross pathological lesions revealed granulomas in the uterus and the trachea (Fig.Respiratory System granulomas filled with cellular debris. and that they play no role in the epizootiology of this disease. Paling et al. Melioidosis was also diagnosed in a 7-year-old female dromedary from the UAE that showed signs of wasting disease and severe emaciation before it died (Wernery et al. diaphragm (Fig. Samartsev and Arbuzov (1940). mycoides. Choy et al. (2000) reported that several dromedaries and alpacas which were brought to the Northern Territories of Australia have died from melioidosis. mycoides as a cause of pulmonary changes in the camel should therefore be interpreted with reservation. Refai (1992) was able to identify the following isolates from the anatomical sites given: 101 Mycoplasma arginini: nose lung mediastinal lymph nodes Acholeplasma laidlawii: respiratory tract nose Acholeplasma oculi: Of great significance are the reports by B e r s and forenbeeck (1991) andWerneG et al. Hutyra et al. the mediastinal lymph nodes (Fig. In Egypt. is of the opinion that dromedaries are most likely not susceptible to CBPP.55) and massive caseous necrosis of three quarters of the lungs (Fig. The visceral pleura of this llama was also altered. Bares (1968). Although it has not yet been possible to isolate M . liver and kidneys.56). (1946). Basic differences of opinion exist whether camels are susceptible to contagious bovine pleuropneumonia (CBPP) caused by Mycoplasma mycoides. All earlier publications implicating M . (1997). who reported finding very low (non-specific?) antibody titers using complement fixation against M . macrophages and neutrophils surrounded by a few multinucleated giant cells. 57). rnycoides from pulmonary pathoanatomical changes in camels. who were the first to diagnose melioidosis due to Burkholderia pseudomallei in dromedaries. 58). Curasson (1947) and Turner (1959) are of the opinion that camels are not susceptible to contagious bovine pleuropneumonia. As melioidosis is widespread among the Aborigines in Australia (Asche. mycoides in dromedary sera from Chad. However. those scientists who purport that camels are susceptible to this disease have not supplied any proof of their theory either. (1978) identified antibodies against contagious caprine pleuropneumonia (Mycoplasma strain F38) in 49% of the dromedary sera examined in Kenya. thickened by fibrinoserous material. This has also been reported by Davies (1946). .. 1991) and deaths due to Burkholderia pseudomallei have occurred in humans there. Most opponents believe that the proponents have confused pulmonary changes due to Pasteurella with those due to M .

922 camels. Pneumonia has been observed in dromedaries associated with the following diseases: . 1947). If pneumonia occurs. The results of the two studies are compared in Table 25. Samartsev and Arbuzov (1940) consider this disease to be of no significance in camels. The authors presume that this single case of melioidosis was caused by a very rainy season that occurred in 1997 in the UAE. it is usually in conjunction with systemic disease and not as an independent illness. but there was no evidence of the disease. mallei the animals developed characteristic nodules and ulcers in the nasal wall and in various organs 1 to 1 15 days p. (1987) investigated nasal swabs from 219 healthy Indian dromedaries. horses and giraffes is possible.102 Bacterial Diseases Figure 55 Melioidosis lesions in the trachea of a dromedary Figure 56 Melioidosis lesions in the lung of a dromedary Figure 57 Melioidosis lesions in the mediastinal lymph nodes of a dromedary Figure 58 Nodular melioidosis lesions on the diaphragm of a dromedary Histopathological investigations showed an acute necrotic caseous pneumonia (Fig. Transmission by contact to dromedaries. Pneumonia in dromedaries in the UAE is rare. Shigidi (1973) examined nasal swabs and bronchial lymph nodes from 64 slaughtered Sudanese dromedaries. This is most certainly a result of the adequate management of the racing and breeding herds implemented in the Emirates. When dromedaries were inoculated with B.i. Camelids are also susceptible to Burkholderia mallei (Curasson. but there are no records of natural glanders in camelids. and Chauhan et al.59) and a necrotic lymphangitis. Mass malleinisation and clinical observationwas carried out on 45.

0.2.7 er animals (lamb. colibacillosis. .5 Enterobacter spp. 2. 6. pneumonia in adult Neisseria spp. 4. 61).7 0.7 tritus are seen.7 Aspergillus spp.9 membranes in the alveoli (Fig.0 24.7 sis of the lungs as well as perinatal as4. omphalitis.6 thrombi.9 sociated with pneumonia. 1973 and Chauhan et al. Table 25 Bacteriological results o f nasal swabs and bronchial lymph nodes from Sudanese and Indian dromedaries (Shigidi. 3.1 2. hyaline Klebsiella pneumoniae 11. selenium and vitamin E deficiency.4 dromedary calves deserves special menStaphylococci tion. 1983). In addition to a severe dromedary (see 2.5 calves.5 26. This jority of these cases also develop pleuritis type of aspiration pneumonia due to the (Fig. monkey) and in humans 8. is observed only in conjunction with other diseases. 5. 60). hemolyticum As stated above.4) and with aspiration suppurative bronchopneumonia.5 dromedaries in the UAE. the compactness of the lungs is E. and is most probaActinomyces pyogenes 5. clostridial enterotoxemia.6 10. as in young animals. 1987) Bacteria Isolated Sudan n=64 % 30. Bronchopneumonia is improper application of medication is relaregularly associated with leucosis in the tively frequent.4 10. Histologically.2 India n=219 % Aerobic bacteria Hyaline membrane disease in premature Coagulase-negative 2. the maof oral medication given with a bottle.9 13. coli 1.7 phages due to fibrin exudation and cell deHemolytic Diplococci 3.Respiratoty System Figure 59 Lobularly chronic productive pneumonia in a dromedary caused by Burkholderia pseudomallei 103 1. hyaline membrane disease.. During autopsy of the dromedary Staphylococcus a ureus 2.1 Streptomyces phyxia. readily apparent. This disease is regularly asArcanobacterium 0. desquamation of alveolar macroB-hemolytic Streptococci 3. (Jones and Hunt.9 bly related to a hypofunction and atelectaa-hemolytic Streptococci 5. arterial Rhodococcusequi 8. The disease has been observed in othDiphtheroids 15. pyodermatitis.

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1986). Domenech et al. 1986. 1987. the majority of reports on brucellosis utilize serological methods of identification. Al-Ani et al. all three known Brucella species can cause infection in camels (Higgins. Especially OWC are frequently infected with brucellosis.. the prevalence is 3. which are non-motile and non-spore-forming. Extreme care must be exercised when working with Brucella organisms. I Epidemiology and Clinical Signs jc Brucellosis is characterized by abortion. Brucellosis in NWC is rare (Fowler. 1968)and 5. In developing countries. 1991. The incidence of brucellosis in camel populations appears to be related to breeding and husbandry practices (Richard. 1980) respectively. the growth of other Brucellae is enhanced by enriched media. The spread of brucella during sexual activity plays a subordinate role. In areas of extensive animal husbandry in the Sahel. however. whereby the causative agent then enters via the upper gastrointestinal tract. A survey of the prevalence of brucellosis in Africa was published by Chukwu (1985). sheep. but they are also able to grow on nutrient agar. 1964).. In countries with more extensive forms of husbandry. 1998). melitensis is widespread in Africa and the Middle East and B. camelids. brucellosis remains widespread in domesticated and wild animal populations and presents a great economic problem for tropical animal husbandry (Seifert. On tropical dairy farms the rate of infection can reach 80%. particularly when they are in contact with infected ruminants (Abo El-Hassan et al. abortus. Infections through the mucosa of the respiratory tract or the eyes are also possible.8% (Graber.1 Brucellosis Through intensive health control measures. Radwan et al. dogs.Brucellosis is also one of the most important zoonoses in the tropics. In humans. is 15% (Pal'gov and Zhulobovski.4 Urogenital System .4. Etiology Brucellosis is a contagious disease caused by the bacteria of the genus Brucella. 1998). However. The infection rate in some regions of the former USSR. Brucella bacteria are Gram-negative coccobacilli.1. 1980). pigs. Except for B. ovis and B. Madkow. Barsoum et al. 1. Theoretically. As can be seen in Table 26... 1992). (1992) and Ghoneim and . it is surmised that B. where Bactrian camels are kept on large farms. The disease has a worldwide distribution and affects cattle.. abortus is widespread in the former USSR. and occasionally horses. Similar differences in the seroprevalence have been reported from Saudi Arabia by Radwan et al. Humans are at risk through consumption of unheated milk (WHO/FAO. The infection occurs via the mucous membranes or skin or by ingestion of contaminated foodstuffs.. Kiel and Khan. goats. 1995. as in Chad or Ethiopia. the disease referred to as undulant fever or Malta fever is a serious public health problem. biotype 2. 1992. Solonitsyn (1949) reported mixed infections with various Brucella species in Bactrian camels in Russia. the rate of contamination has been estimated between 25 and 30% (Seifert. 1995).5% (Richard. 1989. which require media enriched with serum or blood. many industrialized countries have succeeded in eradicating brucellosis. . (1982) estimated the yearly losses in stock due to brucellosis to be 6%. Radwan et al. and to a lesser extent by orchitis and infection of the accessory sex glands in males. 1992).

9 10.0 8.3 3.4-12.6 10. 1. Baumann and Zessin Bishof Bornstein Bornstein Bornstein et al. .9 30.6 4.0 8.0 5.8 0 x X x x x x x x x x x x X x X X X x X X X X x x X x x X x X x X X X x X X x x x x x X X X Ethiopia Kenya x x x x x x X X Chad Tunisia Nigeria x X X X 10 .o 10.2 4.9 12.9 f 15.9 4.5-1 1.0 m 26. 4.0 32.0 6.3 23.0 f 30 .8 3.0-7. El-Nahas.0 6.3-7.3-1.0-1 1 . Elmi Domenech Richard Kagunya and Waiyaki Waghela et al.9-5. Nada Nada Zagloul and Kame1 Zaki Abbas et al.1 10 Bacterial Diseases Table 26 Summary of literature regarding the occurrence of antibodies t o Brucellae in OWC arranged by country Country Author Year Number of camels examined Prevalence % Serology R C S M B T F T x A T x X R T Egypt Abou-Zaid Ahmed Ayoub et al.5 4. El-Sawally et al.1 5. 0. 5 8 &.0-38. 1.5 24. Bares Graber Burgemeister et al.4 5.4 5.75 8. Abu Damir et al. Agab 1998 1939 1978 1964 1996 1982 1963 1984 1990 1985 1948 1987 1984 1993 1998 1978 1987 1971 1971 1987 1980 1982 1981 1990 1992 1979 1984 1988 1988 1982 1977 1980 1978 1978 1982 1968 1968 1975 1979 422 200 216 200 300 175 780 37 200 238 740 453 Sudan Agab Ali and Ghedi Bornstein and Musa Mustafa and Awad El-Karim Mustafa and Hassan Osman and Adlan Somalia Ahmed and lbrahim Andreani et al. Okoh 250 102 310 137 802 250 1039 47 234 514 977 762 174 172 543 316 52 and 150 milk samples 232 10. Wilson et al.1 m 2.0 2.3-14. Anonymous Baumann et al.4 59 . 14.8 31 . Hamada et al. 5.3 14.9 81 .6-10.5 13 . Fayed et al.3 3.75-5.

0 Monaolia Shumilov Libya Ben Faraj et al.8-5.1 1.0 14. Wernery and Wernery x x x X X x x X x x X X X x x x x x x x X Oman UAE 1995 1994 1998 1990 X X x x x x x x x RBT = rose bengal test CFT = complement fixation test SAT = serum agglutination test MRT = milk ring test m =male f =female * =see page 115 Amjad (1993). studies by Wernery and Wernery (1990) in the UAE have shown that the incidence of brucellosis among racing dromedaries not yet certified for breeding is three times higher than in breeding stock (2% compared to 6%). racing dromedaries are usually given non-pasteurized cow milk.Uroaenital Svstem Table 26 (cont.0 6.2 8.0 3. The opposite situation had been expected. Gameel et al.8 8. Al-Khalaf and El-Khaladi Harby and lsmaily Afzal and Sakkir Moustafa et al.8-3.76 0.5%) in contrast with nomadists (21. The authors surmise that this is due to inherent differences in feeding. In the Emirates.673 666 967 315 210 953 215 235 116 2630 2536 698 and 209 milk samples 550 392 racing 7899 196 breeding 348 racing 1.8 2. agropastoralistsreported a higher prevalence of brucellosis (31.0 8. Mathur and Bhargava Zowghi and Ebadi Al-Ani et al.0-17.) Country Author Year Number of camels examined 109 500 27 54.75 4.6 0. According to the system of camel husbandry in Sudan. Jawad Radwan et al. 1993 and 1998).O-3. India Iran Iraq Saudi Arabia Kuwait Kulshrestha et al. which is not given to breeding stock.7 3. Remarkably.3 15.5 8. Radwan et al.4%) (Agab.01 2.8 3.They reported a higher incidence of camel brucellosis in intensive farming than in free-grazing desert camels.0 3. Radwan et al.0 7.6 x x x x x Prevalence % R B T x Serology C S M * F A R T T T x X X 111 Niger Russia Bornarel and Akakpo Saley Pal’gov and Z h u lobovsky Solonitsvn 1982 1983 1964 1949 1974 1990 1993 1975 1979 1988 1998 1984 1983 1992 1995 1989 8. Various herds of cows were .

isolated B. Sharing this conviction. lymph nodes and hygromas of infected camelids from different countries. retained placenta and reduced milk yield as is common in cattle and sheep. Radwan et al. abortus from Bactrian camels in Russia.. vaginal swabs. melitensis.8% reactors. 1954 a and b. Interestingly. isolation of Brucella organisms from camel samples has proved less successful. The highest prevalence was in 1991 with 5. Infections may also cause stillborn calves. 1986. However. who examined a large camel herd with 2536 dromedaries in Saudi Arabia from which a 12% abortion rate and a Brucella seroprevalence of 8% were reported..biovar 1and 2 twenty six times from a total of 100 milk samples from seropositive Saudi Arabian dromedaries. B. (1995). melitensis. Zowghi and Ebadi (1988) cultured 3500 lymph nodes from 300 slaughtered dromedaries from Iran for Brucella organisms. In the herds examined. 2% of all animals aborted in the first half of the pregnancy.01%. The hematology parameters as well as the enzyme activity remained within normal limits. This may be a result of the difference in the placental attachment (Fowler. (1998) reported on a serological survey in dromedaries and a brucellosis eradication campaign in the eastern region of the UAE during a 5-year period. The results were negative. the authors were successful in isolating B. Pal'gov (1950) was able to isolate B. Although camels appear to be very susceptible to BruceIZa infection. 1981). Radwan et al. The authors are of the opinion that the B. During their investigations. 1995. biovar 1 five times from the milk of Libyan dromedaries and four times from aborted fetuses and a vaginal swab. Malta fever was diagnosed in 30% of the camel handlers and milkers and the same B. since camel milk is not pasteurized. as described by numerous authors (Ostrovidov. Both tests were negative. whereas the lowest was in 1996 with 0. Zaki (1943) both inoculated guinea pigs with milk samples from seropositive dromedaries and cultured the milk samples in vitro. B. seropositive racing dromedaries exhibited no reduction in performance during the racing season.. aborted fetuses. 1996). Brucella abortus biovars 1and 3 were isolated from camels in Senegal (Verger et al. Radwan et al. Gameel et al..1 12 Bacterial Diseases shown to have an incidence of brucellosis of Up to 40%. Fazil and Hofmann. Moustafa et al. According to various researchers. 1963. Retained placentas have not been described in Camelidae. abortus from the gastric fluids of five aborted fetuses. 1998). biovar 1 and 3 were isolated from these lymph nodes in 1%(3/300) of the camels. 2 and 3 from aborted camel fetuses. Fifteen percent of the herds were seropositive to brucellosis. melitensis have been isolated from milk. The samples were obtained from herds with an increased incidence of abortion. Fazil and Hofmann. This poses a severe health risk for man. whereby abortion is its most obvious manifestation (Acosta et al. Only recently have attempts at isolation of BruceZZa from milk been successful. Since no camels have been culled due to brucellosis. melitensis. 1979). melitensis. melitensis . 1972. 1981. it is believed that the reduction in camel brucellosis was caused by the reduction in brucellosis in sheep and goats. AlKhalaf and Al-Khaladi (1989) examined cultures of 209 milk samples from Kuwaiti dromedaries. biovars 1 . The lower incidence of infection in the breeding camel cows when compared to the racing dromedaries in the UAE indicates a spontaneous recovery among currently non-reproductive dromedaries. melitensis infections in the dromedaries originated from neighboring sheep and goat herds. brucellosis in breeding camelids occurs in all of the known forms. Gatt Rutter and Mack. WHO/FAO. Agab et al. (1993) were also able to isolate B. abortus and/or B. (1992) were able to isolate B.

1994.there was a moderate. The bacteria were re-isolated 45 to 65 days No lesions have been described so far in later from the cranial and genital lymph aborted camelids and in brucellosis-posinodes.organs for these bacteria are the pregnant ranging camels in eastern Sudan (Agab et uterus. which was then and bilateral lacrimation were observed. Hyinfected with B. slight lameness largement of the bursa. l.bacteria into the conjunctival sac.ine glands. 1996).. sheep and goats (Fowler. a vagnal swab and an sues.with reddening. 1972).tive camelid males. A three days p. udder. lympholy 30% of the 1449 alpacas tested had a pos. which showed follicular hyperpla.glands. from the placenta and all fetal specimens Brucellosis is not a major disease in as well from the dam’s mammary gland NWC. 1984).. but a severe B. but more conveniently . atrophy of medul. sera. abortus. The authors also observed an erature. 6 x lo6 drobursitis was often observed in brucelbacteria) developed only mild clinical losis-positive dromedaries causing an ensigns. They histories of abortion. edema and necrotic foci in ing that both isolates of B. Nada and Ahmed (1993) described inguinal lymph node in dromedaries with lesions in non-pregnant dromedaries. in llamas in the United States. Near.i.Urogenital System 113 biovars were cultured from aborted sheep Pathology Very little is known about the and goats sharing the same premises. testicle. biovar 3 was recovered from organisms in camelids. melitensis outbreak numerous lymph nodes. It is worth mention. melitensis was isolated curred between the Bursa ovarica and the twice from milk samples of seropositive ovary and in several cases also between camels in the UAE (Moustafa et al. The predilection 3 different specimens obtained from free. lymph nodes. multifocal... B.In an experimental infection trial ganisms (Gidlewski et a .increased number of ovariobursal adhely recovered B. abortus biovar the uterus epithelium. B. Lesions may be found in these tismary lymph node. 2000). from the placenta. the Bursa ovarica and the salpinges. pathological changes caused by Brucella B. filled with a clear amber-colored fluid. as well as fibrosis of 3 from Senegal and Sudan were the only the endometrium and atrophy of the uteroxidase-negativebiovars reported in the lit. 1998). presence of hygromas found inflammation of the uterus lining or testicular lesions. Reduced appetite. The adhesions ocan Indian camel. Brucella organisms can be recovered 1998). Fortylary cords and sinusoidal congestion. Agab et al. it was found that llamas are susceptible to B.tained abundant necrotic and mineralized ver. subacute placentitis itive plate agglutination titer. the llama aborted an eightmild interstitial hepatitis was also observed month-old fetus. A pregnant llama was sia of cortical and paracortical areas with infected by inoculating viable B. (1998) have recent. abortus was isolated (Abu Damir et al. accessory male sex al. causing Non-pregnant dromedaries artificially a severe induration of the latter.The Brucella or. Over 25% of with marked loss of trophoblastic epithethe alpaca handlers were seropositive to lial cells. and histological lesions similar to those milk or tissue or detection of antibodies in found in cattle. abortus (wild strain.bursae. The chorioallantoic stroma conbrucellosis and some developed Malta fe. abortus and Diagnosis :i: Brucellosis is usually diagthat they develop positive serologicaltiters nosed in the laboratory by culture of blood. joint capsules and ganisms were isolated from a supramam. abortus active germinal centers.cytic and histiocytic. Ramadan et al. It was felt that sheep were the source debris and the swollen capillaries were exof infection in this alpaca herd (Acosta et panded by large numbers of Brucella oral. melitensis from a hygroma of sions and hydrobursae... Histologically occurred in a herd of alpacas in Peru.

1996). trypanosomosis. 1996 believe that the Serum or tube agglutination test detects a higher percentage of reactors to brucellosis than other assays due to its greater sensitivity to IgM than IgG. Wernery. 1992). El-Sawaly et al. Wernery and Wernery. The absence of a visual positive reaction in low dilutions has also been observed in 1. or infections with Campylobacter or Trichomonas fetus (Wernery and Amjad Ali. 1978).Herd 1: 3751 head: CFT 4. It is known that false-positive (unspecific) reactions with various other bacterial species can occur (Bisping and Amtsberg. 1963.. In order to eliminate unspecific reactions in the serum agglutination test. It was concluded that the elimination of non-specific reactions to Brucella in camelid sera is essential for the correct diagnosis. Zhulobovski and Pal'gov (1954) observed prozones in some sera of Bactrian camels in Russia and Nada (1984) in dromedaries from Egypt. 1982. such as salmonellosis. 1992. 1989.This is true for both acute and chronic infections. the authors recently utilized a commercial brucellosis ELISA for cattle with good results. Fayed et al. In the serum agglutination test an end titer of 1:20 (40 I ) U was regarded as suspicious according to different researchers (Arbusov.. The labeled second antibody was produced in cooperation with the Institute for Medical Microbiology in Munich.. Salem et al. of which the tube agglutination test (TAT) using 5% NaCl phenolized solution must be included for the serological diagnosis of camelid brucellosis. The animals were immediately slaughtered. Yersinia enterocolitica. Other researchers have recently used ELISA for the detection of Brucella antibodies.6%.Herd 2: 54. Nada et al. Zhulabovski and Pal'gov. not only in camel sera (Azwai et al. 1970. No brucella organisms were isolated. 1998).. He examined two herds with the following results: . Pal'gov 1950. but also in camel milk (Straten et al. Sunaga et al.. Tserendash and Shumilov.3% and SAT 0.. difficulties may arise in the diagnosis of brucellosis. The camel milk ELISA seems to be an important alternative to the conventional serodiagnosis of camelid brucellosis. The Coombs test is necessary to verify the diagnosis of brucellosis in these cases. Wernery and Wernery (1990) utilized a 5% solution of phenol sodium chloride. but nowadays anticamel IgG is commercially available. In addition to this cross-reactivity with other bacteria that make the serological diagnosis of brucellosis more difficult.. Several researchers have evaluated the different serological tests for the diagnosis of camel brucellosis (Abo El-Hassan et al. (1983) reported that five dromedaries imported into Japan had positive complement fixation (CFT) and slow agglutination reactions. 1991. 1940. serotype 09 was identified. Pal'gov and Zhulobovski. He tested Bactrians in Mongolia where brucellosis is widespread among camels.0%. In an attempt to overcome the difficulties in the serological diagnosis of brucellosis in camel sera using traditional methods. However.. Abou Zaid. Waghela et al. It is also important to apply more than one test. 1993. 1964. Abou-Zaid.An incorrect diagnosis of brucellosis may occur when based on serology alone.673 head: CFT 3.114 Bacterial Diseases ~ in pure culture from the stomach and lungs of aborted fetuses. Abortion and reduced fertility in the camel frequently have other causes.. 1988). Shumilov (1974) determined that the CFT was four times more sensitive than the agglutination test. Ghoneim et al. however. 1996. 1998). Many authors regard the CFT as being the most sensitive and specific test for brucellosis (Gatt Rutter and Mack.5% of all positive dromedary sera in the UAE. Atwa (1997) and Abou Zaid . 1990. 1954. Ghazi. 1991. 1997). .7% and SAT 1.

6% and 95. the "test and slaughter" and "vaccination" policy is recommended. the classical neutral pH antigen has to be replaced by a buffered (pH 3. 1998). In addition to this parenteral treatment. the RBPT has to be used with serum-antigen at a 3:l dilution. All treated dromedaries also became negative within 16 months after treatment. (1997) established a MRT that can also be used to detect antibodies in camel milk. When using the CFT. He found that the RBPT and the CFT demonstrated equal ability in detecting positive and negative sera as well as prozone reactions. Using the TAT. The greatest danger comes from replacement animals. The authors used a combination of two tests to identify seropositive dromedaries the rose bengal test (RBT) and the standard United States of America buffered plate agglutination test. Seropositive animals should be slaughtered and the entire herd tested until all reactors are eliminated.. (1995) treated 202 seropositive dromedaries with a combination of oxytetracycline (25 mg/kg body weight) every 2 days for 30 days and streptomycin (25 mg/kg body weight) every 2 days for 16 days. The researchers named this test a modified MRT because Brucella-negative cow milk is added to the camel milk. The MRT results summarized in Table 26 should therefore be interpreted with great caution. 1997). This method should be implemented when the disease is serologically and bacteriologically confirmed. the standard test tube (STT)and the D-tec ELISA were less reliable for the detection of antibodies in comparison with the buffered acidified plate agglutination test (BAPAT). The authors adopted these tests due to their sensitivity.. However. abortus. camel milk cannot be used to detect lacteal brucellosis antibodies using the conventional milk ring test (MRT) because camel milk lacks the agglutinating substance required to cluster fat globules (Straten et al. the CFT. Mohammed (1996) evaluated the rose bengal plate test (RBPT). This regimen of treatment was effective in eliminating the shedding of Brucella organisms through milk. for optimal sensitivity. In Camelidae. Infected vaccinated animals remain a severe hazard to public health. the tube agglutination test (TAT). 115 . the authors successfullyeradicated the disease from the farm that caused 12% abortions. simplicity and applicability in the field. (1995) examined a large camel farm comprising 2536 dromedaries in Saudi Arabia for Brucella antibodies. Straten et al. With these two methods. and the complement fixation test (CFT) for the diagnosis of brucellosis in camels. as in other animals. After this procedure. the standard plate test (SPT) and the rivanol test (Fowler. a vaccination program may then be implemented to protect the entire herd from re-infection.5) antigen to achieve optimal results.Urogenital System (1998) found agreement between five different serological tests ranged between 80. the card test. During intensive investigations. Treatment and Control For the eradication of brucellosis in animals. milking camels received 10 mL oxytetracycline as intramammary infusions in each teat every 2 days for 8 days. In llamas experimentally infected with B. 1995).6%. Radwan et al. this will be achieved when two to three successive tests are negative. the 1:lO diluted sera have to be inactivated at 54°C for 30 minutes and the cold fixation technique has to be applied. it was found that on a camel farm in Saudi Arabia 34%of all Brucella-seropositivemilking dromedaries were Brucella shedders. Selective Brucella medium was found to be the optimal culture medium for the growth of Brucella organisms from fresh camel milk and camel tissue (Radwan et al. producing a typical colored creamy ring when antibodies to Brucella bacteria are present. Radwan et al. In contrast to cattle milk.

which could be improved up to 65% with corresponding improvements in management. The fertility rate of dromedaries in Saudi Arabia lies between 80 and 90% with only 1% permanent sterility (Arthur et al. abortus strain Buck 19 (Chichibabin. The majority of these bacteria are opportunistic. the long gestation period of 13 months. Mukasa-Mugerwa (1981) reported a dromedary fertility rate of only 50%. the fetuses possess an epidermal membrane and they exclusively develop left-horn pregnancies. All five camels seroconverted after one week and their antibodiesdeclined 6 to 7 weeks later. According to Wilson (1989). These special features were unknown for a long time and were discovered only during the last decade. however. In the last decades there has been intensive research undertaken to clarify the causes of uterine infections in the horse and cow and to identlfy a causal relationship between the bacteria isolated in the uterus and endometritis. the long interbirth interval (>24 months) and the early slaughter of breeding stock. trypanosomosis. In a large field study encompassing many Asian and African countries. In general. Cumelidue are very fertile animals. Further relevant information can be obtained through endometrial smear preparations and uterine biopsies (Ricketts. This is due to the late first pregnancy (at five years of age). Agab et al. However.1 16 Bacterial Diseases Both inactivated and attenuated Brucellu vaccines have been used successfully in OWC. tuberculosis.A third group from the UAE investigated the causes of uterine infections (Wernery and Kaaden. Intensive research has been carried out over the last 10 years on the reproductive physiology of Cumelidue. 1997). Nutritional deficiencies. melitensis Rev 1(Radwan et al. The camels tested negative 14 weeks later. After vaccination no further abortions were reported. His experimental dromedaries attained a fertility rate of 100%. which receded after 8 months in young stock and after 3 months in adult camels.. the dromedary birth rate under natural conditions is very low. Dromedaries were vaccinated with B.4. the reproductive biology presents some very important particularities not seen in other domesticated animal species.Yagil(l985)reported similar figures. such as uterine inflammation and discharge. 1999). Young dromedaries received a full dose of the vaccine and adults a reduced dosage. 1989). 1995). 1985). Bactrians and dromedaries produce fertile hybrids and NWC interbreed as well. Both groups developed Brucellu antibodies after vaccination.A comprehensive compilation of scientific papers concerning the reproductive tract of OWC has recently been gathered by Beil(l999). This was done on NWC by Fowler and Bravo (1998) and on dromedaries by two groups from the UAE (Skidmore. Tibari and Anouassi. ecto. only a few of these microorganisms are primarily pathogenic.they are induced ovulators. 1971) and with B. 1994. With advanced technology it is even possible to enter a completely new field the production of hybrids between OWC and NWC (Skidmore et al.and endoparasites as . It is therefore important to view all bacteriological results together with the clinical presentation of the genital tract.2 Infections of the Uterus In Camelidae. 1995). Camelids have a unique ovarian cycle . (1995) vaccinated five dromedaries with a reduced dose (5 x 108CFU in 2 mL) of B. abortus strain 19 (S 19)against brucellosis. 1.. he determined that only three calves are born per breeding female. although dromedaries are supposedly very fertile. A great number of bacterial species have been isolated from the equine and bovine uterus. when kept under conditions of intensive husbandry.. The author estimates a number of reasons for the low birth rate.

62). contrary to those found in horses and cattle. A variety of bacterial species have been isolated from the uterus of infertile camelids. the scientists from Dubai suggest following the bacterial classification for horse and cattle formulated by Ricketts (1981) and Arthur et al. More intensive studies of breeding dromedaries in the UAE have recently been performed by Wemery and Amjad Ai (1989). There were only a few reports on reproductive failure except for brucellosis in Bactrian camels. are the most commonly acquired reproductive failures resulting in infertility (Tibary and Anouassy. In addition to the classical venereal microorganisms Campylobacter fetus and Trichomonas fetus that cause sterility in dromedaries through endometritis. Wemery (1991) and Wemery l and Wernery (1992). These lesions are characterized by the presence of lymphoid granulomatous infiltrations of varying size (Fig. but it is often unclear whether they play an important role in primary uterine infections. In order to evaluate the role of various microorganisms in the development of uterine infections in dromedaries. Wernery (1991) was able to prove that the bacterial species isolated from the dromedary uterus are identical to those found in the mare and cow.Only a few scientists have examined uterine bacterial infections in Camelidae. Epidemiology and Pathology + Uterine infections in Camelidae. 1987).Urogenital System 117 well as recurrent endometritis can reduce fertility. 1997). Granulomas consisting of mononuclear cells have also been described in non-pregnant dromedaries by Nada and Ahmed (1993) and Tibary and Anouassi (1997). The UAE scientists were the first to isolate Campylobacter fetus and Trichomonas fetus from the uterus of sterile dromedaries suffering from endometritis. They primarily focus on dromedaries used for slaughter (no information on reproduction is available [Merkt et al.. with the exception of Taylorella equigenitalis and StrqrJtococcus zooepidemicus which were not isolated. These find- ings could be of major clinical implication and may be associated with a particular form of endometrial lesions seen in many biopsy samples taken from dromedaries with endometritis. as in other domesticated animal species. (1985) (Table 27). Actinomyces pyogenes also appears to play an important Figure 62 Lymphoid granulomas in the uterus of a barren dromedary (HE stain) .

The aborted fetuses showed in- flamed umbilical cords. Ali et al. coli (non-hemolytic) . Wernery (1991) - role in this disease (Nawito. Nawito (1973). 2 E.. The camels aborted after a 5 to 6-month pregnancy.Hassan (1990)..Pseudomonasaeruginosa (non-venereal strains) Heqazy e t al. Anthracoid organisms Wernery and Amjad Ali (1989) Nawito ( 973). A w a d et aI. Hegazy et al.Fusibacter sp.Hegazy e t al.118 Bacterial Diseases Table 27 Classification of bacteria and protozoa isolated and cultured from the equine and bovine genital tract juxtaposed with the microorganisms found in the genital tract of camels Venereal infections due t o bacteria and protozoa Horse. Zaki and Mousa (1965). Clostridium sporogenes 8.21.Nawito (1973). Klebsiella pneumoniae Awad et al. (1987).2. .Hassan (1990) - 7.Wernery and Amjad Ali (1989). Staphylococcus aureus Nawito (1973).Staphylococcus albus 3 E. (1983) 8. Wernery (1991) 4 Campylobacter fetus . brucellosis and glanders were excluded as the cause of abortion. Wernery 1 1 (1991) Hegazy e t al. Wernery and Amjad Ali ( 989). Streptococcus zooepidemicus Nawito (1973)?. 1973. (1987).Hassan (1990) (Capsule type 6.68) 6. (19831. (19781.Wernery and Amjad Ali (1989).Hassan (1990). Streptococcus pyogenes was isolated f r o m the aborted fetuses and their membranes.Awad et al. Eidarous et al. 5. 2. (1979). Actinomyces sp. (1978)? 1. (1983) 3.Wernery and Amjad Ali (1989). Proteus sp. Taylorella equigenitalis 2.Hegazy et at. 1992). Ali et al.Bacteroides fragilis 9.Enterobacter aeroqenes Contaminants and commensals 1 Enterococcus faecalis . (1979). (19791. Pal'gov (1950) observed abortions i n Bactrians i Kazakhstan over a 3-year perin od.Wernery Wernery (1991) and Amjad Ali (1989). Neisseria sp.Ali et al.Wernery (1991) Zaki and Mousa (1965). (1978).7. Pseudomonasaeruginosa (1990). (1987) 5. Wernery and Amjad Ali (1989) 5.Hassan 3.Wernery and Amjad Ali (1989). 6. 1978.5) Nawito (1973). Cattle Camel 1. (1979). 1979. Hegazy et al. (1987). (1979). Tuberculosis. (1978).Hegazy et al.Awad et al. Trichomonas fetus Wernery (1991) Non-specific bacteria in coniunction with endometritis Awad e t al. coli (hemolytic) . Al-Ani et al.. 4. Klebsiella pneumoniae (Capsule type 1.Wernery (1991) 4.Pseudomonas fluorescens 7.Eidarous et al.Eidarous et al.Ali et al. hemorrhages of the epicardium and enlarged spleens and livers. (1983). (1979).Eidarous et al.

S t ~ ~ h ~ l O ~ O ~ ~ ~ s 6x SPP. Staphylococcus aureus Streptococcus spp. Staphylococcus aureus Streptococcus spp. Powers et al. coli C. Aerobic Bacilli Diplococcus E. 1992) With endometritis Staphylococcus spp. l x . coli 6x . (1990) studied uterine infections in llamas. Table 29 Uterus pathology of llamas compared with cultural growth Grade of Uterus IA IB II A II B 111 A. successful diagnosis and treatment of infertility depends on the evaluation and interpretation of all results gained through vaginoscopy. The llama specimens were also classified on the basis of a grading system used for mare endometrial biopsies.E. B Uterus Patholow Normal Mild endometrial changes Few lymphocytes Minimal gland fibrosis Endometritis Endometritis Moderate to severe gland fibrosis Growth 2 No Growth 2 1 3 0 0 4 15 0 . as in equines and bovines. of which 21 had a culture-positive uterus. . the followingbacterial species were cultured: 7x 6x . In camelids. 119 To what extent opportunistic microorganisms are involved in the etiology of infection in the dromedary uterus has not yet been determined.mixed culture 9x - Actinomyces pyogenes . Serratia marcescens Without endometritis Staphylococcus spp. the inherent difficulties in the interpretation of the bacteriological results become apparent. the results of which are seen in Table 29. Aerobic Bacilli Diplococcus E.Fusobacterium necropherurn 1x .Streptococcus spp.Uroaenital Svstem Table 28 Microorganisms isolated from 98 infertile dromedary cows with and without endometritis Wernery and Wernery.Bacillus spp. uterine cytology and eventual biopsy. sporogenes Campylobacter fetus Pseudomonas aeruginosa K/ebsiella ozaenae Salmonella spp. When the bacteria isolated from dromedaries with and without endometritis are compared (Table 28). In 27 of the barren llamas. uterine culture. 3x . They examined 90 animals with fertility problems and discovered uterine infections in 45 (50%). Scientific interest has also turned to the NWC following the intensive study of OWC in the last few years. coli C sporogenes .Bacteroides spp.

Uterine infection should be suspected in any animal that has a history of repeated breeding. The restraint in crouching position is the only possible way to examine the animal in the field. 63). stained on Testsimplets slides (Boehringer Mannheim. Figure 64 Uterine smear from a dromedary with endometritis due t o Campylobacter fetus.120 Bacterial Diseases Figure 63 Uterine swabbing. the clitoral fossa and the urethral orifice were taken. Germany) . the dromedary is swabbed in standing position with i t s tail fixed upwards preventing it from crouching Diagnosis ’!l. CameZidae can be restrained in lateral recumbency or sternal crouching position or placed into a rectal palpation chute (Fig. Wernery (1991) followed the procedures used for the isolation of TuyZoreZZu equigenifulis in horses. In case of suspected endometritis swabs should be taken from the endometrium and cervix. Swabs of the endometrium. The vagina and the cervix orifice of the camel can be examined through a vaginal speculum and swab specimens can be obtained. Thorough examination of the reproductive tract of camelids requires restraint of the animal to avoid any injuries to the veterinarian or the animal. Evaluation of a female breeding camel should begin with a good history of her reproductive record. For research purposes.

clostridiosis. . Laila et al. Various infectious agents have been associated with abortion in camelids. parenteral ad- Table 30 The incidence of endometritis in slaughtered dromedaries Author Year Country Total Endometritis Percentage Nawito Hegazy et al.brucellosis. .. 1973. In the dromedary. a variable histological picture associated with stages of estrus cycle cannot be described.6 86.camelpox. So far no reports are available of uterine biopsies taken in connection with uterine cytology and uterine culture from living OWC. 25. The results of these investigations exclusively stem from slaughtered camels with no reproductive history (Table 30).0 74. 121 Histological investigations of the uterus have been performed on camelids by various scientists in connection with the follicular waves (Fowler and Bravo. Since camelids do not cycle as most animals. Beil. . Abortion rates in Camelidae are low.chlamydiosis.0% (24/96). However. from which a variety of different bacterial species have been isolated (Table 31).0 4.53% (94/2075). . 1992) who f o n d 4. Treatment and Control Treating camelid uterine infections follows the same protocol as for equines and bovines. In most of the cases. Histological changes of the uterus in connection with an endometritis have been reported by various scientists (Nawito... Fetaih Al-Ani et al.. 1987.leptospirosis. Hegazy et al. Fetaih. Bacillus cereus has been recently isolated from the placenta and different organs of an aborted fetus of a dromedary (Wernery et al.The fetal membranes revealed severe hemorrhagic necrotizing placentitis and edema. Al-Ani et al. no confirmed diagnosis was made. During recent years. 1998. Laila et al. The results from slaughtered camels show that they can suffer from different forms of metritis. 1991. The following diseases are considered responsible for abortions in OWC and NWC: .6% (97/130) and 4. no biopsies were taken to evaluate the extent of inflammation and duration of the endometrium.toxoplasmosis. 1973 1979 1987 1991 1992 Egypt Egypt Egypt Egypt Iraq 2075 96 130 78 50 94 24 97 67 2 4. abortion rates may range between 2% and 18%. Several diseases have also been implicated in abortions in camelids.53 25. bovine viral diarrhea. In a recent incident.Urogenital System The author also used cytological techniques to identify the presence of uterine infection (Fig. four alpacas aborted and Enterobacter cloacae and Klebsiella pneumoniae were isolated from different tissues (SAC. 1999). although in many cases a thorough investigation was carried out including testing for leptospirosis.0% (2/50) cases of endometritis in slaughtered camels from Egypt and Iraq. . enzootic abortion agent and toxoplasmosis. 86% (67/78). 64).0 . The treatment may be grouped into local application of drugs into the uterus. 1996).trypanosomosis. . 1979. but generally very little is known. 74. 1999). but their prevalence is unknown except for brucellosis. veterinary journals have published several small reports dealing with abortions in NWC outside their native countries.

0 (a501 ' 3 2 . coli Staphylococcus albus E. (1979) 25 Egypt (24196) Chronic catarrhal endometritis Fetaih (1991) Egypt Aerobic Bacilli Streptococcus epidermidis Staphylococcus aureus E. coli Proteus morgani Klebsiella pneumoniae Corynebacterium pyogenes Non-hemolytic 5treptococcus 25 (24196) 0. coli Hegazy et al. E.5 (31/2075) Staphylococcus aureus Staphylococcus albus Streptococcus spp. coli P-hemolytic Streptococcus 1. coli I Micrococcuspyogenes Staphylococcus aureus P-hemolytic Streptococcus E. (1979) Egypt Nawito (1973) Egypt E. Streptococcus epidermidis Staphylococcus a ureus Corynebacterium pyogenes 2 2 1I 1 2 2 1 1 1 3 3 Acute suppurative metritis Chronic nonsuppurative metritis Fetaih (1991) Egypt Fetaih (1991) Egypt Al-Ani et al. (1979) 25 Egypt (24196) Authors Fetaih (1991) Egypt Corynebacterium pyogenes Streptococcus epidermidis Staphylococcus aureus Aerobic Bacilli Streptococcus spp. coli Proteus morgani Alcaligenes faecalis Bacillus spp.24 (5/2075) 18 16 6 6 4 3 2 1 Hemorrhagic endometritis Hegazy et al. (1992) Iraq 4.122 Bacterial Diseases Table 31 The frequency o f bacterial isolates in different forms of metritis in dromedaries Metritis Bacterial isolates % of uteri with changes Fetaih (1991) Aerobic Bacilli Egypt Staphylococcus aureus P-hemolytic Streptococcus Streptococcus epidermidis Corynebacterium pyogenes E. Proteus morgani non-hemolytic Streptococcus E. coli Number of bacteria isolated 4 3 3 2 2 1 Acute suppurative endometritis Subacute suppurative endometritis 5 4 3 3 3 2 2 1 1 2 2 1 4 Catarrhal endometritis Nawito (1973) Egypt Hegazy et al.

Even after specific treatment following sensitivity .72 (15/2075) Laila et al. coli Aerobic Bacilli Pseudomonas aeruginosa Proteus morgani a-hemolytic Streptococcus 6 83. (1987) Egypt Pyometra plus macerated fetuses Chronic active metritis Nawito (1973) Egypt 0. E. coli Streatococcus eaidermidis Staphylococcus aureus Streptococcus epidermidis Streptococcus spp. This procedure should be repeated daily for 3 to 5 days until the uterine culture is negative. coli Staphylococcusalbus P-hemolytic Streptococcus Streptococcus epidermidis Streptococcus pyogenes Proteus Staphylococcus aureus Staphylococcus albus P-hemolytic Streptococcus E.3% 5 2 4 3 2 2 2 2 1 1 1 1 1 Necrotic Hegazy et al. the uterus should be massaged to reduce the volume of pus which must be drained through a catheter. In NWC up to a 100 mL and in OWC up to 1000 mL should be infused. Before applying any antibiotics. Parental administration of antibiotics may accompany the infusion procedures in severe uterine infections. In severe pyometra cases.Uroaenital Svstem Table 31 (cont. (1970) endometritis Egypt Hydrometritis Laila et al. (1987) Egypt Endometritis with abscessation Nawito (1973) Egypt 0.9 (39/2075) Laila et al. In order to achieve an optimal distribution of the medicine.3% 66. Antiseptic solutions such as Lotagen@at a dilution of 1 to 4 in physiological saline or phosphate buffer should be infused through an artificial insemination pipette. Local administration consists of uterine lavage or infusion with weak disinfectants and/or appropriate antibiotic solutions. non-hemolytic Streptococcus E. the uterus may be massaged per rectum. (1987) Fetaih (1991) Egypt Pseudomonas aeruginosa Staphylococcusaureus Streptococcus spp. before infusion of any drug. a sensitivity test should be performed on the isolated organisms. or both.6% 33.) Metritis Authors % of Bacterial isolates uteri with changes 123 Number of bacteria isolated 5 7 10 5 5 Pyometra Nawito (1973) Egypt 1. coli Sarcina Staphylococcus aureus 75% 25% 1 ministration.05 (1/2075) Corynebacterium E.

coli a-hemolytic Streptococci Treatment Enrofloxacin’ Furazolidonez Neomycin3 Furazolidone Chloramphenicol4 Furazolidone Furazolidone Neomyci n Ampicillin5 Furazolidone Furazolidone Furazolidone Neomycin Enrof loxacin Enrofloxacin Neomycin Neomycin Ampicillin Enrofloxacin Gentamicin6 Furazolidone Preanancv no no no no Yes Yes no no Yes Yes Yes no no Yes no no no no no no Suppliers: ’Bayer. 1999.4. ChZamydia psittaci is known to cause enzootic ovine abortion and epizootic bovine abortion (Beer. E. 4Antarres Vet. ‘jFarvet Lab. psittaci can affect the respiratory and the intestinal tracts. coli E. C. (1990) reported that 22 of the 36 llamas (67%) that were treated became pregnant. Products. Undiluted Lugol’s iodine may be employed as the last resort for severe uterine infections. The bacterial species isolated. psittaci affects various animal species and humans. The role of this bacterium in OWC is unknown. 1999). psittaci causes disease in NWC (Schroederet al.. While C.. coli Pseudomonasaeruginosa E. C. coli Aerobic bacilli E.. the nervous and reproductive system and the joints and eyes. coli E. coli E. SBristol. coli Staphylococcus spp. coli a-hemolytic Streptococci E. coli a-hemolytic Streptococci Staphylococcus spp. Powers et al.K. Goepner. coli E. The authors attained a 30% fertility rate following antibiotic treatment of the uterus in dromedary cows that had been infertile for 2 to 5 years. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 Bacteria isolated E coli . coli a-hem0 Iytic Streptococci E. treatment is not always successful. 2Smith Kline Beecham. . coli E. 1980). 1. trachomatis is mainly limited to humans. Goepner et al. the antibiotics used in the treatment and the success rate are summarized in Table 32.3 Chlamydiosis Chlamydiosis in livestock is caused by Chlamydia psittaci and is characterized by a variety of clinical syndromes. Diplococcus Streptococcus Aerobic bacil Ii E. Wernery and Kumar (1994) had less success in treating endometritis in dromedaries.124 Bacterial Diseases Table 32 Treatment and the resulting reproductive success in dromedaries with bacterial endometritis ______ No. However. a-hemolytic Streptococci E. However. the value of this treatment is controversial.. Holland testing. 3lntervet U. it is known that C. 1998.

and a suspected chlamydia1 pneuDifferent authors have identified antibodies monia were observed in one vicuiia in Gerto Chlamydiae in dromedaries. Genus 1: Chlamydia with species trachomafis. Chlamydia spp. Schmatz et al. Gram-negative. Sheep are usually infected by vaginal discharge containing Chlamydiae and through contact with aborted fetuses.Urogenital System 125 able to identdy antibodies against Chlamydia in racing (15. suis and muridarum and Genus 2: Chlamydophila with species psittaci. The authors are of the opinion that this organism does not have any influence on pregnancy in the dromedary since no increase in the abortion rate was observed in the herds studied. Burgemeister et al. keratoconjunctivitis.. Some of these animals then develop a subclinical intestinal infection. Germany (Goepner et al.. pneumoniae. Wemery and Wemery (1990) were tivitis. Eulenberger. Germany) . Chlamydiae are classified in the order I Rickeftsiales. iridocyclitis and uveitis (Fig. (1975) zig. They were also unable to identify any positive reactors using a Chlamydia ELISA (Abbott Laboratories) on the uterine swabs taken from 28 seropositive dromedaries. abortus. (1978) 1 % brought to the zoo. pecorum. Chlamydiae are intracellularbacteria. Dr. family Chlamydiaceae and two genera. 1999). keratoconjuncTunisia. order I1 Chlamydiules. while serovar 2 causes polyarthritis.7% dromedaries with a positive re.-induced abortion in one Transmission by arthropods is also possible. K. The outbreak was char1 in Egypt and Djegham (1988) 4. Figure 65 Keratoconjunctivitis in an alpaca with chlamydiosis (courtesy of Prof. caviae and felis. non-motile and they possess a unique development cycle. Serovar 1 causes abortions and genital and enteric infections. psittaci infection of dromedaries seems to be close occurs throughout the world. the source of Epidemiology and Pathology 1 C. alpaca. from the genital and respiratory tracts. The bacteria contact with sheep and goats. 1988). Giraud et al.disease was introduced by a male alpaca action in Tunisia.0%) dromedaries in the UAE. In the UAE. interstitial pneumonia and meningoencephalomyelitis.4% also in acterized by conjunctivitis. The found 7.0%) and breeding (24. 65). Isolates of C. Chlamydiosis was reported in al(1954) discovered two positive camels out pacas from a zoological garden in Leipof nine in Chad. psittaci from cattle and sheep are grouped into two main antigenic groups: serovars 1 and 2. polyserositis. with an inare shed in feces and other body discharges fection rate of up to 50%. many. whereby large numbers of organisms are excreted with the feces (Morgan et al.

Antigen ELISA. Some of the affected animals also develop torticollis. The complement fixation test was commonly used for the detection of antibodies to C. in certain breeding herds in the UAE.4. The histologicalexamination of the brain in the young dromedaries suffering from torticollis demonstrated intracerebral hemorrhages and perivascular cellular infiltrates that were infected with microorganisms. The calves affected no longer suckle. Popovici et al. An inactivated vaccine for sheep was used to control the disease. (1970) were the first to report on a Bedsonia (ChZumydia) outbreak in llamas in a zoo in Bucharest. However. Figure 66 Urinary retention in a 2-week-old dromedary calf . During the outbreak it was extremely important to I separate any sick animal from the healthy herd. Treatment and Control Tetracyclines and chloramphenicol are the most effective drugs for the treatment of chlamydiosis because they inhibit the multiplication of Chlamydiae. urinary retention without urethral obstruction is seen (Fig. recurrent urinary retention is seen in 2 4 week-old dromedaries. Of the 53 crias born in this zoo over a period of 12 years. 32 died from chlamydiosis. immunofluorescent and immunoperoxidase stainings are faster methods for the diagnosis of chlamydiosis. Upon autopsy. Young llamas died of encephalomyelitis. 1. 67). psitfacibut is now being replaced by an antibody ELISA. More recently molecular biological methods have been introduced. These lesions could be readily seen macroscopically and indicated the presence of an infectious encephalitis and meningitis. The healthy alpacas were vaccinated twice within 3 weeks and thereafter every 6 months. (1999) stated that treatment with antibiotics stopped the acute disease.4 Urinary Retention in Young Dromedaries Annually. Urine-filled cysts of varying size are found in the kidneys caused by the urinary reflux (Fig. Similar changes were seen in the meninges.126 Bacterial Diseases Many stillborn crias were born and several young animals developed arthritis. Diagnosis !mi Cultivation of Chlamydia organisms is possible in mouse brain. 66). but had no effect on chronic or arthritis cases. Goepner et al. embryonated hen’s eggs and in tissue culture. exhibit fever of up to 41°C and die within 4-6 days.

M. Med. gth Sci.. Pays trap.. It is not yet clear whether a causative relationship exists between the urinary retention and CNS pathology.A. Abo El-Hassan. 40 (3): 231-233. The cauda equina was examined in a number of dromedaries revealing a severe demyelination of the spinal cord and the afferent nerves (Fig. Cong.e.E.M. Rev.A. D. . Giza 39 (3):875-884.G.T. 68). Vet. 1998. copper). Yassin and A. A. Assiut University. Fac. References Abbas.Presumably the infection is secondary to a deficiency syndrome (i. 1991. Prevalence of camel brucellosis using different serological tests.M. Mammam. Vet.M. Abou-Zaid. T. H. 1987.A. Awad and S. Med. Youssef. Survey for certain zoonotic diseases in camels in the Sudan. S. Barsoum. Elzubir. J. Egypt: 690-707. Some studies on camel brucellosis. Sameh. B. vitamin B. M. Elev. Further studies are required to identify the cause of this disease in young dromedaries.Uroaenital Svstem Figure 67 Renal cysts in a 2-weekold dromedary calf secondary t o urinary retention 127 Figure 68 Severe demyelination of the cauda equina and afferent nerves in a 2-week-old dromedary Pseudomonas putidu was regularly isolated from these histopathological lesions. R. vit. Mid..

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Leptospiren. Blackwell Wissenschafts-Verlag. Rep. Trop. I.-R. Sci. Mid. 1943. U. Wernery. B38: 523-528. Gathuma and D. Sunaga.A. Rev. UAE. Y. 3 (2): 153. M. Grayon. Abu Dhabi. Sc. 1 (2): 85-87. Tierarztl. Ser. 1982. Snow and J.O. Brucella infection among ewes. Physiology. D. J. Japanese J. R. Proc. Pays trop. R. Wschr. Zhulobovski. Zagloul. Diagnosis of brucellosis in camels. Inst. . 96: 497-498.H.R. Comp. 1997. van M. Br.E. Mohamed and M. Pathology and Artificial Breeding. Fac. The barren camel with endometritis. Med.. Of. Camel Newsletter 12 (9): 27-28. 1978. and K.A.. Anim. Salim. 9 7 134-135. The diagnosis of Brucellosis in female camels (Camelus dromedarius) using the milk ring test and milk Elisa: A pilot study. Dolan. Veterinariya 1: 116-117. 42: 117-125.G. and 0. 1986. and Res. Cairo University. Mayhew. Isolation of Trichomonas fetus and different bacteria.J. and A.und X Enzootischen Bovinen Leukosevirus (EBL) bei Dromedarstuten (Camelus dromedarius). Theriogenology in camelidae. UK: 155-158. 1983. Vet. Wilson. Wilson. of Vet. Trud. vit. U. U. Wernery. Hlth. tieriirztl. The bacterial flora of the cervical canal.P. 1965. 1990. Yagoub. uterine horn and fallopian tubes in native cows and she-camels. Zaki. J. Mid. M. Epiz. and Amjad Ali. 8. Brucella abortus dorigine bovine au Senegal: identification et typage. Allen. U. Higgins. Solonitsyn. R. Rev. 1985. Haust. Verger. J. WHOIFAO.132 Bacterial Diseases New World camelids: Camelus dromedarius Lama guanicoe. 1990. Kumar. Tech.O. and Y. Geneva 740: 132. Wschr. Zaki. Mid. Verlag Karger. vit. 1988.. Medicine. tech. A. Yagil. Rev. Camel Prac. 1949. Proc. Path. 58: 145-151. Epidemiologische Aspekte bedeutender Kamelkrankheiten in ausgewahlten Gebieten Kenias. Tani and K. sci. Abu Dhabi Printing and Publishing Co.M. Basel. Incidence of brucellosis among farm animals in Assiut governorate. Rev. U. Wernery.L.S. Elev. A. 32 (1):25-32.. Wernery. U. Waghela. E. Field and D. Mina. Eds: W... 1996. Further reading Ahmed. Cooper. and B. 14: 117-122. Schwartz. Kamel. Ali. Shumilov. A serological survey of brucellosis in camels in north-eastern province of Kenya. 1985. and A. Fortpjl. 4 (2): 165-168. Camel Prac. Elev. Chlamydien. abortus antibody prevalence in the one humped camel (Camelus dromedarius) from Eastern Sudan. Detection of Yersinia enterocolitica infection in camels serodiagnosed as brucellosis.V. M. Wernery. Uterine infections in the dromedary camel. Vet. Med. 1979. H. R. Brucellosis in camels. Wernery. Reproductive disorders in dromedary camels due to infectious causes and its treatment. R. Kaaden.. Sagna.H. 1: 229-232. and J.K. Camel Prac. Tibary. Vet. Der praktische Tierarzt 11: 974-987.6th report of the expert committee on Brucellosis. 1948. vkt. SOC. Anouassi. C. Bacillus cereus abortion in a nine year old dromedary camel . 1954.J. 1991. Ebadi. 1970. Pays trop. K. Newmarket. and R. J. 7 (2):383-386. Palgov.H. and Mousa. abortus infection in buffaloes.N. M. 1997. camels and pigs in Egypt. Tserendash. Elev. A. S. Wernery. F. Camel Conf. Brucellosis in camels in Iran. Isolation of the organism from milk.M. A.V.F. J. J. J. Fazil. I. Assiut Vet. LA. BVD/MD. Berlin. Infectious Diseases of Camelids. Wade: R. Alma-Ata 6 17. int. Z. C. Mukai. 45 (2):247-250. 1996.T. The Desert Camel. Reproductive performance of the one humped camel. Kagunya. Serology survey for Br. B 266: 649-656.A case report. J. Pays trop.J. and W. and Res. IBR/IPV . Wernery. Prod. Roettcher. 1989. 10 (1):28-29. Bacterial infertility in camels (Camelus dromedarius). Anatomy. A. R. Some studies on post partum period in the she camels. Straten. Dtsch. U. No Title. The empirical base. Bercovich and Zia-Ur-Rahman. M. Publications.R. 1989. lStInt. 1995. 1992. Zowghi. and Res. Lond. VeterinariyaMoscow 26 (6): 16-20. Zaki. and R. Wernery. Dtsch. M. Isolation of Campylobacter fetus. Doutre and F.A. 43 (2): 167-171. 1994. ewes and camels. A review. Seroepidemiologische Untersuchungen zum Nachweis von Antikorpern gegen Brucellen. M. and A. Thesis.

Pal'gov. Dalafalla. Hamid. Planchenault and J. Vet.B. D. Inst. Osman. Rev. Vet. camels. M. M.X. Med. Dis. 9: 115-117.A. Investigacion preliminar de la brucelosis en alpacas.O. Thesis in Veterinary Science.. M. 1988. Centre . 10: 211-217. goats and sheep in the Sudan. Wang. Marafic.F. University of Khartoum. Lima 12: 135-137. Arshad. Zakia. Fayza. The occurrence. A.M. J. Epiz. Elhag. Wang. Survey of brucellosis among cattle. with emphasis on Brucellosis. I. Halima.A.. Y. 1958. J. El Sheikh. and A. Epidemiology of camel diseases in eastern Sudan. 1993.. D.Est. Chen. M. Richard. Suliman and A.C. A.M. Vet. Faculty of Veterinary Science. Med. 6 243-247.B. Production cameline . Moro Sommo. Rhyan. B a n g and Z. Y. Streptococcal abortion in camels.D. Pathol. A. Bull. Proc. A serological survey of camel brucellosis. 3 7 77-82. Aj?. 6 234-240. A. 9: 36-40. 1 : 8-9. Dis. Res. Miller and M. K.. and Vet. 1986. Experimental Brucella abortus induced abortions in a llama: pathologic effects. Project de D6veloppement de l'6levage dans le Niger. Sero-surveillance of brucellosis. Sudan 1. Pakistan Vet. 1988. IEMVT. Qinghai J Anim Sci b Vet Med.Anim.L.H. Mousa. 2000. A. . L.M.Rapport final. N.. O.N. E. Gilsdorf. Khan. Giovannetti. Sudan: 184.J. The nature of human brucellosis in Kuwait: Study of 379 cases. Vet. Khogali and A. Ahmad and A.F. Gidlewski. H. 1985. Yie. 1989-1990.Uroaenital Svstem 133 Ajmal. 1954. Special Issue on Camel: 87-89.S. T. 1989. Rev. Cheville..O.N. Fac. of Kazakh Res. 1957.D. J. Sci. M. Infect. Comparison of four serological tests in diagnosis of camel brucellosis. GansuJ. H. epidemiology and control of animal brucellosis in the Sudan..

5. In smears made from abscesses. are affected (Manefield and Tinson. but can also injure the mucous membranes of the oral cavity. A multiplicity of skin diseases has been described and there are confusing reports regarding their presentation and etiology. Etiology + The French veterinarian Nocard first described Coynebacterium pseudotuberculosis in 1888.1 Pseudotuberculosis (Caseous Lymphadenitis) Pseudotuberculosisin sheep and goats occurs worldwide. 1984 a and b. Gram-positive rod almost resembling a coccus. hepatitis. 1991). ActinobaciZZus Zignieresi (Daneji et al.C. The severe allergic reaction accompanied by swelling that many camels exhibit following the subcutaneous application of certain medications must also be considered (Schwartz and Dioli.. irregular ovoid. 1991). cervical. the bacteria show a marked pleomorphism. The minor bacterial skin infections are caused by Coynebacterium pyogenes. However. Nocardia asteroides. Many reports do not mention whether the bacteriological samples were obtained from a closed or open abscess or from wounds. Pseudotuberculosis is widespread in OWC and the organism has also been isolated from abscesses in alpacas (Barsallo et al. superficial lymph nodes and musculature frequently observed in camels are most likely due to the animals' preference for the leaves and small branches of the thorny acacia. may be confused with abscesses (Bergin. 1. 1996). It is a short. Eighty percent of Australian feral camels. Streptococcus spp. abscesses of the cranial. arthritis. there is no doubt that Tylopodae in general tend to develop abscesses (Straws. which browse on sharp thorns and branches. As mentioned earlier.. They include pseudotuberculosis. viral and mycotic pathogens. It is theoretically possible that parasitic cysts. mastitis. thoracic and popliteal lymph nodes are seen without noticeable superficial injury. the following chapters particularly deal with skin diseases that are of economic importance in camelids. camels are very sensitive to oil-based vaccines (see Fig. It sometimes also causes pneumonia. C. coli. It is characterized by abscessation of one or more lymph nodes. E. Lindsay and Lloyd. The abscesses in the subdermis. 1986). However.. The long thorns (up to 5 cm) not only penetrate the skin and cause deep-seated infections. for example due to Onchocerca fasciata.The general opinion that wound healing in camels is slower than in other mammals is not true. 1992). StaphyZococcus aureus dermatitis and dermatophilosis. and Fusobacterium necropherum. Greenwood. pseudotubercuZosis also affects horses and produces an ulcerative lymphangitis in cattle. Lloyd et al. 21). Infectious skin diseases in camelids are caused by many different bacterial. 1996). orchitis and subcutaneousabscesses. For routine isolation. pseudotuberculosis colonies are small. white and dry and . 1990. Such injuries are more frequent in free-grazing breeding and racing dromedaries than in racing dromedaries that are kept in the paddock the entire year. 1987. Frequently.. Purohit and Chouhan (1992) determined that camel skin is well vascularized with good wound healing. It is a chronic disease caused by Coynebacterium pseudotuberculosis (ovis) (Behrens. 1991). sheep or ox blood is used and the plates should be incubated at 37°C for at least 48 h.

C.. Ismail et al. Dominic et al. (1966) purport that Histoplusmu furciminosum is responsible for an outbreak of pseudotuberculosis among Bactrian camels in the Soviet Union. renule. Shigella spp. play essential roles in the development of caseous lymphadenitis. In contrast to pseudotuberculosis in sheep and goats. pseudotuberculosis outbreak in 21 dromedaries in 6 Egyptian villages that also affected cattle and buffalo. (1977) were able to isolate the following bacterial species in Ethiopian dromedaries: I 135 Streptococcus 57% (Lancefield Group B) . There was a generalized lymphadenopathy without abscess formation in the lymph nodes. The isolation of C. El-Sergany et al. Guinea pigs that were injected intraperitoneally with cultures of C. pseudotuberculosis.strain sheep/goat and strain horse/cattle. At least two toxins. (1985) believe that Actinomyces pyogenes is of similar importance in the pathogenesis of pseudotuberculosis as C. 1985). For example. and E.. The disease occurred in 1958 when camels were walked from Central Asia to several farms near Moscow. C. 1989). 1959. Wernery and Kaaden. 10% . two distinct strains have been identified .C.lnteaument can be surrounded by a narrow zone of hemolysis. UAE (Tarek and AbuBakr. the chest and the external lymph nodes. pseudotuberculosis was not isolated in 15%of infected goats showing typical lesions (Lindsay and Lloyd. Refai. Serologically. 1976). Epidemiology 1 Camel pseudotuberculosis has been observed in Iran (Esterabadi et al.China (Chen et al. pseudotuberculosis from abscesses poses certain difficulties as the colonies resemble streptococcal colonies and are frequently overgrown by accompanying bacteria. Mycelium and Cryptococcuslike organisms were detected in the draining lymph nodes. Only the first strain has been found in camels. At least two toxins are produced by the organism and may vary between strains. 1990. McGrane and Higgins. 1992). Sadykov and Dadabaev. The lesions were observed in the pre-shoulder lymph nodes. C. 1985. 1986). C. The authors also reported abscess formation in the musculature and subdermis over the neck. Hoste et al.. The toxic cell-wall lipid is associated with the virulence of the bacterium and the hemolysin causes hemorrhages.C. equi. pseudotuberculosis. The infection is spread via ingestion. 1992). pseudotuberculosis. pyogenes 6. 1991). inhalation or directly through wounds in sheep and goats. (1985) reported a C. (1989) were also able to isolate Stuphylococcus uureus.. 1995) and East Africa (Dioli and Stimmelmayer. pseudotuberculosis 37”/0 . pseudotuberculosisdied 3 weeks later with multiple abscesses. 1975). 1934. Ethiopia (Domenech et al. Cryptococci were also observed in macrophages. 1991.7% - Apart from C. Saudi Arabia (Radwan et al. Radwan et al.stuphylococcus spp. pseudotuberculosis is a pyogenic. 1984). The primary manifestation was edema of the elbows. facultative intracellular bacterium. 1985).Australia (Bergin. This was associated with a bloody exudate. C. a toxic cell-wall lipid and a hemolysin.India (Purohit et al. 1977. Kenya (Bergin. increased vascular permeability and enhanced bacterial invasion. C. tail and joints.. Russia (Spesivtseva and Nosko. The afflicted animals concurrently suffered a severe infestation of ticks (Hyulomma) from which the authors were able to isolate C. Hoste et al. coli in 15%of 2500 dromedaries in Saudi Arabia. Spesivtseva and Nosko (1959) and Dalling et al. pseudotuberculosis is not always the only bacteria isolated from the abscesses in camels. Egypt (Caprano. pseudotuberculosis alone was isolated from the non-ulcerative lymph . The authors also reported ulceration of some of the lymph nodes... 1986). It penetrates the tissue and produces filterable toxins.

After 40 days. Following its entry through the skin or mucous membrane. If opened. (1996) observed multiple abscess formation in camels experimentally infected with C. Clinical Signs and Pathology The incubation period of C. The lymph nodes released a thick. Afzal et al. Re-infection of the experimentally infected dromedaries after they had recovered from the disease did not produce any lesions. pseudotuberculosis. The mucous membranes of the oral cavity might be damaged by acacia thorns and/or by dry and hard stems from desert plants. Abou-Zaid et al. 1987. However. 1966. (1996) isolated pure cultures of C. Extensive caseous necrosis in lymph nodes and other organs (especially lung) develop in sheep and goats. from the rest. The microscopic lesions described by Nashed and Mahmoud (1987) consist of caseous necroses of the lymph nodes with a lymphoid and epitheloid reaction. pseudotuberculosis bacteria are then transported via the afferent lymphatics to the regional lymph nodes in which lesions may develop.. pseudotuberculosis ovis was isolated in pure culture from 62. Most abscesses are enveloped by well-developed connective tissue capsules.136 Bacterial Diseases nodes. secondary infection with coccal organisms can be expected. especially at the base of the neck and in the prescapular lymph nodes (Schwartz et al. (1994) detected lymphadenitis in 10.. there is some confusion whether the samples were obtained from closed or open abscesses. closed.. C. Skin lesions caused by acacia thorns. Camels infected with the sheep strain and the dermonecrotic isolate produced lymph node swelling only. Giant . 1989). Six of the camel isolates and a sheep strain used as control produced necrosis of rabbit skin and redness. In an experiment. caseated creamy pus and/or calcified material. the abscess extrudes thick. pseudotuberculosis and Staphylococcus uureus were isolated from the ulcerations. The generalized cutaneous form is also seldom observed (Dalling et al. contaminated injection needles and nodular worms may inadvertently result in damage to the skin and thus create portals of entry for Corynebucteriu. A few cases have been seen in dromedaries whereby the abscessesbreak through the ribs and the organism enters the lung. These pathological changes have never been described in camelids. The affected adult camels revealed enlargement and abscess formation in the superficial lymph nodes.9% (37/339) dromedaries from Egypt. though C. In comparison. Nashed and Mahmoud. 1987). 70). yellow cream-like pus. pathological changes in the internal organs due to C. whereas the strain without dermonecrosis produced multiple abscesses in the experimental camels 40 days after infection. pseudotuberculosis abscesses ranges from 25 to 40 days in sheep and goats.1% cases and associated with Staphylococcus uureus and Streptococcus spp. In most cases a concentrically lamellated (onion ring) pattern of the abscess develops in sheep and goats (Behrens. one of each isolate (with and without dermonecrosis and the sheep strain) was inoculated into the base of the ear of experimental camels. pseudotuberculosis from 1 racing cam1 els from the UAE suffering from lymphadenitis. ticks.Pathognomonic for the disease are cold. producing severe bronchopneumonia with pulmonary caverns (Fig. Lymphogenous and hematogenous distribution of the infection from the primary site to internal organs and tissues may occur latently. Eldisougi. Afzal et al. pseudotuberculosis may not always be the sole cause of lymphadenitis in camelids. 69). 1984). 1982). C. pseudotuberculosis are rare in camels (Radwan et al. Different scientists conclude that C. painless abscesses up to the size of a lemon or orange in the external lymph nodes (Fig. Stowe (1984) reported that in open abscesses.

The successful toxoid vaccine used in sheep and goat pseudotuberculosisis also intended for trials in camels (Bergin. tetracyclines and cephalosporines. El-Sergamy . Since erythromycin is more able to penetrate the tissues. Anonymous. Bergin (1986) suggests a combination of penicillin and erythromycin to treat pseudotuberculosis in camels.. Treatment and Control @!I Affected animals serve as reservoirs of infection. The abscess will eventually subside with no relapse. Afzal et al. pseudotuberculosis. 1983.lnteaument 137 Figure 69 Pseudotuberculosis in a one-year-old dromedary cells were not observed.. Another possibility of treating pseudotuberculosis is the intravenous injection of 20 mL dimethyl sulfoxide (DMSO) and 20mL Baytril@for 12 days. 1986).Several scientistshave started research in the production of a vaccine against pseudotuberculosis (Han et al. (1994) revealed acute serous. 1977. Corynebucteriu are extremely sensitive to penicillin. yet the pus in the abscess prevents the medication from reaching the bacteria. Pseudotuberculosis remains one of the most important bacterial diseases in camelids (Domenech et al. Histopathological examinations of the affected lymph nodes by Abou-Zaid et al. 1995). 1992). They should be separated from healthy ones. The infected material must be destroyed and contaminated equipment disinfected. providing Figure 70 Pulmonary cavern caused by C. (1996) are of the opinion that their experiment indicates that a vaccine against lymphadenitis of camels might be developed based on a sheep strain of C. pseudotuberculosisin a dromedary strict aseptic procedures are employed. Pseudotuberculosis occurs primarily in camels more than 3 years old (Schwartz and Dioli. acute suppurative and chronic suppurative lymphadenitis. Ripe superficial abscesses should be lanced.

the major one in livestock being mastitis in cattle. Figure 71 Staphylococcus aureus abscess in a 6-weekold dromedary . A crater is revealed when this pus is removed.facial or periorbital eczema in sheep. easily removable scab that covers a small amount of pus. piglets. . It may infect the skin of different animal species under the following names: . The abscesses can become quite large and. 1991. Larger abscesses are frequently encountered between the forelegs of the animal. . The disease begins with a folliculitis. It also produces systemic diseases like botryomycosis in equines.impetigo or subcorneal pustular der- matitis of piglets. St. sheep. Since the affected lymph nodes seldom develop abscessation. 1994)with an infection rate between 10% and 60%. 1998) that was diagnosed with botryomycosis. Staphylococcal dermatitis is of greater importance.pyoderma in goats. . chronic inflammation of the skin primarily caused by Staphylococcus uureus and occurring mainly in young dromedaries. uureus is a potential pathogen and can cause a wide range of pyogenic conditions. pyoderma in camels is a suppurative.. Pyoderma is one of the major infectious skin diseases in OWC. yield a whitishgreen pus (Fig. It may also be present in the alimentary and genital tract.2 Staphylococcus aureus dermatitis Stuphylococcus uureus is a commensal bacterium of animals and humans that mainly occurs on the skin and the nasopharynx. pseudotuberculosis in this country is more of an aesthetic problem than a health problem. cattle. dogs. goats. uureus has also been isolated from abscesses of an alpaca (Fowler.folliculitis and furunculosis in horses. Abou-Zaid et al. sheep and goats.dermatitis of the udder in goats. For the reasons mentioned at the beginning of the chapter. when lanced. pyemia of lambs and polyarthritis in young animals. Epidemiology and Pathology Difficult to treat medically..138 Bacterial Diseases et al. 71).5. St. These have a small. . a purulent granulomatous lesion. which frequently progresses to a furunculosis with individual or grouped 3-5 mm big abscesses. The disease also occurs in dromedaries in the Emirates. 1. the disease is seen much more frequently in breeding than in racing dromedaries.

Ismail less than 4 months old. As in caseous lymphadenitis. the ab9. have been iso7. The pus 2. the cause. can lose 4. causing septicemia and/or severe bronchopneumonia with pericarditis The same bacterial species were isolated and hydropericardium (Fig. kin (1968) called the condition “contagious the pathogenic qualities of the staphylo. Fusobacterium necrophorum. head.11. condition or might succumb. scesses located between the front legs of 10. Affected animals are disturbed. from the abscesses was yellow and creamy. Actinomyces pyogenes. and Staphylococcus spp. coli. Staphylococcus aureus. the camel calves may rupture into the tho. among other factors. Often several 5. calves of a herd are affected.. These lesions con. 1989). aureus . 72). spp. ylococcal disease is widespread among The disease can be chronic and difficult to Bactrian camels in Central Asia. racic cavity. Klebsiella spp. chest. leg and abdomen: These abscesses were warm and painful 1.Sadykov and Dadabaev (1976) identified fenses (Schels. 8. colonized with Staphylococcus aureus can be According to Buchnev et al.Integument Bornstein (1995) also described similar Only a few reports of bacteriological studlesions as lymphadenitis in camel calves ies of skin abscesses in camels exist. Pseudomonas aeruginosa. staphpresent in addition to the furunculosis. Streptococcus pyogenes.et al. C. E . The etiology of factors that can harm the host organism this disease was largely unknown until and protect themselves from the host’s de. Streptococcus 6. Semushtreat depending on. (1990) from wither fistuAn exudative eczema with pustules also lae in 93 pack camels in Egypt. shoulder. (1987). pseudotuberculosis.skin abscesses” which can affect 5 to 20% coccal strain present. Proteus mirabilis. by El-Seedy et al. The disease presents as a puru- 139 Figure 72 Pericarditis and hydropericardium caused by St. 3. lated from these lesions. and often as big as an orange. (1990) isolated the following bacterial sisted of several abscesses found at the species from non-draining abscesses of the base of the neck and between the front legs. Staphylococcus aureus of the Bactrian camel population and instrains possess a multitude of virulence duce a mortality of 15%. Proteus vulgaris. Clostridium perfringens.

neck and shoulder. In various tests. 1989). (1977) have studied the pyogenic affections of the one-humped camel in Ethiopia. As can be seen from Table 33. StaphyIococcus aureus and Streptococcus B have been isolated from these lesions. St. the bacterial counts increase 50 to 100 fold in pathological skin lesions. E. ulcers and other skin lesions. The results are summarized in Table 33. cameli. whitish pus. which was caused by Sf. This also prevents the industrial production of a vac- Table 33 Bacterial species isolated from skin lesions from dromedaries in the UAE Bacteria Isolated Abscesses: Open and Closed Staphylococcus aureus Staphylococcusspp. affected animals should be isolated and treated. In some cases. Pseudornonas spp. Actinornyces pyogenes C. The strain has been named St. and ripe abscesses lanced and drained. aureus was isolated from 71% of the abscess specimens. St. aureus was found in small numbers on the skin of healthy dogs (Schels. Since pyoderma is difficult to treat with antibiotics. Affected skin lesions should be cleaned daily with 5% Lotagen@ solution. the authors have regularly produced auto-vaccines for the afflicted dromedaries. pyogenes citreus. aureus strains. a sensitivity test should be performed on all isolated strains. coli aerobic bacteria Total 82 7 5 3 0 Skin Lesions Wounds/ Ulcers 12 6 1 0 0 3 2 1 2 5 Others 7 25 0 0 4 3 5 2 2 7 55 4 3 3 4 4 115 32 . Pyogenic septicemia is a frequent complication and many Bactrian camels have died from the disease. However.140 Bacterial Diseases lent lymphangitis in Bactrian camels. The auto-vaccines were developed for the individual animal or for a small group of animals from the same herd. aureus strains are very resistant to antibiotics. affecting the superficial lymph nodes of the head. abscesses containing 500 mL of pus have been reported. Samartsev (1950) reported an infectious pustular dermatitis in camels in Kazakhstan. bacteriological studies were performed on abscesses. pseudotuberculosis Derrnatophilus congolensis Streptococcus spp. wounds. Lancing the abscess reveals thick.5 to 2. Domenech et al.0 cm in diameter and disappeared after one month without treatment. Since some St. Treatment and Control In order to control the disease. Several staphylococcal strains have been isolated from Bactrians from different areas. In severe cases. During the course of 15 years. all strains possessed identical properties. Proteus spp. Pyogenic dermatitis also plays an important role among young dromedaries in the Emirates. The production of an individual autovaccine is necessary as there are many different immunological and virulence factors present in St. Their study showed two well-defined skin diseases: "mala" or lymphadenitis and "maha" or "doula" or cutaneous necrosis caused after ulceration of skin abscesses. The pustules were 0. parenteral antibiotic administration should be tried.

salt deficiency Contagious skin necrosis Streptococcus asalactiae Skin necrosis. Australia and New Guinea. 1. aureus. b 1939 Edelsten and Pegram 1974 Author Cross Curasson Countw India Africa India India Somalia Somalia Ethiopia Desianationllsolates Strer. Wardeh Gitao et al. aureus vaccine is based on a general non-specific stimulation of the immune system. It is widespread in Africa. 1977 1981 1982 1989 1990 1992 1993a 1990 Kenva Mauritania Kenya UAE 1998 UAE 1998a.lnteaument 141 cine. urine Contagious skin necrosis. 1989). Only a few animals required a booster injection after 14 days. Dromedaries suffering from St.tococcus Cutaneous streptothricosis Actinornyces (Nocardia) cameli Nocardia farcinica Streptothricosis Contaaious skin necrosis Skin necrosis Contagious skin necrosis. Gitao et al. Sixty percent of the dromedaries vaccinated showed initial improvement within the first few days. Fazil and Hofmann Schwartz e t al. The major problem in the treatment of pyoderma is being able to adequately increasing the body’s own defense mechanisms (Schels. Domenech et al. congolensis Derrnatophilosis Derrnatophilosis 0. the abscesses underwent exsiccation and reduced in size. The remarkable success of the St. aureus dermatitis were successfully treated in this manner. various bacterial species Skin necrosis Actinornyces carneli Skin necrosis on hind leas. All cases of St. Gitao Gitao Wernery and Ali Joseph et al. a paraimmunization. as well as a specific immunization against all of the antigenic exotoxins and other virulence factors of the dermatopathogenic strains of St. b Saudi Arabia Dermatophilosis 0. Streptothrix SPP.5. aureus dermatitis were given 5 to 8 mL of a formalin-inactivated vaccine subcutaneously. It was also possible to inoculate the unaffected animals prophylactically and so inhibit the spread of the disease. Phagocytosis resumes following neutralization of anti-phagocytosis virulence factors of the pathogenic Staphylococci.3 Dermatophilosis The infection ascribed to Dermtophilus congolensis is a typical epidemic in the humid tropics. consolensis Dermatophilosis Derrnatophilosis . In the Americas. the in- Table 34 Contagious skin necroses in the dromedary and their isolates Year 1917 1918 1920 1936 1947 Mason 1919 Leese 1927 Peck 1938a.

bloodcontaminated exudate (exudative dermatitis) (Losos. 1992). mycotic dermatitis. humans and certain non-domesticated species such as the zebra and red deer. thereby allowing growth of a new layer of epidermal cells (Seifert. 73). The hyphae produce motile spores (zoospores) that are predominantly released during the rainy season and are transmitted either by direct contact or by vectors (ticks.The disease is known under different synonyms. equidae. (1998a. 1992). The crusts can be removed. lumpy wool disease of sheep and strawberry foot-rot of sheep.. subdivided by transverse and longitudinal septae (Gitao et al. by Gitao et al.. although there is only one published report dealing with cases in NWC (Thedford and Johnston. congolensis was isolated . resulting in a bulging of the slowgrowing epidermis away from the corium. Drying of the serous exudate forms a crust that is a distinguishing characteristicof this disease. 1992). (1998) in Ethiopia and by Bornstein (1995) in Kenya.. 1990). The latter studied the morphological and biochemical properties of different strains. flies). Dermatophilosis also occurs in OWC and NWC. 1989). 1 The mycelial fungi are distinguished by their branching hyphae. Dermatophilosis in dromedaries has only recently been reported by Wernery and Ali (1990)in the UAE. Canada and the USA and sporadic reports have appeared from Europe (Seifert. Figure 73 Skin necrosis on the hind leg of a dromedary from which D. 1992).A similar strain was identified from scabs originating from limbs of dromedaries in the UAE suffering from skin necrosis (Fig. 1998). Hybrid European cattle are extremely susceptible. Dermatophilosis is transmitted to man by contact with infected animals (Bucek et al. congolensis strain was recently isolated from dromedaries' skin lesions in the UAE (Joseph et al. The hyphae developing from the spores in the epidermis attack the hair sheath. 1984). A review of the literature in 1976by Abu Samra et al. A non-hemolytic D.Supposedly the thorns of the acacia and grain awns are also able to transmit the spores (Wilson.142 Bacterial Diseases fection has been reported in Argentina. found no mention of a natural infection with Dermatophilus in the camel. revealing a wet reddish area that secretes a thick. Dermatophilosis occurs primarily in cattle. African zebus less so and NDama cattle of West Africa only slightly (Seifert. Etiology and Epidemiology Dermatophilus belongs to the order Actinomycetales. although various authors have reported streptothricosis-like organisms (Table 34). 1986). This causes an exudative inflammatory reaction. There are distinct genetically determined differences in resistance to the disease in cattle. streptothricosis. small ruminants. b) and Gitao (1992) in Sudan. by Samuel et al.

there are distinct differencesbetween infections involving short or long hair. Similar differences in the development of the skin lesions in horses have been described in camels by Gitao et al. 1982). Dermatophilosis is divided into a winter and summer type. a raw area with a serosanguinous exudate is exposed (Figs. particularly over the dorsum of the back (Thedford and Johnson. These clinical signs are seen in areas with long hair 143 From these results it may be assumed that contagious skin necrosis and streptothricosis are identical to dermatophilosis. The matted hair tufts can be easily detached leaving a wettish pink. Abu Samra et al. (1976) was able to prove that the dromedary is susceptible to an experimental infection with D. 75 and 76).Integument Figure 74 Derrnatophilosis in a racing dromedary: the matted hair stands erect. raised areas covered with thick scabs. Heavy wool cover over the back in high moisture climates predisposes lamoids to this disease. necrosis and hyperkeratosis of the cells in the epidermis characterize the typical lesions. Long hairs in the vicinity of the exudate become matted yielding the characteristic "paint-brush affect. The lesions ranged from nodules to thickened. D. Congestion and edema of the dermis. As in the horse. These areas become covered with a suppurative exu- date in cases of severe infection. (1998a and b). High humidity and the behavior of the female dromedaries during urination leading to chronic wetness of the hindquarters have been implicated in the etiology of skin necroses (Schwartz et al. congolensis showing .The different forms of the disease have also been seen by the present authors in dromedaries in the UAE. (1990) who differentiated between an early or acute form and a chronic form of dermatophilosis. 1989). 1990). 74). Lesions consist mostly of crusting. The histological lesions of dermatophilosis were described by Gitao et al. hyperemic wound surface (Fig. Upon removal of the scabs. There is accumulation of exudate on the surface of the skin and infiltration of neutrophils in the dermis and epidermis. D. congolensis has produced severe cases of wool rot in llamas. Dermatophilosis of short-haired areas occurring on almost all areas of the body was described by Wernery and Ali (1990).. congolensis. degeneration. Clinical Signs and Pathology ill ferent manifestations of dermatophilosis in the horse are dependent on the length of the hair and the place of infection (Pascoe.

Gram-stained smears of scab material show Gram-positive microorganisms arranged in rouleaux form (Fig. Gitao (1993b) developed an ELISA for the detection of antibodies against dermatophilosis in camels.144 Bacterial Diseases Figure 75 Dermatophilosis in a dromedary bull Figure 76 Dermatophilosis in a dromedary bull. Infected dromedaries . It is planned to use this test in the field. Treatment and Control 111 Successful treatment of dermatophilosis with terramycin or procaine penicillin and streptomycin has been reported. Diagnosis . The test detected antibodies to dermatophilosis21 days after the experimental infection with D. bacterial filaments or coccoid zoospores are found in the epidermis down to the stratum basale. septated. Some of the crusts have been removed revealing a raw bleeding area. The plates should be incubated at 37°C for up to 5 days in a CO2 atmosphere. congolensis. 77). these lesions are seen in areas with short hair branching. The bacterium is comparatively easy to culture and grows well on sheep and ox blood agar.

1934. Corynebacterium pseudotuberculosis and "Mala" (lymphadenitis)in camels.T. Comp. G..: 135.M.A. Peru. The research work done for the preparation of vaccine against camel abscess. Barsallo.S. H. Abu-Samra. Shang and Caimude. E. Calle and B. G. of Kuwait seminar.. Proc.A. Rev. Sakir and M. Atkins. A. Barsallo. Sansyzbaev. Vet. 1995. Selim. Majid Hussain. 1987.lnteaument Figure 77 Dermatophilus congolensis: smear from underneath a scab of a dromedary. The lesions should be fully healed within 4 weeks. tech. 1976. Corynebacterium pseudotuberculosis infection and Lymphadenitis (Toloa or Mala) in the camel. Verlag Paul Parey.Agentesbacterianos en procesos respiratorios que causen mortalidad en alpacas.A.J.. 1994. 1984. Bomstein. Report of Ministry of Agriculture. Skin diseases of camels in: Camel keeping in Kenya. F. As dermatophilosis is on the rise in camelids. S. Hlth. Z. S. J. Vet. Purasitol. Pospisil. K. Med.J. Evans. J. Microbiol.. Abd EL-Samea. in FA0 the camel: Development and research.R. Shalka.. the establishment of a vaccine should be considered. Parasitol. Bucek.. 1998a) and because it is a zoonosis. Anonymous. Technical Science Service. Anim. 1987. sci. A. Samame. 6 (2): 492495. Chavera. M. Cong. Bull. 1992.Z.H. (Cuzco) 113: 53. Zagazig: 600-604.J. 1984a. 28: 158-162. Prod.M. Microbiol. M. Behrens. Bergin. J. Lehrbuch der Schafkrankheiten.O. Private report: 1-26.S. Trop. 86 (2): 157-172. Off. M. Shearing of badly affected areas with long hair is often an important additional method of further reducing the development of lesions.J. 1995. 1996. M. Berlin und Hamburg. Y. Chen. int. Sexto Congr. The scabs are removed and the areas cleansed daily with a n iodine solution for 7 days.N. No title.. L.Y. Experimental infection of domesticated animals and the fowl with Dermatophilus congolensis.Z. Epiz. Moster and B. B39: 495-502.. S. J. Afzal. Mahgoub.H.. Sec. Path. Experimental Dermatophilosis.. S. References Abou-Zaid. C. Lymphadenitisin camels. J. Epidemiological survey of corynebac- . Tulepbaev and A. Imbabi and E. Perus. Piers Simpkin and D. Villena and C. Kuwait 20-23 October 1986.Abscesos en alpacas. M. (Cuzco) 113: 53. Range Manugment Handbook of Kenya 3 (8):7-13. 1986. Grampositive rnicroorganisms arranged in rouleaux form (XI 000) 145 are treated twice with Terramycin LA intravenously.J. Yousef and M. 2ndVet. S. 1984b. Caprano. Han. Ed. Buchnev.A.E. Med. Sexto Congr. Isolating clinically affected animals and controlling ectoparasites are methods used to break the infective cycle. T.. sometimes in connection with dermatophytosis (Gitao et al.

SOC. A. Egypt.E. 1998. Narimani and M.. M. Epiz. Rev.. Praxis 9: 389-402. 128 (9): 215.G. Agab and A. M. ASS. Symptomatologie . Enany. C. (Supplement to Rec. Important camel diseases in the one-humped camel in Eastern Africa. A. M. Lymphadenitis in Egyptian camels with special reference to bacteriological and parasitological affections.M. The Camelid. Encyclopaedia of Veterinay Medicine. Chen and Y. Richard.R. Agab and A. Ogunsan.. 1984. Shouman.. Lotfi. 17 (3): 743-748. tech. Z. Vet. Gitao. Green and Son.O. Hlth. Rev. Schwartz and M. Ismail. 1981. Soufy. Shang. Anim.A. Ofl.. C. M. Epiz. an "all purpose" animal. P e p de Fabregues and D. Trop. G. Tindall and Cox.. K. 1991..A. Balliere. W. 50: El-Sergany. G.. Cross.E. Rev.R. Hoste. 1990. 1996. E l m Mkd. 1975.T. Enany and M. Trait6 de pathologie exotique v6t6rhaire et compare. Gitao. G. 81-92. Elev.T. vkt. H. Evans and D.G. Clinic Path. 12 (2): 639-645. The epidemiology and control of camel dermatophilosis..H. 0 int. Contagious skin necrosis of Somali camels associated with Streptococcus agalactiae.R. x . Anim.. Boddie and J. Shash. Nigeria. Prod. 1918. Une maladie du dromadaire analogue au farcin du beuf. Le chameau et ses maladies. Pays trop. Gansu. Sadri. Pays trop. Curasson. Dalling. Hygiene et maladies du dromadaire en Afrique occidentale franeaise Gor6e (SEN). H. Cockrill. Pays.146 Bacterial Diseases teriosis of Bactrian camel in Subei County. J. Dioli (Eds). F. 28: 315-316. 46 (1-2): 309-311. Guidot and D. Curasson. 155-164. Mkd. J. and R. 1991. sci. Natural Dermatophilus congolensis infection in camels (Camelus dromedarius) from Kenya. Eldisougi. Trop. R. 1966. 1992. T.A. El-Sayed and M.G. 1947.S. Tieriirztl. Elm. Actinobacillus lignieresi infection in camels on the Sokoto plains. Sci. Experiment on immunization against corynebacteriosis of the Bactrian camel. 1917. Greenwood. 1974. Edelsten. v6t.M. Z. Microorgan- . Gitao. El-Jakee. Oedematous skin disease of camel in El-Sharkia Governorate. C. Outbreaks of Dermatophilus congolensis infection in camels (Camelus dromedarius) from the Butana region in Eastern Sudan. and R. Nasser. Z. Diseases of camels. Ismail. A pictorial guide to diseases. Sci. 1920. Path. 1983.J. Rec. C. El-Seedy. Bacterial species implicated fistulous wither affecting one-humped camels in Egypt. Khalafalla. Ezzat. Prod. A. 6: 255-256. A. tech.A. Spruell. Vigot Freres. Anim. Gitao.G. Hassanain. London.F. 1998a. Gitao. C. Verlag Joseph Markgraf Scientific Books:pp. Egypt J. 103: 307-312. J. health care and management. H. J. An enzyme-linked immunosorbent assay for the epidemiological survey of Dermatophilus congolensis infection in camels (Camelus dromedarius). Gitao. H. Esterabadi. Ames. Khalafalla. A. C. Hofmann. and R. Uppsala: 496-502. Djang and E. trop. M. M. Abdel-Ghani. A.J. Bull. El-Seedy and M. Ofl int. 1993a. vkt. M. Editeurs: 86-88. Tech. Richard. 1st int. H. M. Gansu 2 47-58.Z. Rev. The Int.: 145-146.R. Le dromadaire et son &levage.J. Iowa State University Press. Vet. T. Laila and M. Haltung und Krankheiten des Kamels.. 1758) in Kenya. Curasson. Han. 1 (1-2): 1 309-311. Atkins.E.Anote on the diseases of camels in Saudi Arabia. 17 i 8 (3): 749-755. Paris: LI. Fowler. Conf Appl. M. F. Fazil. A. Med.tech. 1985. Rev. Daneji. Proc. Imprimerie du gouvemement g6n6ral. G. Mkd. Vigot Freres. Entessar. 1936. Hedayati. F. Comp. Robertson. Cent.E.G. Zagazig. Rev. The camel and its diseases. Path. comp. 1985. int. 4 (1):25-45. Sci. El-Sayed. Dermatophilosis in camels (Camelus dromedarius Linnaeus.A. Gansu J. M.: 51-54. Med. C.I. Dioli. Epiz. H. M.G. sci. J. 1990. Archives de l'Institut Razi 2 7 61-66. Vet. Suppl. Domenech. M.J. Pegram.G. 94) 71: 491-496. B. Abd El-Rahmen.Etiologie. W. vet. Edinburgh 1:585. G. Ismail. J. Scandinavian Institute of African Studies.G. 1998b.G. 30 (3):251-258..Y. Les maladies pyogenes du dromadaire en Ethiopie. Med.. Medicine and surgery of South American Camelids. Control of pseudotuberculosis in zoos. 1993b. Hlth. Stimmelmayr.M. 1992.G. Curasson. Acta Agriculturae Universitatis. Egypt Med. An outbreak of a mixed infection of Dermatophilus congolensis and Microsporum gypseum in camels (Camelus dromedarius) in Saudi Arabia. 1990. 1977. I.

and A. Bacterial and mycotic diseases of int. JAVMA 185 (10):1137-1141. J.M.H. 18: 82-86. Tagungsbericht: 80-83.. 1939. and L. H. Tarek. A. Chouhan. 128: 86. E.A. The Vet. Peck. Pseudo-actinomycosisor S t r e p totrichosis in the camel.Z. J. and A. Kazakh Res. 46 (51):1355-1360. 141: 529-547. N. Wade: R. Publications. Thedford.G. 1991. Tierurzt 11: 985-989. and Res. The T.G. M. I. and M. Trop. 1950.W. A. Wernery and M. 3 0 145-147. R. Br.S. G. 1992.J. Bacteriological study of Ethiopian isolates of Dermatophilus congolensis.J.J. Tareke. Rebleza. Corynebac- terium pseudotuberculosis infection in camels (Camelus dromedarius) in Saudi Arabia. A compendium.) in British Somaliland. Eds: W. Infectious and parasitic diseases of farm animals. The relationship of salt starvation to contagious necrosis and lameness in camels. Vet. Infectious pustular dermatitis in camels. Purohit. 1989.I. Vet. Pract. Erfahrungen bei der Behandlung der Pyodermie des Hundes mit Autovaccinen.. E. 1991. Bacteriological studies on dromedaries lymphadenitis in United Arab Emirates.I. 1996. Mayhew. Ther. 1985. Proc. J. I. 18 (1): 77-90.F. Vet. Rec. Wilson.H.S. S. E. 1968. G. R. J. A. Microbiological and histopathological diagnosis of rare cases of Corynebacterium infection in camels. N. health care and management.G. Jackson. and Abu-Bakr. R. S. Food Anim. D. A. Erkrankungen junger Neuweltkamele i Tierpark Berlin-Friedrichsm felde 11. Dermatophilosis caused by a nonhaemolybc Dermatophilus congolensis strain in dromedary camels in the United Arab Emirates. S. 33 (50):1052-1054.M. UK: 59-64.J. 1938a. J. 1992. Vet. Higgins. Lymphangitis in the camel (two cases). D. Dioli. 21: 229-230. Higgins.Integument 147 isms associated with closed abscesses of camels in Egypt. Notes relating to the camel. D.R. 1990. Allen. H. Practice 6 (5): 23-24. 1976. Mayhew. Proc.E.R. Proc. Med. Samuel. Purohit.J. H. T. Gustav Fischer Verlag Jena. Epizootic lymphangitis in camels. Vet. Avon. and W.J. Noskov. Tinson. Infectious tropical diseases of domestic animals. 1987. 1989. 1998.R. 5 (3): 145-157.S. 5 (2):247-248. Hungerford Vade Mecum Series for Domestic Animals: pp. J. Zag. Nov. 1-3 in Stuttgart. Infectious diseases of New-world camelids (NWC). Snow and J. H. Agr. H. Trudy Vses. 1989. and A. McGrane. Rec. Vet. Hlth. N. Salt intake in relation to cutaneous necrosis and arthritis of one-humped camels (Camelus dromedarius. North A m . Sadykov. H. Strauss. and D. A pictorial guide to diseases.A. Allen. . Samartsev.F. U K 365-370.S. Eds: W. C.I. Schwartz. Vet. J. A. Trop. Higgins. F.n.J. Institute 5: 190-197. A. Kiros. Mason. El-Magawry. 1984. G. Assiut. 1990. Sunitha. Wirtu and T. 1982. 1938b. Vet. 1919. Mahmoud. G.F. Wolfe Publishing Ltd. 127 478. Wound healing in camels. Losos. A colour atlas of equine dermatology. Wade: R. 1992. Snow and J. and W. N. Radwan. Hawari.G. 1998. Dadabaev. Vet. Der prakt. U. Ectoparasit. Hlth. F.G. Schels.R. Choudhary. Nashed. Schwartz. Rec. Lindsay. Slater and P. Stuttgart.J. Camel Conf. Med. Sabine. lSt Camel Conf. Sel'khozgiz Moscow. Pro Veterinario 9 (1): 3. J. Tropentierhygiene. Publications. SSR. 1986. 32 (1):34-42.J. and A. 1992. Joseph. Vigot Freres. The onehumped camel in Eastern Africa. bacteria and fungi. 1 s t int. Semushkin. Schwartz and A. Diagnosis of caseous lymphadenitis in goats. Clin. Comp. Paris II. 1959. 1985. Refai. The Bath Press. Newmarket.J. Anim. Spesivtseva. camels in Egypt. 298. Inst. Antimicrobial drug interactions. Giza 38: 53-62.R.F. Alma Ata (SUN) s. 240. Johnson. Path. AlBekairi and R.R. Camels. Arbeitstagung der Zootierarzte im deutschsprachigen Raum.. Verlag Josef Margraf. Rec.: 73-78. Ali. Lloyd. L. Stowe. Prod. Diagnosis of camel diseases. Vet. Infectious diseases of the camel. Chouhan and R. Lloyd.S. Seifert. S. A treatise on the one-humped camel in health and disease. and Zh. and S. Peck. 14 (50):409-410. Rec. Newmarket. Vet. Eine fotographische Dokumentation wichtiger Kamelkrankheiten in Kenia. On camels with pus lymphangitis (staphylococcosis) in Kazakh. Lindsay. 1927. Caseous lymphadenitis in goats in England. 14: 86. sanit. 1990. Pascoe..D. Prod.R.W. S. Camel Prac. Manefield. Anim. viruses.H. M.G. Peck.F. Leese.M.

M. M. Further reading Abubakr. Tieriirztl. 1995. Camel Prac.T.148 Bacterial Diseases Wardeh. Wu. 1990. Kaaden. Diagnosis of Corynaebacterium pseudotuberculosis infection in Bactrian camel with indirect hemagglutination test. J. Wemery. and Res. 1981. Gansu 2: 53-58. Fadlalla. B.O. 1984.E. Berlin.. clinical observation and etiology of contagious skin necrosis in camels (Camelus dromedarius) in the Sudan.F. U. and 0. Camel Prac. J. Camel production in the Islamic Republic of Mauritania. 1986. London and New York.S.N. 3 (2): 95-98. (1):107-1009. Shen. The camel. U. Umschau 45 (3): 209-210. .Y. 1999. Xinjing Animal Science b Technology 4: 2630. Huang. J. Ali.-R. S. Blackwell Wissenschafts-Verlag. Camel Newsletter 5: 11-17. Corynebacterium abscess in camels in Bahrain.E. 1989. B. M. 1996. and D. Mohamed. Acta agriculturae Universitatis. Dermatophilose in Renndromedaren Fallbericht. and G. Pustules in camel. Nayel and M. Infectious Diseases of Camelids. R. Wilson. Incidence.Y. and M. Shen.I. 1987. Wemery.G. 3: 4-5. Gansu J Anim Sci b Vet Med. Yagoub. and Res. Comparison of biochemical reactions of some pseudotuberculosis strain isolated from corynebacteriotic camels in different districts of China. Longman.

rapid milking (milker on each side). immunoglobulins. 1998).In true ruminants the reservoir for milk-water is lost for cooling and via fecal and urinary excretions.. EL-Agamy et al.This may explain why there are so few publications regarding mastitis in the camel. 1996). sheep and goat populations. 1980a. However. Farah. These and many other features make the camel favorable over other ruminating domesticated animals. and retention of the calves of the best milkers in the herd. Kappeler. in many parts of the world the prejudice against the camel family still exists.6. These covers might reduce injuries to the teats and the udder and protect against gross contamination. which can only be achieved by regular milkings (3 to 4 times daily). There might be several reasons why mastitis is more uncommon in camelids than in other domesticated animal species used for milk production. the lack of drinking leads to cessation of lactation or to a very concentrated high fat and low water content milk after a short period. sheep and goats. It is estimated that good milk camels can produce 30 to 40 liters of milk daily. lactoferrin and lactoperoxidase.1 Infectious Mastitis In the drought-stricken areas of the world where continuous severe drought decimates cattle. the more likely explanation why udder infections in camelids are less frequent lies in the m l itself. 1998. 1998). dromedaries are known to produce well over 20 liters daily with a lactation period lasting 8 to 18 months (Al-Sultan.The milk is also unaffected by acid and will virtually pass untouched through the acid environment of the human stomach to the in- testines. These proteins have been shown to have higher concentrations or higher activity in camel milk . where it is available for absorption. The lactation period can last over 2 years. This twin duct anatomy with its narrow streak canals might in some way protect against infection. The streak canals are very narrow and a 1mm tomcat catheter is required for penetration. Pakistan and the Middle East. Ramadan et al. Milking camels are often fitted with udder covers to restrict suckling. In cattle. The mammary glands of both OWC and NWC possess four quarters and one teat per quarter. However. These inhibitors are proteins and have been described as lysozyme. 1984. It is of short duration and milking must be as fast as possible. One of the most remarkable features of dehydrated camels is the ability to continue lactation and to secrete milk that is highly diluted with over 90% water content (Yagil and Etzion. Each teat has two streak canals that enter into separate teat and gland cisterns. 1996. Each teat is associated with a non-communicating double gland. Lactating camels will therefore guarantee ample food with the desired content for their offspring and humans alike. Nomads are aware of this fact and thus milking is carried out on both sides simultaneously. only the camel survives and continues to produce milk. Large concentrations of insulin and vitamin C have been found in camel milk. Inflammation of the udder occurs less frequently in the camelids than in other domesticated animals (Leese.1. ELAgamy. Camel can secrete 20 L of milk daily for at least 10 days without drinking water. Fowler. 1987.b). 1992. However. Barbour et al. In India. Several scientists ik have found substances in camel milk that inhibit the growth of pathogenic bacteria (Kosparkov. which are already well characterized... 1975. the let-down of milk must be stimulated by massage or calf suckling. 1927.

8 x the affected quarter and. found that 81% of secretions are watery. . the mammary in the Negev desert.150 Bacterial Diseases 101 dromedaries from eastern Sudan were studied to evaluate the value of the CMT. Quarter samples from samples from the third dromedary were which St. who exam. Somalia (Arush et al.E.cies. (1995). Similar results sterile. aureus matic cells in the milk samples occurred si. subacute Staphylococcus spp.lence of mastitis in 146 adult Indian dromined 391 udder quarters from Sudanese edaries using the CMT and cultivation. Staphylococcus aureus. Abdurahman Bakhiet et al.. found bacteria in 45% (22/49). coli were the most important organisms tion in milk production.and coagulase-negative Staphylococci were multaneously with a bacterial mastitis. Both the SCC dary milk samples was confirmed. (1987) reported chronic uni.lated.microorganisms. Quarters from in cattle.. (1992).were the most frequently isolated udder grenous mastitis with lymph node enlarge. Saudi Ara. 1985. peptidoglycan recognition protein (PGRP).India (Kapur et al. Ra. using the California mastitis test (CMT). with madan et al. (Quandil and Ouadar. SCC ranged from 1.. Sudan. 1984.. (1994) Mody et al. Of 160 milk samples originating from 7 They showed that in the majority of the clinically healthy Bactrians.86 milk samples from clinically healthy tinged (Tibary and Anouassi. Sudan (Obied. The 391 milk samples from Thirty subclinical cases of mastitis were than in bovine milk. 22. Micrococcus spp.found to be positive for bacteria. A simi. Guliye (1996).. Milk mean SCC values. in 2 cases. 1997). a sec.7% revealing 2 or more bacterial spelateral mastitis in 3 dromedaries’ lactifer. Streptococcus dysagalactiae and keratin. This obstruction caused a reduc. alReports of inflammation of the though a significant number of quarter camel udder have appeared from various milk samples had elevated values from countries. dromedaries. It was found that the mean values of all three tests were generally higher for quarters infected with major pathogenic bacteria. 1987). the somatic cell count (SCC) and the adenosine triphosphate (ATP) tests for the detection of subclinical mastitis. (1992). who invesment (Bolbol. (1985) examined 205 milk of subclinical mastitis in Bactrian camels samples from dromedaries in Saudi Arabia were reported from Abdurahman (1996). man et al.0x O5 to 11..higher SCC and CMT values. Hafez et al. yellowish or blood. an increase in so. In acute cases. Peracute (Kapur et al.106 cells/mL.the infection status of the camel udder. aureus was isolated showed the highest mean values. 1982)have been described in tigated subclinical mastitis in dromedaries the camel. Barbour et al. such as Egypt (Mostafa et al. 1982). Kappeler (1998) found a novel minor whey protein. As the main organisms found. enlargement of isolated. Abdurahman et al.camels were positive for bacteria. 1983) and the samples from 49 healthy dromedaries in UAE (Quandil and Ouadar. seems to occur more often than is realized. 1984). a correlationbetween mastitis and which cocci were isolated had significantly the number of somatic cells in the drome. Quarter milk samples with ondary bacterial infection with Pasteurella bacterial isolates had significantly higher haernolytica and Staphylococcus aureus. (1998) investigated the prevaand Abdurahman et al.40.. ous ducts blocked by accumulations of Bacillus spp. which has a beneficial influence on establishing favorable gut microflora in the newborn and seems to especially inhibit the growth of Gram-positive bacteria. who examined milk et al.and the CMT are of value in predicting lar observation was made by Abdurah. St.5% were dromedaries examined. 1991)... 1982). which no pathogenic bacteria were iso1987). and Streptococcus spp. indicating that subclinical mastitis bia (Barbour et al. 1984) and gan.

epidermidis. Quandil and Ouadar. 1991. Hashi. The authors also tested the pathogens for their antimicrobial susceptibility and found gentamycin and chloramphenicol highly effective. Treatment 611 When mastitis occurs. Staphylococcus. Farah and Ruegg. There are divergent opinions as to which bacteria are potentially the primary causal organisms of infectious mastitis in the camel. 1982. 1987..Udder 151 found.. Streptococcus spp. The streak canals can be easily traumatized when using bovine an- .. Mastitis treatment should be based on culture and sensitivity and the treating person must be fully aware of the anatomical particularities of the camelid’s mammary gland. It is also of great significance that BruceZZa organisms have been isolated from fresh camel milk (Radwan et al. The authors did not find any correlation between the SCC and an udder infection. . Aerobacter and E .. 1998) and OWC udders. Micrococcus. 1992) and cases of human brucellosis have been attributed to the consumption of raw camel milk (Mousa et al.In NWC. necrosis and abscessation might be observed with discharge of greenish pus. ..Bacteroides spp. coli.Micrococcus spp. Al-Ani and Al-Shareefi (1997)failed to isolate any fungi from 50 milk samples. 1987). prompt attention is necessary to avoid severe damage to the mammary gland or even loss of the animal. Pathology srl Very little is known about the pathological alterations occurring during infection of the mammary gland. Numerous authors believe them to be primary causative organisms in the pathogenesis of mastitis in the camel (Barbour et al. Ramadan et al.. 1988) (see also chapter Brucellosis). From the multitude of bacteria isolated from milk samples taken from camels with mastitis. 1985. coli. reddened and painful to the animal on palpation. St.Pseudomonas aeruginosa. Obied et al.. E. So far no mycoplasmas have been isolated from NWC (Fowler.. . of which 28 possessed bacterial pathogens including Staphylococcus spp. 1989..Klebsiella pneumoniae. Barbour et al.. aureus and Coynebacterium pyogenes were the main causes of chronic mastitis.. were responsible for subclinical mastitis. Klebsiella pneumoniae. Al-Ani and Al-Shareefi (1997) described some of the lesions observed histologically in mastitis. Aerobacter enterobacterium. (1985) views Micrococcus as an important causative agent of mastitis whereas Obied (1983) did not consider this bacterium pathologically relevant. whereas St. coli to be the main bacterial species causing mastitis.. Several scientists have studied the properties and products of camel milk (Whabi et al. Pasteurella huemolytica. The affected udders are often swollen. Mostafa et al. no specific bacteria that cause mastitis have been reported. . Very little is known about fungal mastitis. Farah.. .C. 1985. These bacteria were isolated as both pure and mixed cultures from milk samples of camels with mastitis (Kapur et al. perfringens. Streptococcus spp. The following bacteria were considered secondary agents: . 1996).. In chronic mastitis.Actinomyces spp. 1984. (1996) found Streptococcus. Hafez et al. Barbour et al. .E.. Hassanein et al. coli and Micrococcus spp. 1984. Several bacteria species were isolated from peracute NWC mastitis including E. but Quandil and Quadar (1984) cultured Candida albicans from milk originating from subclinical mastitis samples. Pasteurella haemolytica and Streptococci were found most frequently. Al-Ani and Al-Shareefi (1997) found that 38% of lactating camels from three different herds in Iraq suffered from mastitis. 1987. Staphylococcus aureus. hard. 1987). and Coynebacterium.

J. Comrn. Abbas and G. of Tech. Vet. E.. 24-26 Octobre 1994.. Dromadaires et chameaux. Commercial mastitis infusions are Ampiclox@. A 39: 648-655. U K 48-50. F. o Dairy Res. Valente.Y. Before the infusion is carried out. Studies on the compositional and hygienic quality of the milk of Bedouin camels (Camelus dromedarius) of the Negev . Hussein. Anim. Sh. 1994. M. Res. Guliye. Bull. Hlth. Frerichs. CH-8092. Acta Vet. Somali Acad. Br. R. J. Ruppanner.A.. A1 Mukayel. J.S.M. In severe cases. Farah.. and Res. O. Arush. f Farah. W. Nabbut. A. M. Before infusion. 1998. Vet. Camel milk. Sud. S. 1997. Sh. 4: 99-104. Z. Mastitis in Camelus dromedarius in Saudi Arabia. Working Paper 3 7 1-9. 1996. Mastectomy in she-camel. camelid society. El-Agamy. of Food Science. Barbour. 20 (1): 9-14. 36 (4): 423-431. Veterinary care of camels in Saudi Arabia: Mastitis in camels. of Food Protection 47 (11):838-840. Assaf. vet. Instit. Frerichs and H. A. Scand. El-Agamy.P. Actes du colloque. 1992. Antibacterial and antiviral activity of camel milk protective proteins. Al-Nakhli. Agab. Aqab and B.S. Medicine and surgery of South American Camelids.. Camel Pruc.M. Zoot. Cooray and S. 1985. Kh. scient. Trop. H. Al-Shareefi. Orbenin LA@ and Mastalone@. A. Ruegg. It is also important to follow the withholding time of milk after treatment. M.. O. Noaukchott. Mastitis in camels (Camelus dromedarius) in the Sudan. ETH-Zenhwn. Fac.K. The nozzles of the bovine infusion tubes are too big. E. Camelforum. 1992.H. Husb. Al-Sultan. Anim. Laboratory of Dairy Scient.E. Bolbol. Al-Ani. H.K. the udder or the infected quarters should be emptied. Inhibition of pathogenic bacteria by camel milk Relation to whey lysozyme and stage of lactation. Prod. Short communication. 31 (1): 58-59 Barbour. Astroem. O. 59: 169-175. 1991. 7 4 2901-2904.Sh. Zakrisson. 1982. Abbas. 1992. O. 1984. 10: 215.M. Agab and LE.S. 1995. Assiut. Mamoun. The creaming properties and size distribution of fat globules in camel milk. J. Bornstein.. J.A. Peracute and sometimes acute mastitis require parenteral treatment with antibiotics along with local infusion. Med.A.R. M. Fowler. Al Nakhli and A. Abdi and G. and M. Ed. 1996.I. E. Zurich. Abdurahman. Bornstein.: Bonnet. H.H.I. Camelids should be restrained and then rolled on their sides with the hind legs roped back.. A. 1996.R. J. Nabbut. Champagne and R. N. O. Relations between udder infection and somatic cells in camel (Camelus dromedarius) milk.A. animaux laitiers. Ismail. Prevalence of mastitis among camels in Southern Somalia: a Pilot Study. 1984. which should be infused according to the manufacturers' recommendations. P.. C. the teats should be cleaned and disinfected with an alcohol wipe. Properties and products. Antimicrobial factors. Indagine sulla diffusione delle mastite del dromedario (Camelus dromedarius) in Somalia. Vet. Abdurahman. Z.A. References Abdurahman. W. Iowa State University Press. H. N. Ames.A. J. 3'6 meeting of British Vet. vet.152 Bacterial Diseases tibiotic mastitis ointments. Streak canals should only be penetrated with a 1mm tomcat catheter to avoid any injuries. Osman. LFO. E. Dairy Sci.M. B. The detection of subclinical mastitis in the Bactrian camel (Camelus bactrianus) by somatic cell count and California mastitis test. Compagnucci and H. Abdurahman. Prod. R. This is sometimes difficult to do when there is a lot of pain. S.. Vet. 14-16 November 1996. 4 71-76. Camel mastitis in Western Sudan. Abdurahman. Swiss Federal Inst. 1998. med. 1996. and M. Mogadishu. 17 (3): 173-179. Arts and Science. Bakhiet.M. Studies on mastitis in lactating one humped camels (Camelus dromedarius) in Iraq. 4 (1):47-49. 1991. C. Sc. Camel's colostrum. the exudate should be removed from the gland three to five times daily by gently massaging the udder.The ultrastructure of cells and cell frag- ments in mammary secretions of Camelus bactrianus. J.K. Mauritanie: 177-1 79. Relationship between udder infection and inflammatory parameters in Sudanese camels (Camelus dromedarius).

Y. M. tional supplement among chronic pumonary Vet. Mal. and Z. S. Prasad. Anouassi. Narimani and M. lnst.A. A. S.S. K. Sa1996.. Camel prod. Preliminary observation on Ramadan. Suchitra Sena. Shang and Caimude. H. 1988. Univers. Singh. elus dromedarius) caused by Corynebac. 1927. Ragab.. 59 (8):650-651. drought conditions on the quality of camels’ Leese. Fazig. 1 (3):837-844. Y. S.. Idris. Kosparkov. J. Molla. 1982. K. and B. Ramadan. 47 (1 & 2): 117-128.S.S. R. sci. Plebani. l?. 4 7 159-166.. UAE. Fayed. 8. Studies on mastitis in farm 1992.V.O. Sadri.. Dis. a clinical pathological study. 1998.S. A. Prajapati. Pays trop. Biochem. Entessar. El-Amrousi and R. Zurich. 10: 211-217. Gadir. F.P. and J. Field investigation. Res. G. A.Sc.A. Rev. Biochemical studies on Sudanese Kapur. J. 24-26 Oct. Paris 11. 67A: 207-209.int. Etzion. Mid. Epidemiological survey of corynebacteSayed. Velona.E.E. A.M. Z.M. 12 (23): in camelidae. Rev. A peracute case of mastitis in a she-camel J. camel.M. Gansu. land. 12947. M. Milk yields of Escherichia coli. Esterabadi. Z. Hafez. C. B 34: 340-342. Meeting on camel dromedarius) in eastern Ethiopia.A. J. tech. Bekairi and P. 7 (1): 97-100. M. Epiz. Mostafa.H. T. S. 1 Hashi. Physiol. Chen and Y. and Vet. sis on protective proteins.: she-camel milk for detection of subclinicalmas51-54. 1989. A. Sci. Working paper. Sci.A. ExObied. Supp. R. Abu Dhabi. . analysis of camel milk proteins with emphaUAE. R. Safwat. Etzion. H. 1983. associated with Klebsiella pneumoniae and Yagd. 1984.1998. Jain and M. Cavagni. Pate1 and C. Assiut vet. and A.Udder 153 desert. Mousa. G.. 1987.. Bagadi and M. B. chez la camelle (Camelus dromedarius) dans G. A.P.. S. camels (C.I. ISt analytical studies. 1983.Z. Of. Egypt Vet. Algasnawi. Elev. 1998. and Z. A. 30. Patholo239-241. Y. ETH No.. Asbrucellosis in camels in central Saudi Arabia. A.Z.M. Ismail. and M. Chen. 1980a. Dairy Res. S. 93. El-Danaf riosis of Bactrian camel in Subei County. J.Antibacterial properties Comp. 1999.A. V. 2 7 61-66. Abdalla and A.B. Switzerland. Sud. University of Khartoum. Radwan. Etude baccamel. Prevalence and bacteria isolated from mastitic milk of rural etiology of mastitis in camels (Camelus camels in India. Abd-El-Rahman. Thesis. A. R. camel in health and disease. A. med.Tibary.M.S. Utility of raw camel milk as nutrithe somatic cell content of camels’ milk..G. A. A. Zh. 19: 140-145. A. of camel’s milk. Anatomy. 61 (1):55-58. Arch. 1987. Infect.M. Beretta. 135 (11):705-707. A. E. camel in Iran. Gaiascha. Obied. The nature of human brucelCorynebacterium pseudotuberculosis from losis in Kuwait: Study of 379 cases. 1975. 1997. 1987. J. Mastitis in Camelus dromedarius and hani. Anim. Abu Dhabi PrintKappeler.M.. Scotles Emirats Arabes Unis.. the camel. siut Vet. Isolation of Marafic. Whabi. May Prac. Proc. Z. University of Aberdeen.. Vet. Bey. D. l?R. A. med. 1984. CorA clinical case of mastitis in she-camel (Camnell Vet. Quarzazate. Soliman and M.T. Med.. Further reading Mody. J.S. El.. El-Abdin camel milk production and composition.M. Workshopon the young Quandil. gy and Artificial Breeding. Han. clinical and periment on immunisation against Corynelaboratory findings of camel mastitis. El1984. dromedarius) in drought areas.F.A. Shouman. Serological and bacteriological study of animals in Al-Hasa. Ouadar. Han. titis. Diss. Hedayati. 77 (2): 132-150. M. A. E. A treatise on the one-humped milk. N. lnd.O. Acta Agric. Mriologique de quelques cas de mammites Restani.Theriogenology terium pyogenes.Y. Rev.I. vit. S. Morocco. Awadelsied and O. Shang.K. 2: 47-58.M..V. Physiology. Int. Veterinarnoi Sanitarri 51: Yagil. A.Hassan. Compositional and structural ing and Publishing Co. and Res. 1987. J. The effect of 37-40. Vigot Freres. 2-3. Khanna and R.. Fiocchi.O. Poiesi.I. 1980b.A.Med. lnt. Khogali and A. A study on antimicrobial susceptibility of Almaw.K. bacterium pseudotuberculosis of the Bactrian Thesis. A.J. 2000. J. andfuture perspectives.S. A.J. tuberculosis patients. Ass.A1Ain. camel milk collected from Butana Area. Razi. 1975. Mukhtar. Mina. A. Vet. Elhag.A. Gansu J. Chronic obstructive mastitis in Hassanein. lnst. Examination of raw Gansu.

Cross-reactivity between milk proteins from different animal species. Bacteriological quality of camel's milk with special reference to mastitis. Clinical and Experimental Allergy 29 (7): 997-1004. Younan. Streptococcus agalactiae infection in Kenyan camels (Camelus dromedarius). Morocco. and A. Sci. .G. N. Sci. M. J. Pustules in camels. Med.Anim. 24-26 Oct. Huang. Assiut Vet. Gansu J. 1999. Matofari. J.L. 1987. 2 8 194-198. and Med. Xinjiang Anim. Ugazio and C. 1993.EI-R. Int. Saad. B. 3 4-5. Shen.W. Galli.G.M. Wu.Y. 4: 26-30. 1981. 73. and Techn. Workshop on the young camel. and J.. Thabet. Quarzazate. 1999.154 Bacterial Diseases A. and D. Comparison of biochemical reactions of some pseudotuberculosis strains isolated from corynebacteriotic camels in the different districts of China.S.

stiffness and the characteristic disturbduced simultaneously. particularly deep punc. In CNS and then producing the descending most cases.7. Cattle are resistant to tetanus infections. Through to tetanus. The spores multiply in disease similar to tetanus in their book. tetani spores can then are the most sensitive of all species. C. Dromedaries of ma occurs to the initial site of infection any age may develop clinical signs. chronic form of the disease occurs. it is introduced into tissues clinical signs of tetanus (Seifert. massive toxin production following severe Etiology and Epidemiology %I Clostridiurn infection.released following multiplication and lysis tibodies to tetanus have been detected in of the bacteria in the organs and may reach dromedaries with no disease. The highly active neurotoxin is external wounds are very common and an. some of them sefrequent puncture wounds due to the long vere. with spread from the site of infection into the the exception of humans. After the Almost all mammals are susceptibleto teta. C. Small fied tetanus antibodies in dromedaries that amounts of material contaminated with did not exhibit any signs of the disease. Tetanus in camels is considered to be anaerobic environment. 1987). which provide a suitable cally in Fig. tetani is also able ances of mastication. leading to great loss. 1992). and/or received external injuries. tetani into the wound if.agnosed only 4 cases of tetanus among es. 1920. producing the typical ascending clinical signs of tetanus. Curasson. the toxin may directly breach the tetani. Ramon and Lemetayer (1934) identihard thorns of the acacia bush. thereby reaching the spores. Schwartz and Dioli (1992) described a C. Tetanus in cam.1 Tetanus .there into the liver and spleen (idiopathic ty of OWC and NWC is unknown. tetani susceptibility to the tetanus toxin. How- 1.noise or physical contact. but there is a wide variation in the tissue falls. Reflex activity is into vegetate for months in the wound until creased and the animals may suffer a tetansuitable conditions for growth develop. Rabagliati (1920) diusing rubber bands). an anaerobe with terminal spheric blood-brain barrier. the tissues only under certain conditions.acute form is supposedly very similar to troduction of C. aerobic bacteria are also intro. The toxemia often occurs in sheep following castration or insigruficant (Rabagliati. Dromedary owners in East Africa call this especially when the oxygen partial pres. neck for example.000 Egyptian dromedaries over 3.(Blood and Radostits.oxygen partial pressure of the surrounding nus.These relationships are shown schematiture wounds. The This may occur immediately following in. 25. 1990). Since tetanus). is found in soil and feces. Infection with tetanus in camelids oc. especially when 1947. Mustafa. it may be the central nervous system by retrograde concluded that camelids are quite resistant axonal transport.blood vessels and lymph system and from elids is rare and the degree of susceptibili. 78. An acute and sure is reduced in the surrounding tissues. be it This may be the case when a second trau.5 years.the "stiff neck syndrome". through wounds. the strictly anaerobic C.g.The initial injury may even have long healed. ic seizure at the slightest provocation. classical tetanus with muscle spasms. Horses can multiply.although the majority of the animals had curs via a contaminated wound. cropping of the tail (e. tetani spores may be introduced into the puncture channel.

and the other half i. 1995. antibiotics and chlorpromazine 2. The typical jaw spasms. Abu Bakr (1992. Liver Neurotoxin Spinal Cord Central Nervous System Tissue Infection Lymphatics Massive Neurotoxin Neurotoxin Figure 78 Development of ascending (slight infection) and descending (massive infection) forms of tetanus ever.000 IU of tetanus antitoxin. Rabagliati (1920) and Morcos (1965) have described similar clinical signs. All sick animals should be placed in a quiet. darkened box-stall and good nursing is invaluable during the acute period of spasms. One llama suffering from tetanus was given the treatment recommended for tetanus in cattle: tetanus antitoxin at a dose of 225 IU/kg body weight (half i. stiff neck. During the acute phase of the disease muscle relaxants might also be used. the following clinical signs describe a racing dromedary suffering from tetanus (tetanus occurs sporadically in racing dromedaries in the UAE).156 Bacterial Diseases Slight Spores Blood Vesse Is Spores Spleen. Specific tetanus antitoxin is available and should be used in valuable animals. Closfridium tetuni is susceptible to penicillin and a full dose of this antibiotic should be administered for 7 days. erected ears and fixed stare. only individual animals are affected. The dose is unknown for camelids. 1965).).m. The camel was recumbent for 3 weeks while it was treated.000 I of tetanus antitoxin in conjuncU tion with tranquilizers or barbiturate sedatives have been effective in the treatment of horses. Both animals recovered within 12 days. If animals are unable to drink or eat. a drooping nictitating membrane and all four extremities extended sideways (sawhorse). Clinical Signs As clinical signs of tetanus in NWC and OWC are very similar. 1961 to 1962a). but 300. . Morcos (1965) treated two dromedaries in Egypt for tetanus with Combelen@ and penicillin. The author is of the opinion that the quick recovery of the dromedary was primarily due to the Combelen@ therapy.v. and two cases in llamas in the USA (Keller. antibiotic treatment and artificial feeding via a gastric tube.2 mg/kg/6 hours as a tranquilizer (Fowler. Other signs included dyspnea. Two cases of tetanus have been reported in alpacas in Peru (Moro Sommo. wound debridement. rigid tail and stiff gait developed 14 days later. Only one dromedary was given 2 x 30. Control and Prevention The UAE dromedary recovered within 3 weeks following intravenous application of 2 x 100 mL tetanus antitoxin during the first 72 hours. 1995).one case of tetanus in a llama in Argentina (Toucedo. 1998). artificial feeding via a gastric tube is recommended. Lopez and Snyder. a stiff tail. Both authors observed stiffness of the neck muscles. increased muscle tonus in the entire body. personal communication) described a racing dromedary that initially had a deep laceration on the hind foot.

Listeria monocytogenes can also infect humans via food including soft cheeses. The bacteria are readily cultured on ordinary media and some strains grow only at 4°C. particularly the pons and the medulla ob- 157 1. Two adult llamas contracted encephalitic listeriosis in New York with abortion. They were confined to the brain and the spinal cord. f i Epidemiology Listeriosis has a worldwide distribution. 1961 to 1962b. non-spore-forming. Five serotypes and a number of subtypes have been identified. three of them only through the cold incubation. monocytogenes. abortion (llama) (Mc Laughlin et al. 1965. Three animals had developed encephalitis from which L. The course of the disease is usually 3 to 5 days (Moro Sommo. monocytogenes was isolated from the brain... Some cases develop u i nlateral facial nerve paralysis in association with drooping lips. An emergency vaccination with a live Listeriu vaccine was administered which stopped the further spread of the epizootic (Mayer and Gehring. 1991). ears. decaying vegetation and silage with pH of over 5. monocytogenes was isolated from one of the llamas. A listeriosis outbreak in a German zoo occurred in 1975 during which six llamas died.Nervous System Tetanus toxoid vaccines are readily available and should be administered before any surgery. eyelids and paralysis of the jaw and pharynx. The other three llamas died from septic listeriosis from which the organism was isolated from different organs. 1998). which interferes with mastication and swallowing.4 to 0. Listeriu can multiply and it is commonly implicated in outbreaks of listeriosis in cattle and sheep. The surface of the leptomeninges was rough. running into . The disease occurs most frequently in sheep. 1975).The mortality rate can reach 100%. It is. Haenichen and Wiesner (1995) described two cases of septic listeriosis in 10 day-old alpacas after feeding poor-quality corn silage. It was mentioned that heavy rains had flooded the zoo and there was an acute outbreak also in other ungulates. 1991). measuring about 0. 1994). Only individual animals are commonly affected. Tapia Cano. 1991).5. dark red and thickened with a ti layer of yellowhn ish exudate.L. 1989).. more common in regions with cold temperatures and it is often associated with the feeding of poor-quality silage with a pH higher than 5. Not only meningoencephalitis is caused by L. Butt et al. Microscopic changes are confined to the white and/or gray matter of the brain stem. monocytogenes is a medium seized Gram-positive rod. It causes sporadic outbreaks in NWC (Fowler. otitis media and intema with suppurative meningoencephalomyelitis (llama) (Van Metre et al. L. Llamas respond to toxoid vaccination with a rise in titer. 1975. ataxia.5 pm in diameter. Clinical Signs and Pathology Listeriosis causes a meningoencephalitisin NWC with circling.5. objects and fever. Silage is not fed to OWC and this might be the reason why OWC do not contract listeriosis. and facial paralysis followed by death (Butt et al. Listeriosis has been reported from NWC but not from OWC. Hamir and Moser (1998) described lesions found in a 2-year-old female llama at post mortem. 1993) and septicemia with thrombocytopenia and hepatopathy (llama) (Semrad. From this outbreak different serovars were cultured. but also septicemia with polyarthritis (alpaca) (Wisser. milk and poultry meat and coleslaw. but both were positive in the immunofluorescent test.2 Listeriosis Listeria bacteria are widely distributed in the environment and can be isolated from soil. goats and cattle. Mayer and Gehring. In silage. trembling of the head.7. depression. plants. however.

monocytogenes. and E. lnvest. Ber. Haenichen. Zootiere (Tunis)1 7 307-312. Lemetayer. Med. thesis. and G. Hamir and Moser (1998). Rabies must always be considered in the differential diagnosis. and M. 1998. Moro Sommo. 1998. . Fac. (Lima) 16-17 160-162. lesions and immunofluorescence of Listeria monocytogenes in brainstem lesions. 116 (18):275-277. J. 1961-1962b.S. 1965. Weldon. Seifert. and H. 81: 251-258. Morcos.E.E. Erkr.N. Treatment of tetanus in the camel.C. Erkrankungs. Moro Sommo. M. Vet. Ramon. 1 1 Tetanus. 1920. 17thlnt. I. perivascular infiltrationsof mononuclear cells and microabscesses can be detected. G. France 55: 18-22. Med. 1934. A. Path. The authors also observed a multifocal acute necrotizing splenitis and on immunohistochemistry there was a positive immunoperoxidase reaction to L. M. H. 1995: 2-4. Mayer. and J. Stuttgart. Cornell Vet.G. Veterinary Medicine. H. Semrad. OIE 55e Session g6n6rule OIE. Hamir. Lopez.158 Bacterial Diseases longata. Medicine and surgery of South American Camelids. Investigacion de Listeria monocytogenes en la medula oblongata de alpacas aparentemente normales. A pictorial guide to diseases. Iowa State University Press. 1947. Gehring.R. G. Immunohistopathological findings in an adult llama with listeriosis. Bacterial diseases of the camel and dromedary.C. Keller.. are of the opinion that the encephalitic form of listeriosis in NWC is not manifested as microabscesses in the brainstem. Lockjaw in a llama. 2: 132-134. Univ. 1965. Enfermedades 1 infecciosas de las alpacas. Singh.Gustav Fischer Verlag Jena. Med. F. M. Infectious diseases of alpacas. Curasson. Verhund. McLaughlin. B. Vet. Vet. Treatment and Control signs have developed the prognosis is poor. Paris.und Todesursachen bei Neuweltkameliden. 1991. Vet. Ames. Rec. Greer and S. S. Vet. (Lima): 129.J. Editeurs: 86-88. and H.T. JAVMA 204 (2): 213-216. Infeccion a Clostridium tetani en una llama.E. monocytogenes. Sur l'immunit6 antitetanique naturellement acquise chez quelques especes de ruminants. Equine Pruct. Radostits. 1998) are two fast methods for the diagnosis of listeriosis. 1965. Schwartz. Moser. Le chameau et ses maladies. 1975. the liver and spleen should be cultured. M. Fuc. T. 33: 10-12. Culila Newsletter Dec. D. 1993.Sc. Vet. 1961-1962a. M. C. Specimens of choice are brains from animals with CNS involvement. A. Penicillin at a dosage 44. The onehumped camel in Eastern Africa. If primary isolation attempts fail. Tropentierhygiene. 1994. 17 (4): 26-31. Tapia Cano. Encephalitic listeriosis in two adult llamas (Lama glama):clinical presentations.H. Listerial abortion in a llama. G. San Marcos (Lima): 1-45. Mayor. London: Bailliere Tindall. A. References Blood.Biol.J. Ther. Nac. aborted placenta and fetuses.D. Listeriose bei Lamas. health care and management. H.M. A live vaccine has been successfully used in a German zoo. 1995. Vet. Tetanus in the camel. M. Wiesner. Diugn. 143: 477-479. and O. however. Syrnp. D. I11 Tetanos. Butt. r. samples should be incubated at 4°C for several weeks and re-cultured weekly. Snyder.000 IU/kg twice daily for 1or 2 weeks may be tried. thrombocytopenia. J. 1992. D.B. 1992. Rev. Diagnosis '8 Listeriosis can be confirmed by isolation and identification of L. med. (Argentina)27 (13):432-436.A. An. 1987. 7* edn.. Praxis 23: 515-520. Guc. I m munofluorescence and immunohistochemistry (Hamir and Moser. Premier Congr. B. S. 1990. blood parasitism and hepatopathy in a Llama. Tetanus in a llama.B. comp. O. Nac. Dioli. In the medulla oblongata. Fowler. office internationale des epizooties. Step. SOC. Toucedo. Rabagliati. Rev. Septicemic listeriosis. but as a suppurative meningitis. 1995. Enfermedades infecciosas de las alpacas. Tierk'rztl. Vigot FrPres. dela Hunta and C. Verlag Josef Margraf. 5: 105-106. Huxtable. Seunc. In the septicemic form.R. 1995. Mustafa.

1989. Sero-prevalence of agglutinins to Listeria monocytogenes in Nigerian domestic animals. 42 (3):383-388. 1927.O.M.C. Int. Paris 11. Ippen. 1989.Nervous System 159 Van Metre. Oni. G. ed.B.A.N. Bailliere Tindall. Berlin: Institut fiir Zoo. J.. A. Parish and D. Barrington. O. A treatise on the one-humped camel in health and disease. JAVMA199 (2): 236-240. Leese. 1991. vkt. Pays Trop. Mkd. Sai'du. Elm.M. Further reading Higgins. A. Erkrankung Wildtiere. J.O. S.Polyarthritisbei septikaemischer Listeriose eines Alpakas. Rev. The camel in health and disease. . R. 1986. Otitis media/interna and suppurative meningoencephalomyeltis associated with Listeria monocytogenes infection in a llama. D.S. A.und Wildtierforschung:83-88. Symp. Proc. Adesiyun. Vigot Frhres.. Adekeye and S. Wisser. Tumas.

Viral Diseases .

6 23. the authors prefer to keep them under this heading. foot-and-mouth disease.0 23.Viral Diseases ~~ 163 With the exception of the camelpox complex. Although all camelid species possess multiple physiological and anatomical similarities. Salama et al. Mattson Puntel et al. Table 35 Virus isolation and identification of viral antibodies in camels (except camelpox) . Bovine viral diarrhea virus could come under "Viral Infections Causing Disease".papillomatosis. a grave lack of information exists regarding viral diseases in camelids.3 93.g. and it is believed that they do not differ in their susceptibility to viruses. . A great number of sero-epidemiological virus studies have been performed in the camel. .camelpox. Awad et al. Picton Galbreath et'al.a summary of the literature arranged alphabetically by disease DiseaseIVirus Adenovirus BAd Vlll Isolate 7649 Anti.6 13.llamas.0 0. . whereas equine herpesvirus (Em-1)has been reported as being pathogenic to camelids. Although several viral diseases mentioned under the chapter "Nonpathogenic Viral Infections" might cause mild clinical signs in camelids (e.ecthyma contagiosum. . as very little is known about its pathogenicity in dromedaries.0 . Hafez and Ozawa Afshar and Kayvanfar Eisa Abu Elzein Abu Elzein Stanley Simpson Year 1989 1993 1994 1994 1999 1981 1986 1986 1988 1992 1993 1973 1974 1980 1984 1985 1990 1979 X X x x x x x x x x African horse Sickness X .13 llamas Argentina X 5.9 5.0 81.rabies.equine herpesvirus. .Antigen body Prevalence (%) 1. .influenza.6-14.4 14. Baba et al. Only a few viruses appear to cause disease in camelids. They include: . rinderpest. A summary of the viral antibodies and isolates found is given in Table 35.9 Egypt Sudan Egypt Sudan East Africa Nigeria Egypt Iran Sudan Sudan Sudan Yemen Botswana - 0 x x x Bluetongue disease - X - - x x x x x 4. .6 16.0 10. comparison of NWC with OWC is important to indicate any possible familial susceptibility.Borna disease.0 llamas -llamas Country Nigeria USA USA Author Olaleye et al. alpacas USA 5. It is worthwhile to mention that bovine herpesvirus1 (BHV-1) does not seem to cause diseases in camelids. Foreign Animal Report Binepal et al. bluetongue).3 5.2 5. but the authors still prefer to keep it in the chapter "Nonpathogenic Viral Infections".rotavirus. Salama et al.

2 alpacas ) 0. 1980 Bornstein et al.7 15. 1980 1993 1997 1998 1975 1980 1987 1988 1988 1990 1987 1991 1993 1993 1994 1998 1999 1999 - Bovine herpesvirus (BHV-1) IBWIPV - 0 x x x x 0 0 0.0 4.0 0. Rosadio et al.0 1.0 5.0 9.0 0.4 llamas 11.77 0.O alpacas 52. Germany (Zoo) Schueppel et al.0 - 0 0 0 X 0.8 0.0 0.5 racing ) 2. Ostrowski Year 1982 1984 1987 1990 1993 1998 1999 1999 1975 1976 1994 - X 0 X 0.0 X X - Malignant catarrhal fever - X 0 . Tunisia Oman Sudan Somalia Djibouti UAE Bovine diarrhea virus - - X X X X X Bovine herpes mammilitis virus Arsentina Oman USA Peru Egypt Tunisia Oman Sudan Djibouti Somalia UAE Peru USA Peru USA USA UAE Argentina Argentina Burgemeister e t al. 1987188 Bornstein 1988 Bohrmann et al. Bornstein and Musa Bohrmann et al. Bornstein Wernery and Wernery Rivera et al. 1999 Hedger et al.5 llamas 5. 1988 Wernery and Wernery 1990 Hegazy e t al. 1995198 CVRL Annual Report 1998 Puntel et al.0 alpacas 13.9 6.0 alpacas . Picton Mattson CVRL Annual Report Puntel et al.4 0.3 6.) DiseaselVirus Bluetongue disease Antiaen Antibody X X X X X Prevalence (%) 23. 1994 Hegazy et al. Stainley Picton et al.0 Country Israel Saudi Arabia Peru Yemen USA UAE Argentina Saudi Arabia Author Barzilai Hafez et al. 1993 Tantawi et al. Puntel e t al.7 llamas .0 llamas 58. 1975 Hedger et al.4 breeding ) 0.2 breeding ) 3.6 racing ) 11.0 4.0 67. CVRL Annual Report Puntel et al. Zaghhana Burgemeister et al.0 NWC NWC NWC 3.llamas 16.5 5. Hedqer et al.llamas 0.164 Viral Diseases Table 35 (cont. Williams et al. Picton Rivera et al.7 llamas ) 16.0 21.7 3.0 0.05 llamas Borna disease x X X - X X X X X X Germany (Zoo) Altmann Germany (Zoo) Altmann et al. Rivera et al.

8 99. Fowler Azwai et al. Nigeria Nigeria Nigeria Singh Maurice et al.3 2.NWC alpacas llamas llamas llamas (exper.C. Jenkins Rebhun et al. Olaleye et al.0 alpaca 0.Asl. Lvov et al.0 . SOMAC-SAREC Yamnikova et al.0 llamas x x x 4. El-Amin and Kheir Olaleye et al. 1969 Tulepbaev 1969 Moro 1971 Dashtseren et al.0 0.7 B Influenza-like Influenza x X X 0 - - 00 .6 12.C. Abu Elzein et al. Wernery and Kaaden Kinne and Wernery Khalafaila et al.0 NWC - Country ~ Author Year o - - x X X X o - X X X X X X - X 37. 1991 Gitao 1994 Azwai et al. Wernery et al.0 TI O.Antigen body x x X 165 Prevalence (%) 0.9 sick herds 0-68 healthy herds .SA X 0 - 1995 1997 1998 1998 1998 1979 1985 1988 1991 1996 1998 1880 1980 1986 1987 1999 1982 1985 1989 1989 1982 1. House et al. - - Equine herpesvirus-1 (EHV-1) X x X X X - FMD virus O.5 18.993 1996 1998 1980 1990 1995 1998 1998 1989 1989 1989 1967 1968 0.) Bactrian Peru Kazakhstan Russia South America Mongolia Kenya Somalia Sudan Kenya Libya UAE Saudi Arabia South America Libya USA USA USA USA USA UAE Afghanistan Oman Niger Egypt Arclentina Mongolia Sudan Nigeria Nigeria Somalia Mongolia Mongolia UAE India Somalia UAE UAE Sudan Nigeria Nigeria Nigeria Egypt Chad 1940/47 Preston Smith Buchnev et al.) Disease/Virus Ecthyma contagiosum Anti.A. Papillomatosis x X X - X X x x x x x Parainfluenza - 1 2 3 3 - 22. Richard Moussa et al.0 0. Munz et al.SAT2 0 Influenza A A A x X 0 x 2. 1986 Moallin and Zessin 1988 Ali et al.Viral Diseases Table 35 (cont. CVRL Annual Report Sadana et al.6 X 0 0.7 0. Puntel et al. Anchlan et al. Pursell et al.5 3. Bildfell et al. 1984 Munz et al. CVRL Annual Report Pringle Hedger et al.

45. 1985 Bornstein and Musa 1987 Djibouti Bohrmann et al. Haji Samartsev and Arbuzov Dhillon Scott and MacDonald Singh and Ata Singh and Ata Maurice et al. Rivera et al.0 29. Saluzzo et al.0 Rinderpest X X 0 x x 0 x X - 0.6 0.0 81. Wernery and Wernery Picton Scott et al. 1988 Sudan Bornstein et al.3 81.0 5.0 80.8 66.0 0.2 Chauhan et al.0 R i f t Valley fever x X X - x x x 22.0 33.7 7. Chauhan et al. Olaleye et al. 1980 Arush 1982 Richard et al. Eisa Slama Davies et al.0 alpacas 0. 1993 UAE Wernery and Kumar 1993 UAE Afzal et al. 1996 India Kumar and Jindal 1997 Nigeria Olaleye et al.1 17.3 42. Abou Zaid 1986 1987 1990 1993 1963 1978 1981 1984 1985 1987 1996 1932-33 1940 1959 1962 1967 1967 1967 1968 1982 1985 1991 . 1975 Frigeri and Arush 1979 Hedger et al.0 - - experimental 9. 1993 South America Miller 1994 Niger Bloch and Diallo 1995 Israel Per1 et al.) DiseaselVirus 3 3 3 3 3 3 3 3 3 Rabies Anti.0 66.166 Viral Diseases Table 35 (cont.7 37. 1981 Somalia Arush 1982 Oman Ata et al.8 alpaca similar Country Tunisia Somalia Oman Somalia Niger Sudan Author Year x x x x x x x x x - - X X X X X x llama Respiratory syncytial virus Retrovirus Bovine leukosis - 0. Imam et al.5 0. Taylor Wilson et al. 1988 Somalia Bornstein 1988 South America Moro Sommo 1958/59 Mauritania Bah et al.Antigen body X X X X X Prevalence (%) 80.0 Burgemeister et al.7 experimental 0. 1989 India Peru UAE USA Kenya Egypt Sudan Tunisia Kenya Mauritania Nigeria India Russia India Kenya Egypt Sudan Chad Kenya Kenya India Eqwt X 0 0 0 0 0 0 llamas .

) DiseaseNirus Rotavirus Anti. Saidi et al.Although many have been isolated from camels and their ticks. . which are widespread in the tropics and subtropics. . Togaviridae. Year 1983 1987 1999 1998 X x x x - - x = positive. Bunyaviridae Dhori virus Wanowrie virus. Anderson and India Casals Country Year 1982 1982 1988 1973 1973 1975 1979 1980 1980 1990 1996 camel ticks camel ticks Egypt Iran Russia UAE Iraq Egypt Oman Williams et al. At the end of the section on viral diseases we report on "Unusual Arboviruses". Converse and Yemen Moussa Arabian Peninsula Al-Busaidy et al. The results do not indicate whether the exposure has produced manifest disease or how severe the disease response may be. Iraq. Hoogstraal Suleiman et al. Puntel et al. Serological results have a limited predictive value since they only confirm whether or not the animal has come in contact with a viral agent and has produced antibodies. their significance to camelids is not yet known. Morrell et al. 0 = negative Unusual Arboviruses Origin Kadam virus. Flavivirus camel ticks Quaranfil virus camel ticks Akabane virus.0 alpacas 87. Mohammed et al. The sero-epidemiologicalstudies have confirmed that the camel produces antibodies against a great number of pathogenic viruses without developing the disease. Thogoto virus. Dhori virus Congo hemorrhagic virus serology camel ticks Author Saudi Arabia Wood et al. Scrinaeour et al.Antigen body Prevalence (%) 50.= not done.7 llamas 167 Country Morocco 5. America Argentina UAE Author Mahin et al. Tantawi et al. Kuwait. Many can severely affect humans. Rivera et al.Viral Diseases Table 35 (cont.

In Niger. 4) Kumar. rabies virus (Zyssavirus serotype 1)and the 1959). Rhabdoviruses are rod or bul. camels. cattle. Little is known about the epidemiologsegment of single-stranded RNA and there are five structural proteins.subject.. Three types of rabies have been difand viral proteins accumulate here. Ata lysis and death.The sylEpidemiology Rabies is an infectious vatic form plays the greatest role on the disease transmitted via the saliva of infect.2. Oman rabies-related viruses (Lagos bat.Rabies-likediseases with hindquarter parephagus dipterids in Africa. Although rabies in dromedaries has supEtiology The rabies virus belongs to the posedly been observed in many African family Rhabdoviridae. which are isolated from birds and hemato.and Asian countries (Richard 1980 and virus. Replication oc. 1990). Mokola. cotton generally transmitted by the bite of a dis. 1997) and Israel (Per1 et al. the sylvatic Negri bodies. Niger are biologically and antigenically different (Bloch and Diallo.Arabian Peninsula. South America sis have been reported by Arush (1982) and and Australia. Mauritania (Bah et al. 3. 1993). It causes encephalitis. the have appeared from Morocco (Chevrier. 1993. Rabies is a fatal disease for humans and all however. 1996).ferentiated. (Ata et al.. rabbits and cats are elids are susceptible to rabies and the dis. Recent reports of rabies in camels groups.India (Kumar and from seven other viruses of this group Jindal.1 Rabies . The genus Lyssavirus includes the 1986).. Rabies is most probaed animals and is characterized by disturb. Bloch and Diallo (1995) reportvores or vampire bats only sustain the cyed that a rabid dog was responsible for a cle of infection. It can only be presumed man usually occurs through a bite.The genome consists of a single daries. 1990).et al.bly transmitted by the red fox in the UAE ances of the central nervous system. sheep and goats are ease has been extensively studied in NWC less susceptible.rats and prairie wolves are extremely suseased animal. the UAE (Wernery and Duvenhage = Zyssavirus serotypes 2. Radostits. 1993) and by wild dogs in Yemen bies virus from animal to animal and to (Stanley. Opossums are most probably not susceptible to rabies (Blood and due to its zoonotic aspect.1 Viral Infections Causing Disease JUIIII(1UIi Warm-blooded mammals as well as birds are susceptible to the rabies virus.ceptible. 1993. depending on which animal tuting the inclusions seen histologically as species serves locally as the main reservoir and vector: the urban form. Cam.ical interdependencies of rabies in the curs in the cytoplasm of the infected cell camel. 1981).. there are substantial variations in other warm-blooded vertebrates which is susceptibility to the virus. which includes the genus Lyssavirus and the genus Vesiculo. rabies outbreak in 7 camels in a herd of 40. consti. Afzal et al. Foxes.very susceptible.that these animal species are the vectors of vores and man are the final hosts and do rabies on the Arabian Peninsula as there is not normally play a role as vectors. 2.dogs..and Oman (Wernery and Kumar. Within the rabies serogroup. 1995). little has been published on this rabies and bovine ephemeral fever sero.1. Carni. The transmission of the ra. form and the bat form (paralyssa). 1993). Herbi. para.Somac/Sarec (1982) in Somalian dromelet-shaped.very little available research.

1990. trembling and sternal recumbency. 1968). The animal showed the "silent fury" of rabies with weakness. An immuno- Figure 79 Rabid dromedary: the attempted yawning is typical for rabies . Anonymous 1990a.After an incubation period of 3 weeks to 6 months (Higgins. Peck (1966). The intracerebrally infected mice showed paralysis 12 days after the infection and the brains were positive for rabies in the fluorescence test. which can last one or two days prior to death. affected lamoids died 6 to 8 days after the development of clinical signs. Direct fluorescent antibody testing of hippocampus. Experimental rabies has also been produced in llamas (Tamayo. the following clinical signs are seen in cases of the "raging fury": restlessness.. 1995). The latter form is seldom seen in the camel (Leese. Reid-Sanden et al. 1986).Blood and Radostits (1990) consider these motions to be aphonic bellowing. 1993). the rabid dromedaries lie on their sides and flail with their limbs. Miller. 1990b. 79). 1 aggression. Curasson 1947. Krebs et al. cerebellum and medulla for rabies was negative. 1992. Post mortem examination revealed a mild edema around the spinal cord at L7. However. During this stage. 1958-1959). 1927. only dogs were responsible for outbreaks in alpacas in Peru (Moro Sommo. 1958-1959. Per1 et al. Krebs et al. 1994. skunks and bats. This excitative state lasts 1 to 3 days in the dromedary and is followed by the paralytic phase. They include dogs. (1981) have described two forms of rabies in the dromedary: the "raging fury" and the "silent fury". Transmission of rabies from alpaca to alpaca by bites has also been reported (Franco. several vectors are responsible for the spread of rabies.. (1996) reported an unusual form of rabies in an %yearold dromedary belonging to a herd of 150 camels in Israel. itching/ scratching together with self-mutilation. raccoons. Mustapha. foxes. Mustapha (1980) and Bah et al. but the mouse inoculation test was positive. Clinical Signs and Pathology :. 1905) and there are several reports from the United States (Moro Sommo. biting and snapping. The incubation period in NWC that had been bitten by dogs was between 15 days and 3 months. The attempted yawning is a typical symptom of rabies in the dromedary (Wernery and Kumar. hypersalivation and muscle tremor. During the paralytic stage.. 1993.Viral Infections Causing Disease 169 In America. 1980). 1991. Krebs et al. the dromedary attempts to yawn continuously (Fig..

Anorexia.170 Viral Diseases Figure 80 Foreign bodies found in compartment 1 in a dromedary with rabies histochemical investigation of the camel's brain was also negative. facial paralysis and pharyngeal paralysis characterize paralytic rabies in NWC. the aggressive form is also usually recorded and seldom the paralytic syndrome (dumb form). 1998). In NWC. The only visible abnormality is congestion of the leptomeningealblood vessels. rabies virus antigen-containing cells were detected. Animals may Figure 81 Non-suppurative. It is worthwhile mentioning that lamoids suffering from rabies cannot spit due to the paralysis of the pharynx (Fowler. penmates and offspring and selfmutilation. the spinal cord should be included in the diagnostic procedures. The major signs of furious rabies in lamoids are attacks on people. circling. salivation. but when the lumbosacral to thoracic sections of the spinal cord were tested. The rabid animals may also bite inanimate objects. non-purulent encephalitis in a dromedary with rabies . The authors stress that in rabies-suspicious camels. There are no consistent macroscopic lesions in animals that die of rabies.

Negri bodies can be demonstrated in impression smears prepared from fresh glycerol-saline preserved brain tissue or histologically in formalin-fixed tissue (Fig. 81). The rabies virus causes a nonsuppurative. small batteries. 1996). There is focal and diffuse gliosis. neuronal degeneration and intracytoplasmic inclusions (Negri bodies) in the neurons.. The standard method of making a diagnosis of rabies is to demonstrate rabies virus antigen in impression smears of fresh brain by immunofluorescence. euthanize it for laboratory examination. pieces of glass or porcelain have been found in compartment 1 in dromedaries (allotriophagia)(Fig. nonpurulent encephalitis with perivascular cuffing by mononuclear cells (Fig. The most significant microscopic lesions of rabies are in the central nervous system and cranial and spinal ganglia.In all of the rabid dromedaries examined by the authors. massive viroplasms of rabies virus antigen conglomerates of varying sizes were seen immunofluorescently in the brain. The third diagnostic method for rabies is the isolation of the virus by intracerebra1 inoculation of brain suspension into weaned mice. Veterinary officials should be notified and they should decide whether to confine the animal and keep it under observation for a period of 14 days. Isolation of the virus is confirmed by histopathological examination of the mouse brain and by immunofluorescence. but the distribution of lesions or virus antigen varies and it is recommended that tissue samples be taken from a variety of sites in the brain and spinal cord (Per1 et al.Viral Infections Causing Disease 171 be emaciated and there may be self-inflicted wounds or injuries sustained during fights. 82). 80). The hippocampus is commonly used for the diagnosis of rabies. Figure 82 Rabies in the dromedary: masses of virus antigen in the hippocampus (immunofluorescent stain) . Animals should be euthanized in such a way as to avoid any damage to the crani- um. 83). and then. particularly Ammon’s horn (Fig. Diagnosis Any abnormal behavior of camelids should be considered suggestive of rabies. Foreign bodies such as nails. Suspicion of rabies is heightened when the affected animal comes from an area where the disease is known to be endemic. only if it develops overt signs of the disease. The diagnosis of rabies can only be made on dead camelids. This method is very sensitive and it may take up to 4 weeks or even longer to obtain a result. stones.

however..0 mL bies is a viral disease that can be effective. Seven months post vaccinapermanent cell line cultures are available. Kalanidhi et al. m munoprophylaxis is possible with both Serological tests were performed four live attenuated virus vaccines in foxes and times on the dromedaries during a 13 vaccines from inactivated virus. Fowler (1998) stresses that no single test should form the basis of a definitive diagnosis of rabies in NWC. A range of highly effective. Active i ..sults following application of an inactivatment for rabies infections in animals.shot of an inactivated rabies vaccine at 14 bies vaccines for animals prepared from days post vaccination can be regarded as virus grown in a variety of primary and satisfactory. It is recommended that antibody titers equivalent to at least 0.declined to low levels or disappeared altosponse to vaccination is an important fac. Germany) As mentioned earlier.subcutaneously) to a small herd of dromly controlled by vaccination. Dahme.gether. Young herbivores should be vaccinated at the age of 4 months and/or 9 months if the dam has been immunized. 1996). Boosters should be administered annually. The response of dromedaries to a single tivated vaccines. These tests are mainly performed to assess a response to vaccine or to identify virus isolates. Ra. Similar results are shown by Sihvo- .172 Viral Diseases Figure 83 Rabies in the dromedary: Negri bodies in the hippocampus (HE stain. Sihvonen et al. 1992. The results are summarized mesticated animals can be given only inac. He recommends histological investigations. tor in protection against rabies infection. 1998). Several serological tests like ELISA may demonstrate antibodies to the rabies virus. fluorescentantibody staining and rodent inoculation for the diagnosis of rabies in NWC.5 W/mL be obtained to protect animals from rabies (Barrat et al. inactivated ra. 1993). All do... courtesy of Prof.edaries in the UAE are presented below. Killed rabies vaccines have been used with success in OWC (Wernery and Kaaden. spinal cord samples should be included in all investigations (Per1 et al.in Table 36. The duration of protective immunity to challenge with rabies virus generally varies from 1 to 3 years.ed aluminum hydroxide vaccine (1. tion.month period. Some serological reTreatment and Control There is no treat. rabies antibody titers had A neutralizing antibody produced in re. 1998) and in NWC (Fowler. 1995. safe and thermostable.

3 9. 24 hours before vaccination 14 days after vaccination 173 7 months after vaccination 13 months * ** nen et al.5 7. Tubingen.5 0.1 < 0.1 < 0.1 < 0.5 13 0.1 7.1 4 0. RFFIT)* before and after rabies vaccination with an inactivated aluminum hydroxide vaccine (1.1 c 0.1 < 0.5 c 0.1 0.1 0.5 1.1 c 0.1 14 c 0.1 23 c 0.5 0.5 0.1 21 c 0.1 2.1 < 0.1 8 < 0.5 IU/mL are considered protective against rabies in cattle (Barrat et al.1 15 16 < 0.1 c 0. (1993) in reindeers.5 0. The data shows that one dose (1mL) of inactivated rabies vaccine induces good.5 < 0.1 < 0.1 5.2 0.1 2.1 17 0.1 c 0.1 4.1 5.5 < 0.5 < 0.1 < 0.1 4.5 0.5 1.1 < 0.1 3. Germany Titers higher than 0.5 3 c 0. France and Federal Research Institute for Animal Virus Diseases.1 0.1 19 20 0.1 1. Killed rabies vaccines administered to llamas produced titers that are considered protective in other species. 1992).1 c 0.5 < 0.1 c 0.1 < 0.1 < 0.1 < 0.1 18 0.1 18.1 18.5 c 0.1 7 0.1 Performed by Rhone Merieux.Viral Infections Causinu Disease Table 36 Serological test results (Rapid Focus Fluorescent Inhibition Test.3 < 0.1 < 0. Fowler (1998) recommends administering only killed rabies vaccines (also to NWC) as a modified live virus vaccine (MLV) given to 290 alpacas following an outbreak of rabies caused postvaccinal paralysis in 10% of the vaccinees within 14 to 30 days.1 c 0.1 5 6 c 0.5 < 0.. a booster dose of vaccine is necessary 6 to 8 months after primary vaccination to guarantee sufficient protection against rabies.1 < 0.5 0.3 c 0.3 9 10 < 0.1 25 < 0. Titers are given in international units (IU/mL)**.1 22 < 0.1 < 0.5 < 0.1 4.1 < 0. Therefore.5 < 0. or in the individual animal's response to the vaccine.1 < 0.1 11 12 0. but shortterm serological conversion in dromedary camels.1 28.5 0.5 < 0.O mL sc).5 0. Llamas have contracted rabies in a num- . (1998) presume that the reason for this discrepancy may lie in the difference of camel breeds used in the study.1 c 0. Lyon.5 0.1 2.5 0. The duration of the immunological response to vaccination was quite different in dromedaries from India.1 3. The authors showed that an inactivated tissue culture rabies vaccine induced a much longer lasting immunity.1 4. Animals 21 to 25 are controls Dromedary after vaccination 1 c 0.1 < 0.5 2 0.5 0.5 0.1 1.5 0. Kalanidhi et al.5 0.1 c 0.1 c 0.1 24 < 0.3 18.1 c 0.

174 Viral Diseases ber of different areas in South America and should therefore be vaccinated annually. Since the virus has been detected in nasal secretions. Diagnosis of BD can also be confirmed by serological methods using indirect i m munofluorescence in infected cell cultures. sheep and a variety of other animal species.1. The virus replication occurs in the nucleus of infected cells. the mode of transmission is still unknown. it was classified by the International Committee on Taxonomy of Viruses as a member of the newly established family Bomaviridae. The disease is restricted to localities in Central Europe. Diagnosis BDV can be isolated from homogenates of infected brain or cerebrospinal fluid by infection of embryonic rabbit or rat brain cell cultures or by intracerebral inoculation of rabbits. BDV-specific antibodies have recently been shown in sera and cerebrospinal fluid from human patients suffering from psychiatric disorders. dogs. However. Among the rabies-related viruses. (1994) also confirmed the disease by immunohistochemistry. Schueppel et al. the host range of the virus includes horses. 84). . Clinical Signs and Pathology In two German zoos. Although the virus shares some physicochemical and physical properties with members of the order Mononegavirules. sheep. are also useful for a diagnosis of BD. Duvenhage is antigenically closest to Zyssavirus serotype 1and rabies vaccines afford the greatest protection against this virus. The animals later died as a direct result of the disease. and least protection against Mokola virus. if present in neurons. camels. Viral antigen might also be detected by immunohistochemical methods. Altmann et al. saliva and urine. cats. In two of these four a i nmals.. especially those inducing the "silent fury". 2. Under natural conditions. 1976. intranuclear inclusion bodies (Joest-Degen bodies) were detected in the hippocampus typical of a BDV infection. Schueppel et al. Furthermore. The lamoids affected did not develop any neurological signs. It would be interesting to determine if camelid rabies viruses from different countries share the same antigenic structure. it might be possible that the infection occurs by direct or indirect contact. genus Bornavirus. and also very likely humans. 1994). Recently. 1975.Positive labeling for BDV was observed in the nuclei of ganglion cells of the hippocampus. Gyrus dentatus and Corpus striatum in the vicinity of inflammatory infiltrates (Fig. ii . Rabies viruses isolated from camels in the UAE were indistinguishable from the Zyssavirus serotypes. BD was diagnosed in NWC in Germany (Altmann. Intranuclear JoestDegen bodies. Epidemiology i:ij Many animal species and different cell cultures can be infected experimentally with BDV. Etiology The viral etiology of BD has been known since 1927. llamas and alpacas that were affected by BD exhibited anorexia and severe weight loss at the beginning of the outbreak. Borna disease virus (BDV) was shown to be an enveloped virus containing a single-stranded RNA of negative polarity. All virus isolates seem to be antigenically identical but there are obvious differences in the degree of virulence. Four alpacas revealed a non-suppurative meningoencephalitis. Diagnosis of BD was confirmed by histopathological investigations.2 Borna Disease Borna disease (BD) is a progressive viral polioencephalomyelitis predominantly affecting horses and donkeys (rarely other Equidae).. cattle.

Fall.A. Radostits. Anonymous.E. Brun. Fowler. Extraordinario 3: 59-60. Epidemiologic de la rage au Maroc. 132 68-69. Vet. and O. M. Verhandhngsber. M. Ass. Assoc. M.I. Paper read at Proc. Lippmann and I. A. H. Rec. 1 7 53-60. A probable outbreak of rabies in a group of camels in Niger. D. vkf.A. Med. N. Brote de rabia en alpacas de m a hacienda del Departamento de Puno. Oklahoma J. M. Editeurs: 86-88. Blood. 1975. H. Le chameau et ses maladies. 34 (3):263-265. Centers for Disease Control.M..O.. D. Vigot Freres. Rep.A. Salman. E. Rev. Centers for Disease Control. Rabies in a llama. Chevrier. Curasson. Anonymous. 29 (3-4):121-129. Khan and R. S. Mkd. Org. Verhandlungsber.O. Chamoiseau. vet. Pan-American Hlth. 1992. Die wichtigsten Erkrankungen der Alt. Al-Ismaily. Symp. F. 7th ed. References Afzal. Oklahoma Morb. Biha and S. Kronberger. 1993. 1947. D. Precausta. Vet. El-Ahwal.L. 263 (16):2766.A. 1976. Rabies in a llama. Medicine and surgery of South American Camelids. 1981. L. Vet.: 24. K. M. Zootiere. Altmann. I. G.-F. Rev. Elm. 1991. Lacoste and P. Rabies problem and eradication in U. Bah. F. Rabies in a llama.R. G. Mkd. 65 (38): 294. Wkly. Cattle vaccination against rabies. Wkly. Anonymous. 39 (12):203-204.H. Schueppel. F.10. 1969. 1993. R.. La situazione sanitaria del dromedario nella Repubblica Democratica Somala.. Ames. Centers for Disease Control. Un foyer de rage Cameline en Mauritanie. Microbiology 46 (1-3): 281-283. Arush. 1990a. Altmann.A. . Med. Guillemin.S. 1959. and I. Vet. Rec. Erkr. Bollettino scient@ca della facoltd di zootecnia e veterinaria 3: 209-217. Pays trop. Epidemiol. Innsbruck 127-132.und Neuweltkamele. Elm. J. Mort. Bloch. Zootiere (Tunis) lnt. Diallo.. A.M. Franco. Tageldin. 17fh Symp Erkr. 1990. Iowa State University Press.O. Bol. Clinical signs and clinical pathology of rabies in the camel. 1968. 133: 220. J. Rec. Am. Barrat. Veterinary Medicine. London: Bailliere Tindall. 1990b. Egypt Vet.91. Immunity duration and challenge three years after vaccination.C. 1982. lnt.M. 18. 1998. Altmann. Bornasche Krankheit (meningo-encephalomyelitis simplex enzootica equonun) bei Neuwelttylopoden und Equiden. Rabies in the Sultanate of Oman. Ata. 12 (2): 115-120. 1995. A1 S u m r y and S.Viral Infections Causing Disease Figure 84 Positive labeling for BDV of the hippocampus in an alpaca 175 Treatment and Prevention ji'i BD is a reportable disease and controlled by a stamp- ing-out policy. Pays trop.

1986.. Assoc. 207 (12): 1562-1575. 1990. Berlin. Dromedary pathology and productions.A. 203 (12): 1721. Infectious Diseases of Camelids.N. J. A. J. Kaaden. Vigot Freres. Rabies surveillance in the United States during 1994. Smith and D. Am. Llamas 8 (3): 49-55. Krebs. Elev.1. Richard. N. G. 1982.176 Viral Diseases Higgins. R. Vet. U. Smith. 34 (3): 263-265. Rabies antibody titres in vaccinated reindeer. Fishbein. Camel research project report by a Somali/Swedish Mission. Chamoiseau.3 Camelpox Camelpox occurs in the dromedary and the Bactrian camel and has also been experimentally induced in NWC (Kinne and Wernery.W. Krebs. Sudan and Stockholm 12 (18-20): 409-430.. Blackwell Wissenschafts-Verlag. 1993. and M. ed.. J. W. D. Kumar.1. Cron. ber. Assoc. Childs.. La rabia experimental en la llama. 1970. 6 on camels. 6 camels. 1992). Peck. Encyclopaedia of Vet. Srinivasan. Perl. Rev.F.B. 1998. Mohamed Lemine Ould Biha and Sidi Mohamed Ould Ahmed Fall.W. M. Med. J. Miller. 1997. Pox-like lesions in camelids may also be induced by a yet-unnamed parapoxvirus and papillomavirus.E.. Veterinarski Arhiv 68 (3): 81-84. Kinne und M. March 10-26: 18-23. K. 197 (12): 1576. Childs. 1995. Strine. Projet de developpement de l'elevage dans le Niger centre-est. Somac/Sarec. 2. J. J. Seroconversion and duration of immunity in camels vaccinated with tissue-culture inactivated rabies vaccine. Med.-F. Erkrg. The camel in health and disease.J. Vet. van Straten. Am. ed. Anim. Anim. 1994.Antigennachweis bei Alpakas (Lama pacos) sowie bei einem Faultier (Choloepus didactylus) und einem Zwergfldpferd (Choeropsis liberiensis). Mahnel and Mum. 1996. Nieminen. 1958-59. Kumar. 1981. Schwartz and Dioli. Paris H. 1990. S.. Sihvonen. Med. 2000).E. IEMVT. 2 2 269-272. 1966.S. Bornavirus .E. 22: 273-274. International Science Foundation (IFS). Rabies in the U. E. Tribulus. 1982 to 1986. Jerusalem.E. Provisional report No. Orgad.. 1905. Bulletin o the Emirates f Natural History Group Vo13. J. 29 (1): 34. A. AX. 1927. Rabies in a camel -A case report.J. J. Richard. U. Strine. Leese. Un foyer de rage camline en Mauritanie. Further reading Sidya Ould Bah. Boddie and J. 1979. Wemery. T. L. lSt Edinburgh. Stanley. Spruell. Israel.C. Kalanidhi.W. Sheikhab and U. Balliere Tindall. . EL. Med. Trop. J. 201 (12): 1839. T. K. Soveri. Am. 1992. Prod. Vet. Verh. vkt. Rabies surveillance in the United States during 1991 (a llama). Reid-Sanden. I. Mandel and J.. Symposium of Vet. Rabies in Yemen Arab Republic. IFS Provisional report No. Acta vet.G. P. Krebs. 1980. scand. 399. 1987. Med. Holman. E.: 5-21. Richard. Med. Vet. M. J. A. C.W. 4-8 Aug.D. 8tkInst.-R. (Lima) 13-14 35-40. Vet. Samina. Robertson. Fac. 34: 199-202. Lab. Dobbins.W. Maisons Alfort.. Med. Strine and J. Rupprecht and J. M.S. T. Am. Green and Son: 577. A treatise on the one-humped camel in health and disease.S. Mustapha. Assoc.E. 1994.. 1996: 14. G. Rabies surveillance in the United States during 1992 (a llama). and 0. Dalling. Rev. Hines. J. I. Prod. 1993. Hind limb paralysis associated with rabies in a camel (Camelus dromedarius). B.K. Hlth. Rabies on rise. In Intern. Hlth. Jindal. A. D. Trop. T. T. Bissa and V. Reinacher. Zootiere 36: 189-193. Wernery. Moro Sommo. Khartoum.W. Manuel des maladies du dromadaire.A. Jakobson. Pays trop. 1986.E. U. Schueppel. and B. 1980. Mid.. Childs. Sobre un brote de rabia en alpacas. Kulonen.E. Diagnosticians. 1993. 1995. 1999. U. M. Assoc. Wernery et al. Foundation for Science. 1980. and N. The camelpox virus causes a proliferative skin disease that primarily affects younger animals (Rohrer. Rabies surveillance in the United States during 1989.S. Stockholm: Int. Tamayo.

(1985) showed. Antibodies different African countries possess differ. (1998). it diseases. . abrasions of the skin. 1994). 1992). doublestranded DNA virus that represents 1 of 1 spe1 cies currently assigned to the genus Orthopoxvirus. Wernery et al. an important factor in the produc. This results in a second1992. lymph nodes is followed by a primary Differences in the virulence of camelpox viremia and multiplication of virus in orstrains have also been suggested (Munz. forcing a greater virus pressure and further viral multiplication in the draining virus doses onto the camel populations. ary viremia and subsequent infection of Pfeffer et al. that there is a high prevalence of antibodDNA restriction enzyme analyses have ies to camelpox in herds kept by nomadic shown that camelpox virus strains from pastoralists and by ranchers. which are divided into two subfamilies: Chordopoxvirinae. Munz et al. Camelpox virus (CaPV)is a large. milder course (Pfahler and Munz. which infects vertebrates and Entornopoxvirinae.were found in five out of six camel herds in ent genomes. (1986) reported 95% tion of vaccines and in performing test ex. (1998) found a prevalence betion appear to develop a lifelong immuni. which was confirmed in 72. Hafez et al. elpox has not been observed (Doerges and During the dry season. by aerosol infecPox is the most frequent infectious viral tion of the respiratory tract or mechanical disease of the camel and therefore the transmission by biting arthropods. 1995). Wemery and Kaainfected with the poxvirus through small den. 1989). 1995.. using the SNT. Wer. Animals that have recovered from infec. Epidemics occur in regular cycles dependent on the rainy season and relationship of the density of the insect population to the number of immune camels in the population. Several most widely reported. 1997.positive cases in Sudan. Camelpox is most probably not a zoonosis. 1992..Davies et al.g. sons. The infective agent of camelpox is the Orthopoxvirus cameli.000 dromedaries Etiology li. enveloped. Munz. In those infecpopulation builds up during rainy sea. An exception is the Australian (e. Epidemiology Camelids may become 1982. 1997a and dromedary population where. it usually follows a Heucke.tween 88% and 100% in 1. Poxviruses are the largest and most complex viruses and have a brickshaped appearance.gated. Otterbein.Pfeffer et al. Jezek et al.5% by Khalafalla et al.the skin. gans and tissues. produce generalized pox infections and oth.. personal communication.tions characterized by systemic disease.. Munz et al. Even very recent reports of skin eruptions in camel herdsmen could not identify camelpox as the causative agent using current laboratory methods (Kriz. although there was no strains differ in their virulence (Munz. The disease occurs scientists have reported an increase in wherever camel husbandry is practiced camelpox outbreaks during wet seasons (Table 37).*Poxviruses are classified in the family Poxviridae. 1994. Since the camelpox virus has been isolated In both localized and systemic poxvirus from the camel tick ffyalornrna dromedarii. posure experiments (Baxby et al. Otterbein et al. which may explain why virus Kenya using SNT. clinical disease seen in the herds investi1992). so far. 1999). 1975).. 1983. initial multiplication of the virus is now believed that a larger arthropod occurs at the site of entry. which are found in insects. 1992. although clinical observations in various articles have reported the possibility of transmission of Orthopoxvirus carneli to humans.. nery and Zachariah.. ers only a localized form (Wernery. camb) when the disease becomes more severe. 1996.Viral Infections Causina Disease 177 ty. which may exSerological studies in different countries plain the phenomenon that some strains have revealed a high prevalence of CaPV.

1974 Buchnev et al. 1987 . Binns et al. Azwai et al.. for example. Schwartz et al. Baxby Ramvar and Hessami Al Falluii et al. 1983 1998 1994 tested with the ELISA in the UAE. family Poxviridae. Tantawi et al. 1989 Shommein and Osman 1987 Odend‘Hal Ghulam et al. 1974. Mahnel. Guenther. Somalia Kriz Arush Year 1986 1987 1992 1982 1982 Sudan UAE Yemen Shommein and Osman 1987 Khalafalla and Mohammed 1996 Khalafalla et al. Shommein and Osman Leese Cross Chauhan et al. Diagnosis f:i Various authors have concerned themselves with the characterization and systematization of the camelpox virus (e. Chauhan et al. Bartenbach. The results have shown that the camelpox virus is a typical representative of the genus Orfhopoxvirus. the vuccinia/variola virus subgroup of poxviruses. 1973.. 1990. Chandra et al.g. 1992. 1973.. In Libya. based on morphological. Hafez et al. Roslyakov. Davies et al. chemical. Renner-Mueller et al. 1992Wernery et al. 1998 Kaaden et al. Munz 1992. Chauhan and Kaushik Khanna et al. The systematization and laboratory differentiation was of great importance in demarcating the orthopoxvirus from the pura- Russia Vedernikov 1893 Vederni kov 1902 Amanzhulov et al. physical and biological characteristics. (1996) investigated 520 dromedaries from 6 different herds and found only 10% positive animals. the cell-mediated immunity seems to protect animals from disease rather than circulating antibodies (Fenner et al. KroPP Gitao ~ Ethiopia India Year 1983 1992 1974 1974 1978 1987 1909 1917 1985 1986 1987 1996 1972 1972 1979 1975 1982 1982 1985 1997 1996 1989 1987 1991 ~~~~~ Country Author Saudi Arabia Hafez et al. 1988).178 Viral Diseases Table 37 Outbreaks o f camelpox. 1997ah Odend’Hal 1983 Iran Iraq Kenya Libva Carter and Azwai Mauritania Wardeh Morocco Fassi-Fehri El-Harrak et al. 1995. 1998). arranged by country and author Country Afghanistan Bahrain Egypt Author Odend’Hal Higgins et al. Mahnel and Bartenbach. Hussein et al. Serological investigations are of little value for the evaluation of the immune status o f camel populations since it is known that in orthopox infections. The virus is closely related immunologically to other representatives of this group such as. Al-Hendi et al. Niger Oman Pakistan ~ Richard 1986 Ba-Vy et al. 1930 Bauman 1930 lvanov 1934 Sarmatsev and Praksein 1950 Vyshelesskii 1954 Likhachev 1963 Borisovich and Orekhov 1966 Buchnevand Sadykov 1967 Semushkin 1968 Vedernikov 1969 Borisovich 1973 Marennikova et al. Wilson et al. 1972.. Tantawi Tantawi et al.

Newer methods include the ELISA technique with monoclonal antibodies. 1974. Johann and Czerny (1993) and Pfeffer et al.Czerny et al. 85). Mahnel. 1995) (Fig. Utilizing a relatively simple set pattern. Another advantage of this method is that embedded tissue blocks can be inves- Figure 85 Electron microscopy of camelpox (left) and parapox (right) in a dromedary (courtesy o f Prof.Viral Infections Causina Disease 179 pomirus. Germany) Figure 86 Acute lesions o f camelpox within the dermis. CaPV-antigen detection by immunohistochemistry is a new method for camelpox diagnosis which can easily be performed in laboratoriesnot possessing an electronmicroscope (Fig. (1998) have described various laboratory methods for the diagnosis of camelpox. 1972). laboratory methods also permit the differentiation of other closely related orthopoxvirus species (Baxby. ELISA. They include electron microscopy. as both viruses can be found in the same camel (Werneryand Kaaden. 1993). Some criteria used to differentiate between viral species include the inoculation of embryonated eggs. the intracutaneous test in rabbits and the feather follicle test in chickens. fibrocytes and endothelial cells . 1992)and a dot blot assay using digoxigenin-labeled DNA probes (Meyer et al. 86). Munz et al. (1989).. In addition to the diagnosis. 1986. DNA restriction enzyme analysis (Munz et al. immunohistochemistryand polymerase chain reaction. 1974). immunohistochemistry is of particular interest for histopathologists because it visualizes the morphological changes induced by the poxvirus. Positive staining of CaPV-antigen (golden-brown granula) is found in macrophages. cytopathic effects in cell cultures (Bedson.. Mahnel..

87). Buchnev and Sadykov (1967) have described abortions in camels caused by the Orthopoxvirus cameli and they have isolat- . 88a and b). thus making it suitable for retrospective studies (Kinne et al. In more severe cases presenting with generalized clinical signs such as fever. 1998). lassitude.. diarrhea and anorexia. Clinical Signs and Pathology ” Following an incubation period of 9 to 13 days. pustules develop on the nostrils and eyelids as well as on the oral and nasal mucosa in mild cases (Fig. the erup- tions are distributed over the entire body (Fig. b Generalized camelpox in a dromedary and a guanaco after experimental infection with Orthopoxvirus cameli tigated years after they have been made.180 Viral Diseases Figure 87 Camelpox on nasal mucosa Figure 88a.

b Camelpox lesions in the trachea and lung of a 9-monthold dromedary ed the virus from the aborted fetuses. 1995. Classical lesions in the skin start as erythematous macules. Vesicles develop into .Viral Infections Causins Disease Figure 89 Camelpox with secondary Staphylococcus aureus infection 181 Figure 90a. which develop into papules and vesicles. Mortality can reach 28% in generalized forms of the disease (Jezek et a . bacterial and mycotic infections can complicate the course of camelpox (Fig. 1998). 89). Kinne et al.. 90a and b) (Wernery and Kaaden. 1983).Secondary l. Pox-lesions were also observed in the trachea and lungs of young dromedaries (Fig.

1986). animals in milk and rubbing the mixture consisting of sparse foci of pulmonary con.(Samartsev and Praksein. varied in diameter from 1to 10 Higgins. Buchnev ture had been partly or completely obliter. 1995. vich. the details regarding Immunohistochemical examination of the virus strain and the safety and effecthese foci showed numerous poxvirus anti. pustules contributes to the raised borders Although camelpox has a great economof pustules. The disease caused scat. The pulmonary lesions.also applied for pox lesions of the skin tules might take 4 to 6 weeks with or (Nothelferet al.particularly in the minimize secondary infections it is advisstratum spinosum. Borisoated with necrosis and fibrosis (Fig.tiveness of the vaccine are insufficient.. HE-stained lung sections revealed Reports of the existence of a camelpox confluent foci of proliferated alveolitis and vaccine first originated in the Soviet Union bronchiolitis in which the normal architec. fibrous tissue and mature collagen. they beImmunohistochemistry technique was come covered by crusts. Camel owners recogas an edema. only a few scientists have infiltrations.However. 91). After the pustules have ruptured. 1973. in order to looning of keratinocytes. (1998) described nizing the importance of camelpox have camelpox lesions of the respiratory system created numerous names for this disease.Treatment and Control i There is no treatacterized by swelling. Poxviruses are generally epitheliotropic and the skin lesions are char..Even today.ment for camelpox infections. esopha.and Sadykov. Sedov. Perivascular mononuclear cell ic significance.182 Viral Diseases pustules with depressed centers and raised gen-positive cells in the bronchial epithelia erythematous borders. Rupture of these cells able to treat severe cases by local applicaleads to the formation of vesicles. 1973). solidation. 1998). Healing of pus. neutrophils and eosinophils concerned themselves with the production are often observed in the dermis as well of a specific vaccine. the so-called pock. Figure 91 A consolidated focus consisting of a mixture of tissues including some residual alveoli. without scars. Pfeffer et al. mm. Kinne et al. in dromedaries. Marked tion or parenteral administration of broad hyperplasia of epithelial cells surrounding spectrum antibiotics and vitamins. 1950. (Fig. vacuolation and bal. Note the infiltrating mononuclear cells and the cytoplasmic and nuclear debris (HE x220) . 1909.on the calves’ scarified lips (Leese.calves by dissolving scabs from affected gus and lungs. 1967. 92). these owners protect their tered focal lesions in the trachea.

1998). However... All three groups were successful in producing a camelpox vaccine. 1998). Because of the antigenic relationship between the camelpox virus and the vaccinia virus. Wernery and Kaaden. It is imhs portant to mention that the vaccine producer recommends a booster dose in 6 to 9-month-old camels to avoid any vaccine breakdown because of maternal antibodies.. Saudi Arabia (Hafez et al. several clones were selected and clone A28 is now used because of its safety and good immunity (ElHarrak et al. Mayr (1999) states that inactivated pox vaccines do not possess a protective efficacy against any poxvirus infection. the authors have stressed that only a small number of camels were used in t i long term experiment. 1991. 1995).. Newer reports of attempts at producing a vaccine come from Morocco (EL-Harrak et al. El-Harrak. 1992. Klopries. Attenuated virus strains were employed in Saudi Arabia and in the UAE. Because of the inability of the vaccine virus to multiply in the host. 1992)and the UAE (Kaaden et al. Wernery et al. 2000). 1992. It also protects NWC against camelpox (Wernery et al. Wernery and Zachariah 1999. it is possible to immunize camels with known vaccinia strains. (1975) were able to . A pox vaccine can only be protective when the vaccine titer is greater than 107. but this vaccine did not protect camels from a camelpox infection. Higgins et al. Kaaden et al.. This vaccine has to be administered annually. EL-Harrak. Wemery and Zachariah (1999) showed that a single dose of Ducapox@ given at the age of 12 months can protect dromedaries from camelpox infection for 6 years and even longer. not enough specific pox antibodies can be produced. X I 20) 183 Buchnev and Sadykov (1967) immunized camels with an aluminum hydroxide vaccine.. 1991... The UAE attenuated camelpox vaccine (called Ducapox@= Dubai camelpox vaccine) has been used since 1994with success (Wernery. 2000).. Ducapox@ commercialis ly produced in South Africa. An inactivated vaccine was developed in Morocco and has been used in prophylactic campaigns since 1991.0TCID50 and if the animals are revaccinated after 3 to 5 weeks. 1994). Wernery et al. In further developments. In a recent experiment. 1993. 1997a. Note the intralurninal necrotic mass (ABC method. The UAE group established a permanent fetal dromedary skin cell line (Dubca) for the isolation of the camelpox virus (Kaaden et al. 1995. and Baxby et al. (1992) brought an outbreak of camelpox in Bahrain under control with the Lister strain.Viral Infections Causing Disease Figure 92 Proliferated and desquamated bronchial epithelium with numerous cells showing labeling for poxvirus antigen.

. Diss. Kaushik. J. B 36: 537-546. Isolement et identification du virus de la variole du dromadaire au Maroc. Carter. 1975. A slow-spreading mild form of camelpox infection. Balliere. Switzerland. 1996. El-Harrak. Camb. Lancet 2 1063-1065.B. Vet. Hassanien. R.1996: 23-36. J. Chauhan.G.D.N. M. Y. Path.-P. Buchnev. S. Arush.K. 6 (2): 487-495.. H. Little-known infectious diseases in animals. H. Moscow: 32-42.A. References Al-Falluji. 1985. 1996. Br. D. Proc. Rev.K. Ba-Vy. Chauhan. development of an inactivated vaccine and . l(1):10-16. Camelid Soc. 1985.D. and R. Camel pox. Microbiol. Burford. B.143581-582. 41: 71-73. Atema and A. 1 Bedson. 1987. 1917.C.36... Borisovich. R.A. Rev. Vet. and S. Shony. Proprikt6s d'une souche d'orthopoxvirus isol6e des dromadaires du Niger. S w la variole du chameau de la region d'Oural. 22: 95-98.. Czerny. M. J. Bull. Sadykov. K.C. Baxby.S.M. Chauhan and S. London. Comp. Z . Vet. 75: 381-385. Loutfi and F. 1973. Woldehiwet and U. 1. Hyg. Me'd. C. Part 11: 152-153. Bartenbach. Hyg. Cross. Mbugna. J. Camel Newsletter 3: 10-14. November 14-16.794 3: 50-52. H. Tindall and Cox. Baxby. Charakterisierung und Systematisierung eines Kamelpockenvirus.K. S. Infectious diseases of camels in the USSR. J. J.N. Bauman.M.R. Miinchen. Moscow.C. Smallpox-like viruses from camels in Iran. 1982. 1987. Tulepbaev and A. Sel'khozgiz. J. Dis. Differentiation of smallpox and camelpox viruses in cultures of human and monkey cells. Comp. Brit. 1930. It should be mentioned.O. G. Gillet. med. R. Mungai and T. D. ve't. Wemery. Binns. Elm. Azwai. were able to withstand test exposure to camelpox.S. V 1930.M. 1986.M. S.D. Hyg.S. Vet. Infection and Immunity 1 (4): 617-621. K. Arbuzov. 95: 633-635. Sansyzbaev. 1973. 148: 541-546. 1967. sci. Prevalence of different diseases in camels (Camelus dmmedarius) in India. Davies. S. Mahnel.A. Vet. infect.. Vet. identification and characterization of camelpox virus in Iraq. E.S. Chauhan.F. Shaw.A. and M.S. H. Tantawi and M. The camel. J. Garg.G. R. D. 1979. Kolos. Abstract in Bull. Gameel and M. Ann. The prevalence of antibody to camelpox virus in six different herds in Kenya. trop 42 (1):19-25. M. Orekhov. Epiz. Rech.. 1989. Y. 1998. R. N.K. Immun.184 Viral Diseases show that dromedaries in Iran. C. 72: 251-254.P. f 1967.. 1996.. Mos. H. Serology of Orthopoxvirus cameli infection in dromedary camels. Virol.N. 1975. 1998.N. Camb. Camel Newsletter 14: 34-45. Br..C. Wemery. Of. Baxby.F. 83: 267-272. tech.. Borisovich. Camelpox and smallpox. Mumford and U.Z. La situazione sanitaria del dromedario nella Repubblica Democratica Somala. S. Analysis of the camel pox virus thymidine kinase gene. Vet. Gupta. Analysis by ELISA and Western Blotting.G. and R. Camel pox: A review. A. Amanzhulov. R. Bollettino scientifica della facoltli di zootecnia e veterinaria 3: 209-217. 1989. Ind. Kaushik. Proceedings o the 3rd All-Union Conference on Virology.. Camb. Epidemiological studies of viral diseases of livestock in Haryana State. Richard and J. Samarzev and L.. Al-Hendi. R. 1974. Carter. M. however. Med. Isolation. Ramyar. Satiya and R. A. 1972. Hessami and B. Response of camels to intradermal inoculation with smallpox and camel pox viruses. M. Immunity and infectious diseases in the dromedary camel. Pays.. The camel and its diseases. Establishment of an ELISA for the detection of orthopox viruses based on neutralizing monoclonal and polyclonal antibodies. F. 19 (1):65-78. 1972. J.. Abuelzein.E. Med. Inst. M. Buchnev. Wilson. D. Kaushik. vaccinated with the vaccinia strain EA8. J. 1966.Isolation of camelpox virus in India.M. F. Bertin. Pasteur 29: 96. El-Harrak. H. Contribution to the study of camelpox. S. Chandra. 1992. Meyer and H.. R.E. Davies. Ghaboosi. Characteristics of a Kenyan camelpox virus. Isolation of camelpox virus. Kulshreshta. A. 1994. Veterinayia. Dated in Vet. The Lancet 9: 1253. C.H. 1991. Kulshreshtha and R. cow and Leningrad. Azwai. that the vaccination program against human variola using vaccinia virus was terminated worldwide by a recommendation implemented by the WHO in Geneva. int.

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prophylactic application in Morocco. Int. meeting on camel production and future perspectives, May 2-3,1998, A1 Ain, UAE: 736. Fassi-Fehri, M.M. 1987. Les maladies des camelides. Rev. Sci. Tech. Of.int. Epiz. 6 (2): 315-335. Fenner, F., R. Wittek and K. R. Dumbell. 1988. The orthopox viruses. Academic press, New York Book 100-133. Ghulam, M., M. Z. Khan and M. Athar. 1998. An outbreak of generalised pox among draught camels in Faisalabad city. J. Camel Prac. and Res. 5 (1):127-129. Gitao, C.G. 1997. An investigation of camelpox outbreak in 2 principal camel (Camelus dmmedarius) rearing areas of Kenya. Rev. Sci. Tech. Ofice Intl. des Epiz. 16 (3): 841-847. Giinther, G. 1990. Isolierung und Charakterisierung des Kamelpockengenoms. Inst. Virologie, Hannover. Hafez, S.M., A. Al-Sukayran, D. dela Cruz, K.S. Mazloum, A.M. Al-Bokmy, A. Al-Mukayel and A.M. Amjad. 1992. Development of a live cell culture camelpox vaccine. Vaccine 10 (8): 533-537. Hafez, S.M., Y.M. Eissa, A.M. Amjad, and A.K. Al-Sharif and A. Al-Sukayran. 1986. Preliminary studies on camel pox in Saudi Arabia. Proceedings of the 9th Symp. on the biological aspects of Saudi-Arabia, 24-27 March. Higgins, A. 1986. The camel in health and disease. Bailliere Tindall. Higgins, A.J., R.E. Silvey, A.E. Abdelghafir and R.P. Kitching. 1992.The epidemiology and control of an outbreak of camelpox in Bahrain. int. Proc. lSt Camel Cod. Eds.: W.R. Allen, A.J. Higgins, I.G. Mayhew, D.H. Snow and J.F. Wade: R. and W. Publications, Newmarket, UK: 10-104. Hussein, M.F., S.M. Hafez and M. Gar El-Nabi. 1987. A clinico-pathological study of camelpox in Saudi Arabia. lothSymp. on the biological aspects of Saudi Arabia, 20-24 April. Ivanov, P.V. 1934. Camel breeding. Kazakhskoe kraevoe izdatel'stvo, Alma-Ata. Jezek, Z., B. Kriz and V. Rothbauer. 1983. Camelpox and its risk to the human population. J. Hyg. Epidem. Microbiol. Immun. 27 (1): 29-42. Johann, S. and C.-P. Czerny. 1993. A rapid antigen capture ELISA for the detection of orthopox viruses. J. Vet. Med. B. 40: 569-581. Kaaden, 0.-R., A. Walz, C.-P. Czerny and U. Wernery. 1992. Progress in the development of a

camel pox vaccine. Proc. of the lstint. Camel Conference. Eds.: W.R. Allen, A.J. Higgins, I.G. Mayhew, D.H. Snow and J.F. Wade: R. and W. Publications, Newmarket, UK 47-49. Kaaden, 0.-R., U. Wernery and M. Klopries. 1995. Camel fibroblast cell line DUBCA and its use for diagnosis and prophylaxis of camel diseases. Proc. o the Intl. Con$ on Livestock f Production in Hot Climates,Muscat, Oman:A49. Khalafalla,A.I., M.E.M. Mohamed and B.H. Ali. 1998. Camelpox in the Sudan. Part I and Part II. J. Camel Prac. and Res. 5 (2): 229-238. Khalafalla, A.I. and M.E.H. Mohamed. 1996. Clinical and epizootiological features of camelpox in Eastern Sudan. J. Camel Prac. and Res. 3 (2):99-102. Khanna, N.D., P.K. Uppal, N. Sharma and B.N. Tripathi. 1996. Occurrence of pox infections in camels. Ind. Vet. J. 73 (8): 813-817. Kinne, J., J.E. Cooper and U. Wernery. 1998. Pathological studies on camelpox lesions of the respiratory system in the United Arab 1: Emirates (UAE). J. Comp. Path. 1 8 257-266. Kinne, J. and U. Wernery. 1999. Experimental camelpox infection. In: Meeting of the European SOC. vet. Pathol., Nantes, France, 14-17 of September 1999. Klopries, M. 1993. Etablierung und Charakterisierung einer Kamelhautzellinie (Dubca). Vet. med. Dissertation, Miinchen. Kriz, B. 1982. A study of camelpox in Somalia. J. Comp. Path. 92: 1-8. Kropp, E.M. 1985. Kamelpocken - eine synoptische Darstellung sowie der Nachweis von Antikorpern in ostafrikanischen Dromedarseren mit einem ELISA. Vet. med. Diss., Miinchen. Leese, AS. 1909. Two diseases of young camels. J. Trop. Vet. Sci. 4: 1-7. Likhachev, N.V. 1963. Goats and sheep pox virus. Guidance on vet. virology. Sjurin V N . ED., Kolos, MOSCOW: 622-625. Mahnel, H. 1974. Labordifferenzierung der Orthopockenviren. Zbl. Vet. Med. B 21: 242-258. Mahnel, H. and E. Munz. 1987. Zur derzeitigen epizootologischen Lage bei den Tierpocken. Tierurztl. Umschau 42 (1):5-14. Mahnel, H. and G. Bartenbach. 1973. Systematisierung des Kamelpockenvirus. Zbl. Vet. Med. B 2 0 572-576. Marennikova, S.S., L.S. Shenkman., E.L. Shelukhina and N.N. Maltseva. 1974. Isolation of camelpox virus and investigation of its properties. Acta. Virol. 18:423-428.

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Mayr, A. 1999. Geschichtlicher iiberblick iiber die Menschenpocken (Variola), die Eradikation von Variola und den attenuierten Pockenstamm MVA. Berl. Munch. Tierarztl. Wschr. 112 322-328. Meyer, H., N. Osterrieder and M. Pfeffer. 1993. Differentiation of species of genus Orthopoxvirus in a dot blot assay using digoxigeninlabeled DNA-probes. Vet. Microbiology 3 4 333-334. Munz, E., E.-M. Kropp and M. Reimann. 1986. Der Nachweis von Antikorpem gegen Orthopoxvirus cameli in ostafrikanischen Dromedarseren mit einem ELISA. J. Vet. Med. B 33: 221-230. Munz, E., S. Linckh and I.C.E. Renner-Mueller. 1992. Mektionen mit originarem Kuhpokkenvirus und kuhpockenihlichen Erregern bei Mensch und Tier: Eine Literaturubersicht. J. Vet. Med. B 3 9 209-225. Munz, E. 1992. Pox and pox-like diseases in camels. Proc. lSt Camel Conference. Eds.: int. W.R. Allen, A.J. Higgins, I.G. Mayhew, D.H. Snow and J.F. Wade: R. and W. Publications, Newmarket, UK:43-46. Munz, E., C.K. Otterbein, H. Meyer and I. Renner-Mueller. 1997. Laboratory investigations to demonstrate a decreased virulence of two cell adapted African camelpox virus isolates as possible vaccine candidates. J. Camel Prac. and Res. 4 (2): 169-175. Nothelfer, H.B., U. Wemery and C.P. Czemy. 1995. Camel Pox: Antigen detection within skin lesions-immunocytochemistry as a simple method of etiological diagnosis. J. Camel Prac. and Res. 2 (2): 119-121. Odend'Hal, S. 1983. The geographical distribution of animal viral diseases. Academic Press, New York 99. Otterbein, C., H. Meyer, I. Renner-Mueller and E. M u . 1995. Charakterisierung zweier afrikanischer Kamelpockenvirus-Isolate.

ruses isolated in Dubai. Veterinary Microbiolog~ 49: 135-146.

Mitt. Oesterr. Ges. Tropenmed. Parasitol. 1 7
7-16. Otterbein, C.K. 1994. Phaeno- und genotypische Untersuchung zweier Kamelpockenvirusisolate vor und nach Attenuierung durch Zellkulturpassagen. Diss. Med. Vet. LudwigMaximilians-Universitat Miinchen. Pfahler, W.H.E. and E. Munz. 1989. Camelpox. Int. J. Anim. Sci. 4: 109-114. Pfeffer, M., H. Meyer, U. Wernery and 0.-R. Kaaden. 1996. Comparison of camelpox vi-

Pfeffer, M., U. Wemery, 0.-R. Kaaden and H. Meyer. 1998. Diagnostic procedures for poxvirus infections in camelids. J. Camel Prac. and Res. 5 (2): 189-195. Ramyar, H and M. Hessami. 1972. Isolation, cultivation and characterization of camelpox virus. Zbl. Vet. Med. B 19: 182-189. Renner-Mueller, I.C.E., H. Meyer and E. Munz. 1995. Characterization of camelpox virus isolates from Africa and Asia. Vet. Microbiol. 45 (4): 371-381. Richard, D. 1979. Study of the pathology of the dromedary in Borana Awraja (Ethiopia). Diss. Med. Vet., Universitaet Creteil. Richard, D. 1980. Dromedary pathology and productions. Provisional report No. 6. Camels. International Science Foundation (IFS), Khartoum, Sudan and Stockhoh 12 (18-20): 409-430. Richard, D. 1986. Manuel des maladies du dromadaire. Projet de dkveloppement de l'klevage dam le Niger centre-est. Maisons Alfort, IEMVT. Rohrer, H. 1970. Traite des maladies a virus des animaux. Paris, Vigot, France. Roslyakov, A.A. 1972. Comparison of the ultrastructure of camel pox virus, the virus of poxlike disease of camels and contagious ecthyma virus. Voprosy Virusologii 17, Zoovet Institut, Alma-Ata, Kaz. SSR. Abstract: Vet. Bull. 42,512 1: 26-30. Samartsev, A.A. and S.T. Praksein. 1950. Camel pox study. Proc. Kazakh Res. Vet. Institute 5: 198-200. Schwartz, H.J. and M. Dioli. 1992. The onehumped camel in Eastern Africa. A pictorial guide to diseases, health care and management. Verlag Josef Margraf. Schwartz, Sabine, H.J. Schwartz and A.J. Wilson. 1982. Eine fotographische Dokumentation wichtiger Kamelkrankheiten in Kenia. D r prakt. Tierarzt 1 :985-989. e 1 Sedov, V.A. 1973. Official communication: measures for the prevention and eradication of camelpox. Veterinariya, Moscow. Vet. Bull. 1974,44,295 12: 63-64. Semushkin, N.R. 1968. Diagnosis of camel diseases. Sel'khozgiz Moscow. Shommein, A.M. and A.M. Osman. 1987. Diseases of camels in the Sudan. Rev. sci. tech. Ofiint. Epiz. 6 (2): 481.

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Tantawi, H.H., M.S. Saban, I.M. Reda and H. ElDahaby. 1974. Camel pox virus in Egypt. I. Isolation and characterization. Bull. Epiz. Dis. Afi. 22 315. Tantawi, H.H. 1974. Comparative studies on camelpox, sheeppox and vaccinia viruses. Acta Virol. 18: 347-351. Tantawi, H.H., H. El-Dahaby and L.S. Fahmy. 1978.Comparativestudies on poxvirus strains isolated from camels. Acta Virol. 22: 451-457. Vedernikov, V. 1893. Camel diseases. Archives of veterinary medicine, St. Petersburg I, V 149. Vedernikov, V. 1902. cited from Curasson (1947). Vedemikov, V.A. 1969. Pox. Epizootiology. Sosov R.F. ed. Kolos, Moscow: 158-164. Vyshelesskii, S.N. 1954. Pox. Particular epizootiology. Sel'khozgiz: 195-212. Wardeh, M.F. 1989. Camel production in the Islamic Republic of Mauritania. Camel Newsletter 5: 11-17. Wernery, U. 1994. Neue Ergebnisse zur Diagnose, Prophylaxe und Therapie wichtiger bakterieller und viraler Krankheiten beim Kame1 (Camelus dromedarius). Habilitationsschrift zur Erlangung der Lehrbefahigung an der Tierarztlichen Fakultat der Ludwig-Maximilians-Universitat Miinchen. Wernery, U. and 0.-R. Kaaden. 1995. Infectious Diseases of Camelids. Blackwell Wissenschafts-Verlag, Berlin. Wernery, U., H. Meyer and M. Pfeffer. 1997a. Camel pox in the United Arab Emirates and its prevention. J. Camel Prac. and Res. 4 (2): 135-139. Wernery, U., 0.-R. Kaaden and M. Ali. 199%. Orthopox virus infections in dromedary camels in United Arab Emirates (UAE) during winter season. J. Camel Prac. and Res. 4 (1): 51-55. Wernery, U. and R. Zachariah. 1999. Experimental camelpox infection in vaccinated and unvaccinated dromedaries. J. Vet. Med. B. 46 131-135. Wernery, U., J. Kinne and R. Zachariah. 2000. Experimental camelpox infection in vaccinated and unvaccinated guanacos. J. Camel Prac. and Res. 7 (2): 153-157. Wilson, A.J., H.J. Schwartz, R. Dolan, C.R. Field and D. Roettcher. 1982.EpidemiologischeAspekte bedeutender Kamelkrankheiten in ausgewahlten Gebieten Kenias. Der praktische Tierarzt 11:974-987.

Further reading
Binns, M., J. Mumford and U. Wernery. 1992. Development of camelpox virus as a vaccine vector. Proc. lSt Camel Conf. Eds.: W.R. Int. Allen, A.J. Higgins, I.G. Mayhew, D.H. Snow and J.F. Wade: R. and W. Publications, Newmarket, U K 97-99. El-Harrak, M., C. Loutfi and B. Harif. 1994. Isolation and characterisation of camelpox virus in Morocco. 2nd int. conference on vaccines, new technologies and applications, March 21-33, 1994, Virginia, USA 2-8. El-Harrak, M. and C. Loutfi. 1999. La variole du dromadaire chez le jeune. lnt. Workshop on the young camel, Quarzazate, Maroc, a t . , 24-26, 39. Gitao, C.G., P.N. Nyaga and J.O. Evans. 1996. Pathogenicity of sheep skin-cell-propagated camel pox virus in camels (Camelus dromedarius). lnd. J. o Anim. Sci. 66 (6): 535-538. f Guake, L.K., Z . Dubba, K.H. Tumba and R.M. Abugaliev. 1964. No title. Vet. Moscow 41: 115-116. Meyer, H. and H.-J. Rziha. 1993. Characterization of the gene encoding the A-type inclusion protein of camelpox virus and sequence comparison with other Orthopoxviruses. J. Gen. Virol. 74: 1679-1684. Munz, E. et al. 1986. Serological and etiological investigations on camelpox in African dromedaries. Proc. Y h Con$ lnst. Trop. Vet. Med. Kuala Lumpur, Malaysia: 75-76. Wernery, U. 1999. New aspects on infectious diseases of camelids. J. Camel Prac. and Res. 6 (1): 87-91.

2.1.4 Contagious Ecthyma
Parapoxviruses are not related to orthopoxviruses and there is no crossimmunity as such between the two viral species. Contagious ecthyma (OW) causes a localized, vesiculo-pustular exanthema with a worldwide distribution. It is a disease in sheep, goats and wild ruminants (Buettner et al., 1995).In sheep, it is regarded as one of the most serious viral diseases.
Etiology Contagious ecthyma virus is a member of the genus Parapoxviridae. The

188 Viral Diseases or "scabby mouth", as contagious ecthyma is also called, has been described in OWC from many different countries. In Kazakhstan this disease is called "Auzdyk" in the Bactrian camel, and has been intensively studied by Tulepbaev (1969 and 1971). The opinion that the disease is not contagious and due to the consumption of thorny Separation of the parupoxviruses into four plants has been a long held belief among distinct groups has been based on natural camel owners (Borisovich and Orekhov, host range, pathology and more recently 1966).Later it was realized that the thorny on restriction endonuclease and DNA/ plants damaged the lips, allowing transDNA hybridization analysis. The latter mission of the parupoxvirus (Buchnev et al., studies have shown that the purupoxviruses 1987).Roslyakov (1972) showed, using elecshare extensive homology between central tron microscopic studies, that the ultrastruregions of their genomes, but much lower cture of this parupoxvirus is similar to the levels of relatedness within the genome virus found in contagious ecthyma and termini (Mercer et al., 1997). named the latter virus "Derrnovirus curneli" Parupoxvirus ovis (ORFV), the causative and the disease "pustular dermatitis of the agent of contagous ecthyma in sheep and camel". Kokhoo (1982) also studied the bigoats, has also been described in dogs, ological characteristics of this virus. OWC, NWC and seals (Hartung, 1980).All Other reports of outbreaks of contagious three purupoxviruses, as anthropozoonoses, ecthyma in OWC have originated from Ruscan also be transmitted to humans (Liess, sia (Buchnev et al., 1969), Mongolia (Dasht1962; Hartung, 1980; Hartmann et al., 1985; seren et al., 1984),Kenya (Munz et al., 1986; Mahnel and Munz, 1987; Mercer et al., Dioli and Stimmelmayr, 1992; Gitao, 1994); 1997). Only the recently reported PVNZ Somalia (Kriz, 1982; Moallin and Zessin, has yet to be recorded as infecting humans. 1988);the Sudan (Ali et al., 1991; Khalafalla, 1998); Libya (Azwai et al., 1995; Azwai Epidemiology 1. The ORFV can cause a et al., 1998);UAE (Wernery et al., 1997) and disease in OWC and NWC (Ali et al., 1991; Saudi Arabia (Abu Elzein et al., 1998). Gitao, 1994; Wernery and Kaaden, 1995; Camel contagious ecthyma occurs mainly in young animals up to 3 years of age. Fowler, 1998). Contagious ecthyma in the camel is very Several scientists from different countries difficult to differentiate clinically from true have recorded the morbidity and mortality camelpox. Contagious pustular dermatitis rates (Table 38), which differ extremely.
Table 38 The morbidity and mortality rates of dromedaries suffering from contagious ecthyma Author(s) Dashtseren et al. Munz et al. Ali et al. Gitao Wernery et al. Abu Elzein et al. Khalafalla Year 1984 1986 1991 1994 1997 1998 1998 Country Mongolia Somalia Sudan Kenya UAE Saudi Arabia Sudan Camels examined 478 700 600 30 700 Age in months
% Morbiditv

current members of the genus Parupoxvirus are: - Parupoxvirus ovis (ORFV), - bovine papular stomatitis virus (BPSV), - pseudocowpoxvirus (PCPV), - parapoxvirus of red deer in New Zealand (PVNZ).

% Mortalitv
0 0 0 0 0 0 8.8

-

Adult 10-80 Adult 100 / 10-20 14 6 8 100 16 20 Young and adults 24 12 60.2

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NWC are also susceptible to contagious Very little is known about the transmission of the parapoxvirus. It is believed that ecthyma virus (Preston Smith, 1940 and natural transmission occurs by direct con- 1947; Moro, 1971; Ramirez, 1980; Thedford tact or indirectly from the environment or and Johnson, 1989; Fowler, 1998).Affected fomites. New findings indicate that the NWC develop typical proliferative lesions carrier animal is probably very important of the epidermis at the commissures of the in the spread of the disease in sheep. Con- mouth, which might spread to regions of siderable evidence has shown that k-the face and perineum. It is also possible fected flocks grazing on pastures abundant that crias become infected when they suckin thistles, on which no sheep have grazed le their dams that have developed lesions for many years, still succumb to the dis- on their teats. ORFV from lamoids has proease (Lewis, 1996).Azwai et al. (1998) found duced severe ulcerating lesions on fingers, that the seropositivity rate (ELISA) in limbs and face in man (Fowler, 1998). Libyan camel herds with clinically affected dromedaries was 38% (and was related to Clinical Signs and Pathology Two to 6 clinical signs) and in apparently healthy days post infection, primary lesions develherds was between 0% and 7Yo. Gitao op at the point of entry of the virus to the (1994)believes that the common practice of body. The lesions consist mainly of localkeeping all camel calves in the same shel- ized skin lesions of different magnitude, ter at night could be responsible for the severity and location. Single or multiple spread of the virus by contact, and he also primary pox lesions develop on the skin of proved that the outbreaks in camel calves the lips and muzzle. They frequently exoccurred when parapoxvirus infectionswere tend to the skin of the eyelids and other also observed in goat kids raised nearby. parts of the head as well as to the buccal Similar observations were made by Munz cavity, such as the palate and the gums beet al. (1986) and by Robertson (1976) who low the incisor teeth. The lesions develop examined ORF infections in alpacas. Abu as reddish papules that change to yellowElzein et al. (1998) reproduced camel con- ish pustules within a few days before betagious ecthyma experimentallyin suscep- coming nodular, ulcerated and hemortible dromedaries, but experimentally-in- rhagic. Secondary bacterial and fungal infected sheep were refractory to the camel fections as well as myiasis may aggravate virus. On the other hand, experimental in- the lesions on the lips and mouth. Enlargefection with the ovine ORFV in drome- ment of some superficial lymph nodes is daries did not produce any disease in this also often observed. animal species (Wemery, pers. corn.). WerMicroscopic examination of the affected nery and Kaaden (1995) reported three 8- skin reveals parakeratosis, acanthosis, balmonth-old dromedaries in the UAE that looning degeneration of keratinocytes and developed and died from a mixed infec- inflammation and edema of the dermis. tion of true camelpox and parapox during The lesions are often accompanied by focal the course of an experimental camelpox ulcerations, neutrophilic and eosinophilic vaccination program. The camels used as infiltrations and superficial bacterial and control animals were artificially infected fungal colonies.Microscopic lesions are diwith the camelpox virus. They might have agnostic in early and acute stages, when developed a super infection with the con- cytoplasmic inclusion bodies are found in tagious ecthyma virus or were latent carri- swollen epidermal cells but disappear in ers of the virus. Both viral species were older lesions (6 days or more). Contagious ecthyma in camels is usualseen situated next to one another upon ly characterized by local pox-like lesions electron microscopy (see Fig. 85).

190 Viral Diseases

Figure 93 Camel contagious ecthyma in a young dromedary (courtesy of Dr. Khalafalla, Sudan)

any lesions on the udders of the dams or on the skin of any adult camel. The morbidity among the young Kenyan dromedaries reached 100%. The disease was also described by Dashtseren et al. (1984) in Mongolian Bactrian camels, but without any deaths. The authors described small elevations around the mouth, which within 4 to 12 days developed to larger papules about 4 m m in diameter. These skin lesions became confluent and within 2 to 5 months scabs developed 5 to 15mm thick, occasionally subdivided by many furrows. The percentage of adult camels that developed the disease lay between 10-80% in Mongolia and 10-20% in Kenya.
Diagnosis iri As it is extremely difficult to differentiate camel contagious ecthyma from true camelpox, mange or dermatophilosis, it is important that biopsies of fresh proliferative lesions are submitted to a veterinary diagnostic laboratory for diagnosis. Electron microscopic examination of biopsies or crusts is essential since virus isolation on the chorionallantoic membrane of chick embryos and in tissue cultures requires many passages. A recently developed PCR for the detection of parapoxvirus infection can also be recommended, especially when electron microscopy shows negative results (Buettner et al., 1995). Indirect immunofluorescence, ELISA and western blotting technique for the detection of antibodies to camel contagious ecthyma can be used (Azwai et al., 1995), but are unreliable indicators of the immune status of the animal as it is known that immunity is mainly dependent on cellular mechanisms.

on the face (Fig. 93). Recently, further reports have indicated that severe generalized forms of parapoxvirus infections seen in East African dromedaries cannot be differentiated from true camelpox (Mahnel and Munz, 1987). Munz et al. (1986) described an outbreak of parapox in a 450-head dromedary herd in Kenya. Primarily, proliferative lesions on the lips were seen occasionally spreading to the nasal and oral mucosa. There was a tendency to generalization in calves and young dromedaries. Initially, papules emerged; then progressed into pustules before encrusting. The scabs finally became dark brown in color and dropped off after 6 to 10 weeks. In severely affected dromedaries, round, black hairless areas with slightly thickened epidermis remained up to 6 months. Some animals also developed edema of the eyelids, lips and alae of the nose or even the entire head. Similar clinical signs have also been reported by Moallin and Zessin (1988) from Somalia, and Gitao et al. (1994) observed swollen and edematous cervical and mandibular lymph nodes in many Kenyan dromedary calves. The majority of the skin lesions became infected with thick yellowish pus beneath the scabs. The authors did not detect

Treatment and Control I/;\ Treatment is unrewarding as contagious ecthyma is caused by a virus. Management of infected animals plays a very important role. Because of public health considerations and the sometimes chronic form of OW, animals

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suspected of harboring the virus should be kept isolated from the herd until they recover fully. Stocking density should be reduced as much as possible and attention directed at reducing any secondary infection. Systemic treatment with high doses of synthetic penicillin against staphylococci is probably the best approach. Veterinarians examining or treating camels suffering from ORF should always wear gloves. Neither vaccination nor natural infection produces a long-lasting immunity. Recovered sheep, for example, are only immune to re-infection for about 8 months after a primary infection. Attenuated vaccines are routinely used in sheep and goats and might also be used in camelids. Studies by Dashtseren et al. (1984) have shown that neither vaccinia virus nor the parapoxvirus ovis vaccines protect camels against parapox disease. However, the authors have achieved protection against this disease using a camel parapoxvirus strain adapted in eggs. Vaccinated camels were protected for at least 6 months. It seems to be possible that a bivalent vaccine against two of the most important viral diseases of camelids can be developed in the future. References
Abu Elzein, E.M.E., E.R. Coloyan, A.A. Gameel, R.O. Ramadan and A.I. Al-Afaleq. 1998. Camel contagious ecthyma in Saudi Arabia. J. Camel Prac. and Res. 5 (2): 225-228. Ali, O.A., S.A.M. Kheir, H. Abu Damir and M.E.S. Barri. 1991. Camel (Camelus dromedarius) contagious ecthyma in the Sudan. A case report. Rev. Elev. Mid. vit. Pays trop. 44 (2): 143-145. Azwai, S.M., S.D. Carter and Z. Woldehiwet. 1995. Immune responses of the camel (Camelus dromedarius) to contagious ecthyma (Orf) virus infection. Veterinary Microbiology 47 (1-2): 119-131. Azwai, S.M., S.D. Carter and Z . Woldehiwet. 1998. An immunological study of contagious pustular dermatitis in camels. Int. meeting on camel production and future perspectives. May 2-3,1998, A1 Ain, UAE: 108.

Borisovich, Y.F. and M.D. Orekhov. 1966. Camel pox. Veterinaryia, Moscow. Dated in Vet. Bull. 1996,36,794 3: 50-52. Buchnev, K.N., R.G. Sadykov, S. Zh. Tulepbayev and A.A. Roslyakov. 1969. Smallpox-like disease of camels Auzdyk. Trudy Alma-Ata Tinskogo Zootekhnicheskogo Instituta 16: 36-47. Buchnev, K.N., S.Z. Tulepbaev and A.R. Sansyzbaev. 1987. Infectious diseases of camels in the USSR. Rev. sci. tech. Of.int. Epiz. 6 (2): 487-495. Biittner, M., C. von Einem, C. Mclnnes and A. Oksanen. 1995. Klinik und Diagnostik einer schweren Parapocken-Epidemie beim Rentier in Finnland. Tierarztl. Praxis 23 (6): 614618. Dashtseren, Ts., B.V. Solovyev, F. Varejka and A. Khokhoo. 1984. Camel contagious ecthyma (pustular dermatitis). Acta virol. 2 8 122-127. Dioli, M. and R. Stimmelmayr. 1992. Important camel diseases in the one-humped camel in Eastem Africa. A pictorial guide to diseases, health care and management. H.J. Schwartz and M. Dioli (Eds.). Verlag Joseph Markgraf Scientific Books: pp. 155-164. Fowler, M.E. 1998. Medicine and surgery of South American Camelids. Iowa State University Press, Ames. Gitao, C.G. 1994. Outbreaks of contagious ecthyma in camels (Camelus dromedarius) in the Turkana District of Kenya. Rev. Sci. Tech. 13 (3): 939-945. Hartmann, A.A., M. Buettner, F. Stanka and P. Elner. 1985. Sero- und Immunodiagnostik bei Parapoxvirus - Infektionen des Menschen. Der Hautarzt 36: 663-669. Hartung, J. 1980. Lippengrind des Schafes. Tierarztl. Prax. 8: 435-438. Khalafalla, A.I. 1998. Epizootiology of camel pox, camel contagious ecthyma and camel papillomatosis in the Sudan. Proc. Int. Meeting on camel prod. and future perspectives, Al Ain, UAE, May 2-3,1998: 105. Khokhoo, A. 1982. Biological properties of camel contagious ecthyma virus. Thesis, Veterinary Institute, Bmo. Kriz, 8.1982. A study of camelpox in Somalia. J. Comp. Path. 92: 1-8. Lewis, C. 1996. Update on orf. In Practice 18 (8): 376-381. Liess, H. 1962. Lippengrind (Ecthyma contagiosum) der Schafe als Zooanthroponose. Zbl. Bakteriol. Microbiol. Hyg. A183: 1969-1983.

192 Viral Diseases
Mahnel, H. and E. Munz. 1987. Zur derzeitigen epizootologischen Lage bei den Tierpocken. Tierarztl. Umschau 42 (1): 5-14. Mercer, A., S. Fleming, A. Robinson, I? Nettleton and H. Reid. 1997. Molecular genetic analyses of parapoxviruses pathogenic for humans. Archives of Virology. (Suppl. 23) 13: 25-34. Moallin, A.S.M. and K.H. Zessin. 1988. Outbreak of camel contagious ecthyma in Central Somalia. Trup. Anim. Hlth. Prod. 2 0 185-186. Moro, M. 1971. Ectima: En: La Alpaca. Enfermedades Infecciosas y Parasitarias. Bol Divulgacion Instito Veteranario de Investigaciones Tropicales y de Altura. Unva Nac San Marcos, Lima, Peru: 30. Munz, E., D. W i n g e r , M. Reimann and H. Mahnel. 1986. Electron microscopical diagnosis of Ecthyma contagiosum in camels (Camelus dromedarius) First report of the disease in Kenya. 1. Vet. Med. B 33: 73-77. Preston Smith, H. 1940. Los camello Peruanos, anguenidos, alpacas ectima. Ministr. Agric. Bol. (Lima). Preston Smith, H. 1947. Ectima de 10s animales del Peru, dermatitis pustular contagiosa. Ganaderia (Peru) 1 (1):27-32. Ramirez, A. 1980. Ectuina contagioso en alpaca. En aspectos santarios en la alpaca. Curso sistema de production pecuaria en 10s altos Andes. Assoc. Peruana Prod. Anim., Lima, Peru: 94. Robertson, A. 1976. Handbook on animal diseases in the Tropics. 31d ed. British Veterinary Association, London: 9-11. Roslyakov, A.A. 1972. Comparison of the dtrastructure of camelpox virus, the virus of poxlike disease of camels and contagious ecthyma virus. Voprosy Virusologii 2 7, Zoovet Institut, Alma-Ata, Kaz. SSR. Abstract: Vet. Bull. 42,512 1: 26-30. Thedford, R.R. and L.W. Johnson. 1989. Infectious diseases of New-world camelids (NWC). Vet. Clin. North Am. Food Anim. Pract. 5 (3): 145-157. Tulepbaev, S. Zh. 1969. Sensitivity of domestic and laboratory animals to the virus of smallpox-like disease of camels (“Auzdyk”). Trudy Alma-atinskogo Zootekhnicheskogo Instituta 16: 41-42. Tulepbaev, S. Zh. 1971. Pox-like disease (”Auzdyk”) of the camels in Kazakhstan. Diss. Kand., Alma-Ata. Wemery, U., 0.-R. Kaaden and M. Ali. 1997. Orthopox virus infections in dromedary camels in United Arab Emirates (UAE) during winter season. J. Camel Prac. and Res. 4 (1): 51-55. Wemery, U. and 0.-R. Kaaden. 1995. Infectious Diseases of Camelids. Blackwell Wissenschafts-Verlag, Berlin.

Further reading
Guo, S.Z. 1988. Serological comparison of the pathogens of aphthosis in camel, sheep and goat. Chinese J. Vet. Med. and Techn. 5: 35-37. Khalafalla, A.I., H Agab and B. Abbas. 1994. An outbreak of contagious ecthyma in camels (Camelus dromedarius) in eastern Sudan. Trop. Anim. Hlth. Prod. 26: 253-254. Khalafalla, A.I. and M.E.M. Mohamed. 1997. Epizootiology of camel contagious ecthyma in eastern Sudan. Rev. Elev. Mid. vkt. Pays trop. 50 (2):99-103. Khalafalla, A.I. 1999. Camel contagious ecthyma and its risk to young calves. Int. Workshop on the young camel, Quarzazate, Maroc, Oct., 24-26,45. Mustapha, I.E. 1980. IFS Provisional report No. 6 on camels, 399. Stockholm: Int. Foundation for Science.

2.1.5 Papillomatosis
Papillomas (warts) are benign neoplastic growths of the skin and mucous membranes and are observed worldwide in humans and a variety of animals. They are caused by species-specific pupillornuviruses that have also been associated with the development of squamous cell carcinomas. Cattle are more affected by warts than any other domestic animal species: 6 types of bovine papillomaviruses having been identified. More than 70 pupillornuvirus serotypes are recognized in humans and cattle, while only 1virus type has so far been identified in each of the other animal species. The papillornuvirus can also affect camels and cause typical skin lesions (Munz et al., 1990; Munz, 1992; Wernery and Kaaden, 1995; Khalafalla et al., 1998; Kinne and Wernery, 1998; Khalafalla, 1998).

The lesions were difficult to differentiatefrom true pox and parapox infections as generalized forms of papillomatosis had also been observed. ropes and contaminated instruments may transmit the virus. 94). The virions are about 50 nm in diameter. Figure 94 Papillomatosis in a young drome- dary (courtesy of Prof. The pathological picture of camel papillomatosis has been described by several researchers (Munz et al. The authors found most cases of camel papillomatosis during the rainy season. (1980) reported a rare case of papillomatosis in a dromedary in India. Dioli and Stimmelmayr. 1998). 95). Khalafalla et al. In the early stages of papillomatosis. Grooming equipment. was removed surgically without complications. Munz et al. These lesions that were examined by electron microscopy contained papillomavirus-like particles (Fig.3 to 4 c m in diameter and are usually pedunculated without affecting the health of the camels. Khalafalla et al. Sadana et al. Wernery and Kaaden. spherical with icosahedral symmetry and possess 72 capsomeres composed of at least 3 proteins. the lesions appear as rosy. Cases of papillomatosis in young dromedaries have also been reported in the UAE (Wernery and Kaaden. (1998) believe that there is a close relationship between papillomatosis and camel contagious ecthyma.. It is believed that this growth was not papillomatous. The wart lesions appear as round cauliflower-like papillomas 0. Munz et al. Kinne and Wernery (1998) described papillomatosis in a small camel population of 10 dromedaries in the UAE of which 3 camels displayed proliferative. Transmission of papillomavirus between animals usually occurs via abrasions or microlesions of the skin. Munz. only individual lesions on the lips and nostrils that. in which the skin lesions usually undergo vesicle and scab formation. as pedunculate warts. Germany) .. 1998). Generalized forms have not been observed. are commonly found on the lips and submandibular area without impairing the affected animal's health (Khalafalla et al.. which are quite distinct from pox lesions. pedunculated warts on and in the mouth. such as electron microscopy. However. 1998. Epidemiology '1 Papillomatosis has only been reported in OWC. hyperemic elevations of the skin. The wart. (1990) reported an outbreak of papillomatosis in Central Somalia primarily affecting animals from 6 months to 2 years old. 1992.Viral Infections Causing Disease 193 Papillomaviruses are classified within the genus Papillomavirus within the Papovaviridae family. The disease usually occurs in camels less than 2 years old and the wart lesions. but rather a tumor (fibropapilloma). where it is rare and of little economic significance. Kinne and Wernery. 1990. 1995). Dioli and Stimmelmayr (1992) found a relationship between camelpox and papillomatosis in Kenya. coinciding with outbreaks of contagious ecthyma. located on the fetlock of a 15year-old dromedary and weighing 2 kg. could clarify the disease agent. 1995. This clinical picture is quite distinct from that produced by camelpox and parapox. Only laboratory procedures. were easily differentiated from other diseases involving pox viruses (Fig. Mechanical transmission by arthropods might also be possible.

para. Some camels had lesions on the ears. x220) .the affected epithelium is hyperplastic with excessive folding that leads to the formation of proliferative outgrowths. but mortality was zero. The epithelial hyperplasia is characterized by marked acanthosis. Virus antigen is visible in a few nuclei of the upper stratum spinosum and in numerous cells of the stratum granulosum and corneum (PAP-method. inguinal and genital regions and on their legs. eyelids. Microscopically.and hyperkeratosis with Figure 96 fapillomavirus-antigenpositive labeled cells of the epithelium of a wart. The morbidity was high.194 Viral Diseases Figure 95 fapillomavirus-like particles from a wart in electron microscopy (XI25.000) (1990) described an outbreak of papillomatosis in Somalia where many dromedaries revealed pustules and scabs on lips and nostrils and generalized proliferative small and large nodules and tumor-like lesions.

Khalafalla. development of a specific vaccine for each individual herd is recommended.S. 1992. J. H. Mahajan and K. Infectious Diseases of Camelids. 1998.C. Indian J.R. Z.H. J. usually by aerosols. S. J.. camel production and future perspectives. meeting on . Berlin. clear cytoplasm and large pleomorphic keratohyalin-like granules (hollow cells). Snow and J.F. Mayhew. A. 5 (2): 201-205. Epidemics occur particularly in poultry. W. C and D. Due to the antigenic variants of the papillomavirus.I. 43-46. 96). Wade: R. B. and W. A. A. UK: pp.J. pigs and equines. 1998.. Camel papillomatosis in Somalia. A1 A h . U. Note on papilloma in a camel. severe outbreaks were reported among Bactrian camels in Mongolia (Lvov et al. Dioli (Eds..I. camel contagious ecthyma and camel papillomatosis in the Sudan. Group A is the most important one. B and C which are transmitted directly.1998. seals and whales. which might turn hyperplastic. UAE: 105. a 2. 1982.. Kinne and Wernery (1998) were the first to develop an immunohistochemistry method using polyclonal rabbit-antibovine-papillomavirusserum (Fig. Group D differs biologically from A. e..Viral infections Causina Disease 195 elongation of the rete ridges. Anchlan et al.G. Kinne. and R. Humans are infected by all four groups of Influenzaviruses: A. the affected animals were treated with a formalinized autovaccine produced from surgically removed warts.. A pictorial guide to diseases. Mohamed. Proc. E. Epizootiology of camel pox.R.). C and D. Med. May 2-3. Although ruminants in general and camelids as intermediates are not considered susceptible to the influenza virus. Higgins. of which D comprises tick-borne viruses. Blackwell Wissenschafts-Verlag. Etiology w The influenza viruses belong to the family Orthomyxoviridae. Also in camels. Mahnel and M. but only Group A viruses produce epidemics. health care and management. However.: int. Reimann. M. Int.J. in two outbreaks of papillomatosis in the UAE. Stimmelmayr. J. and U. A.K. lSt Camel Conference. Satija. Important camel diseases in the one-humped camel in Eastern Africa. However. Camel Prac. Vet. Khalafalla. In animals too. Camel Prac.6 Influenza The family Orthomyxoviridae (lnfuenzaviruses) consists of four genera. Wernery. B 37: 191-196.M. Wernery.H. A. H. B. self-limiting disease and therefore neither prevention nor treatment is usually necessary. I. 50 (9): 793-794. Publications. Allen. 5 (1):157-159. Papillomatosis in camels in the United Arab Emirates. and Res. Camel papillomatosis in the Sudan. wart lesions are often self-limiting and fall off within 3 to 6 months. but infections have also been observed in minks. i Papillomas can usually be differentiated by their typical microscopic features. Sadana. and Res. Munz. 1995. Schwartz and M. Anim. Pox and pox-like diseases in camels. Kaaden. Munz.1.g. Abbas and M. 1992. 1996). and 0. Treatment and Control I Papillomatosis is generally a mild. The dromedaries were given between 3-7mL (depending on body weight) of the wart vaccine subcutaneously. Newmarket. 1993.The warts receded within 8 to 10 days. Sci. J. Yamnikova et al. These ridges extend deep into the underlying dermal connective tissue. Verlag Joseph Markgraf Scientific Books: 155-164. Virions are 20 to 120 nm in diameter and are surrounded by a host cell-derived envelope with "spikes" formed by the glycoproteins of hemagglutinin and neuramini- References Dioli. Eds. Dhori and Thogota (see under Unusual Arboviruses). E. Within the stratum granulosum individual and/or clusters of cells might appear with swollen. 1990.-R. 1998. Moallin. 1980. D.E.

There was a mucous ocular and nasal discharge. These test camels were confirmed to be free of pre-existing specific influenza antibodies. although the challenge virus strain was re-isolated and the experimental animals seroconverted. bronchitis. occasionally with fatality.6% and cachexia 6. isolated from Mongolian patients during the same time as the influenza epidemics in camels. 3 to 4-year-old Bactrian camels were infected experimentally with the HlNl influenza isolates from affected camels. Viral-protein synthesis occurs in the cytoplasm of host cells and during replication. intratracheal or intramuscular route.. The isolates were identified by the hemagglutination test as HlNl influenza A viruses. Groups of three camels were each infected by either the intranasal. but true recombinations have also been described. 1993). The clinical course lasted about one week. pneumo- Figure 97 Bactrian camel with nasal discharge caused by influenza . Genetic reassortment may occur in mixed infections with viruses of the same species resulting in antigenic shift. nia and fever. but the disease has been observed in two-humped camels. The outbreaks started in 1979 and were caused by HlNl influenza A virus. no severe clinical signs were observed after the experimental infections.1%... Further clinical signs during the acute stages involved a dry cough. In three independent experiments performed between 1985 and 1986. The clinical signs observed were as follows: lethality 9. were found to be highly related in all genes sequenced to the camel strains. Nineteen outbreaks of severe respiratory diseases were recorded in camels between 1978 and 1988 in 61 farms in different parts of Mongolia (Lvov et al. 1982. One of the outbreaks involved about 4. A total of 34 healthy. Four influenza A viruses of the same subtype HlN1.The questions still remain as to how the viruses were introduced into the camel population and how they spread and attained pathogenicity in a formerly non-susceptible species. It is believed that the camel influenza isolates were derived from an UV-light inactivated reassortant vaccine (PR8x USSR/77) prepared in Leningrad in 1978 and used in the Mongolian population at that time (Anchlan et al. The experimentally infected Bactrians developed clinical signs similar to those found during natural Epidemiology 81 Influenza A outbreaks have not been reported in NWC. exhibiting hemagglutination inhibition titers between 1:16 and 1:128. abortion 2. The outbreak occurred on 61 camel farms between 1978 and 1988 in different parts of Mongolia.000 camels affected with severe respiratory symptoms.7%. Yamnikova et al. 1996). Thirteen virus isolates were obtained from a total of 92 nasopharyngeal swabs cultured in the allantoic fluid of infected embryonated chicken eggs.196 Viral Diseases dase in a ratio of 4:l or 5:l.

Praha may infect camelids.89'0 of fore essential to carry out virus isolation Sudanese camels positive for the influenza and identification or serological tests. equine rhinoviruses. Specimens for virus isolation should be A virus.Viral Infections Causina Disease 197 infection (but milder): fever. A rapid diagnosis in equines and camels are kept in close vicinity. the inhave a high pathogenicity for other species fluenza outbreaks in Mongolia proved that (Scholtissek. Influenza viruses should be culcurred in horses: H7N7 (influenza A/ tured in embryonated eggs or in Madinequine-l/Prague/56) and H3N8 (influen. els have been reported by Auguadra (1958) and Somac-Sarec (1982) without any at. as virus excretion might be very (N) have been identified. camels are kept in close vicinity is the The influenza outbreak in Mongolian UAE.Diagnosis In horses. In this country. collected in virus transport medium and only one combination HlNl occurred. intempts to isolate the virus. the rapid various African countries. it is dromedaries in northeastern Nigeria.for the detection of antibodies to the intremely cautious in countries where horses fluenza virus. 12 different collected after the onset of pyrexia and hemagglutinins (H) and 9 neuraminidases coughing. The virus is identified by es when mutations in the gene sequence hemagglutination and subtyped using HIT result in amino acid substitutions. No further outbreaks among Bactrian the countries where valuable horses and camels have been reported since. particu. USA) and should also binations of influenza viruses (antigenic be tried in camelids with influenza-like 11. Among influenza viruses.4. However. for example. It is thereAmin and Kheir (1985) reported 7. 1998). shift). The authors re. El. In vaccinated animals or in aniinfluenza B virus taken from slaughtered mals that have overcome the disease. Sero.7%for the diagnosis. other influenza serotypes than Miami and Influenza-like epidemics in Somali cam. as not is done with the Directogen FLU-A test kit only antigenic drift occurs but also recom. The HIT is also used larly in the hemagglutinin.6% of the samples positive ature are sufficient to make a preliminary for the influenza A virus and 12.Darby canine kidney cells (MDCK).extremely difficult to diagnose. Antigenic shift gives rise to new inbronchitis and discharge from nose and fluenza viruses which might result in paneyes (Fig. the authors have excamels is convincing evidence that a reas.Severza/equine-2 /Miami/ 63).(Becton Dickinson.perienced annual outbreaks of respiratory sortant between two human strains has disease in racing dromedaries caused by caused severe epizootics among camels. sent cooled to the laboratory as soon as Only two combinations have so far oc. Major antigenic al passages may be required in order to isodrift has been observed among H3N8 virus. spread. the harsh cough and high temper(1989) found 0. Olaleye et al.respiratory diseases like EHV-1 and EHVtion with rhinitis and conjunctivitis. Nasopharyngeal swabs have to be lian influenza outbreak in Bactrian camels.late the virus.fluenza must be differentiated from other ported respiratory symptoms in conjunc.short. equine arteritis logical studies to identdy antibodies to the virus. Furthermore.possible. All infected animals recov. 97).with specific antisera.Prague revealed no positive cases (CVRL fore be adopted. because new strains may Annual Report. coughing. Safety requirements HIT with the equine strains Miami and for cold-adapted reassortants must there. One must be ex. a serologiwhich are not regarded as natural hosts for cal survey on 500 UAE camels using the influenza A viruses. Streptococcus equi equi (Strangles) influenza virus have been performed in and Rhodococcus equi.1995). In the Mongo. One of ered. However. . coccal infections.demics in susceptible populations.

S. Potential hazards associated with influenza virus vaccines. 1985. Annual Report. by agargel diffusion test.int. Preliminary survey for antibodiesagainst respiratory viruses among slaughter camels (Camelus dmmedarius)in northeastern Nigeria. Agab and Abbas (1998) reported a mortality rate higher than 30% in dromedary calves caused by diarrhea. Rev.K. which include enterotoxigenic E. L. J. Sudan.and coronaviruses have been identified as having characteristic localizationson the mucosal epitheliumof the jejunum. Dachtzeren. ital. 1998.. 6 (1): 87-91. Vladimirtseva. Kheir. sci.. Parasif. Field and laboratory investigations have indicated that there is not a single etiology. O. S.A. Biol. Bel-Ochir. Z. ileum (rotavirus)and colon (coronavirus). 1 ) Further reading Wernery. vdf. Rev. trop. Nymadawa. but in case of an outbreak. However. Sci. Yamnikova. Scholtissek. . The presence of viruses in the feces is not always indicative of manifest disease. Scholtissek. the serological diagnosis of infection in a vaccinated population is complicated by the presence of vaccine-induced antibodies. P. Stand. coronavirus. Treatment and Control The most effective means of control in the face of an influenza outbreak are vaccination and restriction of movement of animals. Omolabu. Epidemiology i Very little is known about the cause of neonatal diarrhea in camelids. Mdd. Archives of Virology 141 (8): 1553-1569. Yamnikova. Pays frop. Elm. Ludwig. March 10-26: 18-23. family Coronaviridae. P.S.In Sudan for example. Epiz. Grippe 0 influenza del dromedario Somalo. 8 (3): 779-783. and S. Agafonova. 1989. 1995.S. Zhadanov. Viral replication leads to the loss of function of the villous epithelium. I. Miyasnikova. med.. New aspects on infectious diseases of camelids. Lvov and C. P. and Salmonella spp. A reassortant HlNl influenza A virus caused fatal epizootics among camels in Mongolia.A. U. Mandler.H. Dachtzeren. Dubai. D.A.M. Camel Prac. S. Nymadava.G. genus Rotavirus.7 Neonatal Diarrhea Neonatal diarrhea in calves is one of the greatest sources of loss in animal breeding. El-Amin. On a clinical basis it is not usually possible to differentiate between the common known causes of diarrhea in newborns. 38 (2): 127-129. Camel research project report by a Somali/Swedish Mission. Central Veterinary Research Laboratory. Virology 197 558-563. LA. tech. J. 1982. Mendsaikhan and C. viruses and parasites. Dev. Coronaviruses belong to the order Nidovirales.: 19. Bel-Ochir and V. 1982.K. U. M. The cause is complex and usually involves an interplay between enteropathogenic bacteria.coli (ENTEC). S..198 Viral Diseases clinical signs. No influenza vaccines have been administered to camelids. J. Detection of influenza antibody in animal sera from Kassala region. D.H. Rota. 84: 55-58. Ludwig. CVRL. 34: 215-222. 1984). but there is agreement that the most common cause of death in camel calves up to 6 months of age is diarrhea (Khanna et al.D. Olaleye. S. D. Shemyakin. 2. 1993. Z. Voprosi Virus0127 401405. Previous H l N l influenza A viruses circulating in the Mongolian population. P. P. Somac/Sarec. causing the clinical signs (Freitag et al. There are only few reports that camelids might be susceptible to both ro- References Anchlan. vaccination programs should be considered. Cyptosporidia spp. 1999. 1992). Lvov.A. Auguadra. Baba and S. 1958. Arch.. S. 1996.1. Each rotavirus is named after the species in which it occurs.V. Scholtissek..A. Etiology d Rotaviruses are classified in the l family Reoviridae. rotavirus. Of. E.E. C. Persistence of genes of epidemic influenza viruses. and Res.

composed of conventional antibodies. but Rivera et al. 1998. ELISA tests are more reliable and sensitive than electron microscopy and are nowadays widely used for the diagnosis of viral neonatal diarrhea. 1993. totaling 25% of serum IgG. Attempts to isolate rotavirus from eight positive fecal samples using MA 104 cell line (fetal monkey kidney) were unsuccessful up to the eighth blind passage. At present. .7% (342/390). Rota.).IgG2 and IgG3 consisting of dimers of short heavy chains. ELISA and Latex agglutination (Khalafalla. Immunoglobulins (Ig) are divided into classes or isotypes (IgG. (1985) showed that alpacas are also susceptible to rotavirus. 2000 in prep. IgM. However. . Mattson (1994) believes that neonatal diarrhea in NWC occurs with a lower incidence than in cattle.unpublished). This proves that dromedaries are susceptible to rotavirus infection. Rotavirus has not been isolated from NWC. (1983) found in serological studies of Moroccan dromedaries that 50% of the animals (27/55) had antibodies to rotavirus. Diagnosis Rota. 1 out of 117by ELISA and 1 4 out of 87 by electron microscopy were positive for group A rotaviruses. Most of the positive samples were recorded in early winter (October). 1995): . totaling 75% of serum IgG. A seasonality of rotavirus infection in camel calves was observed. Neonatal diarrhea is often caused by a secondary immunoglobulin deficiency and it is therefore important to comment in this chapter on the passive transfer of immunity. which are characterized by a normal Fc region without CH1 domain. Rotavirus antibodies were also detected by Puntel et al.and coronaviruses such as SNT and HIT. pigs and sheep.2. Most studies on animal immunology deal.. however.3).IgGl binding strongly to protein A and G. of which IgG2 and IgG3 lack the light chains (Fig. IgE..and coronavirus particles can be demonstrated in preparations of fecal samples from diarrheic calves by transmission electron microscopy. In the UAE. which indicates that this species is highly susceptible to rotavirus. 98) (Hamers-Casterman et al. Azwai and Carter. corona-like agents were detected by electron microscopic investigations in fecal samples of dromedary calves with diarrhea.and coronaviruses were detected in fecal samples in UAE dromedary calves suffering from diarrhea using electron microscopy (Mohamed et al. It is worthwhile mentioning that IgG antibodies in camelids differ from all other known antibodies and contradict all common theories on antibody diversity. Chang-Say et al. three subclasses of camelid IgG have been identified (IgG 1. IgM or IgA (Table 39). (1999) in 390 llamas from 9 farms located in 3 different Argentinean provinces. Rotaviruses were detected in a number of fecal samples from eastern Sudanese camel calves suffering from diarrhea using electron microscopy. The genome of the camel rotavirus was analyzed by polyacrylamid gel electrophoresis (PAGE). Mahin et al. The antibody prevalence was 87. These tests also have the advantage of handling larger numbers of specimens. IgA..Eight out of 200 samples examined by Latex agglutination test. with IgG. Several methods are used for the detection of antibodies to rota. Ijaz et al. (1987) detected antibodies to rotavirus in alpacas. IgD) and further subdivided into subclasses. Virus isolation in cell cultures is difficult and often fails. in comparison with group A human and equine rotavirus isolates.Viral Infections Causina Disease 199 tavirus and coronavirus. The results indicated that the profile of the camel rotavirus RNA was different. but attempts to isolate the virus in cell culture failed (Mattson. 1994). Coronaviruses have been seen by electron microscopic examination of feces in two llamas with diarrhea.

G3 G1. G2**. 1999) Species Horse Cattle Sheep Pig Alpaca Llama IgG subclasses Ga. In dromedaries at least five IgG isotypes have been detected: IgGla. (1997) described that llamas possess IgGla and IgGlb conventional antibodies and at least three heavy chain antibodies: IgG2a. G l b (conventional) GZa. 1999) . 2000. IgG2b and IgG3. G4 IgM M M M M M IgA A A Al.. G2b) G1 (Gla). G3 -* Garmendia and McGuire (1987) Ghahroudi et al. G3** -* -* -* -* -* * ** Gla.200 Viral Diseases Table 39 IgG. G l b (conventional) G2a. IgG2c. G3. G2b. G(T) GI.) Ghahroudi et al. (2000) describes how different antigens (cell-lysateor haptens conjugated to carrier proteins) induce a variable response of different camelid isotypes. correspond to llama isotopes) (Nguyen and Muyldermans. has in the meantime been reported by Woolven et al. Gc. 1993). IgM and IgA subclasses in different domesticated animals (after Huelsebusch. (1999). Gb. G2. A2 Source Tizard (1992) G G la. (1987) Hamers-Castermanet al. (1993). = not identified = heavy chain antibodies Grover et al. A2 Al. commun. G(B). IgGlb (conventional antibodies) and IgG2a. G2. in press). show a Figure 98 Structure of camelid IgG molecules (Huelsebusch. (1999) M M A Camel G1. (1993) Nguyen and Muyldermans (pers. It has been demonstrated that up to 75% of all serum proteins in camelids were IgG molecules lacking light chains (HamersCasterman et al. G ~ cG3 (heavy chain) . IgG2c and IgG 3 (heavy chain antibodies. G2 3 subclasses G + associated protein G1.G3 (heavy chain) Gla. Carter and Azwai (1996) Ungar-Waron et al. A recent paper by Linden et al. G2 (GZa. which only consist of heavy chains. An existence of a fourth heavy chain antibody. (1983) Azwai et al. G2c. G l b G2a. (1997) Woolven et al. IgG 2 and IgG3.G2b.

Fig. 99). For IgG. Moreover. principally IgG. 1987) .. (1999) that antigen-specific llama VHHs are stable at extreme temperatures. 1999. CDR: complementary determining region molecular weight of 100 kD. The camels therefore must obtain passive immunity by intestinal absorption of IgG from the colostrum. Immunoglobulins. Lauwereys et al. 1998. for IgM it is 3 to 5 days... Fig. since the rate of decay of antibodies in serum is fast. 1998. because their smaller size improves biodistribution and allows better tissue penetration. Riechmann and Muyldermans. Hoelzer et al. In the latter respect. 100 demonstrates that newborn dromedary calves have very little demonstrable serum IgG prior to ingesting colostrum.Viral Infections Causina Disease 201 Figure 99 Molecular structure of variable heavy chain domains of camelid heavy chain IgG antibody (A) and common IgG antibody (B). are transferred from the dam by colostrum intake after birth. it was also shown by Linden et al. In general. Protection is afforded rapidly. VH: variable heavy domain. These antibodies and their antigen-binding domain (referred to as VHH) have advantages over common antibodies. the third complementary determining region (CDR) loop can be inserted deep into the active site of an enzyme.. 2000). it seems that camelids possess a unique class of antibodies which show a great advantage over common antibodies in applications where enzyme neutralization.. Passive acquisition of antibodies is an important survival mechanism for the newborn. Failure of passive transfer (FPT) of maternal immunoglobulins is the most important immunologic deficit in veterinary medicine because it is significantly correlated to numerous infections in postnatal life. size or stability is an issue (Nguyen et al. Although the neonate camelid is i m munocompetent at birth. it is immunologically na'ive and therefore dependent on 9 F 10 5 10 15 20 25 30 Days after parturition Figure 100 Serum immunoglobulin values in dromedary mothers (solid triangle). 1994. Camelids have a thick-layered epitheliochorial placenta which prevents transplacental transfer of IgG. The transfer of maternal antibodies from serum to colostrum to the intestinal tract and finally to the neonatal vascular system is a complex process with many sites for disruption. dromedary calves that have ingested colostrum (solid circle) and dromedary calves that have not ingested colostrum (square with central dot) (Graph modified after Ungar-Waron et al. Two of the six llama VHHs were able to bind antigen at temperatures as high as 90°C. enabling it to neutralize enzymes fully (Muyldermans et al. the half-life is 9 to 21 days.

commercially available for NWC: Llama-STM. septicemia. Levels between 5 and 6 g/ dL are equivocal and levels over 6 g/dL indicate a successful passage of IgG. (1992) were the first to examine this problem in dromedaries. while the average IgG concentration of the dams’ sera on the day of parturition was 23. Fowler (1998) described serum protein levels in NWC. 1999). As in other domesticated animals. USA). Newborns that fail to acquire adequate passive immunity are at greater risk of developing diseases such as diarrhea. The Ig concentrations of colostrum of camelids are seen in Table 40. IgGs decline rapidly and reach low levels 2 weeks after birth.6 i 15.26 0. Studies have determined that the concentration of IgG in NWC colostrum is approximately 220 mg/ mL (Bravo et al.5 mg/mL. Serum IgG concentrations stabilize at a plateau around 4 months after birth. In bovines the mechanism of IgG transfer involves an active IgGl specific receptor. 1999).7 mg/mL were reached in newborn dromedaries 18 to 30 h after birth. (1987) Ungar-Waron et at.56-84. and it is believed that based on the predominance of IgG in camelid colostrum (7: 1IgG vs IgM).. Pullman. In NWC as in OWC the lowest level of globulins is reached 3 to 5 weeks postpartum. Although the newborn calf is immunocompetent at birth. It was calculated that a 10 kg cria would require 20 g of IgGs to obtain an IgG level of greater than 9 mg/ mL. the efficacy of immunoglobulin absorption in camelids declines in a linear fashion over the first 24h of life.81-6. WA.202 Viral Diseases passively acquired humeral immunity.02 (192) Authors Garrnendia et at. Ungar-Waron et al. As in other domesticated livestock neonates. The calves’ own antibody production does not start before 2 weeks. VMRD Inc.. The maximum IgG levels of 21. the endogenous antibody production is not sufficient to obtain a protective immunoglobulin level within the first month of life. a cria would need to consume approximately 100 mL of colostrum.9 2 7. meaning that the critical period of calves for infections lies between 2 and 5 weeks. To obtain 20 g of IgG from colostrum with an average IgG concentration of 220 mg/mL. (1987) and Hannant et al. Several methods are available to measure passive transfer such as zinc sulphate turbidity (ZST).25 (lgl) 1. After the peak IgG level is obtained. Total protein levels of less than 5 g/dL are suggestive of FPT. (1987) Karnber (1996) El-Agarny (1998) El-Agarny (1998) .4 25. Successful passive transfer is achieved when neonates have IgG serum levels of greater than 9 mg/mL at 48 h of age (Barrington et al. The single radial immunodiffusion (SRID) is Table 40 Colostrum IgG concentrationsin rng/rnL of carnelids (after Huelsebusch. omphalitis and pneumonia. sodium sulphate precipitation (SSP. 1999) SDecies Alpaca Camel IQG 10-280 70-220 58. and a marked increase in serum IgG above 10 mg/mL is found between 1and 2 months. None of these tests measure serum IgG concentrations specifically. 1997). Assessment of passive immune status of compromised camelid neonates is essential to enable prompt administration of IgG. enteritis. a similar selective transfer of IgG into camelid colostrum occurs. arthritis. indicating that the immune system has matured.1 2 11.23 mg/mL) (Huelsebusch. very low IgG concentrations were observed in 68 camel calves before intake of colostrum (0.

1997).zinc sulfate turbidity (ZST). . Hutchison et al. Bethyl Laboratories.Viral Infections Causing Disease 203 the only method that specifically measures serum IgG concentrations. TP and G (after Bourke. The anti-camel-IgG antibodies were raised by immunization of layer hens with camel IgG and were subsequently extracted from the egg-yolk. 1999. 1999). Montgomery. The calves did not suckle. If no camelid colostrum is available. This syndrome was caused by copper deficiency. .. in press) described a secondary IgG deficiency in young dromedaries in the UAE which died from septicemias.. Literature on camelid IgG deficiency is limited. and animals with diarrhea should be separated from healthy ones. Table 41 IgG status in carnelids based on ZST.globulin (G).and hardly any reports exist on FPT in OWC. the amount of circulating IgG acquired from colostrum is primarily dependent upon two factors: the amount of IgG in the colostrum and the efficacy of its absorption by the calf.2 ance at later ages. Redmond.5 > 5. but consumed variable amounts of sand as compensation for the copper deficit. Fluid may be given orally or parenterally depending on the degree of dehydration. 1987. Barrington et al. Farms.. 1992. 1976). an important tool in tackling FPT (Huelsebusch. Garmendia and McGuire. Kennel and Wilkens. Few reports indicate that FPT is the major factor in neonatal mortality in alpacas (Garmedia et al. Murphy. Successful immunoglobulin transfer is associated with low infection rates and high likelihood of survival (McGuire et al. Treatment Treatment of diarrheic camelids should primarily aim at rehydration and the correction of electrolyte imbalance.3-1. It is common practice to establish a colostrum bank and feed 10% colostrum in milk during outbreaks of neonatal diarrhea. as death mainly occurs due to dehydration. Therapeutic administration of IgGs to provide protection against a number of pathogens has an important place in veterinary medicine.. 1996) IgG transfer status Nil or low Moderate Adequate ZST I c 30 30-40 >40 TP gldL c5 5-5. Triple J. USA and Llama Vet-RID. Bourke (1996) has studied the application of three tests for the determination of the passive immune status in llama neonates: . and it also modulates the occurrence of mortality and severity of enteric and respiratory disease in early life and perform- . Antibiotics may be administered to control secondary bacterial infections. However. 1987. Erhard et al. Many important factors exist which influence the level of serum IgG achieved by the newborn.. 1995b. 1998. Hutchison et al. TX. For NWC the test is commercially available in two kits: Llama IgG Test Kit. goat colostrum (up to 20% of body weight) may be administered to lla- The study indicates that all three tests can be used to assess the IgG status in neonatal camelids. The ingestion of colostrum is essential for the survival of the newborn. An ELISA has recently been developed for the quantification of camelid IgG in blood serum.5 G gIdL c 0. as seen from Table 41.total protein (TP). (1995a) compared these tests on 528 llama plasma samples and found that each test kit provided significantly different IgG levels when compared to the other. (2001.25 0. FPT is the major determinant of septicemic disease. This procedure will provide passive protection for a 2 to 3-week period of risk. USA. WA.This assay is designed as an indirect ELISA carried out in 96-well microtiter plates.2 > 1. Wernery et al.

ma is commercially available at Triple J.. sobre Camelidos Sudameriwarmed to 37°C. Bonnet. S. F. 26: 145-149. Chronic weight loss in an immunodeficient adult llama.E. Espenkotter. DeterViral Neonatal Diarrhea in calves is difmination of serum IgG levels in camels by a bovine specific sandwich ELISA. Abbas.M. Immunity and infectious diseases in the dromedary Fowler. ELISA for camel IgG and measurement of colostral transfer. F.W. 1995.D. Hamers. 1996. Determination of passive immune status in llama neonates. Farms.H.H.B. Eds: W. Nature 363: 446-448. D.J. Iowa State University Press. Parish and F. Wyns.A. Camel's colostrum. Immunodeficiency in South American Camelids. 1984. 1999. Grover. Mechanism and isotypes involved in passive immunoglobulin transfer to newborn alpaca (Lama pacos). 1987. J. Ghahroudi.A. Camel Prac. 1997. Vet. significantly reduce the prevalence of rotaMauritanie: 177-179. Anderson.P. 1997.C. McGuire.A. cases of viral Neonatal Diarrhea in camelid Aus der Praxis. E.. Reporte preliminar sobre prevalencia de camelid plasma intravenously. Wetzel and E.. Bajyana Songa. R. Pugh and D. Srivastava. M.M. Wade: R. Woldehiwet. 1999. Azwai. J. Proc. Res.E.B.M. 1993. Biochem.M. Monoclonalantibodies against camel (Camelus dromedarius) IgG. Brit.G. 109: 187-195. Dabbag.. Hamers. S. L. Camelid SOC. . Belknap. A.E. S. J. Bendahman and R. K. Carter and Z. alpacas and their crias. Am.R. Assoc.C. Publications. A.Burford: 39-45.204 Viral Diseases camel. Camel Newsletter 14 (4): 53-58. Schickel and M. Y. Path.. and Res. 1998. Dromadaires et chameaux. DeMartini and T.N. Bowen. G. Preliminary studies on camel serum immunoglobulins. Atarhouch. Hannant. Pugh and November 14-16. M.M.E. Ames.. Comp. Peru: 37. Immunoglobulin G concentrations in periparturient llamas. Bravo. 1997. Azwai. 1992. Mumford. H. S.K. 45 (1-2): 175-184. Garmendia. Snow and J. D. Vet. 48: 1465-1471. Wernery and J. urztl. and S.. Umschau 39 (10): 731-736. Med. Proc. and T. In Freitag. Kaura. Vet. J.F. 1993. 17 (13): 3512-3520. S. H. Muyldermans. J. Vet. Ind. Proceedings of the 3rdBr. 6 (1):15-18. Stangassinger. Garnica and M. Mayhew. mas as a substitute (Pugh. 1987. Am. and W. Erhard. The isolation and characterization of camel (Camelus dromedarius) immunoglobulin classes and subclasses.H. Maternal vaccination may be an al. Llama hyperimmunplascanos V. H.D. 211 (3): 295-298. Garmendia. T. Higgins. EMBO J. 4 8 1472-1476.M. A.El-Agamy.. Carter. Muyldermans. Carter. It should be virus influenza tip0 A rotavirus en alpacas. Barrington. J. A. and 8. and corona diarrhea in affected animals. ten complex and the disease has a rapid course. S.I. D. 1998. J. D. Camel ficult to control because the etiology is ofPrac.Comparison of llama VH sequences from conventional and heavy-chain antibodies. it is also possible to give 20 to 40mL of Chang-Say. 1996.N.Burford.. 1998. S. and S. Hamers and S. Ed. For the treatment of FPT. Bourke. Antimicrobial factors. Medicine and surgery of South American Camelids. Zur Prophylaxe der Rotacalves. 1997). Kouider.1996 23-36.E. G.. Actes du colvaccines 1to 3 months before calving can loque. Am. 1992. Camelid SOC. J. Robinson. J. and Res. Incidence and causes of morality in pastoral camels.M. Samame. References Agab.D. Y. Garry. 24-26 Octobre 1994. Camel Conf. Failure of passive immunoglobulin transfer: a major determinant of mortality in newborn alpacas (Lama pacos). 2 0 238-240. Allen. C. G. The use of commercial animaux laitiers. Azwai. U. 6 (2): 185-190. Tyler. Parish. N. S. McGuire. given over a 30 to 60 min time frame and Convencion Int. J. Noaukchott. 1 s t int. Epidemiological studies on camel diseases in eastern Sudan: 11. Naturally occurring antibodies devoid of light chains.. J.C. G. E. S. Res. Prasad and S. USA. 1985. Vet. M. I. Newmarket. Palmer.M. 1983. UK: 93-95. vaccination programs should thereCorona-Virus-bedingten Kalberdiarrho..G. PW. IgM and light chains. H. Rivera and H. Tierfore be considered. Small Ruminant Res. Redmond.. Biopkys. Cuzco. ternative approach. WA. Fowler. P. Desmyter. Immunology and Imrnunopatk. Barrington. Vet. Hamers-Casterman. C.

Ruuls.A. 1998. Schudel. 1994. Keefe.N. A. Detection of coronavirus-like agents (CVLA) in diarrhoea of neonatal calves born to racing camels. Hutchison. Vet. N. McGuire. 1999.M. de Genst. Gorde and S. Untersuchungen iiber die Versorgung von neugeborenen Kamelfohlen (Camelus dromedarius) mit ImmunglobulinG. Wyns and S. USA. Carillo and A. Causes of mortality in farmed llamas in North America. D. Eds: W. Blanco Viera. M. Mahin.A. J. Serological survey of viral antibodies in llamas (Lama glama) in Argentina.M. 1992. J.R. 5 (2): 187-188. Puntel. Kamber. Ravnak.. Maenhoudt and P.A.B. A. R. Wilson.P. Johnson. Murphy. J. 8.A. A.A. Bos. u Hohenheim Tropical Agricultural Series. Pugh.R. Huelsebusch. Fondevila. I. 198-201.W. Quackenbusch..J.E. Wernery. Invest. C. S. Calf mortality in Indian camels. Sequence and structure of VH domain from naturally occurring camel heavy immunoglobulins lacking light chains. and J. Am. Methods 240 185-195. I? Davis and C.. Chr.J. D. Mohamed. Belknap. Ellis.E.. T. Publications. J. Camel heavy-chain antibodies: diverse germline VHH and specific mechanisms enlarge the antigen binding repertoire.Viral Infections Causing Disease 205 Hoelzer. W. Mayhew.H. J. W. R. F. van der R. Comparison of physical chemical properties of llama V-HH antibody fragments and mouse monoclonal antibodies. J. Snow and J. M. A l Ain. SOC. Al-Masri. van Wassenaar. 2000 (in prep. EMBO J. North America: Food and Animal Practice 10 (2): 345-351. 169: 713-718.J. Assoc. J. de Geus. Vet. Mohammed. R. Elev. 1992. EMBO J. 1983.G. 1998. 7 515-519. trop. Chadli.M. S.M. L.G. Potent enzyme inhibitors derived from dromedary heavychain antibodies. MN. 2000. 46: 157-161. 292-297. and Res. 1976. Sahani. Hoelzer. Harmsen. T. L. Dar. Pastoret. and Immunopath. Muyldermans. 1st Int. Muyldermans. Llama Assoc. J.T. A. Belknap. Biochemica et Biophysica Acta-Protein Structure and Molecular Enzymology 1431 (1): 3746. G. Clin. Margraf Verlag.K. Allen. 36 (3):251-252. Cockerell. P. M. Nguyen. Riechmann.J.M. meeting on camel production and future perspectives. Herlekar. M. Pays. Higgins.E. Khanna. B.D. Ahmad. 1998. Prepartum care of the pregnant llama and neonatal care of the cria. J. 5: 1983-202.M. L.. 1999. Verrips and 1. Ijaz.. Weikel. J. neonatal care and congenital conditions. Perinatal and neonatal care of South American camelids. Linden. N. Tandon and M.). T.. Switzerland.H. Viral Diseases. W. Saldanha. de Ron. 1992. Theriogenology. Failure of colostral immunoglobulin transfer in calves dying from infectious diseases. W..L.H. Kennel. Geky.K.E. Pfeiffer and J. Muyldermans. Vet.H.-R. 2000. Stok.M. Immun. U K 89-92. V. Med. M..A.B.. Agents associated with camel diarrhea in Eastern Sudan. Alkarmi. Clinics of North America: Food Animal Practice. lmmun..J. Mattson. V. and E.A. M.H. Muyldermans. Res. L. Barbosa and R. R. E. F. J. I. Comparison of two commercially available single radial immunodiffusion kits for quantitation of llama immunoglobulin G...K. S. Linden.K.S.B. Camel Cord. Neb. 1995a.C. J. Protein Engineering 7 1129-1131.D.R.F.P.J. L. Johnson. Hamers. Al-Mugheryi.. Frenken. TC. 19 (5): 921-930. Atarhouch. Rochester. Wilkens. Single domain antibodies: comparison of camel . Int. D. Med. W. Induction of immune responses and molecular cloning of the heavy chain antibody repertoire of Lama glama. Frenken. Zurich University. M6d. J. Vet. van der. Proc. Kaaden. Proc. Salman. 1998. Wyns and S. Proceed.G. 1996. A.K.A. Vet. Schwers. 1994.I.K. Necropsy findings from the database of a major insurer. Hamers. Immunoglobulin G stats of camels during 6 months post natum. Hutchison.B. 1997. Marcovechio. Med. de Geus. Obstetrics. Corn. Ghahroudi. E. Garry.A. M. L.. Annual Meeting. S. R6ceptivit6 du dromadaire (Camelus dromedarius) a l'infection par rotavirus. 17 (13):3512-3520. J. Vet. and W. D. 2-3 May 1998. Hart and 0.Y. 1995b.A. Hoover and G. Hastfor ings. Garry. ODonnell. G. Verrips. Kinne. E. B. Collins and T. B. Wade: R. A. R. S..Anote on camel IgG antibodies. Vet. Stok.F. Camel Prac. 1999. Rev. F.L. 1999. Pugh. Prospective characterisation of the clinicopathologic and immunologic features of an immunodeficiency syndrome affecting juvenile llamas. M. Newmarket.I.. Diagn. J. pp.. Muyldermans and U. Desmyter. 49: 209-227. N. A. L. U. and S. Thesis. L. ve't. M. Int. Lauwereys.

Methods 231 (1-2): 25-38. Znt. Rivera. Sheriff. 24-26: 34. . 1999. L. 24-26: 43. M. 3 (9): 752-757. Bos. Huelsebusch. Both viruses are members of the genus Varicellovirus within the family Herpesviri1' due.W. W. Rebhun et al. Zmmunol. Almaty..K. A. Maroc.. Oct. Thesis. Quarzazate. Workshop on the young camel. Workshop on the young camel. 2. 1985. 24-26: 17. Camel Prac.. Res.. Philadelphia. J. St.A.B.E. E. P. and EHV-4. B. In: Vet. H. Struct Biol. Clinics of North America: Food Anim. Camel calf losses in pastoral herds of northern Kenya-a system comparison. Purohit.N. M. 1999. Vet. van der Logt and l?J.. Leipold. Cambillau and M. Workshop on the young camel. in press. The crystal structure of a llama heavy chain variable domain. Etiology At least seven different herpesviruses were isolated from horses. 1999. Quarzazate. Copper deficiency: A predisposing factor to septicemia in dromedary calves. Abraham and Renate Wernery. Kaufmann. Med. The most important pathogens are EHV-1. lnt. Nagpal. 1988. characterization and quantitation in sera of dams and newborns. Camelid SOC. M. Chr. Gandega. Pract. Constantine. Aissa and B. the causative agent of equine abortion and neurological disorders. Workshop on the young camel. A. and Res.. Sahani.8 Equine Herpesvirus Interestingly. the etiological agent of equine rhinopneumonitis. Serological survey of viral antibodies in the Peruvian alpaca (Llama pacos).. D. Proc. C. J. Workshopon the young camel. M. S. 43 (3): 198-203. B. Maroc. Faye.P. Quarzazate. 24-26: 32. G. 1999. 1985. Immunoglobulin-G status of camels during 6 months post natum. Penn. 24-26: 33. R. o 2nd Camelid Con5 f "Agroeconomics of Camelid Farming". Woolven. Maroc. lmmunogenetics 50: 98-101. USA: p. J. Tegoni. Bildfell et al. Nat. 1999. Further reading Berrada. Bengoumi. Biol. Zsr. U. Thedford and Johnson. B. Ali. 1989. Trainin. 3 (9): 733-736. Znt. Frenken. Bourgeois.. Bristol: 50-64.W. India. Hiraga and L. Equine herpesvirus type 1 (EHV-I) produces rhinopneumonitis and abortion in horses and the disease has also been reported in OWC and NWC (Jenkins.. Johnson. Congenital defects in the llama. Tizard. 2001. A. 1999. Fikri. Spinelli. 2000. Wernery. Am. 8-12 Sept. H. 1991.1. J. 1987. 1992.K. Workshop on the young camel. Maroc. Oct.lnt. T. J.. Redefining the minimal antigen-binding fragment. Quarzazate. Nat. Quarzazate.R. lnt... 1996. Kinne. 1994. U. 24-26: 35. H. Ameghina. The neonate Proceedings of the Br... House et al. Dromedary Ig G: purification. Oct. Workshopon the young camel..N. Madwell and E. Quarzazate. 1999. no herpesvirus unique to camelids has been identified so far. Vet. 1999. 498. 10 (2): 401402. de Ron. Anguille. Diseases and pathological conditions of camel calf in eastern Africa.. Verrips. I. Oct. Hidane. Kazakhstan. New aspects on infectious diseases of camels. and Anim. Ungar-Waron.S.. J. College of Vet. lnt. Veterinary Immunology-An Introduction. 1999. Torres et al. Morbidity and mortality rate in dromedary calves. Maroc. Quarzazate. Saunders Co. M. Sci. Oct. T. Maroc. Molecular characterisation and immunobiology of camel serum and lacteal immunoglobulin classes and subclasses and their role in immunity... 4 8 189-191. Maroc. Oct. Dioli. Nicholls. and K. W. S. Bengoumi and K. B. Wernery. Gluckman and Z... Frenken. Struct. Kataria.. Disease prevalence and calf mortality in camel rearing areas in Bikaner. The structure of llama heavy-chain constant genes reveals a mechanism for heavy-chain antibody formation. Diarrhkes nkonatales du chamelon dans les provinces Sahariennes du sud du Maroc: Etude bactkriologique. C. 6 (1): 87-91. Elias. L. Tandon. Rajastan. 1999. 1994. 1987. 24-26: 53. Vet. L. Znt. A. A. Broadbent. and M. Oct.L. J. 1999.. and G. G. 1996.206 Viral Diseases VH and camelised human V H domains. 1996). El Abrak.

(1996) cultured EHV-1 from the brain of a Bactrian camel suffering from severe neurological disease prior to death.. zebras and antelopes. 1991) three llamas were experimentally infected intranasally with EHV-1 isolated from the brain of an alpaca with severe neurological signs. camels. it causes a respiratory disease most frequently seen in foals and yearlings. 1998). When herpesviruses infect a non-adapted host. Antibodies to EHV-1 were found in 21 serum samples from llamas and alpacas suffering an EHV-1 infection (Rebhun et al. No antibodies to EHV-1 were found in 500 UAE dromedaries when tested with a sandwich ELISA (CVRL Annual Report.Viral Infections Causing Disease 207 Epidemiology and Pathology EHV-1 has worldwide distribution and although it is considered a disease of equids. Confirmation of the disease can be achieved by virus isolation on a wide . Rebhun et al. 1985. These features are similar to those in EHV-l-induced neurological disease in llamas and horses. EHV-1 infects not only NWC but also OWC.Only 1llama of 270 from Oregon possessed antibodies. One hundred lamoids had been brought to the USA from Chile where they had been in close contact with other llamas. EHV-1 can also cause neurological disturbances associated with encephalomyelitis. 1996). necrosis and edema. These investigations show that NWC and OWC can suffer from EHV-1 infections associated with nervous system signs. Jenkins. These investigations demonstrate a difference between EHV-1 infection in equids and NWC.77% in 390 (3/390) llamas from 9 farms in 3 different Argentinean provinces. (1999) reported an antibody prevalence of 0. 1988). but antibodies to EHV-1 have not been reported in OWC. has been isolated from other animal species including bovines. Efforts should be undertaken to clarify the role of EHV-1 in abortions and neonatal diseases in camelids. In pregnant mares. There are no reports that EHV-1 induces abortions in camelids. gnus and various species of antelopes.. Camelids are susceptible to EHV-1. there was no ocular damage detected in this case. Bildfell et al. whereas in NWC the v h s is believed to replicate in the cells of the mu0 cous membranes of the nasal cavity. torticollis and paralysis. Microscopic lesions in the brain of the Bactrian camel included a non-suppurative meningoencephalitis with vasculitis. In equines. In a subsequent study (House et al. a viremia occurs after initial virus replication. Two of the three llamas developed severe neurological disorders: one died and one was euthanized. This has occurred in both NWC and OWC. The blindness was believed to have been caused by chorioretinitis or optic neuritis. serious disease or death is likely to result (Fowler. where it infects the olfactory nerve and optic nerve and progresses to the central nervous system. The third llama showed only mild neurological signs.. it is a major cause of abortions in late gestation. not only EHV-1 but also other equine viral infections should be considered in a differential diagnosis. With the increase in breeding of NWC in different countries and an increased opportunity for both NWC and OWC to come into contact with equids. Additionally. A herpesvirus indistinguishable from EHV-1 was isolated from dead llamas and alpacas that had suffered from blindness and central nervous system disturbances such as nystagmus. EHV-1 can cause seroconversion in NWC. EHV-1 was only re-isolated from a sample of the thalamus of the llama that had died acutely. Diagnosis EHV-1 infections cannot be diagnosed solely on the basis of clinical signs. EHV-1 infections have been described in a group of 100 alpacas and llamas on an exotic animal farm (Purse11 et al. Puntel et al. However. blindness and death.. In equines. 1988). EHV-1 appears to have followed an unusual pattern in alpacas and llamas exposed to the virus. 1979.

Blanco Viera. 1998. Journal o Zoo f and Wildlife Medicine 27 (3): 409-415.C./Dec. Am.J. D. so far no challenge infection has been conducted after vaccination to determine the efficacy of such a vaccine. Diagn. 1999. J. House. by IFAT and by immunohistochemical staining for viral antigen in endothelial cells of the central nervous system. Pursell.A. Vet.. Isolation of a herpesvirus associated with an outbreak of blindness and encephalitis in a herd of alpacas and llamas. M. An epizootic of blindness and encephalitis associated with a herpes virus indistinguishable from equine herpes virus I in a herd of alpacas and llamas. Vaccination with a killed vaccine to EHV-1 induces antibodies in llamas (Mattson. Dubovi and A.F. References Bildfell. Med. 3: 101-112.A. tech.C. C. R. B. Clin. J. 4 6 157-161.E. W. M.A. Abstr. Pracf.: 19. 175: 473474. Byars et al. Thedford. B. 1996. 1988. Infectious diseases of New-world camelids (NWC). Dubai. Lubroth. Workers Anim.E. 1996. D. Rebhun and J. 15 (1): 155-1 69. However. A. Sangster. D. Of. Central Veterinary Research Laboratory. 1979.: Food and Animal Practice 10 (2): 345-351. 1985: 15-16. Fondevila. 1985. Torres. JAVMA 192 (4): 953-956. int. 5 (3): 145-157. N. D. J.J.D. Live attenuated EHV-1 vaccines are not recommended in camelids.E.R. Torres. x i .W. R. 1991. Jenkins.R. Experimental equine herpesvirus-1 infection in llamas (Lama glama). J.K. Marcovechio.T. Husbandry and diseases of camelids. Llama Magazine Nov. Schudel. 1985. Dubovi. Johnson. Viral Diseases.. ODonnell. E. Torres. including rabbit kidney (RK 13). R i . is Rebhun. 1994. Haines and M. D. R. Jenkins. 1. Alpacas and llamas are susceptible to an equine disease. Clin.G. Epiz.. Serological testing of acute and convalescent sera is also important for the diagnosis of EHV-1 in camelids.J. Dill. Food Anim. Vet. Rev. W. Although steroids and antibiotics were administered to sick lamoids suffering from EHV-1. Vet. E J . North Am.D..208 Viral Diseases range of cell cultures. Serological survey of viral antibodies in llamas (Lama glama) in Argentina. Dubovi and A. A. Fowler. Invest. Gregg. Treatment and Control There is no specific treatment for EHV-1 infection. V. CVRL.H.A. King. J. Mattson. and L. J. Annual Report. Vet. EHV-1 vaccines have not been used in OWC.. L. . Vero and EDMIN (equine dermal cells). Dis. Vet. U. Yason. Carillo and A. St. 1989. Neurological disease induced by equine herpesvirus 1. there was no response. 1994).A. Puntel. Med. Assoc. North America. McGowan. 66th Con5 Xes. E.M.T.. Herpesvirus encephalitis in a camel (Camelus bactrianus).

(1994) isolated an adenovirus from the lungs of a 5-month-old llama with pneumonia and hepatitis. They will be examined in a separate chapter.8% in Somalia (Bornstein.bovine respiratory syncytial virus (BRS) .parainfluenza virus 1. Olaleye et al. As seen in Table 35. However.3%positive reactants to adenovirus among dromedaries kept for slaughter. The authors therefore prefer to keep these viral infections under the chapter "Nonpathogenic Viral Infections". Intranuclear inclusion bodies characteristic of adenovirus were detected in the lung and liver.2. 2. 1987) and 42.5%. Puntel et al.13% (20/390) in llamas on a single farm in Argentina. More than 50% of all references appeared after 1970.1 Respiratory Viruses ..Only 5.Adenovirus . It is interesting to note the high prevalence rate of antibodies to parainfluenza virus 3 in dry desert conditions (El-Amin and Kheir. 2. especially through experimental infection. In northeastern Nigeria. sero-epidemiological viral studies on camelids were primarily performed in the last 2 decades and investigations have reported a number of positive findings on viruses in camelids. The incidence of exposure in llamas appears high. 18. 1975). foot-and-mouth disease. USA. (1989) found 1.400 NWC veterinary references appeared in the world literature (Wernery et al. 81% in Sudan (Bornstein and Musa. 99% in Chad (Maurice et al.000 publications concerning microbiologicalsubjects have been published. some of them have caused mild diseases. 1988). 1993). (1999) found a prevalence of antibodies to bovine adenovirus (Bad VIII) of 5.500 papers have been published on OWC and 2.. 2 and 3 (22. However.6%). less than 1.2. 1985): 81% in Tunisia (Burgemeister et al. Galbreath et al.2 Nonpathogenic Viral Infections The growing interest in camelids is documented in the rapidly increasing number of publications since the 1970s. but the infection is mostly subclinical in nature. Adenoviruses have been isolated from llamas and alpacas with diarrhea in the USA (Mattson. for several viral diseases only antibodies to the virus have been identified. More than 5.infectious bovine rhinotracheitis virus Antibodies to the respiratory viruses mentioned here have been found in camelids all over the world. which have been identified through serological investigations or isolated from the camel tick. Rift Valley fever.A llama that died revealed severe necrotizing enteritis and colitis. 1968). bovine viral diarrhea and bluetongue have been isolated from camelids. most of which are cited in this book. Little is known about the unusual Arboviruses in camelids. 1994). For both NWC and OWC. it was diagnosed as having an immunodeficiency syndrome as well as a secondary adenovirus infection.5%) and the respiratory syncytial virus (0.6% of racing camels in the UAE were positive for parainfluenza 3. rinderpest. 1999).. The same authors have identified antibodies to parainfluenza viruses 1.The epidemiological significance of these results is still unclear and requires further study.2.3 . the prevalence of one of the adenovirus species (isolate 7649) was 93% (Picton. (BHV-1) . Viruses such as African horse sickness. In a serological survey involving 270 llamas from 21 ranches in Oregon. Many of these reports were of OWC used for slaughter with little or no background regarding either their origin or condition. indicating exposure and antigenic response. Because it registered a very low IgG level.3%.

Prevention Adenovirus. seem resistant to BHV-1.The clinical signs of disease in these cases included progressive cough. 77 breeding camels.Both camels and a control camel failed to develop any clinical signs and all three camels failed to seroconvert..210 Viral Diseases The difference in the prevalence of parainfluenza in different countries is probably due to different environmental conditions and management practices (Afzal and Sakkir. BHV-1 was also isolated by the same author from the brain tissue of a 1. the authors believe that additional studies are needed to clarify this issue. but there have been no reports that these viruses can cause clinical signs (Rivera et al. can infect more than 150 species in the suborder Ruminantia. BHV-1 antibodies were found by Rosadio et al. However. However. The authors found the highest prevalence (16. The role of bovine herpesvirus type 1 (BHV-1) in diseases of NWC and OWC is not well established and is therefore referred to in the chapter ”Nonpathogenic Viral Infections”. in contrast. parainfluenzavirus. BHV-1 was also isolated from three separate cases of bronchopneumonia in llamas and also confirmed by immunofluorescent antibody test (IFAT) (Mattson. 1991). When the alpacas were separated from other ruminants. In an experimental trial. the parainfluenza virus has not yet been isolated. intranasal vaccination with live virus vaccines has been shown to be very effective in controlling respiratory tract disease in cattle caused by bovine herpesvirus 1 and para- . while only 0. the authors infected two dromedaries intranasally with a BHV-1 strain that had a titer of lo5 TCID50/mL. 1987. 1994). bovine respiratory syncytialvirus and bovine herpesvirus 1are of minor importance to Camelidae. NWC can also become infected with parainfluenza 3 and respiratory syncytial viruses.7% in llamas and 16. Bornstein et al. Hedger et al. no antibodies were found to BHV1in 804 dromedaries (717racing camels. 1993). It seems that NWC are more susceptible to BHV-1 than OWC. From all this data. The dromedary does not seem to be susceptible to the BHV-1 virus. In other serological surveys of alpacas. Picton. Only Burgemeister et al. (1988).1%. 1998). BHV-1 was isolated from a 3-yearold llama revealing bronchopneumonia in association with Pasteurella haemolytica (Williamset al. HongLi et al.In spite of the high incidence rate. it can be concluded that NWC are susceptible to BHV-1 and develop a disease.. (1987) detected 5% reactors. 1994). a gammaherpesvirus. 1993).8% of Tunisian dromedaries. (1975) found low antibody titers (1:5) in 5.2% in alpacas) when the herds grazed on the same pasture together with cattle. OWC. Bohrmann et al. the prevalence was only 5. All tested llamas were negative. (1993) in Peruvian llamas and alpacas. Histological changes revealed an acute. Since it is known that malignant catarrhal fever virus (MCF).It was not clear if the virus had caused the death of the animal. in Peru Rivera et al. 10 yearlings) (CVRL Annual Report. multifocal neutrophilic bronchopneumonia consistent with an early inflammatory response to a bacterial infection.7”/0 reactors to BHV-1 of 270 llamas were diagnosed in Oregon (Picton. (1996) tested 41 llama sera with a competitive-inhibition ELISA from the USA. (1988) and Wernery and Wemery (1990)were not able to detect any antibodies to the causative bovine herpesvirus (BHV-l). Bornstein and Musa (1987). sheep and goats. In a second serological survey conducted in the UAE (using a sandwich ELISA). although the incidence of infection does not appear to be high.5-year-old llama with acute neurological disease associated with diffuse nonsuppurative encephalitis. (1980). NWC can become infected.

. E. vey on the prevalence of neutralizing anti. Ricerca di antisera.. Musa. int. Baker-Behap. T.int. 102 (5): 372-376. 1994. 1994.. 1998. R.A. parainfluenza 3 in sieri provenienti da aniColor Atlas of Camelid Hematology. Dtsch.A. R. JAVMA 204 (3): 424-426.B. Med. Jessup. Research Laboratory. 1988.A. Rev.Hedger. Trop. Omolabu. Baba and S. Kheir. O. Rev. sci. Vet.R. 21 (4): 443-449. capre e dromedari) della Somala. Presence of antibodies against Rev.J.F. Taylor. Serologic survey of llamas in Comparison of seroepidemiological findings Oregon for antibodies to viral diseases of of antibodies to some infectious pathogens livestock (MS thesis). H. Carillo and velopment of Animal Resources in Sudan. Serological survey of vitoum: 28-34.. 38 (2): 127-129. corpi inibenti la emagglutinazione da virus Wernery.E. D. Vet. tech. Anim. Res. B. H. Bollettino scientifica della facoltd d i malignant Catarrhal Fever in wild and dozootecnia e veterinaria 3: 209-217. Brucella Olaleye. and S.F.. E.L. B 46: 157-161. Vet..K. Bornstein. 1993. A.A. Vet. Leyk and R. R.E. Queval and J. D. 1988. Fowler and R.J. R. Barnett and D.Rivera. Epiz. chez le dromadaire tchadien. 7 84. Hlth. 1994.K. CVRL. North America: Food and Animal Practice 10 (2): bovine herpes virus type 1 (BHV-1)and para345-351. M. W. 13 (3): 107-114. Med. Elm. 12: Arab Emirates.. Africa.E. bodies to bovine viral diarrhea (BVD) virus. Epiz. Gorham.: 19. these two vaccines may be used in these animal species. Fondevila.Mattson. Gray. Sweden. Proc. antibodies to some viral pathogens. Hong Li. B. Blackmali appartenenti a specie diverse (bovini. Goessler. B 34: 364-370. bakteriellen und viralen Infektions1987. sala region. Ameghina.. R. Clin. Wildl.R. dromedario nella Repubblica Democratica Crawford. 1987. 1993. R. reference to findings in other countries of Puntel. 8 (3): mali camel. Yamini. Y. J. Enthe Djibouti Republic. OToole and T. 1979. Viral Diseases. H. Shen. Sakkir. Rec. the Peruvian alpaca (Llama pacos).A. J. Manchego. influenza 3. R. Kennedy. Afzal. S. KharA. Oregon State of cattle in camels of Sudan and Somalia with University. F. influenza virus type 3 (PI-3) in ruminants in Maurice. Preliminary survey for antibodies from camels (Camelus dromedarius) in Suagainst respiratory viruses among slaughter dan. of influenza antibody in animal sera from KasVet. In case of outbreaks in camelids. 1982. M. Schudel. Untersuchungen iiber Vorkommen von Para. Tierarztl.T. Parainfluenza 3 virus in camel and sheep Frigeri. Detection bovine herpesvirus-1 in Peruvian livestock. 779-783.A. Madwell and E. B. . camels (Camelus dromedarius) in north-eastBornstein. Singh. Pays trop. Mkd. Vet. La situazione sanitaria del J. Sudan. 1999.V. D. Pays trop. Knowles. ral antibodies in llamas (Lama glama) in ArBurgemeister. and M. SurELISA. Of.A.A. Elev.. gentina. Clin. Musa and EM. Prevalence of neutralising antibodies to El-Amin. vet. B. U.. Mkd. sci. Liess. Wernery.D. Arush. Am. well Wissenschafts-Verlag. 82: 352-354. M. D.E. Wschr. 1996. Holland. Jama. and B. Rec. Berlin. sitosen. Survey of anti. M. Rivera and A. Dubai. Bares. Corvallis. T. Central Veterinary Rosadio. qu@te l’infection a virus parainfluenza 3 sur 95: 99-102. K. A disease survey of the Soern Nigeria. United the Sultanate of Oman. 132 611-612. Vet. abortus and Toxoplasma gondii in serum 1989. A. tieriirztl. bodies against various infectious disease Some virus diseases of domestic animals in agents in racing camels in Abu Dhabi. Arush. Wschr. Bornstein. Report to Sarec. 1968. Serological survey of viral antibodies in krankheiten bei Dromedaren in Siidtunesien. 1980. Picton. Rev.P. J. Maes.E. V. mestic ruminants by competitive-inhibition Bohrmann. J. R. Dis. Adenovirus-associated pneumonia and hepReferences atitis in four llamas.F. S. Prevalence of antibody to Somala. J. and M. 1988. 48: 189-191. Frey and B. M. 787-792. 1967.R. Thorne. Dtsch. F.S.H. Galbreath. Prevalence of vet.S. Gilardy and D. of. Trapp.R.A. Annual Report. J.. 1975. S. of International Symposium of DeO’Donnell. by agargel diffusion test. D. 1985.Nonpathogenic Viral Infections 21 1 pecore.K. U.E. N. S. Marcovechio. Blanco Viera. 32 (3):437-443.A. 1999.

depending on the virulence of the virus.M. Williams.. 6 (1): 87-91.F. Davis. Plowright.and R.S. insect-borne viral disease affecting horses.Ticks do not play an important role in the transmission . Leptospiren.O. Serotypes 1to 8 are highly virulent for horses and cause up to 95% fatalities. AHSVs affects all equines as well as canines. D. mules and donkeys.A. Invest.P. 13 (2):45-50. A H S is a disease of the vascular endothelium resulting in a variety of different forms of the disease. 1999). of which C.R. the mortality rate reaches 70%. Beede. IEMVT. J.F.Est.M. The virus grows in BHK 21. Stone. C. and M. Further reading Eisa. 126-146.Production cameline . The disease has also been seen in North Africa. Amin. Adenovirus precipitating antibodies in the sera of some domestic animal species in the Sudan. Vet. Etiology The African horse sickness virus (AHSV)belongs to the genus Orbivirus 9: Epidemiology A H S is endemic in eastern and central Africa from where it regularly spreads southwards. It has now been confirmed that there is a strong link between the timing of epizootics of AHS in South Africa and the climatic changes brought about by El Niiio (Baylis et al. Donkeys and zebras are resistant and the disease is often subclinical in these equids. U.und Enzootischen Bovinen Leukosevirus (EBL) bei Dromedarstuten (Camelus dromedarius). Trainer: pp. Virions of AHS contain 10 double-stranded M A genome segments encapsulated in a double-layered capsid... 1990.F.. 2. 3: 258-260. L. Wernery. P. Association of bovine herpesvirus type 1in a llama with bronchopneumonia. E. Evermann. imicola is the most significant vector. It shares many properties with other orbiviruses such as bluetongue and equine encephalosis. Project de DCveloppement de l'Clevage dans le Niger. Dtsch. New aspects on infectious diseases of camelids. Scott. C. These midges can travel hundreds of kilometers on air currents. The size of plaques produced in cell culture indicates the virulence: small plaque viruses are more virulent than large plaque variants. the Middle East and Spain. Dilbeck. Herpesvirus of wild ungulates. It has been known in Africa for hundreds of years. Serotype 9 of AHS is already widespread and occurs in North and West Africa as well as in the Middle East. Karstad and D. With the increasing impact of El Niiio as a result of global warming. Different clinical presentations are seen in the horse. The spread of the disease is greatly influenced by favorable climatic conditions for the breeding of Culicoides midges. 1991. The virus is transmitted by Culicoides spp. 9 7 134-135.A. Vet. 1. Sudan J. 1.H. 1. Seroepidemiologische Untersuchungen zum Nachweis von Antikorpem gegen Brucellen. 1991. 1994). the main vector of AHS. W. Stone. 1985. Chlamydien. including Malignant Catarrhal Fever. R. IBR/IPV.Rapport final. U. Giovannetti. Whetstone and D. 1999. In: Infectious diseases of wild mammals ed.M. J. Husb. and Anim. D. and Res. whereas with serotype 9. Wernery.M. 3 258-260. of the family Reoviridae. Vero and MS cell cultures with a cytopathic effect (CPE). Sci. tierarztl. there is real concern about important insect-borne diseases spreading worldwide. Diagn. Camel Prac.212 Viral Diseases Wernery. 1981. 1972. Whetstone and D. Scott. M. Dilbeck.W.A. Nine different serotypes of AHS are known to give cross-reactions between the serotypes. J. S. Centre . Diagn.G.2 African Horse Sickness African horse sickness (AHS) is a highly fatal. Association of bovine herpesvirus type 1in a llama with bronchopneumonia. Planchenault and J. Wschr. BVD/MD. Richard. Invest. It is believed that the outbreak in Spain in 1992 was caused by midges from Morocco (Coetzer et al.2.. Horses followed by mules are most susceptible to the disease. Vet.

At necropsy. This (unpublished.sickness fever. 1988)..logically. (1986).formed. MS and ma et al. PathoClinical Signs and Pathology Serologi. In Nigeria.specific to allow a preliminary diagnosis in equines. AHSV should be isolated from hedarii).in horses vaccinated 9 years prior were still dary can serve as a reservoir for the AHSV.. positive when tested in the ELISA (CVRL of the virus.scopic lesions of AHS are often sufficiently ceptible horses that subsequently devel. Salama et al. Vero. there is enorwho examined 134 Sudanese and 266 Egyp. is authors believe that camels and dogs are a mixture of the pulmonary and cardiac an important reservoir of AHSV. The A rare third form of AHS. Lastly. 1981a). There are no opment of clinical disease. edematous interlobAHSV in African dromedaries yielded a ular septa. The pulmonaryforrn occurs after an incubation period of 3 to 5 days and is associated with fever and severe respiratory distress. Those animals infested with infected parinized blood during the febrile stage ticks showed no signs of illness. However. and ecchymotic hemorrhages on organ surBaba et al. type 9. (1986) isolated two AHSV lated from the blood and ticks of dromestrains.anterior portion of the body with petechial itive and 5. can be observed in partially bodies detected by Binepal et al. heart failure. from blood of two daries. IFA or tible animals that then developed the AHS. The infected lar. there were no anti. AGID. the horse African dromedaries.specific tests such as CFT.by intracerebral inoculation of suckling vae and nymphs of Hyalomma dromedarii mice. which is usually parasitic to camels (Awad et al. spleen and lymph ticks.Salama et al. con. 1979 and 1980). although the virus has been isoAHS in NWC. there is a marked pulmonary cal studies identifying antibodies to the edema with widened.4% positive faces accompanied by hydropericardium. The cardiac form occurs after a prevalence of 5% in Egypt (Awad et al. 17% carried the AHSV. (1992) and immune animals with an influenza-like serological studies performed by Wernery syndrome followed by total recovery. ELISA.6%. Serotyping of AHSVs is carried out Infected nymphs are also able to transmit by virus neutralization using type-specific the disease later in the adult stage (Foreign antisera. Antibodies studies appear to prove that the drome. No clinical reports of serological investigations of signs of AHS have been described in camelids. (1993) detected 10. Mouse Clinical signs and macrobrain suspensions of the fifth passage of Diagnosis these viruses were injected into two sus. However. . the AHSV can replicate in Hyalomma dromedarii. dromedaries out of 96 with the HIT. All these for the detection of antibodies. Virus isolates are identified by grouptransmitted the causative agent to suscep.should be done on BHK 21.nodes of necropsied horses. ELISA is the best serological test Animal Disease Report. 1992)on 500 dromedaries in form occurs in species such as donkeys the UAE also yielded a negative result for and zebras that are resistant to the develantibodies using the AGID. Of 2089 and from the lung. slightly longer incubation period and is 1981b) and 23% in Sudan (Foreign Animal characterized by intermittent fever and Disease Report. The reservoir host of AHSV is unknown. found 23..mous subcutaneous edema throughout the tian camels serologically. healthy camels in suckling mice. Virus isolation firmed by the mouse inoculation test (Sala. the mixedform. a mild form of AHS. 1988). The AHSV was also isolated in Egypt sis virological investigations must be perfrom dromedary ticks (Hyalomma drome.Nonpathogenic Viral Infections 213 There are four clinical and pathological disease forms seen in equines. to confirm the diagnooped typical clinical signs of AHS. In 24 East forms. respectively. serotype 9.2% pos.

Veterinary Services 16 (4). M.A. 16 (31): 379-390. Amin. wild ruminants.K.A. Animal and Plant. The disease is characterizedby cyanosis of the mucous Awad. 1998. Davies. Meiswinkel. Hassanein. Egypt Bull. The virus is transmitted by Culicoides species.A. Rep. A .M. Since there are many serotypes. Vet. 1994.E. Prod. BTV was the first domestic animal virus to possess a double stranded RNA genome. 1981b. S. the use of a polyvalent vaccine is recommended to protect horses from AHS in endemic regions. The incidence of African Horse ing the last decades to America and AusSickness antibodies in animals of various tralia. Wariru..K. Baba. by a serological survey in some Equidae.A. All 24 serotypes possess cross-immunity. V.M.. Bull. Horse sickness and ENS0 in South Africa. Foreign Animal Disease Report. Binepal. cattle and vaccination. Culicoides midges are nocturnal and will not enter buildings. S. and only affectingsheep.D. Salama.. J. Twenty-four seroReferences types of the virus are known. Camelidae. Infectious diseases of livestock with special reference to Southern Africa. New techniques. 1518-1535. flammation and ulceration of the mouth. inhorse sickness virus in Egypt.A. Since camels seem to be resistant to AHSV there is no necessity for Bluetongue (BT) is an acute arthropodborne viral infection of sheep. El-Husseini and S. edema of head and neck. coronitis. The disease. Prod.S. laminidromedarii in the transmission of African tis. Soi and R. Loxodontidae and Carnivore. B virus (BTV) belongs to the T genus Orbivirus in the family Reoviridae.M. M. Central Veterinary Research Laboratory. Ayanbadejo. U.Med. Annual Report. A sandwich ELISA used at CVRL. Assiut Vet. Racehorses are generally not vaccinated against AHS. No Title. S.214 Viral Diseases Annual Report. Dubai. Hlth. United States Department of Agriculture. Nature 397 (2):574. like polymerase chain reactions (PCR) or genomic probes that are more rapid. O.M. 1992. M. Anim. Anim. EI. Mellor and R.A. Haemagglutination-Inhibiting antibodies against African Horse Sickness virus in domestic animals in Nigeria. Abdalla.: 19. sensitive and specific. Salama and S. Infection of susceptible horses can be prevented to a large degree by stabling them some hours before sunset and letting them out a few hours after sunrise. G. P.C.2. EL.S. B. The role played by Hyalomma membranes of the oronasal cavity. in Africa 29E: 337-340. will soon become available for the diagnosis of AHS.R. 1998). EG.M.S. Cairo: 55-69. Veterinary Research 24 (6):483-487.A. S. 1986. Treatment and Control i cific therapy for AHS.. 1993. Amin.AGID. Horses suffering from AHS should be euthanized and disposed of properly. showed no antibodies to AHSV in 293 UAE dromedaries (CVRL Annual Report. El-Bakry and M. 1981a. Thomson and R. Dubai. Tustin. Afr. Serological studies on African Horse Sickness virus in camels.3 Bluetongue trade or racing. S.91-98. 2 9 285-287. Coetzer.N. 1988. CVRL. The application of insecticides will also have a positive effect on the control of AHS. Hlth. Knide. originally confined to Africa Awad. Salama. Reoviridae) in East Africa. CFT and HIT have been used for the detection of antibodies to AHS in camels. because they might be excluded from international 2. S.. species in Egypt. Oxford University Press 2 pp. US AHS Project 169. An attempt to define the host range for African horse sickness virus (Orbivirus. Health Inspection Service. Olubayo.. 1998). M. Olaleye and O.W. R. 3rd& 4*hAnn. 1979 and 1980.. Baylis. Salama and M. Abdallah. has spread durAly. J. 1999. M. Microbiology 31 (1): 19-23.

In 5. most of the llamas origithe BTV. Infected midges remain infective (CVRL Annual Report. Hafez et al. Paired serum the BTV have also been found in Israeli samples taken after the abortion demon.6% daries have appeared from many different of 89 animals. In Egypt. Twenty-three strated a fourfold increase in BTV antibody percent of the dromedaries examined had titer. The days. the virus replicates in its salivary same area reacted positively to the virus glands. although 35% of sheep from the ed blood.6% and Abu role in the spread of BT. and in Oregon. slight susceptibility of the dromedary to 1993). Ten days after be.ies to the BTV. fy BT antigens in Sudanese dromedaries Reports of BTV seropositive drome. 1998). BTV has been isolated from edaries were found positive to BTV with various parts of the world from a variety of the agar gel immunodiffusion test. Simpson (1979) found a prevalence of 81%of the Epidemiology The distribution of B is dromedary population showing antibodT mainly confined to the tropics and sub. According to Abu Elzein (1985b). Antibodies to distress followed by abortion. Stainley (1990) found that 13%of the game and cattle. as well as epizootic hemorrhagic disease (EHD) virus in deer. Afshar and Kayvanfar (1974) diagcase in a llama associated with respiratory nosed 5.isolated from sheep and camels from this coming infected with BTV. How. (1984) found 67% reactors in Saudi Arabian dromedaries.3%reactors.ELISA.ed in the UAE. Abu Elzein (1984) 14. only able to identify 14. With these conditions. Several serological studies have also Elzein (1985a) 16.9%. that is a been conducted in NWC. which are the most suscep. However. less than 1% 1023 dromof tible species.Nonpathogenic Viral Infections 21 5 ever.9% reactors in Iran. USA. there is only one lence of BT between these countries is unstatement (Fowler. 21% of 114 alpacas possessed anof the sheep exhibit positive titers. (mainly from insects in Australia). Puntel et al.using the immunodiffusion test. have also been detected. (1987). Abu Elzein (1984) was the first to identirole camelids play in the epizootiology of BT. Ostrowski (1999) found 58% serological reMidges live 30 days and feed every 3 to 5 actors in Saudi Arabian camels (an arid country almost identical to the UAE). Hafez and Ozawa (1973) were B is not enzootic in livestock.5% small percentage may be explained by the of 270 llamas reacted positively (Picton. Seropositive dromedaries tropics and to areas with high rainfall in were also diagnosed on the Arabian Peninassociation with a sufficient number of sula. It is worthwhile mentioning that transmit the virus to animals (by biting). (1979) and Eisa (1980)identified opinion that the dromedary might play a 4. In a serological survey conductvirus to sheep. This tibodies to BTV. Although reports of BTV seropositive reason for the great differencein the prevaNWC and OWC exist. In Sudan. BT antigen was detected. the midges can region. dromedaries in Yemen had antibodies to large numbers of Culicoides transmit the this virus. countries. . 1998)of a suspected B T known. where the virus is also nating from Oregon were from areas where T endemic.(1999) did not detect any antibodies to BTV large number of related orbiviruses. it remains unknown what positive titers to type 4. where B is endemic.No BTV was for the rest of their lives. However. In Botswana. although it should be noted that the authors only examined three animals. 86% of the goats and 73% al. After a female gnat has ingest.dromedaries (Barzilai. the author is of the T Eisa et al. and 5% Culicoides. 1982). of which C. In a seroprevavery small prevalence in a country where lence study carried out in Peru by Rivera et 93% of the cattle. irnicolu is the most of 211 camels positive with the competitive important. Based on these results. 1.6%positive dromedaries.

M.Serological survey of Bluetonme in Egypt. Kayvanfar. Radwan. E. dyspnea. int. erosions and necrosis of the mouth mucosa and of the dental pad may appear. cyanotic “blue” tongue. using the Gel Immunodiffusion test.M.int. Afshar. Of. certain cell cultures or susceptible sheep. Bluetongue antibodies in Camels’ sera in Israel. Ah. Karrer and A.: 19.21 6 Viral Diseases in 390 llama sera from 9 farms in 3 different Argentinean provinces. Epizoot. 92 (7-8): 491-500. This can be done by the use of insecticides and sterilization of Culicoides males by irradiation. Beharairi and A. 1982. Considerations on bluetongue in the Sudan. A. Rapport No.4. Abu Elzein. Rec. Fowler. but some may develop clinical signs similar to those seen in infected sheep. Epiz. Res. sci.. and it is therefore often necessary to confirm the disease by either virus isolation or serology. Occurrence of precipitating antibodies to bluetongue virus in sera of farm animals in Iran.E. Diagnosis BT is often misdiagnosed as photosensitization. XVLIII Session Gherale. vet. 1979. Mid.M. although more than 30% of the sheep population have antibodies to BTV. Bluetongue in the Sudan. Elev. but also between different breeds of sheep. and H. Barzilai. Rev. References Abu Elzein. sheep and cattle in the Sudan. AGID and SNT. 1984.I.A. except in one llama with a respiratory syndrome and abortion (Fowler.. lips and ears. 94: 233-235. S. D s i. Bull. S. I. EHD and Orf. A. and hyperemia of the muzzles.Sci. BT in sheep in the USA is much milder than in Africa and the authors have not seen any clinical cases in sheep in the UAE.M.gered areas can make a significant contribution towards the control of BT. E. Int. 1998. Of. 2. A. However. Bull. Central Veterinary Research Laboratory. M. Attenuated vaccines are highly effective.E. Viruses are then identified by serum neutralization or by FA. U. but problems might arise in areas where several serotypes exist.A. Bluetongue in camels: a serological survey of the one-humped camel (Camelus dromedarius) in the Sudan.E. Camb. E.M.H. E. The coronary bands may become inflamed and swollen. BVD/MD. Direct isolation of the virus can be done in embryonated chicken eggs. Incidence of bluetongue virus precipitating antibodies in sera of some domestic animals in the Sudan. Prevention and Control Measures to reduce the Culicoides populations in endan. MCF. Eisa. Serological tests include ELISA. lameness and muscle necrosis. tech. Lameness is an early sign of infected flocks and might be confused with FMD. Off. Abu Elzein. Rev. 0ther signs include a swollen. 1973. -_ 21 (3):2971303. U1ceration. Annual Report. Pays trop. Ozawa. the most effective and practical approach to endemic BT is prophylactic immunization. 1984. Hafez. Bull. Refuah Vet. CFT. Serological evidence for the occurrence and prevalence of bluetongue among ruminants in Saudi Arabia. M. Epiz. 4 (4): 795-801. The virus can also be propagated in suckling mice by intracerebral inoculation. Clinical Signs and Pathology No clinical signs or pathological lesions caused by BTV have been described in camelids. 1980. Al-Mukayel. and Y. Hyg. 83 (3): 539-545. Abd Elrahim. Dubai.E. Cattle are commonly latently infected. 38 (4): 438-442.E. 1985b.M. Medicine and surgery of South American Camelids. 2 (1): 289-295. IBR. 39 (3): 90-93. Vet. 1974. No BT vaccines have been used in camelids. In sheep the disease is characterized by fever. 1985a. Rapid detection of Bluetongue virus antigen in the sera and plasma of camels. 1998). Arab GulfJ. Ames. S. FMD. . 1998. Archives of Virology 79: 131-134. Iowa State University Press. CVRL. Hafez. Eisa. Clinical manifestation of BT possesses an extreme variability not only between different ruminant species.E.I.

Chauhan et al.6 9.4 157.Madwel1 and E. Vet.A. Corvallis. 1995). 101). The affected dromedaries were all above 8 years of age and all exhibited a very high leukocytosis (Table 42). Ameghina. Simpson.caprine arthritis encephalitis (CAE).. several diseases in livestock caused by viruses belonging to the Retroviridae family: .8 7.Nonoathoaenic Viral Infections 217 Ostrowski.0 12.6 8. P A b u Dhabi Int. Oregon State University.F. 48: 189-191.0 12. Rivera. . the authors had diagnosed lymphatic leukemia in UAE dromedaries.3 45. All these sera were negative. 1 (1):43-49.NeutroEosino. S.2 9. 1999. B. Anim. ODonnell. Bluetongue antibody in Botswana's domestic and game animals. .7 949.. 1999. in press. Prod. However. Am. Stanley.1999. Serological survey of viral antobodies in the Peruvian alpaca (Llama pacos).3 7.3 7. There are Table 42 Cases of lymphoblastic leukemia in the dromedary in the UAE WBC RBC x 103/mm3 x lO~/mm3 818. J.3 Cases 1 2 3 4 5 6 7 8 9 10 Hb g/dL 12.5 7.6 6. 2 2 163-164. 1990. Marcovechio.A. . chickens.6 13. 46: 157-161. R. Prod. Prevalence of Bluetongue precipitating antibodies in domesticated animals in Yemen Arab Republic.5 126. B. Wernery and Wernery (1990) examined sera from 986 UAE dromedaries with the agar gel immunodiffusiontest. Vet. Hlth. Carillo and A. Puntel. Fondevila. B.J. Picton. 1979.ovine pulmonary adenomatosis (OPA).enzootic bovine leukosis (BVL). Proc. N. Res.0 217.K.R. .I.7 14. V. Med.9 3. Ten dromedaries affected by lymphatic leukemia within a six year period did not have antibodies to the bovine leukemia virus in their serum or in organ homogenates (Wernery and Kaaden.0 11.0 44. rats. composed primarily of lymphoblasts (Fig. Health management of the Arabian oryx (Oryx lencoryx)reintroduction. Upon 2.8 226. H. Trop. Hlfh.Monophils phils cytes cytes 99 1 0 0 1 0 0 99 100 0 0 0 99 1 0 0 98 2 0 0 94 6 0 0 98 2 0 0 0 0 92 8 98 2 0 0 98 2 0 0 WBC = white blood cells.5 9.4 142.4 Retrovirus Infection Several retroviruses have been isolated which can cause leukemias. RBC = red blood cells. Arabian Oryx Con5 Feb 27-Mar 1. 1 Anim. lymphomas and sarcomas in mice. Serological survey of viral antibodies in llamas (Lama glama) in Argentina. Serologic survey of llamas in Oregon for antibodies to viral diseases of livestock (MS thesis).equine infectious anemia (EIA).0 Differential Cell Count % % % % Lympho. Several serological studies have been conducted in NWC and OWC for the detection of antibodies against BVL and OPA. M.9 10.visna /maedi strain. 1993. Hb = hemoglobin . 1987. V.3 5.1 204.0 11. Blanco Viera.R. All of the dromedaries diagnosed with leukemia died within 6 months.0 8. Schudel. M. J. (1986) found no antibodies to BLV in 283 sera from Indian dromedaries. cats and a variety of other animals. I.2.J. Trop.

During this time. bronchopneumonia and endometritis were seen (Afzal and Hussein. 1 from Table 42) autopsy. no hematological changes were detected. secondary pyelonephritis. Wernery and Kumar. 1996). The blood of both experimental camels was examined regularly over a 1 year period. 1995. Histopathological examinations showed extensive infiltration with neoblastic lymphoid cells in the lungs (Fig. 102). Two pregnant dromedaries diagnosed with leukemia gave birth to healthy offspring with no abnormalities in their blood cell counts. case No. indicating that the disease is probably not infectious.218 Viral Diseases Figure 101 Lymphoblastic leukemia in a dromedary (Sudan black stain. Antibodies to OPA were not detected in a serological survey conducted in Peru where alpacas grazed with sheep (Rivera Figure 102 Neoblastic lymphoid cells in the lung of a racing camel suffering from lymphoblastic leukemia (HE stain) . Ten mL of heparinized blood was drawn from each of two dromedaries with leukemia and given to two test camels intravenously. enlarged lymph nodes. spleen and lymph nodes.

P. Am. Serological survey of viral antibodies in llamas (Lama glama) in Argentina. 201: 1318.A. Rev. Leptospiren.J. Wernery. Ameghina. BVD/MD. R. Serologic survey of llamas in Oregon for antibodies to viral diseases of livestock (MS thesis). Serological survey of viral antobodies in the Peruvian alpaca (Llama pacos). Mersky et al. Mattson.2. Seroepidemiologische Untersuchungen zum Nachweis von Antikoerpern gegen Brucellen.NonDathoaenicViral Infections 219 et al.-R. 1992).H. Morin. Chlamydien. 1987). 46: 157-161. Gupta.O. References Afzal. W. Zakia and A. Fayza. seroconverted.C. 1995. Rivera. Carillo and A. Chauhan. At least .M. Retroviral basis for immunosuppression remains to be proven. M. R. 1994. 1990. Acute prolymphocytic leukemia in the camel. Vogel. Blanco Viera. Vet. B. Vet.5 Foot-and-mouth Disease Foot-and-mouth disease (FMD) is a highly contagious disease occurring almost exclusively among cloven-hoofed animals. Camel Prac. A. 1994. Infectious Diseases of Camelids. Wernery. therefore it is important to ascertain if they can develop the disease or serve as viral reservoirs. Wschr.R. 200 358-362. A serological study conducted in Peru also showed no evidence of antibodies to BVLV (Rivera et al.S. D.. USA. North America: Food and Animal Practice 10 (2): 345-351. Prevalence of different diseases in camels (Camelus dromedarius) in India. there have been several reports that llamas develop lymphosarcoma similar to that induced by BVLV (Mattson. Hussein. Res. and 0. Apparent retrovirus-induced immunosupression in a yearling llama. tierarztl. Underwood. 1986.L. Corvallis.und Enzootischen Bovinen Leukosevirus (EBL) bei Dromedarstuten (Camelus dromedarius). 1995. 1999. J.M. Kaaden. ODonnell. 1992. Med. Elm.E.. M.C. Assoc. Suspicion of a case of lymphocytic leukaemia in a camel (Camelus dromedarius) in the Sultanate of Oman. 2. U. 1992. No antibodies to BVLV were found in 390 llamas from 9 farms located in 3 Argentinean provinces by Puntel et al. Further reading Tageldin. Kumar. K. The rare incidence of lymphatic leukosis in camels detected in the UAE. B. Wernery. J. Picton. 1996. J. 1992).. Opinions vary widely whether camelids are susceptible to the disease or not. Wernery. Fondevila. the similarities of the pathohistological findings and the apparent lack of a retrovirus led us to speculate that the described cases may be related to sporadic forms of bovine leukosis. U.E. Assoc. (1999). Camel Newsletter 3: 10-14. J. Marcovechio. IBR/IPV. Oregon State University. This most feared disease inflicts great economic (productivity and operating) losses worldwide because of international embargos. and R. Satiya and R. and B. Vet. R. Med.Madwell and E.. Kaushik. the susceptibility of camelids to leukemiavirus remains uncertain. Schudel. J. although sheep in that region were infected with OPA (Picton.. U. and Res. and M. Clin. M. Am. but it is not proven that this virus has caused this syndrome (Vogel. 4 8 189-191. 1994).J. B. H. M. V. Am.However..C. Blackwell Wissenschafts-Verlag. D. ve't. Viral Diseases.F. Me'd.N.S. 9 7 134-135. S. J. 1993). 3 (1):49-50. as in dromedaries. 47 (2): 157-158. FMD is caused by a RNA uphfhovirus of the family Picornuviridue. Until a leukemia virus is identified from such cases. Vet. Med. 1987. Berlin. J.. Vet. Pays Trop.. Puntel. and none of the 270 llamas tested in Oregon. Camel 1 Newsletter 1 (9): 22-24. Kulshreshta. 1993.A.K. Dtsch. 1987). Pulmonary lymphosarcoma in a 16 year old dromedary camel-a case report. Al-Sumry. N.K. H. A retrovirus has been isolated from a llama in association with an immunodeficiency syndrome (Underwood et al.

The dromedary did not develop vesicular lesions. usually when animals are in close the ram developed hyperemia of the eyes contact with each other. Two viral strains were isolated importance to know if camels play a role in from these lesions and both were identitransmitting FMDV. Pringle (1880) reported that the disease was widespread and that foot lesions were the most prevalent symptom. who Epidemiology :i FMD was enzootic in observed outbreaks of the disease among parts of Europe.and buccal cavity and the dromedary detain circumstances it may spread over long veloped ulcera on the scarification site and distances. A calf.breaks of camelpox. from Africa. Within the 7 serotypes. affects the lips. 0 and C are the three most common strains in Europe. . of which A. it has been possible to trace the move.from bovine aphthae. be. the goat developed ulcera on the dorsum of the tongue and the upper lip. for example (with a camel popula.000). serotype 0. 0 appears to be the most common and C the least common. but also many dif.any antibodies to the artificial infection. Rohrer (1970) also believes that all and many countries in western Europe are artiodactyl ungulates can develop FMD. seven immunologically distinct serotypes of FMDV have been identified. goat and a dromedary were artificially insheep. the buccal mucosa and the North America. FMD is of great in. The study of the epidemi.known bovine FMDV. 1947) also described outbreaks similar to FMD in dromedaries. (1987) in tion of 800. imports approximately 6. swine and goats. although under cer. the other animals seroconverted use of molecular techniques to characterize 3 weeks later. This observation was based on clinical manifestations of the disease. the disease East. The calf dement of individual strains of FMDV from veloped a vesicle at the inoculation site and one country to another (Kitchmg. Australia. individual strains of virus. They beduction of the FMDV. These countries have However.220 Viral Diseases camels. ology of FMD has been transformed by the However. the Far East and South America. Again the Clinical Signs and Pathology @ Earlier dromedary did not develop any antibodies studies have reported FMD epizootics in following the second viral exposure. 1998). ulthe nomadic herds of Saudi Arabia and cerations were seen between the teeth and neighboring countries. over 60 subtypes have been identified. Leese (1927) was not cause the disease is enzootic in many coun.5 million live animals. After an additional 5 weeks. Some ungulates can harbor the two to three vesicles on the inside of the virus for a long period without developing upper lip. Saudi lowing inoculation attempts with material Arabia. There is no crossimmunity between strains. type 0. Steele (cited from Curasson.lieve that these epizootics were all outterest with regard to NWC and OWC. and still is in the Middle Bactrian camels in Kazakhstan. aerosols. Additionally. Most transmission is via and the goat did not develop any lesions. which spread within lips of four dromedaries. Leese (1918) and Curasson (1947) stringent regulations preventing the intro.able to confirm FMD in dromedaries foltries where camelids are reared. Recent studies by Moussa et al. a the virus are artiodactylids including cattle. mainly sheep and Egypt have shown that dromedaries are goats. feet.fected with this FMDV. It would be of great on the teats. By these meth. The authors described Animals from Africa and Asia bring their ruptured vesicles and ulcera on the upper own FMDV strains. Asia and Australasia. a ram.all four animals were infected with a ods. susceptible to FMD. India. type 0. According to Kowalevsky (1912). The calf ferent wild animals. New Zealand.are skeptical of the earlier reports. free of the disease. After observing thousands of Afghani dromedaries. The natural hosts of fied as FMDV.

Several studies of NWC susceptibility to FMDV have been carried out (Mancini. 1979. but the antibodies disappeared after 6 weeks. 1986). (1993) again showed that.. Konigshofer. Further studies carried out by Abou Zaid (1991) revealed that dromedaries could contract FMD after experimental infection. The authors conducted an experimental trial with FMDV serotypes A79.. the three infected bovine calves as well as the contact bovine calf developed FMD. These investigations showed that camels in contact with cattle or camels with FMD did not contract the disease. 1952. 1979. One camel and three bovine calves were kept as contact animals. 1980). The contact camel did not show any lesions and no virus was isolated.i. These experiments also showed that infected.6% of the sera from Nigerian dromedaries. which are known to carry FMDV for long periods of time. However. Lubroth and Yedloutschnig 1987. However. Moussa (1988) is of the opinion that the substances identified were nonspecific inhibitory substances in the sera. Lubroth et al. 1993) did not develop any signs of clinical signs. Callis and Craig. as opposed to specific antibodies. 1984) while others describe the susceptibility of NWC to experimental infection with FMDV (Moussa et al. 1971. Three camels were infected with FMDV strain 01/3/87 Egypt IDL intradermolingually and the fourth intradermally in the footpad.. Oman (Hedger et al.. The fourth camel that was inoculated with FMDV into the footpad did not develop any FMD symptoms. As with OWC. Four weeks later. esophageal-pharyngeal (OP) fluid. virus detection was negative..NonDathoaenicViral Infections 221 Additional experimental studies on the dromedary by Nasser et al. The camel not showing any lesions did not develop antibodies to FMD. Niger (Richard. 1990. Tantawi et al. but the three bovine calves contracted the disease and the virus was isolated. Paling et al. C and SAT2 in 2. Moussa et al. diseased camels seroconverted to FMDV during the first week. Lubroth et al. camels could contract FMD when intradermolingually infected. 1979). following intranasal infection with serotype 0 FMDV strains. the opinions on whether NWC are susceptible to FMD or not vary widely.. further evidence was provided that llamas are resistant to FMD infection. feces and ruptured vesicles. little is known about the carrier ability of camelids. 1992). Moro. A few surveys suggest that NWC are resistant to natural FMD infection (Mancini. 1971. 1990) in a limited number of animals and with variable results. (1995). However. 0 3 and 01 to evaluate the ability of FMD to infect susceptible llamas exposed either directly to affected livestock or indirectly to llamas that had been . In the second group. The three infected camels showed signs of FMD and the virus was isolated from blood. a second excretion of the virus was noted lasting for a week. In a wellexecuted study by Fondevila et al. Saudi Arabia and Egypt (Hafez et al. At the same time. Unlike cattle. Only Richard (1986) was able to idenhfy antibodies to the FMDV serotypes 0. sheep and goats in various FMD epizootics in Ethiopia (Richard. neither clinical signs nor seroconversion were seen in the infected dromedaries. following intranasal infection with the Egyptian strain Sharkia 0/2/72. 1979.. Similar reports in Saudi Arabia from Hafez et al. Dromedaries kept for weeks in close contact with severe cases of FMD in cattle. whereby the highest titers were observed between the 3rdand 4th day p. Again there was no evidence of humoral antibody production. (1980) and Moussa (1988). but the contact camel did not show any clinical signs. frequently seen in camel serum. yielded only slight or clinically inapparent manifestations.. the virus was re-isolated from the pharynx and the feces over the course of 6 days following infection. 1952. Thereafter. three bovine calves were inoculated with the same FMDV strain and one bovine calf and two camels were kept as contact animals.

but showed no lesions and did not shed the virus. Cumelus buctriunus. Along with the picornuvirus infection. has been isolated from a 2-year-old dromedary in an American zoological collection (Wells et al. bovine calves. continue to carry live FMDV in their . Laboratory methods are therefore necessary for diagnosis. The most effective preventive measure is to prohibit introduction of animals or animal products into FMDfree countries from countries that have the disease. is susceptible to FMD and may transmit the virus to other artiodactylids (Indian elephants are susceptible to FMD. The virus was isolated from two fetuses. An encephalomyocarditisvirus (EMCV). Africans not). Stehman et al. Furthermore. Only 2 of 30 llamas directly exposed to the FMD pigs developed minor lesions. This occurred over a three and a half month period at an average 220 days gestation. Thirty llamas were placed together with the infected pigs and later interspersed with an additional 30 llamas after the exposure to the pigs. (1998) reported a picornuvirus infection in llamas that caused abortion in 15 llamas. virus neutralization and agar gel precipitation. which is a picornuvirus. Many European countries have banned routine vaccinations against FMD because most of the outbreaks have been traced to improperly inactivated vaccines or escape of the virus from the production site. goats and sheep) were then added to the entire group of 60 llamas to detect possible transmission of FMDV from llamas. Treatment and Prevention 1*1: There is no cure for FMD. NWC and dromedaries are not very susceptible to FMD and do not present a risk in transmitting FMDVs to other susceptible animal species. Six pigs were inoculated with three different types of FMDV by different routes. All control animals introduced to the 30 contactexposed llamas failed to develop lesions or antibodies and failed to yield any FMDV. The divergent results from scientists of various countries underline the importance of examining and qualifying the pathogenesis of FMDVs in camelids.. including fetal camel kidney (Farid et al. epicardial hemorrhages and pale foci within the myocardium. The virus was isolated from the heart. These methods include complement fixation test. 1974). 1989). seroconverted and yielded virus in blood or OP fluid. The virus can be isolated on different cell lines. as it is known that immune animals in contact with live FMDV can become carriers. ELISA. It has also caused disease in Bactrians in Mongolia. Diagnosis The clinical signs of FMD are indistinguishable from vesicular stomatitis.222 Viral Diseases directly exposed to affected livestock. ruminants (in particular cattle). however. and that they play no role in transmitting the virus to domestic livestock. Forty susceptible livestock (pigs. It is believed that rodents may have transmitted the EMCV. A third llama from this group also seroconverted.. It is now believed that NWC and dromedaries are more or less resistant to FMD infection. serum neutralizing antibodies to the picornuvirus were found in the fetal fluids as well as in two llama herds with a similar clinical syndrome of diabetes mellitus. There is now agreement that NWC and dromedaries can contract the disease after experimental infection and by very close contact with FMD-diseased livestock. However. vesicular exanthema of swine (culicivirus) and vesicular disease in pigs (enterovirus of the Picornuviridue family). all FMD antibody-positive animals should be considered to be potentially infected. The pandemic serotype 0 virus (now named the PanAsia strain) has currently reached a global extension and has out-competed all other strains of FMD. Gross pathology consisted of excessive pericardial fluid. diabetes mellitus was observed in the adult llamas.

one natural case of VS in lamoids has been reported (Fowler. A treatise on the one-humped camel in health and disease. Anim. Vet. PhD thesis (Infectious Diseases). Mebus. Le Chameau et ses maladies d'aprhs les observation d'auteurs russes. the virus from the outbreak must be isolated and typed to determine whether the field strain is homologous to the vaccine strain being used. P.. Abd El Galil.Med. Multiplication and Titration of foot and mouth disease virus in the Foetal Camel kidney tissue culture. M. Mtd.P.): Veterinary Diagnostic Virology. Paris II. Gomez. A. 1998). A. Le chameau et ses maladies. M. of Vet. 118 89-108. Anales li Cong. K. Susceptibility of Llamas (Lama glama) to Infection with Foot-and-mouthdisease Virus. Tmdall and Cox. Hlth. ve't. Vesicles appeared at the inoculation site at the dorsum of the tongue and the animals developed fever and anorexia (Gomes. Louis. med.. Egypt. 1964). Fluids taken from these vesicles of NWC caused disease in cattle. G. Leese. Mosby Year Book: pp. J. Farid. The llamas even shared the same watering and feeding facilitieswith the diseased cattle and they did not seroconvert to VSV. Leese. 100-103.S. Kitching. Peru: 403406.S. Carrillo. Torres and C.S.J. .A. Are camels susceptible to natural infection with Foot-and-Mouth Disease virus? Internal paper. 1964. London 50. Foot-andmouth disease.O. V.. VS is caused by a rhabdovirus and there are two major types: New Jersey and Indiana. 1971. 1947.J.A. 2. The duration of immunity after FMD vaccination is rarely longer than 6 months (Kitching. Blanco Viera. No reports exist on VS in OWC. Gray. J. P o p . J. Kowaleski. 1989). Marcovechio. 1995. FMD vaccine is an inactivated preparation. M. n . 1927. Health Yearbook. J. A. Craig. Comp.E. Lima. A. However. 1998). Fondevila. Callis. B. Al-Mukayel. Saudi Arabia. FAOWHO-OIE: 178. H. N.J. 1974. Barnett and D. F. Ames. 12: 107-114. 1912.H. H. Fac. Few studies involving the susceptibility of NWC to VSV have been conducted. 86-88. Medicine and surgery of South American Camelids. Hedger. J. Bailliere. FMD vaccines have not been used in camelids. G.R.Studies on some diseases of camels. J. Riyadh. T. 1998. David. R. Konigshofer. Animals immune to FMD after vaccination can still become carriers after contact with field strains during outbreaks. S. Zagazig U i .A. Editeurs: pp. B 42: 595-599.NonDathoaenic Viral Infections 223 pharynx after contact. 1992. Cattle can harbor FMDV for up to 3 years. Tantawi. Lyon 15: 462-466. 1993. Iowa State University Press. Zootechn. A.F. 1998. Heuschele (eds. Farag and A. References Abou-Zaid. attempts to take advantage of new molecular biological technology to produce better FMD vaccines have been unsuccessful. J. "Tips" on camels for veterinary surgeons on active service. Vigot Frkres.A.2. A. and W. Nuc Med V t y Zoot. Ass. A recent history of foot and mouth disease.S. Vigot Freres. Egypt vet.. 1993).M. Med. A Practitioner's Guide St. 1991. Anim.O. Curasson.P. Saber and M. Fowler.6 Vesicular Stomatitis Vesicular stomatitis (VS) is another vesicular disease which is indistinguishablefrom FMD. R. e Hafez.. M. National Agriculture and Water Research Centre.A. 1980. D.E. 34 (3-4): 384-392.A. ODonnell. F. 1918. Box 17285. Puth. Foot and Mouth Disease in Peru.. In countries where vaccines are used. as llamas that had been in close contact with diseased cattle did not contract VS (Thedford and Johnson. It is believed that natural infection rarely occurs. A. and D. Shalaby.M. Two hundred and seventy llamas which were serologically tested to strains Indiana and New Jersey in Oregon were also negative (Picton. M. Schudel. A. Tests on the sensitivity of Camelids to vesicular stomatitis. In:Castro. Some virus diseases of domestic animals in the Sultanate of Oman. Alpacas and llamas have been shown to be susceptible to an experimental infection with VSV.

Med. transmission. S. 11560. Proc. B. Agr.J. 1979.2): 219-229. Med.2. L. Metwally.. L.Z.W. The camel development research. A. Lubroth.. Mancini. S. Prevalence of serum antibodies to the Foot-and-mouth disease virus infection associated antigen (via) in camels. Sutmoller. Daoud. Bol Divulgacion Instito Veteranario de Investigaciones Tropicales y de Altura. I.7 Bovine Viral Diarrhea Bovine viral diarrhea (BVD)and mucosal disease (MD) are epidemiologically different diseases of cattle that have different . IEMVT. 5 7 1-18. Nasser. Case report: Picomavirus infection associated with abortion and adult onset diabetes mellitus in a herd of llamas.M.E. Proc. A. Vet. Colonia Polanco. Vet.E. Ectima: En: La Alpaca. cited from Curasson. Oregon State University. Egypt Vet. Picton. Paling. Am. A serological survey with special reference to foot and mouth disease. 40 (4): 5-13. Res. de I'Office Int. Invest. Moro. Food Anim. The role of camels in the epizootiology of FMD (Foot and Mouth disease) in Egypt In:FAO. 20 (3): 291-296. Yedloutschnig.H.A.J.. Chinese J Vet Med b Tech 5: 35-37. Moussa. A.E. Ass. Vet. l? 1999. 1998. 1984-1985. J. Rev. H. 1971. Culle Hegal 713. Soike and G. J. Rohrer. 5 (3): 145-157. 1970. D. J. 1987.M. and L. Secretion and persistence of foot and mouth diseases virus in faeces of experimentally infected camels and ram. Risk of disease transmission by llama embryos. Med. Clin. Sudan J. M. Foot and mouth disease virus in the llama (Lama glama): Diagnosis. Inst. E. Rev. Encephalomycocarditis virus: epizootic in a zoological collection. D. 1988. J.F. Moussa. Mikiciu. Vet. Clin.J. Taswfik. Steele. Zglich and E.A.M. Gulter. Foot and mouth disease studies in the llama (Lama glama).B. France. Pract. Viral Diseases. 1979. Omar. Projet de d6veloppement de l'klevage dans le Niger centre-est. Jesset and B. Susceptibility of camel and sheep to infection with foot-and-mouth disease. Culhane and P. Del Piero. N. Nac.W. Guo. 1980. Freeman. S. 91: 313-316. 18 (3): 719-728. Mexican US Commission FMD. Mexico. 1993. J. J. Ass.M. Abdeir Metwally and R. Stehman. North America: Food and Animal Practice 10 (2): 345-351. 1994. Diagn. R. Wild. Vet. Med. Moussa. 1984. Paris. 1986. Lima.K. US Anim. 1952. El-Nimr and J. Antiaftosa (Lima) 1(2): 127-145. Amer and S. Br. Baskin. Vigot. R. 6: 58-60.A. E. Zoo and Wildl. A. Thedford. 1989. Corvallis.. U. Dis. Weisensel. 1989. North Am. Further reading Abu Elzein. 13: 65-79. Omer and B. Richard. Manuel des maladies du dromadaire.A. Epiz.. o Kuwait seminar. A.E. Johnson. Dubovi. sheep and goats of the Sudan. 1979. Bol.. Pringle. R. sheep. Morris. R. Haroon. A.W. Maisons Alfort. A. S.. Diss. M.1986. Unva Nac San Marcos. Tests on susceptibility of South American camelids to foot-and-mouth disease. Pathology meeting. Enfermadades Infecciosas y Parasitarias. 1987. Sci. Tantawi.162-173. Res.A. A.R. Detection of foot-and-mouth disease virus carriers among farm animals. Assiut Vet. 1988. Yedloutschnig. Heath.. 15: 351-358. H.R.K. Omar and M. 47 (1.. Vet.. Daoud. f Kuwait: Oct 20-23. N. McVicar. Foot and mouth disease in camels. Egypt. Wells. 2. K. A. The occurrence of infectious diseases in mixed farming of domesticated wild herbivores and domestic herbivores including camels in Kenya: Viral diseases. and goat.M. D. Vet. Universitaet Creteil. A. Richard. and R. R. Techn. Traite des maladies a virus des animaux. Arafa. Saleh. M. Isolation of Foot and Mouth disease virus from camels with ulcerative disease syndromes.I. J. M. Neumann. 1990. Peru: 30. Ensayos sobre la receptividad de 10s anguenidos a la fiebre aftosa.224 Viral Diseases Lubroth. M. Study of the pathology of the dromedary in Borana Awraja (Ethiopia). Mattson. Moussa. F. J. D. 2 (3): 197-203. W. Moussa. Vet. 1947. 1880. Med. Serological comparison of the pathogens of aphthosis in camel. M.J.H. Serologic survey of llamas in Oregon for antibodies to viral diseases of livestock (MS thesis). and susceptibility. El S. Health Assoc.M. A.A. Arafa. Mectious diseases of New-world camelids (NWC).

Mattson. either through mutation of the non-cytopathic to a cytopathic BVDV or through an exogenic cytopathic infection. The clinical disease is typically rapid in onset. 1999). 1987. Together with the viruses of border disease and classical swine fever virus it forms the genus Pestivirus. the fetus is immunotolerant in the early stages of pregnancy. 1988). However.. although both are caused by the same virus. (2000) suggest the following definition for M D "MD is a fatal condition.5% and 15.these findings were confirmed using .Superinfection. i.2%)when compared to racing dromedaries (3. 1993. with infection of a non-immune pregnant animal. It is remarkable that both the non-cytopathic and the cytopathic forms can be isolated from MD cases. It occurs only in those cattle that have suffered a non-cytopathic viral infection in the early stages (40-120 days) of fetal life and in which the virus has persisted as a result of immunological tolerance of the fetus (Thiel et al. (1988) did not identify any antibodies to BVDV in Qibouti. Bornstein et al.7% (Bornstein and Musa. The results of serological studies identifying BVDV antibodies in the dromedary have appeared from Tunisia with 3. Epidemiology Postnatal infection with the virus is acquired by ingestion or inhalation of contaminated material and results in the development of serum neutralizing antibodies.9% positive (Burgemeister et al. The disease was characterized by a profound thrombocytopenia and hemorrhages. On the other hand.4% (Bornstein. The outcome is mainly dependent on the stage of fetal development during which infection takes place. whereas BVDV-2 is largely restricted to the USA and Canada. 1994. This is usually a clinically unrecognizable infection. is believed to trigger MD. or a persistent lifelong infection without clinical signs. While the dam seroconverts without showing signs of disease. BVD can occur at any age in postnatal life as a result of an acute mild infection.. while those from tissues 1 of cattle suffering from MD are usually cytopathic (BVDVc). Strains isolated from newborn calves and persistently infected cattle are generally non-cytopathic (BVDVnc). Etiology Bovine viral diarrhea virus (BVDV) is a small RNA virus of the FZaviviridae." After the persistently infected (p. The virus is widespread in cattle populations worldwide and has also been isolated from NWC and OWC (Evermann et al. from Oman with 6. 1989) and Somalia with 3. 1998). the virus is capable of crossing the placental barrier and invading the fetus. severe clinical disease with agalactia and diarrhea may also occur.NonDathoaenic Viral Infections 225 pathogeneses. 1998).from Sudan with 15.. congenital defects.6%) with their larger breeding herds and closer contact with cattle herds. Brownlie et al.. 1975). Today two genotypes of BVDV are recognized: BVDV-1 and BVDV-2. BVDV-1 has a worldwide distribution. MD is a severe disease with fatal consequences in cattle 6 months to 2 years of age. This congenital infection can result in a wide spectrum of abnormalities: fetal death. In the late 1980s. Using the serum neutralization test. although chronic debilitatingforms can occur.) calf is born. it excretes the virus during its entire life. In a later survey (CVRL Annual Report. with characteristic erosive pathology in the oral/intestinal mucosa from which the cytopathogenic biotype of BVDV can be isolated.. 1980). In contrast. an acute and fatal syndrome of calves was reported in h e r ica.Bohrmann et al. Hegazy et al. Wernery and Wernery (1990) explained the higher incidence of BVD in UAE breeding camels (9. Clinical Signs and Pathology Serological studies indicate that NWC and OWC are susceptible to infection with the BVDV.. mainly of young cattle aged 6 to 18 months. The three viruses are antigenically related.7% (Hedger et al.

. spleen.In another Egyptian survey.4% in 270 llamas from Oregon in the USA. Cattle suffering from BVD and MD show lesions in the alimentary tract. The incidence of BVDV antibodies in 552 camels tested was 0. the authors prefer to keep this chapter under “Nonpathogenic Viral Infections”. Live and inactivated vaccines have been widely used in several countries. Since it is known that BVDV also causes abortions in camels. Diagnosis isi Diagnosis of BVD and MD requires laboratory support in the form of virus isolation. adult dromedaries and calves that have died of other causes are routine- ly virologically screened. neonatal respiratory distress syndrome and acute hemorrhagic gastroenteritis. virus antigen detection and serum antibody determination. In the UAE. through extensive field observations and laboratory studies.4% in breeding camels. In a serological survey conducted in Peru involving 117 alpacas that grazed with cattle and sheep.. (1994) detected 4.5% in racing camels and 6.indicating an MD-like disease. 1999). 1992). brain and kidney on bovine kidney cells causing a cytopathic effect (CPE).. weak calf syndrome with congenital deformities. Live vaccines are not recommended in camelids . So far the results have always been negative (Wernery et al. BVDV was isolated from lymphoid tissues. In another publication.226 Viral Diseases an antibody ELISA. Skin biopsies are the tissues of choice for the diagnosis of BVDV using immunohistological techniques and are always positive in persistently infected animals (Braun et al.3% BVDV positive dromedaries and Zaghhana (1998) found that camels from Egypt exhibited an even higher prevalence (52. 1987) and Picton (1993) reported a prevalence of 4. However. pathological changes consist mainly of erosions and ulcers of varying severity. 1994).05% (8/390) reactors to the BVDV in llamas from nine farms located in three different provinces in Argentina. In both BVD and MD. (1999) found 2. Tantawi et al. The pathological changes in MD are much more severe than in BVD. Investigations in bovines have led to a new understanding of the complex epidemiology and pathogenesis of BVD and MD and one can hope that this will also be the case in the camelid family. BVD infections have been described in dromedary calves from Egypt (Hegazy et al. The MD lesions are often found only in the upper alimentary tract. The presence of neutralizing antibodies to BVDV was 11% Egypt with a peak in of 23% in one area (Hegazy et al. VDV has been isolated from dead llamas that suffered excessive nasal discharge and diarrhea (Mattson. Hegazy et al. In camels these lesions have not been described. A recent study by Puntel et al. as with bovines. (1995) state that the main cause of abortions in dromedaries is the BVDV. This method should also be applied in the diagnosis of this disease in camelids..The virus was also demonstrated by immunofluorescence in different organs.. which can reach 50% in some herds. stillbirths. 1998) causing intrauterine death. extensive studies are necessary to elucidate the entire disease pattern in this animal species. Treatment and Prevention ’ Economic losses caused by BVD/MD mainly arise from prenatal infections. the prevalence of antibodies to BVDV was 11% (Rivera et al. 1993). including the fluorescence test for the presence of the BVDV. it may be necessary to adopt control and vaccination strategies similar to those carried out in cattle. It is therefore essential to remove all persistently infected animals and to vaccinate heifers prior to first breeding.5%)of neutralizing antibodies to BVDV. Over the last years our knowledge about BVD in camelids has increased and it seems that both NWC and OWC can contract the disease. Since only one publication on BVD has been published each on NWC and OWC.

M.E. Orlich. R. I.E. J. References Bohrmann. Berlin-Brandenburgische Rindertag 10/ 2998 (in press). bakteriellen und viralen Infektionskrankheiten bei Dromedaren in Siidtunesien.A. Thompson and A. Lotfia and M.C. U. 1975. Med.. Madwell and E. 1995. Brucella abortus and Toxoplasma gondii in serum from camels (Camelus dromedarius) in Sudan. T. 2000. 48: 189-191.S. SARE report. Am..J.mortalities associated with bovine virus diarrhea virus infection. S. 95: 99-102. Musa and EM. Meeting on camel production and future perspectives. Picton. Serological survey of viral antibodies in the Peruvian alpaca (Llama pacos). N. J.-J. Bacillus cereus as a possible cause of haemorrhagic disease in dromedary camels (Camelus dromedarius).F. M. Musa. U. H. B 34: 364-370.R. 12: 107-114. Oregon State University. Aboellail.. Arab.. J. Corvallis. Pathological and virological studies on calf mortality: B. Vet. Serologic survey of llamas in Oregon for antibodies to viral diseases of livestock (MS thesis). Puntel. B. Dtsch.S. A. Wschr. R. 1999. Camel Conf. 32 (3): 9-15. R.R. A. H. Youssef. P. Proc. J. J. M.R. Marcovechio. Tierarztl. H. Diagn. A. H. Becker. M.. Central Veterinary Research Laboratory. S. Ameghina. 1998.E. North America: Food and Animal Practice 10 (2): 345-351. Bovine virus diarrhea infection causes reproductive failure and neonatal mortality in the dromedary camel. 4 6 157-161. Med. Anim. R. 1988.R. 1994). J. Berry. Al Ain..J. Baszler et al. J..S.A. J. Hegazy. Hilbe and M. 1999.: 19. and B. Intrauterine infection with bovine virus diarrhoea virus on alpine communal pastures in Switzerland. Schimmelpfennig. F. J. Invest. Hegazy. Some virus diseases of domestic animals in the Sultanate of Oman. Saber.H... Rivera. Dubai. Vet. Clin.A. Bornstein. B. H.NonDathoaenic Viral Infections 227 because a variety of adverse effects have been observed using live BVDV vaccines in cattle. Evermann.. In:Allen. M.J. Wemery. V.A. M. Comparison of seroepidemiological findings of antibodies to some infectious pathogens of cattle in camels of Sudan and Somalia with reference to findings in other countries of f Africa. Some studies on bovine viral diarrhea disease in camel. Braun.S. D. Liess. Prevalence of antibodies common in viral diseases of domestic animals among camels in Egypt. M. Egypt Med. Strasser. Baroth. Seifert and J.M. A.S. Serological survey of viral antibodies in llamas (Lama glama) in Argentina. Jama. Carillo and A. 1994. R.. Mattson.F.. Sweden. A. Cumen. In Practice 22 (4): 176-187. Dtsch.A. l S t int. Fondevila. CVRL. 1992.F. Schoenmann. Wschr.V. J.R.A. Yousif and C. R. Saber. Cng. T. 1988. 1994. Assoc. Proc. Khartoum: 28-34..H. Survey on the prevalence of neutralizing antibodies to bovine viral diarrhea (BVD) virus. 1980. Tierarztl. Res. B.L. March 19-23. In Project (91-H-2-4) NAlU? Epidemiological. bovine herpes virus type 1(BHV-1) and parainfluenza virus type 3 (PI-3) in ruminants in the Djibouti Republic. L. Burgemeister. 1999. Barnett and D.. ODonnell. Untersuchungen uber Vorkommen von Parasitosen. Med. Vet.A. Brownlie. Cairo. Hegazy.A. 1987. Bornstein. . 5 265-269. Koenig and M. Med.F.S. Lotfy and T. S. Auftreten von MD nach Impfung. Annual Report. 1998. Blanco Viera.W. Vet. Frey and B. W.A. Vet. 1993. Aboellail. 2-3 May 1998. Vet.K.E. Prevalence of antibodies to some viral pathogens. Diagnostic approaches for the detection of bovine virus diarrhea (BVD)virus and related pesti-viruses.S. Hlth.. Ehrensberger. Hedger. 82: 352-354. S. 1989. Leyk and R. 1 & 2): 493-503. Viral Diseases. Proceedings of 22& Arab Vet. It has been shown that NWC seroconverted after a regimen of three vaccinations using a inactivated-virus preparation (Mattson. Egypt 55 (Nos. Chase.M. Marzouk and R. H. Vet..H. Bornstein. Trop. UAE. W. 1993. 46: 13-17. o International Symposium of Development of Animal Resources in Sudan. Thiel. Fahmy. E. T. M. clinical and pathological studies on some diseases in camel in Egypt. 1987. Bovine virus diarrhoea virus-strategic decisions for diagnosis and control. U. Med. Itman. Int. A disease survey of the Somali camel.. Goessler. Gray. 1993.A. A. Pohlenz. El Sanousi. 3. Inactivated vaccines are safer and can provide good protection. Schudel. B. Tantawi.

Scott et al. Prevalence of antibodies to Bovine Viral Diarrhoea Virus and/or Border Disease Virus in domestic ruminants. It has also spread into Egypt and clearly has the potential to spread elsewhere. Wernery. Eisa. Many different mosquito species can serve as vectors.. Seroepidemiologische Untersuchungen zum Nachweis von Antikorpem gegen Brucellen. Epidemiologic studies of RVF have always been performed during epizootics or immediately afterwards.E. A. Further reading Abou-Zaid. Infectious diseases of New-world camelids (NWC). Leptospiren.In addition to the human health hazards. Infection in humans is primarily due to contact with material from infected carcasses (Hoogstraal et al. North Am. Ames. Food Anim. and R. Wernery. J. Wernery. and W. W. but differences in virulence have been demonstrated.. Chlamydien. R. probably indicating a very large insect population as a vector prerequisite (Huebschle.S. 1990. No significant antigenic differences have been detected between RVF isolates. 1998. Strikingly. and L. Thedford. Kenya and Egypt. It has been accepted that the virus is endemic in indigenous forests. I. Snow and J.W. U. of Vet.R. exacerbated by the 100% abortion rate at all stages of pregnancy. Egypt. UK. Dtsch. where it circulates in mosquitoes and vertebrates spreading to livestock-rearingareas when heavy rains favor the breeding of mosquito vectors. Clin. 80 to 120pnin diameter. 9 7 134-135. Camel Prac.. 1979). 2-3 May 1998.G. all of the RVF epizootics described to date have followed unusually severe rainy seasons. clinical and pathological studies on some diseases of camel. 1997. production and fatalities. and have a host cell-derived. 51-58. U.2. Hegazy.und Enzootischen Bovinen Leukosevirus (EBL) bei Dromedarstuten (Camelus dromedarius). D. 5 (3): 145-157.A. J. Med.A. A. Vet. The virus was first isolated in 1931 in livestock on a farm located in the Rift Valley of Kenya. BVD/MD.H. The bunyaviruses are spherical. Several studies also included the respective local dromedary populations. RVF epidemics have occurred at prolonged intervals in eastern and southern Africa. Al Ain. Fac. and Res. Antibodies to RVF were found in 45% of the dromedaries examined during this outbreak. Newmarket. Publications. B 45: 345-351. This was the case following epidemics in Sudan. bilipid layer envelope through which virus-coded glycoprotein spikes project.E. IBR/IPV. Meeting on camel f production and future perspectives. 1998. Fowler. The authors incrimi- 2. and L. parallel to a drastic increase in abortions in dromedaries. Proceedings o the Int. The virus is now endemic in much of sub-Saharan Africa with epidemics in West Africa. but mostly found in ruminants. 1989. Epidemiological. PhD thesis (Infectious Diseases). M. Epidemiology For more than 70 years.. Johnson.I. Wade. Medicine and surgery of South American Camelids. RVF epidemics regularly cause serious economic damage to animal owners through the loss in . 1983). Fahmy. Zaghana.A. RVF does not occur in very arid areas. (1963) reported outbreaks of RVF in cattle following severe rainfall in Kenya. Iowa State University Press. Mayhew. Camel Newsletter 13 (9): 21-22. Pract.228 Viral Diseases Higgins. New aspects on infectious diseases of camelids.8 Rift Valley Fever Rift Valley fever (RVF) is an arthropodborne viral disease of animals including humans. U. A. 1999. Egypt. Zagazig Uni.F. () Etiology The Rift Valley Fever Virus (RVFV) is a member of the Phlebovirus genus of the family Bunyuviridue. Wschr. Studies on some diseases of camels. tieriirztl. Vet. 1991. Med. Serological survey of some viral diseases in camels in Sharkia Governorate. 6 1 :87-91. 1998. M.

During this period. the WHO received many reports of high mortality in camels throughout the affected area. spleen. Treatment and Prevention Measures such as chemical control of vectors... Many domestic animals and humans had been affected in vast areas of Kenya. 1985). no virological studies were performed to substantiate this supposition. (1996) examined 180 dromedaries with the hemagglutination inhibition test and serum neutralization test in Nigeria and detected 3. (1979) registered 31 RVF reactors in dromedaries. Since no RVFV was isolated from camels during these outbreaks it is not clear if the disease was caused by RVF. Peters and Meegan (1981).. Clinical Signs During the last RVF outbreaks in East Africa. HIT and ELISA. lymph nodes and brain from aborted fetuses for virus isolation on Vero and BHK 21 cells or suckling and weaned mice. Immunization remains the only effective way to protect livestock. Lesions in the livers of young animals also differ in both RVF and Wesselsbron disease. However. naturally infected dromedary.however. with ballooning of the head and upper neck. The authors stressed the involvement of camels in the transmission cycle of RVFV. In this case. Specimens for laboratory confirmation should include heparinized blood. (1978) and Eisa (1981) were able to isolate the virus from a healthy. kidney. swollen eyes and huge mucoid membrane sloughs in the mouth covering some ulcers. Antibodies to RVF can be demonstrated by CFT. the general disease pattern was that of fever and abortion.as severe epidemics were raging in northern Sudan at the time (Eisa et al. or the confinement of animals to mosquito-proof stables are usually impractical or too late. Hoogstraal et al. the epidemic was supposedly carried by Sudanese dromedaries to Egypt (Hoogstraal et al. southern Sudan and northern Tanzania in December 1997 and January 1998. Other than the increased abortion rate during outbreaks of RVF. This is especially true for Wesselsbron disease. Meegan et al. kids and calves and abortion in ewes. (1979) also observed an increased abortion rate in dromedaries during a RVF epizootic in Egypt. Diagnosis Definitive diagnosis of RVF depends on virological and serological investigations. movement of livestock to higher altitudes. Severe RVF epidemics have recently occurred in East Africa (Anonymous. Olaleye et al. which were the predominant features. observed only a subclinical form of RVF. however. liver. Experimental infections with the RVFV have induced no clinical signs in non-pregnant dromedaries (Davies et al. the same authors were not able to determine an increased rate of abortion in infected dromedaries. 1977). 1998). no other clinical signs have been so far observed in camels (Davies et al. AGID. Some descriptions of morbidity and mortality were highly suggestive of camelpox or parapox (Ecthyma contagiosum). In spite of high RVF antibody titers. However. which can also cause mortality in lambs.6% dromedaries in Egypt and Walker (1975) described abortions and deaths in young one-humped camels during RVF outbreaks. .Nonpathogenic Viral Infections 229 nate the RVFV for the increased rate of abortions. The authors therefore prefer to keep this part of RVF under the overall chapter "Nonpathogenic Viral Infections" until proven otherwise. but early neonatal death and jaundice have also been observed.3% positive cases. 1979). RVF is associated with higher mortality and abortion rates.. 1985). Hepatic changes are usually less extensive in RVF compared to Wesselsbron disease. Imam et al. Aly (1979) found antibodies with the HI-test in 15. since other arthropod-borne virus diseases tend to occur under the same climatic conditions. Viral antigen can also be detected by impression smears of infected tissues by immunofluorescence.

40 (3): 215-223. M.W. Davies. 1998. Reit sults of field investigations of the epizooty in Kosti district. CRC Press.2. Anonymous. Tomori and H. Vet.S. and R. Coakley. Study of Rift Valley Fever in camels in Egypt.M. M. 403. F. Rev.int. Isolation of RVF virus from animals. Egypt Publ. the artiodactylids. Lancelot. The authors determined that the attenuated vaccine strain (MVP-22) has yielded satisfactory results in the dromedary. 1996. J. 1987. The disease is characterized by high mortality and is typified by hemorrhagic/septicemic symptoms and mucosal erosions of the entire alimentary tract. Rapport d'execution. Transactions of the Royal Society of Tropical Medicine and Hygiene 73 (6): 624-629.B. Mid. As in other viral diseases already described. Afr. J. Abeid and A. Flu. 18 of 22 dromedaries developed neutralizing antibodies.Sc.I. 1989. Guillaud and Lancelot (1989) have concerned themselves with the production of a vaccine. Med.K.A. Beran G. Adham. Camb.. anim. M. A challenge infection with the R W was not performed. 6: 209-221..G. Ecological and entomological studies. Roach and N. Bact. Rift Valley Fever. 1983.V. La f i h r e de la vallee du Rift en Afrique de l'Quest. 143 (2): 34.E. 2. Mbugua. 86: 229-231. Rift-Tal-Fieber. Egypt. R. 1984. An epizootic of Rf Valley Fever in it Egypt in 1977. 1981.M. Exotische Virusseuchen der Wiederkauer II.M. Epiz. R. 2 Meegan. Rinderpest is an acute or subacute. J. Rec. Umschau 38: 268-273. Chartier. Meegan. Thesis (Micro. is necessary to clarify the pathogenicity of this virus in the camel. M. H. Technical Report Series 1:2-13. Cowdy.I. caprins. Eisa. 1975. 105: 124-125. RVF. Imam. Rev. J. Vet. G. Further intensive research. Animal Health Assoc. foreign animal diseases.. Th..M.Z. Rf Valley Fever in the Sudan. Hyg.9 Rinderpest The clinical presentation and dangers of rinderpest. 0. however. 1979. have been known for centuries. the scourge of cattle husbandry. K. 1963. diagnosis and control committee on foreign animal diseases of United States. Digoutte.230 Viral Diseases Although it has still not been determined decisively whether dromedaries actually develop RVF. H. Martinez and J. J. Olaleye. Bull. ovins.2. 3 265-269. Pays trop. Hoogstraal and M. G. Following a single subcutaneous vaccination. Scott. their prevention. C. Rec.. Different breeds of cattle have varying degrees of resistance to . Danvish. R. and Meegan. sci. Tierarztl.R. Eisa. Rift Valley fever in camels. Path. Bada. Slama.M. O.J. Boca Raton. 1979. O. References Aly. Moussa. SantiProd. Faculty.R. R. cattle. RVF in CRC handbook series in zoonoses. Khalil and F. Among the larger domesticated animals.P.S.). 25 (4): 356-367. Hoogstraal. 1. febrile viral disease of cloven-hoofed mammals. D. Rift Valley fever in Nigeria: infections in domestic animals. Rift Valley fever in Kenya: the presence of antibody to the virus in camels (Camelus dromedarius).. Sidi Thabet 246. Rift Valley fever in Africa.. Vet.. J. J. W. 1979. C. 1977. highly contagious. The Rf Valley Fever epiit zootic in Egypt 1977-78. El Sawi. Eleu. Karamany and M.R. Contribution a l'etude &roepidemiologique de la fikvre de la vallee d u Rf it chez les dromadaires du Sud Tunisien. H. Saluzzo. tech. Epidemic of RVF in Egypt.D. Schmitz. Health ASS.A. Guillaud. Doct.J. J. Of. Walker. Cairo University. J. Ed. the camel appears to be susceptible to RWV.Vet. 1985.F. Essais de vaccination des ruminants domestiques (bovines. 15 (3): 937-946. 1973..A. IEMVT-CIRAD. 1978. water buffaloes and yaks are susceptible to the virus. Huebschle. vit. Peters. 9 4 241-244. 1981. This disease led to the foundation of the first European veterinary faculties and the implementation of laws governing contagious diseases. Koros and H. camelides) contre la fievre de la vallee du Rift avec la souche MVP-12 en Shegal et en Mauritanie.

never been reported in NWC.Individual daries were also affected during outbreaks rinderpest virus strains vary in their path. It is should be instituted for the Eritrean aniclosely related to the viruses that cause ca.The mortality was 20 to 40%. served more than 15 outbreaks of rinderAs in foot-and-mouth disease. Srinivasan (1940) was successful in conClinical Signs and Pathology 4 t r o h g an outbreak of rinderpest among from the turn of the century mention se. as well as vesicles on the lips and der Artioductylu. One bull (bovine) developed rinderpest after being given blood from one of these dromedaries. 1947) saw cases of rinderpest atic region of Russia have reported that among Bactrian camels in the region camels are not susceptible to natural infecaround Baku in 1898. Curasson (1947). Epidemiology :3 The natural hosts for the severe diarrhea occasionally mixed with rinderpest virus are all members of the or. Vedernikov (1905) in Egypt. minal atony. measles and peste-des-petits-ruminants. traveling around India. subfamily problem and that disease control measures Pararnyxoviridae. Littlewood vere diarrhea and hematuria. The dromedaries’clinical signs were similar to those in cattle. one of which later died. Wild animals exhibit varying susceptibility and play an important role in the epizootiology of rinderpest as virus reservoirs. 1983).does not exclude the fact that slight clinical cal reactions in two dromedaries. Tartakowsky (1899) tions. produced rinderpest experimentally in neither observed nor heard of outbreaks four Bactrian camels. various els. epidemics with clinical signs similar to the virus. Leese (1927). susceptible to the rinderpest virus or not. The author However.blood. eruptive skin lesions and. Of the smaller domesticated animals. one of which died. sheep. vesicles and ulcera in the mouth. Conti (1913) too diagnosed rinderpest symptoms in dromedaries in Eritrea. the author obclinical course of 3-5 days (Fowler. Until the middle of the twentieth centuwith cattle blood infected with the rinderpest virus. According to Haji (1932-1933). but experi. Pecaud (1924) in Chad and (1902) and Tschegis (1902) (cited from Samartsev and Arbuzov (1940) in the AsiCurasson. Contrary to all these statements. in one case. The author believed that the epidemic in Etiology iii The rinderpest virus belongs dromedaries was more of a prophylactic to the order Mononegavirales. Natural rinderpest has hard palate that developed into ulcera.Nonpathogenic Viral Infections 231 following clinical signs: fever.mal population. mogenicity in various species.of rinderpest among cattle and buffalo in India. Dhillon mental studies have shown that llamas de.not susceptible to rinderpest. there are pest among dromedaries with mortality differing opinions as to whether OWC are rates of up to 100%. genus Morbillivirus. who reported the big rinderpest epizootic in Niger in 1892. of rinderpest in dromedaries. diarrhea. There is evidence that the primary means of infection is via a virus-containing aerosol (Munz. phocine distemper. dromenine distemper. ocular discharge. Lingard signs may be possible and that these may (1905) inoculated five Indian dromedaries be overlooked. groups have reported that the camel is learned that dromedaries developed se. 1998). Between 1948 and 1958. depression.ulation from infected goats. goats and swine are vulnerable to the disease under natural conditions. he could only elicit slight clini.dromedaries after ”goat blood virus” inocvere outbreaks of rinderpest among cam. The dromedaries developed the ry. . The affected animals had fever.(1959) reported similar discoveries in Invelop a mild febrile response with a short dia.Cross (1919) injected the rinderpest virus into three Indian dromedaries.

Taylor (1968) confirmed these results through further trials and performed additional experiments on dromedaries using the rinderpest virus. virus was re-isolated bethe tween the 3rdand gthday from the blood of the infected dromedary. l. it was not possible to transmit the rinderpest virus from infected dromedaries to cattle or other dromedaries. However. Dromedaries in this region did not develop the disease and antibody studies on 60 dromedary sera with lapinized rinderpest antigen were negative. Experimental infections in dromedaries with the rinderpest virus have yielded further information regarding the susceptibility of this species to rinderpest. . and Abou-Zaid (1991) found rinderpest-neutralizing antibodies in 5. serving as contact animals.7% of the dromedary sera examined from Chad. One of two dromedaries infected subcutaneously with the virulent rinderpest strain RGK/1 developed a slight viremia lasting 6 days. (1985). whereby high neutralizing antibody titers were observed 28 days after experimental infection with the virulent strains. This experiment also showed that infected dromedaries did not transmit the virus to susceptible cattle. did not develop the disease and also developed no antibodies to rinderpest (Provost et a.Laboratory methods in the diagnosis of rinderpest were introduced later.2% of 536 dromedaries in Egypt. Dromedaries that were infected with these strains subcutaneously did not develop rinderpest. Zebus. (1967) found rinderpest antibodies in 7. Scott and MacDonald (1962)confirmed a severe outbreak of rinderpest among wild animals in northern Kenya in 1960. though both animals developed neutralizing antibodies. In order to determine the susceptibility of camels to experimental rinderpest infection. into two healthy 8 to 12-monthold camels. Following experimental intravenous infection with a virulent rinderpest strain (Kabete0). Only one out of ten dromedaries infected experimentally with an aerosol of the rinderpest virus developed signs of an asymptomatic. The results of these experiments were as follows: 1. 3. A slight increase in body temperature was observed following inoculation with the virulent strains. Although the rinderpest infection originated in cattle. further experiments were carried out by Chauhan et al. One camel was given subcutaneous and the other intravenous inoculation. One dromedary developed slight pyrexia. This was the only clinical manifestation that was observed during the experiments. Singh and Ata (1967) also detected antibodies to the rinderpest virus in 10% of the Sudanese and Egyptian dromedaries examined. A post mortem examination of one of the camels infected with rinderpest virus did not reveal any lesions. 2. This animal also developed neutralizing antibodies. Dromedaries given the attenuated vaccine developed only a low antibody titer. 1968). Maurice et al. Chauhan et al. Slight viremia occurred in two out of three dromedaries that were in close contact to a bull infected with rinderpest. Singh and Ata (1967) utilized two virulent and two attenuated (vaccine) rinderpest strains in their experimental trials. Leukopenia and antibodies to the rinderpest virus were observed in the serum of this animal. No distinct clinical signs of rinderpest lesions were detected except a slight hyperemia of visible mucous membranes and mild diarrhea.The authors inoculated 10mL of a 10% spleen suspension collected from a buffalo calf suffering from rinderpest. (1986) examined 283 dromedary sera from India serologicallyand did not detect any antibodies. 4. non-contagious infection.232 Viral Diseases rinderpest were diagnosed on the basis of clinical signs as well as the tendency to spread among other ungulates living in close proximity with the dromedaries.

1994..Fowler. Pusa. J. freeze dried vaccine that is highly efdo not appear to play a major role in the fective (Coetzer et al. used in camelids. 1985. bidity rate reached over 90% with a morFac. agric. A presumptive diagnosis of rinderpest can be made on the basis of the clini. Infectious Diseases of livestock with after inoculation of the camel viruses.. R. closely related to the pestelence of different diseases in camels (Camdes-petits-ruminants (PPR) virus. 86-88. of the submandibular area and diarrhea Chauhan. J.. A serious prophylactic problem: tions are currently being undertaken to reRinderpest in camel. jor clinical signs were sero-mucopurulent Kaushik. might be very difficult in camelids. Inst. Further investigaConti. Ind. R.C. dysviral diseases of livestock in Haryana State. Cross. Tustin. K. 36: cal signs and gross pathology in cattle.camel kidney cells. G. tion of rigid quarantine and animal moveFrom all these experiments it can be as. 1518-1535. therefore they sive. tion of the diagnosis as soon as possible. Indian Vet. 1932-33.K. J. S. was reported in some cases. R. 1919.rinderpest outbreaks are controlled by the velopment of typical clinical signs and le.C. Thomson and R. it South American Camelids. Rinderpest in camels.S. Gupta.C. l ( 1 ) : 10-16. equi was also isolated University Press 2: pp. Swelling Ind. but 603-607. 1959. pnea and abdominal breathing.R. Egypt. R. sumed that OWC are susceptible to rinderPrevention of rinderpest in endemic arpest. H. pest. This is an inexpentors for the rinderpest virus. Camel Newsletter 3: 10-14. lacrimation. (1985) further showed that rinderpest virus can be readily grown on blood which was collected from the exper. 1913. S. Are camels susceptible to blackquarter. highly contagious respiratory syndrome. M. A new epizootic disease has affected thousands of camels in Ethiopia in 1995 References and 1996 characterized by a febrile. Medicine and surgery of as where the disease is not prevalent.Dhillon. imentally inoculated camels at the height of febrile reaction and injected into two Treatment and Prevention * Confirmed susceptible buffalo calves caused the de. 1986.S. eas requires annual vaccination of all especially through contact with infected calves up to 2 years of age with the attenucattle.A. Moderna Zooiatro. C. Strepspecial reference to Southern Africa. Toriproduce the disease in camels (Roger et al.ment controls.. Iowa State Uniis essential to obtain laboratory confirmaversity Press. PhD thesis (Infectious Diseases). PrevaZivirus strains. 1998.slaughter and disposal of all infected and sions of rinderpest in these calves within 6 contact animals as well as by the imposidays of inoculation. 1991. The mor. Med. 2000). Virol.W. Editeurs: pp.1. haemorrhagic septicemia and rinderpest? Bull. Oxford tococcus equi spp.It has not been epizootiology of rinderpest. Kaushik.E. LA .S.. 1994). (1971) reported that the Vet.Curasson.A. Incidence of Rinderpest in camels in Hissar district.9: 13-14.G. Le chameau et ses maladies. It is less likely that they serve as vec.C. The maChauhan. Kulshreshta. Haji. In are. Vigot Freres.Abou-Zaid.E. of Vet. G. Ames.. were isoelus dromedarius) in India. and might develop mild clinical signs. coughing. 1947. no 24: 215. Diagnosis Several handbooks and scientific papers detail the diagnosis of rinder.S. from diseased camels. tality ranging between 5 and 70%. Studies on some diseases of camels. Res. G. lated from diseased camels and a similar disease was reproduced in goats and sheep Coetzer.ated Kabete " 0 strain. A. Kulshreshtha and R. Two morbilSatiya and R. Epidemiological studies of nasal discharge.K. Zagazig Uni.NonpathogenicViral Infections 233 Chauhan et al. Mirchamsy et al.C..

234 Viral Diseases
Leese, A.S. 1927. A treatise on the one-humped camel in health and disease. Vigot Frhres, Paris II. Lingard, A. 1905. Report on the preparation of Rinderpest Serum, Calcutta. Abst. BUZZ. Inst. Pasteur 4 235. Littlewood, W. 1905. Camels are not susceptible to Rinderpest. J. Comp. Path. 18: 312. Maurice, Y., A. Provost and C. Borredon. 1967. Presence d'anticorps antibovipestiques chez le dromadaire du Tchad. Rev. Elm. Mid. vit. Pays trop. 20 (4): 537-542. Mirchamsy, H., B. Bahrami, M. Amighi and A. Shafyi. 1971. Development of a camel kidney cell strain and its use in virology. Arch. Inst. Razi 23: 15-18. Munz, E. 1983. Die heutige Situation auf dem Gebiet der tropischen Tierseuchen, ihre derzeitige Gefahr fiir die Landwirtschaft der Bundesrepublik Deutschland und ihre Bedeutung fiir den Tierarzt. Der prakt. Tierarzt 11: 993-1006. Pecaud, G. 1924. Contribution a l'etude de la pathologie veterinaire de la colonie du Tchad. Bull. SOC.Path. Exot. 17 (3): 196-207. Provost, A., Y. Maurice and C. Borredon. 1968. Note sur la peste bovine experimentale du dromadaire. Rev. Elm. Mid. vit. Pays trop. 21 (3): 293-296. Roger, F., L.M. Yigezu, C. Hurard, G. Libeau, G.Y. Mebratu and A. Diallo. 2000 in press. Investigations on a new pathology of camels in Ethiopia. Samartsev, A.A. and EN. Arbuzov. 1940. The susceptibility of camels to glanders, rinderpest and bovine contagious pleuro-pneumonia. Veterinariya Moscow 4: 59-63. Scott, G.R. and J. MacDonald. 1962.Kenya camels and Rinderpest. Bull. epizoot. Dis. Afr. 10 (4): 495-497. Singh, K.V. and F. Ata. 1967. Experimental Rinderpest in camels. A preliminary report. Bull. epizoot. Dis. Afr. 15: 19-23. Srinivasan, V. 1940. Active immunisation of camels against Rinderpest with goat blood virus. lnd. Vet. J. 16: 259-260. Tartakowsky, M.M. 1899. No Title. Arch. Sci. biol., St. Petersburg 8: 11. Taylor, W.P. 1968. The susceptibility of the onehumped camel (Camelus dromedarius) to infection with Rinderpest virus. Bull. epizoot. Dis Afi. 16: 405-410. Tschegis. 1902. cited from Curasson (1947). Vedernikov, V. 1902. cited from Curasson (1947). Wilson, A.J., H.J. Schwartz, R. Dolan, C.-R. Field and D. Bottcher. 1982. Epidemiologische Aspekte bedeutender Kamelkrankheiten in ausgewahlten Gebieten Kenias. Der prakt. Tierarzt 11:974-987.

Further reading
Alonso, J.M. 1971. Contribution l'btude de la peste en Mauritanie. T h h e (Doctorat de medecine) Paris 6 No 59. Klein, J.M., J.M. .Alonso, G. Baranton, A.R. Poulet and H.H. Mollaret. 1975. La peste en Mauritanie. Med. Mal. infect. 5 (4): 198-207.

Lobanov,V.N. 1967.La peste chez les chameaux.
In:OMS %minaire inter-regional de L'0.M.S. pour la lutte contre la peste, Moscow.

2.2.10 Unusual Arboviruses
Arboviruses (arthropod-born viruses) are primarily vector viruses that multiply in blood-sucking insects and/or are transmitted to vertebrates via the insect's bite or sting. They are widespread in the tropics and subtropics, but their significance in camelids is not known. Wood et al. (1982) isolated the Kadam virus from HyaZomma dromedarii ticks collected from the immediate vicinity of a dead dromedary in Saudi Arabia. It was not possible to determine whether this animal's death was due to the Kadam virus. The pathogenicity of the Kadam virus for the dromedary, cattle and humans has not yet been determined. Five strains of the Quaranfil virus were isolated by Converse and Moussa (1982) from HyaZomma dromedarii ticks collected in Kuwait, Iraq and Yemen. The significance of this finding has not yet been determined. The Akabane virus can cause epizootics and spontaneous abortions, premature births and congenital deformities in cattle, sheep and goats. The virus is widespread in Africa and Asia and appears to be en-

NonDathoaenic Viral Infections

235

demic to the Arabian Peninsula. A Bul saidy et al. (1988) found that 50% of the dromedaries examined in Oman had neutralizing antibodies to the Akabane virus. It has not been ascertained whether the virus causes abortions in the dromedary. Anderson and Casals (1973) isolated four strains of Dhori virus from ticks (Hyulomma dromedurii) found on Indian dromedaries. Additionally, the author discovered neutralizing antibodies to the virus in 48 out of 50 dromedary sera. No clinical signs of disease were observed in the seropositive dromedaries. The virus has also been isolated from dromedary ticks in southwestAsia and Africa. Williams et al. (1973) found three non-classified Arboviruses in Hyulomrnu ticks from Egyptian dromedaries: Wanowrie, Thogoto and Dhori viruses. These viruses have been widely spread by the migratory patterns of the indigenous animals, including the camel caravans. The veterinary importance of these viruses is unknown. A survey for antibodies against flaviviruses in 269 slaughter camels was carried out in Nigeria (Baba et al., 1990). The antibody prevalence against flaviviruses was noted as follows: Wesselsbron: 60.2%, Yellow Fever: 54.0%, Potiskum: 66.2%, Dengue type 1: 4.5%, Banzi: 5.4% and Uganda S: 0%. The importance of the high prevalence of some of the flavivirus antibody in camels was not evaluated, but the authors believe that there is a potential for infected camels to play an important epidemiological role in the spread of these viruses to humans and livestock. Similar findings were reported by Kemp et al. (1973) who isolated the following viruses from camel blood injected into infant mice: Thogoto, West Nile and Wesselbron. Crimean-Congohemorrhagic fever virus (C-CHFV) is widely distributed throughout the arid regions of Africa, the Middle East, southern and eastern Europe and Asia (Hoogstral, 1979). The infection is enzootic, but mainly asymptomatic in many

animal species such as cattle, sheep, goats, camels and hares (Schwarz et al., 1996). Thirty species of ticks, particularly the genus Hyulommu, act both as reservoir and vector. Humans become infected by tick bites or through close contact with infected animals or humans. Several reports deal with the detection of C-CHF-antibodies from different animal species as well as with the isolation of the virus from animals. Causey et al. (1970) isolated 35 virus strains in Nigeria from cattle blood, from liver and spleen of a hedgehog and from four species of ticks and Culicoides spp. C-CHF-antibodies were found in Iranian men (13%), sheep (38%), goats (36%), cattle (18%) and small mammals (3%) with the agar gel immunodiffusiontest, but no positive cases were detected in camels (Saidiet al., 1975). However, C-CHF viral antibody was demonstrated in 14% (600/4301) of camels imported into Egypt by the agar gel diffusion and the indirect fluorescent antibody techniques (Morrill et al., 1990). Hassanein et al. (1997), who performed a serological survey on humans and livestock in Saudi Arabia using the reversed passive hemagglutination inhibition test, found antibodies in humans (0.8%), sheep (3.2%), goats and cattle (O.6%), but no positive cases in horses and camels. The Hyulomrnu tick was most probably responsible for epidemics in Iraq (Tantawi et al., 1980), the UAE (Suleiman et al., 1980) and Oman (Scrimgeour et al., 1996). However, CCHFV was not isolated from camels during an epidemiological survey on ticks conducted in Saudi Arabia (El-Azazy and Scrimgeour, 1997), although camels had the highest rate of tick infestation. The importance of C-CHFV for the camel is unknown. Serological examination for the virus in a small number of dromedaries suffering from hemorrhagic diathesis in the UAE (see 1.1.4) was negative (Wernery et al., 1992).

236 Viral Diseases
References
A1 Busaidy, S.M., P.S. Mellor and W.P. Tayler. 1988. Prevalence of neutralizing antibodies to Akabane virus in the Arabian Peninsula. Vet. Microbiol. 17 (2): 141-149. Anderson, C.R. and J. Casals. 1973. Dhori virus, a new agent isolated from Hyalomma dromedarii in India. Ind. J. Med. Res. 61 (10): 1416-1420. Baba, S.S., S.A. Omilabu, A.H. Fagbami and O.D. Olaleye. 1990. Survey for antibodies against flaviviruses in slaughter camels (Camelus dromedarius) imported to Nigeria. Preventive Veterinay Medicine 10: 97-103. Causey, O.R., G.E. Kemp, M.H. Madbouly and T.S. David-West. 1970. Congo virus from domestic livestock, African hedgehog, and arthropods in Nigeria. Am. J. Trop. Med. and Hyg. 19 (5): 846-850. Converse, J.D. and M.I. Moussa. 1982. Quaranfil virus from Hyalomma dromedarii (Acari: Ixodoidea) collected in Kuwait, Iraq and Yemen. J. Med. Entomol. 19 (2):209-210. El-Azazy, O.M.E. and E.M. Scrimgeour. 1997. Crimean-Congo haemorrhagic fever virus infection in the Western Province of Saudi Arabia. Transactions of the Royal Society of Tropical Medicine and Hygiene 91: 275-278. Hassanein, K.M., O.M.E. Elazazy and H.M. Yousef. 1997. Detection of Crimean-Congo Haemorrhagic Fever virus antibodies in humans and imported livestock in Saudi Arabia. Transactions of the Royal Society of Tropical Medicine 8 Hygiene 91 (5): 536-537. Hoogstraal, H. 1979. The epidemiology of tickborne Crimean Congo Hemorrhagic fever in Asia, Europe and Africa. J. med. Entomol. 15 (4):307-417. Kemp, G.E., O.R. Causey, D.L. Moore and E.H. OConnor. 1973. Viral isolates from livestock in Northern Nigeria: 1966-1970. Am. J. Vet. Res. 34 (5):707-710. Morrill, J.C., A.K. Soliman, I.Z. Imam, B.A.M. Botros, M.I. Moussa and D.M. Watts. 1990. Serological evidence of CrimeanCongo haemorrhagic fever viral infection among camels imported into Egypt. J. Trop.Med. Hygiene 93: 201-204. Saidi, S., J. Casals and M.A. Faghih. 1975. Crimean Hemorrhagic Fever-Congo (CHF-C) virus antibodies in man and in domestic and small mammals in Iran. Am. J. Trop. Med. Hyg. 24 (2):353-357. Schwarz, T.F, H. Nsanze, M. Longson, H. Nitschko, S. Gilch, H. Shurie, A. Ameen, A.R.M. Zahir, U.G. Acharaya and G. Jager. 1996. Polymerase chain reaction for diagnosis and identification of distinct variants of Crimean-Congo hemorrhagic fever virus in the United Arab Emirates. Am. J. Trop. Med. Hyg. 55 (2): 190-196. Scrimgeour, E.M., A. Zaki, F.R. Mehta, A.K. Abraham, S. Al-Busaidy, H. El-Khatim, S.F.S. Al-Rawas, A.M. Kamal and A.J. Mohammed. 1996. Crimean-Congo hemorrhagic fever in Oman. Transactions of the Royal Society of Tropical Medicine and Hygiene 9 0 290-291. Suleiman, M.N.H., J.M. Muscat-Baron, J.R. Harries, A.G.O. Satti, G.S. Platt, E.T.W. Bowen and D.I.H. Simpson. 1980. Congo/Crimean Haemorrhagic Fever in Dubai. An outbreak 1 at the Rashid Hospital. The Lancet 1 :939-941. Tantawi, H.H., M.I. Al-Moslih, N.Y. Al-Janabi, A.S. AL-Bana, M.I.A. Mahmud, F. Jurji, M.S. Yonan, F. Al-Ani and S.K. Al-Tikriti. 1980. Crimean Congo Hemorrhagic Fever virus in Iraq: isolation, identification and electron microscopy. Acta virologica 24: 464-467. Wernery, U., H.H. Schimmelpfennig, H.S.H. Seifert and J. Pohlenz. 1992.Bacillus cereus as a possible cause of haemorrhagic disease in dromedary camels (Camelus dromedarius). int. Proc. lSt Camel Conf. In: Allen, W.R., A.J. Higgins, I.G. Mayhew, D.H. Snow and J.F. Wade. R. and W. Publications, Newmarket, UK 51-58. Williams, R.E., H. Hoogstraal, J. Casals, M.N. Kaiser and M.I. Moussa. 1973. Isolation of Wanowrie, Thogoto and Dhori viruses from Hyalomma ticks infesting camels Egypt. J. Med. Entomology. 10 (2): 143-146. Wood, O.L., M.I. Moussa, H. Hoogstraal and W. Buettiker. 1982. Kadam virus (Togaviridae, Flavivirus) infecting camel-parasitizing Hyalomma dromedarii ticks (Acari: Ixodoidea) in Saudi Arabia. J. Med Entomol. 19 (2): 207208.

Fungal Diseases

Funaal Diseases 239

Most agents of mycoses exist as saprophytes in soil, decaying vegetables and dung. The soil reservoir is the primary source of most fungal infections, which can be contracted by inhalation, ingestion or by contact with infected individuals or equipment. Pathogenic fungi establish infection in apparently healthy hosts and such diseases as histoplasmosis, coccidioidomycosis and blastomycosis are regarded as primary systemic mycoses. Opportunistic fungi usually require a host that is debilitated by stress, metabolic acidosis, malnutrition or neoplasia to establish infection. Prolonged exposure to antimicrobials or immunosuppressive substances can increase the likelihood of infection by opportunistic fungi like Aspergillus, Mucor, Cryptococcus and Candida.

Dermatophytosis (ringworm) is an infection of keratinized tissue (skin, hair, nails) by several genera of fungi called dermatophytes. All domestic animals are susceptible and the fungi are found worldwide. A few dermatophytes (Microsporum [M.] gypseum) normally inhabit soil (geophilic) and can cause disease in animals and humans. Some dermatophytes (M. audouinii) are adapted to humans and seldom infect animals (anthropophilic)and others are primarily animal pathogens (M. canis, Trichophyton fT.1 equinum), but can also cause disease in man (zoophilic). Very little is known about fungal diseases in camelids. This chapter tries to summarize current knowledge of these microorganisms.

3.1

Mycotic Dermatitis
I*

'

I

Etiology Various fungal species can produce infection of the epidermis, of which the species causing dermatophytosis (ringworm) are the most common in camelids (Table 43).

Dermatophytes are a group of closely related fungi that utilize keratin for their growth. Over 38 species of dermatophytes are known and those that affect animals are placed in one of two genera - Microsporum and Trichophyton.

Table 43 Fungi isolated from mycotic skin lesions of camels Derrnatophytes Authors Curasson (1947) Nasser (1969) Torky and Hammad (1981) Khamiev (1981, 1982, 1983) El-Kader (1985) El-Tamavy et al. (1988) Mahmoud (1993) Fadlelmula et al. (1994) Abou Zaid (1995) Refai and Miligy (1968) Kuttin et al. (1986) Mahmoud (1993) Kame1 et al. (1977) Chatterjee et al. (1978) A1 Ani et al. (1995) lvanova and Polvakov (1983) Dalling et al. (1966) Boever and Rush (1975) Kame1 et al. (1977) Fischman et al. (1987) Mancianti et al. (1988) Gitao et al. (1998) El-Kader (1985) El-Tamavy et al. (1988) Abou Zaid (1995) Curasson (1947) unpublished

Trichophyton verrucosum

Trichophyton rnentagrophytes

Trichophyton schoenleinii Trichophvton sarkisovii Trichophyton dankaliense

Microsporum gypseurn

Microsporum canis Others Sporothrix schenckii Candida albicans Penicillium vinaceum Pseudorotium spp. Pseudoarachniotusspp. Allescheria spp. Mycelia sterile Crvptococcus neoformans Chwsosporium

Singh and Singh (1969)

Ramadan et al. (1989) Mahmoud (1993)

Mycotic Dermatitis Figure 103 Microscopic differentiation of the dermatophyte genera affecting camels (after Quinn et al., 1994)

241

Microsporum spp.

Trichophyton spp.

Macroconidiurn

%
Microconidia

Macroconidium

Microconidia

'

Macroconidia

Large thick-walled and divided into septa. Tend to be spindle or boat-shaped.

Few or absent in some species. If present they are cigar or pencil-shaped.Walls are thin. Divided by septa into 3 to 8 cells. Usually numerous, single or in clusters.

Microconidia

Relatively few or absent. If present they are tear-shaped and single on hyphae.

Dermatophytosis is a common skin disease in OWC under 3 years of age with a peak incidence age of between 3 to 12 months. In NWC it is, however, a very rare disease (Fowler, 1998) and only T. verrucosum and T. mentagrophytes have been isolated from NWC so far. Macroconidia and microconidia are produced in laboratory cultures and their differences for Microsporum spp. and Trichophyton spp. are shown in Fig. 103. The macroscopic (culture) and microscopic characteristics of camelid dermatophytes are shown in Fig. 104a-e.All fungal cultures presented here are 14-day-oldcultures grown on Sabouraud agar at 27°C.
Epidemiology In most circumstances, dermatophytes grow only in dead, keratinized tissue; advancing infection halts upon reaching live cells or inflamed tissue. Infection begins in a growing hair or in the stratum comeum where thread-like hyphae develop from conidia. The hyphae penetrate and invade the hair shaft, thus

weakening it. It grows downward as the hair grows upward. The dermatophytes produce clusters of arthrospores,primarily along the outer surface of the hair (ectothrix type) rather than within the hair (endothrix type). The epidemiology of ringworm in camelids is yet unexplored, but it is believed that direct and indirect contact with infected animals and fomites are the modes of transmission of dermatophytes. High humidity, overcrowding and nutritional imbalance (most probably Vitamin A deficiency) are conducive to the disease. As many as 80% of calves show clinical signs in affected herds (Wilson, 1998). Khamiev (1982) examined 200 camels with skin lesions, of which 90 were positive for T. verrucosum, which he named T. camelius. Of these 90 animals, 90% were younger than 2 years. The chlamydiospores of T. verrucosum and T. mentagrophytes may remain viable for up to 4.5 years in hair and cellular debris scraped off animals and left attached to fomites (Fowler, 1998).

242

Fungal Diseases

Mvcotic Dermatitis 243 Figure 104Macroscopic (culture. 1996). neck. The first shows typical lesions that are gray-white in color (Fig. 1995): (a) Trichophyton verrucosum. round alopecic areas. (e) Microsporum canis !I Although camel owners are familiar with ringworm and are able to differentiate this dermatitis from other skin infections. There are two clinical types of ringworm in camels. The disease is zoonotic and handlers often become infected. (b) Trichophyton mentagrophytes. (d) Microsporum gypseum. Figure 105 Typical lesions of ringworm in a young dromedary These lesions are characterized by small. exhibiting typical ringworm lesions on their arms. dermatophytoses are extremely variable in their clinical appearances. (c) Trichophyton schoenleinii. left) and microscopic characteristics (right) of camelid dermatophytes (after Kozlowska and Nuber. limbs and flanks whereby these lesions Figure 106 Ringworm. may initially be confused with mange (Fig. The second is a more generalized infection on head. 106) (Manefield and Tinson. generalized infection of the hind limb of a dromedary . which may coalesce and mainly OCCUT on the legs. neck and head of young animals. 105).

they are best seen with PAS (Marks et al.. (right) from camels suffering from ringworm dermatitis (wet preparation with KOH) . The characteristic hyphal filaments are difficult to see on HE-staining. 1994).244 Funaal Diseases Pathology lri The epidermis is thickened with rete pegs extending downwards. (left) and Microsporurn spp. parakeratosis and acanthosis in the stratum comeum. although growth usually requires 10 to 14 days of incubation. (1984) a fluorescent staining with Acridin Orange can make the identification of fungal spores and septate hyphae easier. Hairs or scrapings from the periphery of suspicious areas are examined for fungal elements in a wet preparation (20% potassium hydroxide. Diagnosis Direct microscopic examination of hairs or skin scrapings might reveal characteristic hyphae and/or arthrospores. dried serum and fungal elements. fungal culture is the most effective and specific means of diagnosis. inflammatory cells. Fungal elements are often detected inside hair follicles associated with microabscesses. 107).. incubation of the slide at room temperature should facilitate the microscopic examination. 1986) and Grocott’s methamine silver stain. According to Hollaender et al. However. folliculitis and trichogranulomas (Fadlelmula et al. A 10 to 20 min. Figure 108 Mycoline agar slide culture of T: verrucosurn (12 days incubation) Figure 107 Trichophyton spp. KOH in water) that has been warmed and squashed out under a coverslip (Fig. Histology reveals hyperkeratosis. The crusts consist of tissue fragments.

Treatment and Prevention 5h' The spread of ringworm can be limited by early diagnosis and separation of infected from uninfected camels. To avoid recurrence of infec.Mycotic Dermatitis 245 Microsporum spp..Camelvac Tricho@ per acetate (0. In these herds the following incidents of ringworm were found: 5-day to 4-month-old Bactrians: 21. 5% salicylic one or two injections with Camelvac Triacid.cho@ (Toleutajewa. when sprayed on infected animals as a so- lution of 1:200.25%) with cop.In these herds.1% 4 years and older Bactrians: 1.58%)and hydroxyquinolines has also recently been successfullyused by may be applied topically as ringworm the authors in several camel herds in the ointments onto the affected areas.300 camel calves were tion.302 Bactrians from 12 farms were investigated. The use of Captan@ has been ad. It is therefore essential that any skin lesions should be carefully investigated and multiple deep skin scrapings (containing blood) should be dispatched for laboratory diagnosis. This vaccine is used with very good with warm soapy water and all scabs success not only for prophylactic but also removed. and Microsporum spp. UAE.The lesions receded within 14 days and vocated (Ainsworth and Austwick. 1994).Definite diagnosis and species identification requires removal of hyphae and macroconidiae from the surface of the colony with acetate tape and microscopic examination with Lactophenol Cotton Blue (LPCB) stain. Culture on Mycoline agar slide is especially helpful when saprophytic contamination is expected.3% .1994). Camelvac Tricho@ (IDT Dessau-Tornau. in camels have been reported from Kazakhstan (Toleutajewa. Camels suffering and fungistatic agents such as iodine. and not all are caused by dermatophytes(Table 43). Germany)has been used in the Republic of Kazakhstan. coal tar phenols (3. from dermatophytoses were healed after 5% sulfur in sesame oil (w/v).5% 5 to 12-month-old Bactrians: 60. Successful vaccination programs against Trichophyton spp. 3. 105)were vaccinated once.1% 13-month to 3-year-old Bactrians: 17. Young dromedaries with ringworm Captan@is a fungicide for ornamental lesions (see Fig. but it causes side effects in camels such as nausea and diarrhea and is therefore not recommended (Schwartzand Dioli. The mixture is stable for one week after mixing and the solution should be applied to the lesions and surrounding areas for 2 weeks. A variety of common fungicidal for therapeutic purposes. 1992). as well as other fungi should be cultured on Sabouraud dextrose agar and on Mycoline agar slide (bioM&ieux) and incubated for 10 to 14 days at 27°C (Fig. it is also essential that stables and vaccinated with Camelvac Tricho@ and no equipment be properly disinfected. A number of keratin-proliferative dermatoses have been seen in camelids. 108). 1994). where 34. Treatment of dermatophytoses with griseofulvin is very effective in cattle (Coetzer et al. 1973) disappeared after 4 weeks. ringworm cases reoccurred for several Lesions should firstly be scrubbed clean years. and Trichophyton spp. plants.

Sabouraud. A. Clinical Findings and Lesions ElKhouly et al. cause mycotoxicosis and are involved in allergic reactions in humans (Quinn et a . Moldy litter and feed are often suspected as sources of infection in outbreaks of aspergillosis. growing molds with septate hyphae. TransOther Aspergillus species that occasionally mission is by inhalation and ingestion of cause infections include A .crobials or immunosuppressivesubstances mated that A .furnigutus. Pickett et al. (1992) reported a disease in racing camels in the UAE with a specific Aspergillosis spp. but may also cause mastitis and rumenitis. niger.. 1994). Pieces of tissue are gently pushed into the agar and the culture is incubated at 37°C for up to 5 days. 1989. fluvus. 1994) . Aspergillosis is especially found in patients debilitated by stress. The identification is done by colonial morphology and microscopic appearance of the fruiting heads.neoplasia. Aspergillus spp. 1994). Immunofluorescent procedures can be used to identify hyphae in tissue sections. and histopathologiwild species. niduluns. Many of the Aspergillus species produce colored colonies (black. Gareis and Wernery.. Aspergillus species can be invasive. Severo et al. are associated with infections of the respiratory system and of the placenta in livestock.Epidemiology IN1 A. Figure 109 Head of an Aspergillus species (after Quinn et at. 109). flavus is inli Tissue scrapings or any other volved in aflatoxicosis. malnutrition or Etiology ti(#'Several hundred species of As. For the isolation of Aspergillus spp. Aspergillus infections are found worldwide in almost all material can be examined directly with domestic animals and birds as well as many KOH microscopically.. l. Aspergillosis is an opportunistic fungal infection and has been reported in alpacas and dromedaries (Bhatia et al. particularly A . A . The colonies usually appear within 2 to 5 days of incubation. 1985. terreus and A. velopment of this fungal infection. dextrose agar is used.. 1983. The agar gel immunodiffusion test (AGID)for serum fungal antibodies is a reliable technique for diagnosis and an improved sensitivity may be possible with techniques such as ELISA. Prolonged exposure to antimipergillus have been described. 1992. but it is esti. furnigutus is an ubiquitous fungus and infection does not often occur in mammals.. are rapidly cal sections should be stained by the PAS stain.. fungal spores.. El-Khouly et al. A . furnigutus is responsible for can also play an important role in the de90-95% of Aspergillus infections in animals. metabolic acidosis. green or yellow) due to pigmented spores (conidia) (Fig.

A. (1983) reported pulmonary asperglcases of mycotoxicoses characterized by losis in a 9-year-old camel from India. body flucamels showed a slight increase in body ids and intestinal contents of necropsied temperature. nodes. In many cases was fed to breeding camels becoming there was a swelling of the throat with en. a cell-culture bioassay (MTT-test). Fusariurn and Scopulariopsis spealso developed bloody diarrhea. aflatoxin was also detected from aflatoxins in a number of milk samples tissues and sera.were concerned about the health hazard of mine whether these findings were due to a camel milk for humans. scribed by Wernery et al. Extracts of the hay samples. Some hay contained high numbers largement of the submandibular lymph (> lo8 CFU/g) of Aspergillus. granuloma in the lung of a breeding drornedary . In some of these Gadir (1991) found aflatoxin M1 and total cases.proper storage resulted in the hay which oped a mild. and conidia were demonstrated in direct Saad et al. (1992) as hemor.ulation to aflatoxins is kept at a minimum. some camels Alternaria. which was the first gatus was cultured from many organs of proven case of natural occurrence of this the dissected camels and fungal hyphae mycotoxin in feed.Elmaraghy (1996) reported aflatoxin conrhagic diathesis (see chapter Endotoxico. SubseConsistent necropsy findings in 40 camels quent analyses of the extracts showed the showed extensive bleeding into the intes.mycotoxin gliotoxin. hemorrhaging. severe watery diarrhea. The dis. Some animals devel. Penicillium. dry cough. (1989) and Osman and Abdelsmears from the lesions. However. In terminal cases. low Several nodules were found in the lung Figure 110 Aspergillus spp. to ensure that exposure of the human popA very similar disease has been de. Heavy rainfall and imand were lethargic.presence of the epidithiodioxopiperazine tines and into the internal organs. Gareis and Wernery (1994) described et al. Bhatia sis). the authors from dromedaries in the UAE. Death occurred 5 to 7 days camels proved to be highly cytotoxic using after the onset of the first clinical signs. fumi.Aspergillosis 247 respiratory and enteric syndrome. The authors claimed that it was not possible to deter. Affected cies. They stress the secondary infection with the fungus or need for continuous testing of camel milk were the primary cause of this syndrome.tamination of camel feed in Libya.white blood cell count and deaths in oneeased camels had a diminished appetite humped camels.moldy.

A necrotizing suppurative pneumonia was diagnosed and branching. Aspergillus niger pyogranulomatous pneumonia with bronchiectasis was reported in an alpaca by Muntz (1999). septate fungal hyphae were detected in the necrotic retina. Numerous abscesses were also scattered over the lung parenchyma. flucytosine. septate fungal elements that resembled Aspergillus species were seen. Drugs used have included thiabendazole. As a stressrelated disease. (1989) with dissemination causing small abscesses and multifocal areas of necrosis in lung. and amphotericin B. The alpaca was euthanized due to poor prognosis. niger was isolated along with high numbers of associated oxalate crystals. 111). Invasive aspergillosis in two alpacas was reported by Pickett et al. the morphology of the hyphae seen in histology sections was compatible with an Aspergillus species. Treatment and Prevention Ill! Treatment of aspergillosis has been unsatisfactory. prevention of aspergillosis can best be accomplished by minimizing factors that lead to stress.In both cases. large numbers of branching. but very little is known about their effect on camelids. It was presumed that the crystals had been produced by the fungus. This caused blindness associated with head tilt and intermittent circling. Gross post mortem examination revealed purulent material in the pulmonary airways from which A. (1992) and Manefield and Tinson (1996). spleen and kidneys. ciliary body and posterior lens capsule of one eye. An Aspergillus fumigatus rumenitis was diagnosed in the UAE in a guanaco suffering from impaction of the stomachs due to an inflamed diverticle obstructing the duodenum (Fig. The application of thiabendazole as an antifungal agent had no effect on the outcome of the disease in racing camels as experienced by El-Khouly et al. but no cultivation of the fungus was attempted.248 Funaal Diseases surrounded by dark colored consolidated pulmonary tissue containing semisolid caseous necrotic material. C. Figure 111 Aspergillus fumigatus rumenitis in a guanaco indicated by the black area in C1 . heart. (1985) and Severo et al. 110) were detected in a breeding dromedary in the UAE which had suffered from generalized camelpox for several weeks and which was treated with tetracyclines for some time. pyogenes was also isolated from the lung. In one of the cases. Aspergillosis granulomas some 5cm in diameter (Fig.

(most commonly C. Clinical Findings and Lesions al. swine and wild animals (Merck Veterinary Manual. 1991).glossitis in infants. horses.. the walls of C1 and C2 were thickened and Etiology lid Candidu albicuns is the usual agent of infection.Candidiasis (moniliasis) is a common sporadic disease of the digestive tract caused by the yeast Cundidu spp. Cundidu infection can also cause bovine mastitis and abortion. 1985)and cases in young dromedary calves in the UAE after prolonged treatment with antibiotics (Wemery et al. 2000. ulbicuns). Dissemination from the intestinal tract to other organs may OCCUI: Infections are more common in young animals and often follow some predisposing factors.. Epidemiology air The isolation or demonstration of C. The disease has been described worldwide in poultry. but other yeast-like species have been identified. ulbicuns is a commensal of the mucous membranes of Figure 112 Yellow pseudomembrane of the small intestine of a camel calf with candidiasis . cats. the intestinal and genital tracts of humans and many animal species. (1985) reported a neonate llama that had developed a yellowish diarrhea. Transmissionof this fungus may be via ingestion of contaminated food or water. mycosis of the oral mucosa (thrush). in press) have been reported. c. A Cundidu infection of a dromedary calf's skin was also observed (not published). dogs. or extended immunosuppressiveor antibacterialtherapy. The development of candidiasis often follows some predisposing factors such as malnutrition. despite antibiotic treatment and electrolyte therapy it died 5 days later. Therefore it is sometimes rather difficult to relate this fungal infection to a disease. ulbicuns from mucous membranes or tissue sections should not lead to a false diagnosis of candidiasis. Cell-wall glycoproteins seem to possess an endotoxin-like activity. In many cases C. albicuns belongs to the normal flora of the digestive tract. skin infections and vaginitis. One case of gastric candidiasis in a neonatal llama in Europe (Hajsiget al. It is known that C. On necropsy. ulbicuns is not very pathogenic.

perfringens rods Figure 114 Histology of the infected mucous membrane invaded by C. the epithelium of the mucous membranes was necrotic and invaded by masses of pseudohyphae and budding yeast cells. but variable amounts of sand and water were seen in the abomasum. Smears taken during necropsy from the intestinal mucosa showed C. On necropsy.250 Fungal Diseases edematous. albicans . (2000. A white-grayish pseudomembrane several millimeters thick was diagnosed. perfringens organisms (Fig. Microscopic investigation showed necrosis of the mucous membranes invaded by yeast Figure 113 Direct smear from the intestine of a camel calf with candidiasis showing C. in press) who reported candidiasis in 8 to 48 hour-old dromedary calves in the UAE. albicans and C. 113). 112). These calvesdeveloped yellowish diarrhea. Similar clinical findings and lesions were found by Wernery et al. Microscopically. albicans budding yeast cells and C.There was no milk in their digestive system. yellow pseudomembranes were found in the small intestines (Fig.

invaded by masses of C. 118). The authors could prove that the calves possessed very low levels of copper and therefore had ingested sand with which they took up clostridial spores. 117).Candidiasis 251 Figure 115 Multiple ulcers in the abomasum of a dromedary cells that were limited to the epithelial tissue (Fig. albicans invasion of the ulcers . perfringens enterotoxaemia. Figure 116 Histology of Figure 1 15 showing C. 115). 116). The same authors have also diagnosed a skin lesion caused by C. ulbicuns organisms (Fig. The 6-week-old camel calf had developed thick crusts near the hump in which hyphae were demonstrated with PAS stain (Fig. multiple ulcers have been observed in the abomasum (Fig. 114). In adult camels that had been treated with antibiotics over a long period. congolensis (see chapter Integument). ulbicuns (Fig. The lesions resemble infections caused by D. The dromedary calves had also developed a colisepticemia and some of them a C.

albicans can be cultured on Sabouraud's agar or ordinary agars. Giemsa or Gram stain. true hyphae may also be visible. The fungal organisms are well stained with LCBP. C. 3 to 6 mm in diameter) or occur in chains that produce pseudohyphae. but no reports exist concerning these drugs in infected . regular. Treatment and Prevention miconazole and ketoconazole have been recommended for intestinal C. like blood and nutrient agars. albicans infections in pigs and bovines. shiny and convex and grow within 24 to 72 hours. albicans are ovoid. albican5 hyphae from the skin of a camel ca If Fungal organisms were numerous in proliferatingtissue. and diagnosis can be made either by culture or examination of mucosal scrapings or tissue sections. albican5 Figure 118 C. C. The colonies are white. at either room temperature or 37°C.252 Funaal Diseases Figure 117 Thickened crusts near the hump of a dromedary calf caused by C. Filamentous. budding yeast ceUs (blastospores.

The camels did not receive any antibiotics. (Rhone Merieux). the camel mothers received copper and selenium treatment and the calves were given lOmL of an E. 20 mL of a C. . coli autovaccine orally. perfringens antiserum i. and proper mineral supplementation are crucial for the survival of young camelids. Prevention of candidiasis can best be achieved by minimizing predisposing factors. Optimal management of breeding herds. and 10mg StegantoxB (Schering-Plough Animal Health) i. twice within 24 hours. It is therefore essential to detect and to remove them.Candidiasis 253 camelids.v.v. including vaccination (see chapter Vaccination Program). In our cases.

NWC seem to be highly susceptible to this fungus.E. 1998). Clinical Findings and Lesions piratory form with dyspnea and coughing.Arthrospores are found in the infective stage and they convert into spherules in animal tissues.Fowler. a dimorphic fungus that is not transmitted from animal to animal. 1981). The life cycle of C. M. arid weather favors the survival of the fungus in the soil. with the dog being the most frequently infected animal (Wolf and Pappagianis.) immitis is the cause of coccidioidomycosis. Coccidioides (C. Muir (1982) reported on a llama with posterior paresis which was euthanized due to poor prognosis. USA) . In the USA.Infection has never been confirmed in Europe and Asia and seems to be en- demic in some areas of North and South America. (1992). immitis was isolated from these lesions.3.000 cases of infection and 70 deaths are estimated to occur annually in humans (Salfelder. There are no reports of coccidioidomycosis in OWC. creating an aerosol that can be carried for long distances. Figure 119 Lung granulomas caused by C. Infection is restricted to specific geographic zones where climatic conditions of hot. At necropsy. The disease is acquired by the inhalation of arthrospores from the environment. 1990). Coccidioidomycosis was described in llamas by Muir (1982) and Fowler et al.4 Coccidioidomycosis Coccidioidomycosisis a fungal infection of the respiratory tract of humans and animals and it may also appear in a disseminated form or as a dermatitis (Fowler. These aerosols are suitable for inhalation of arthrospores. 100. immitis (courtesy of Prof. disseminated visceral granulomas and an extradural pyogranulomatous mass compressing the spinal cord of T-10 were found. as well as the dermal form. have been described. Disruption of soil exposes the organism to winds. immitis has been described by Fowler (1998). C. The disease has been diagnosed in many animal species. with nodular lesions over most of the body surface.

. M.Coccidioidomycosis Figure 120 Thickwalled spherule filled with endospores (courtesy of Prof. The granulomas can range from 1 to 5 cm in diameter or coalesce into large masses. Avoiding dust is the only way to avoid infection with C. NWC characteristically roll in dry soil.E. Treatment and Prevention tericin B is the drug of choicebut with poor response in lamoids. The most sensitive and specific serological test used to date is the agar gel diffusion (Fowler et al. USA) 255 In the disseminated form. chloramphenicol agar. 119). or by microscopic observations of biopsies or during necropsies. immitis. every organ of the body might be infected (Fig. The fungus may be cultured on selective media such as cycloheximide- . Treatment of a llama with this drug over a period of 6 weeks did not successfully eliminate the disease or prevent transplacental passage of the organism to the fetus. agar gel diffusion. creating dust. but t i should be hs restricted to those laboratoriesequipped to handle dangerous infective cultures. fluorescent antibody or latex agglutination. The nodules are gray and firm and contain numerous spherules when microscopically examined (Fig. 1992). Fowler. Vaccines for lamoids have not been established as they have for humans and non-human primates. but this is extremely difficult to achieve. Diagnosis of coccidioimycosis can be made by serological tests like complement fixation test. 120).

Etiology lii There are 11 genera of the order Mucorales with 22 species. The most important genera are Mucor, Absidia, Rhizopus and Mortierella and the most pathogenic thermotolerantMucor spp. are now classified in a new genus: Rhizomucor. The disease produced by any of these genera is called "mucormycosis". These ubiquitous fungi are common inhabitants of soil, manure and rotting vegetation. Infections are secondary to other disorders and might cause granulomatous lesions in several organs of various animal species. Mucormycosis is particularly important as a cause of placentitis and abortion in cattle. Only one genus, Rhizopus spp., has been isolated from a llama (Fowler, 1998).
The llama suffered from a disseminated, multisystemic infection in

association with a facial paralysis of cranial nerve w. During the course of the disease, swallowing became impossible and the llama began to lose weight. An endoscopic examination of the nasal cavity revealed a black membrane with white patches.
Diagnosis M Mucormycosis can be diagnosed microscopically by demonstrating broad, branching, aseptate and irregular hyphae. Fungi can be identified in tissue sections by FA techniques with fluorescein antiglobulins specific for each genus of the Mucorales. In the reported case of the llama, filamentous growth was present on the surface of a necrotic rhinitis, the meninges on the ventral aspect of the brain were inflamed, and granulomas were present in the area of the cranial nerves.

3.6

Miscellaneous Fungal Infections

Table 44 Miscellaneous fungal infections in camelids Disease Oraanism Zygomycosis Conidiobolus (Entomophtho- coronatus ramycosis) Phycomycosis Histoplasmosis Cryptococcosis not mentioned Histoplasma capsula tum Cryptococcus SDecies llama llama dromedary dromedary vicuiia Clinical Sians chronic, eosinophilic dermatitis of the nose nodular dermatosis of external nares ulcers of abomasum miliar necroses of the lung meningitis and pneumonia Authors French and Ashworth (1994) Moll et al. (1992) Satir et al. (1993) Chandel and Kher (1994) Griner (1983)

Several other fungal infections have been described in OWC and NWC but they are rare. They are listed in Table 44. References
Abou-Zaid, A.A. 1995. Studies on ringworm in camels. 3rd Sci. Cong., Egyptian Society for Cattle Diseases, 3-5 Dec., 1995, Assiut, Egypt: 158-163. Ainsworth, G.C. and P.K.C. Austwick. 1973. Fungal diseases of animals. Znd ed. Slough: Commonwealth Agricultural Bureau. Al-Ani, F.K., L.S. Al-Bassam and K.A. Al-Salahi. 1995. Epidemiological study of dermatomycosis due to Trichophyton schoenleinii in camels in Iraq. Bull. Anim. Hlth. Prod. Afi. 43: 87-92. Bhatia, K.C., R.C. Kulshreshtha and R.K. Paul Gupta. 1983. Pulmonary aspergllosis in camel. Haryuna Vet. XXII: 118-119. Boever, W.J. and D.M. Rush. 1975. Microsporum gypseum infection in a dromedary camel. Vet. Med. Small Anim. Clin. 70 (10): 1190-1192. Chandel, B.S. and H.N. Kher. 1994. Occurrence of histoplasmosis-like disease in camel (Camelus dromedarius). Ind. Vet. J. 71 (5): 521-523. Chattejee, A., P. Chakraborty, D. Chattopadhyay and D.N. Sengupta. 1978. Isolation of Trichophyton schoenleinii from a camel. Ind. I. Anim. Hlth 17 (1): 79-81.

Coetzer, J.W.A., G.R. Thomson and R.C. Dustin. 1994. Infectious diseases of livestock with special reference to Southern Africa. Oxford University Press 2 pp. 1518-1535. : Curasson, G. 1947. Le chameau et ses maladies. Vigot Fr&es, Editeurs: pp. 86-88. Dalling, T. 1966. International Encyclopaedia of Vet. Med. Vol. I. Edinburgh Green and Son, London: Sweet and Maxwell Ltd I: p. 586. El-Kader, A. 1985. Studies on skin diseases of camels with special reference to mycotic causes and treatment in Assiut Province. M.V.Sc. Thesis, Fac. Vet. Med., Assiut University, Egypt. El-Khouly, A-Ba., F.A. Gadir, D.D. Cluer and G.W. Manefield. 1992.Aspergillosis in camels affected with a specific respiratory and enteric syndrome. Austr. Vet. J. 69 (8): 182-186. El-Tamawy, M.A., I. Seddik and M. Atia. 1988. Camel ringworm in Upper Egypt. Assiut Vet. Med. J. 20 (39): 54-59. Elmaraghy, S.S.M. 1996. Fungal flora and aflatoxin contamination of feedstuff samples in Beida Governorate, Libya. Foliu Microbiologica 41 (1):53-60. Fadlelmula, A., H. Agab, J.M. Le Horgue, 8. Abbas and A.E. Abdalla. 1994. First isolation of Trichophyton zlerrucosum as the aetiology of ringworm in the Sudanese camel (Camelus drornedarius). Rev. Elm. Mkd. vkt. Pays. trop. 47 (2): 184-187. Fischman, O., P.A. Siguera and G. Baptista. 1987. Microsporum gypseum infection in a

258

Funaal Diseases

grey wolf (Canis lupus) and a camel (Camelus bactrianus) in a zoological garden. MykoS ~ Y 30 (7): 295-297. I Fowler, M.E., D. Pappagianis and I. Irvin. 1992. Coccidioidomycosis in llamas in the United States: 19 cases (1981-1989). JAVMA 201 (10): 1609-1614. Fowler, M.E. 1998. Medicine and surgery of South American Camelids. Iowa State University Press, Ames. French, R.A. and C.D. Ashworth. 1994. Zygomycosis caused by Conidiobolus coronatus in a llama (Lama glama). Vet. Pathol. 31: 120-122. Gareis, M. and U. Wemery. 1994. Determination of Gliotoxin in samples associated with cases of intoxication in camels. Mycotoxin Research 1 0 2-8. Gitao, C.G., H. Agab and A.J. Khalifalla. 1998. An outbreak of a mixed infection of Dermatophilus congolensis and Microsporum gypseum in camels (Camelus dromedarius) in Saudi Arabia. Rev. sci. tech. Of.int. Epiz. 17 (3): 749-755. Griner, L.A. 1983. Camelidae. In L.A. Griner, ed. Pathology of 200 animals. San Diego Zool. SOC., Diego: 501-505. San Hajsig, M., T. Naglio, D. Hajsig and M. Herceg. 1985. Systemic mycoses in domestic and wild ruminants. I. Candidiasis of forestomachs in the lamb, calf, kid and newborn llama. Vet. Arch. 55 (2):53-58. Hollaender, H., W. Keilig, J. Bauer and E. Rothemund. 1984. A reliable fluorescent stain for fungi in tissue sections and clinical specimens. Mycopathologia 88: 131-134. Ivanova, L.G. and I.D. Polyakov. 1983. Trichophyton sarkisovii Ivanova and Polyakov sp. nov., a new species of the pathogenic fungus inducing dermatomycosis in camels. Mikol. fitopatologiya 17 (5): 363-366. Kamel, Y Y , . . M.A. Ahmed and A.A. Ismail. 1977. Dermatophytes in animals, birds and man. Animals a potential reservoir of dermatophytes to man. Assiut Vet.Med. 4 (7): 149-159. Khamiev, S.K. 1981. Camel ringworm. Buyll. Vses. Inst. Eksp. Vet. 42: 14-17. Khamiev, S.K. 1982. Epidemiology of ringworm (Trichophyton infection) among camels in Kazakhstan. Veterinariya9 42. Khamiev, S.K. 1983. Clinical symptoms of trichophytosis in camels. Rev. Med. Vet. Mycolog y 17 (1): 147 (abstract).

Kozlowska, E.A. and D. Nuber. 1995. Leitfaden der praktischen Mykologie. Einfiihrung in die mykologische Diagnostik. Blackwell Wissenschafts-Verlag, Berlin, Wien: pp. 44-57. Kuttin, E.S., E. Al-Hanaty, M. Feldman, M. Chaimovits and J. Muller. 1986. Dermatophytosis of camels. Rev. Med. Mycol. 24: 341-344. Mahmoud, A.L.E. 1993. Dermatophytes and other associated fungi isolated from ringworm lesions of camels. Folia Microbiologica 38 (6):505-508. Mancianti, F., R. Papini and P Cavicchio. 1988. . Dermatofizia da Microsporum gypseum in un Cammello (Camelus dromedarius). Ann. Fac. Med. Vet. Univ. Pisa 4: pp. 233-237. Manefield, G.W. and A. Tinson. 1996. Camels. A compendium. The T.G. Hungerford Vade Mecum Series for Domestic Animals: 240, 298. Marks, R., A. Knight and P. Laidler. 1986. Atlas of skin pathology. MTP Press Limited: pp. 36, 39. Merck, Veterinary Manual. 1991.The Merck Veterinary Manual. Merck and Co. Inc., Rahway, N.J., U.S.A.: pp. 342-343. Moll, H.D., J. Schumacher and T.R. Hoover. 1992. Entomophthormycosis conidiobolae in a llama. JAVMA 200 (7): 969-970. Muir, Susie. 1982. Coccidioidomycosis in the llama: Case report and epidemiologic survey. JAVMA181 (11): 1334-1337. Muntz F.H.A. 1999. Oxalate-producing pulmonary aspergillosis in an alpaca. Vet. Path. 36 (6):631-632. Nasser, M. 1969. The zoonotic importance of dermatophytes in U.A.R. PhD Thesis. Faculty of Vet. Med., Cairo University. Osman, N.A. and F. Abdel-Gadir. 1991. Survey of total aflatoxins in camel sera by enzymelinked immunosorbent assay (ELISA). Mycotoxin Research 7 35-38. Pickett, J.P., C.P. Moore, B.A. Beehler, A. Gendron-Fitzpatrick and R.R. Dubielzig. 1985. Bilateral chorioretinitis secondary to disseminated aspergdlosis in an alpaca. JAVMA 187 (11):1241-1243. Quinn,P.J., M.E. Carter, B.K. Markey and G.R. Carter. 1994. Clinical Veterinary Microbiology. Wolfe: pp. 381-421. Ramadan, R.O., A.A. Fayed and A.M. El-Hassan. 1989.Textbook of dermatology. Vol. 2. 4'h ed. Blackwell Scientific Publications, Oxford 2 (4):pp. 911-915.

Miscellaneoous Funaal Infections 259

Refai, M. and M. Miligy. 1968. Soil as a reservoir of Trichophyton mentagrophytes. J. Egypt. Vet. Med. Ass. 28: 47-52. Saad, A.M., A.M. Abdelgadir and M.O. Moss. 1989. Aflatoxin in human and camel milk in Abu Dhabi, United Arab Emirates. Mycotoxin Research 5: 57-60. Salfelder, K. 1990. Atlas of fungal pathology. Kluwer Academic Publishers: 101. Satir, A.A., M.I. Abu Bakr, A. Abalkheil, A.E. Abdel Ghaffar and A.E. Babiker. 1993. Phycomycosis of the abomasum in Camelus dromedarius. J. Vet. Med. Ass. 40: 672-675. Schwartz, H.J. and M. Dioli. 1992. The onehumped camel in Eastern Africa. A pictorial guide to diseases, health care and management. Verlag Josef Margraf. Severo, L.C., J.C. Bohrer, G.R. Geyer and L. Ferreiro. 1989. Invasive aspergillosis in an alpaca (Lama pacos). J. Med. and Vet. Mycol. 2 7 193-195. Singh, M.P. and C.M. Singh. 1969. Mycotic dermatitis in camels. Ind. Vet.J. 46 (10):855. Toleutajewa, S.T. 1994. Widerstandsfahigkeit des Erregers der Trichophytie der Kamele in der Umwelt und vergleichende Aktivitat von Vakzinen bei dieser Erkrankung. Thesis, Russische Akademie der Landwirtschaftswissenschaften, Moskau. Torky, H.A. and H.A.S. Hammad. 1981. Trichophytosis in farm animals and trials for treatment. Bull. Anim. Hlth. Prod. Afr. 29 (2): 143-147. Wernery, U., H.H. Schimmelpfennig, H.S.H. Seifert and J. Pohlenz. 1992. Bacillus cereus

as a possible cause of haemorrhagic disease in dromedary camels (Camelus dromedarius). Proc. lst Camel Conf. In: Allen, W.R., int. A.J. Higgins, I.G. Mayhew, D.H. Snow and J.F. Wade, R. and W. Publications, Newmarket, UK 51-58. Wernery, R., M. Ali, J. Kinne, A.A. Abraham and U. Wemery. 2000. Mineral deficiency: a predisposing factor for septicemia in dromedary calves. Proc. o 2nd Camelid Conf. Agroeconomf ics of Camelid Farming, Almaty, Kazakhstan, 8-12 Sept 2000, in press. Wilson, R.T. 1998. Camels. The Tropical Agriculturalist, MacMillan: 106. Wolf, A.M. and D. Pappagianis. 1981. Canine coccidioidomycosis-treatmentwith new agent. Cal$ Vet. 5: 25-27.

Further reading
Abdel Samed, G.H. 1983. Yeast flora in the digestive tract of the one-humped camel. Thesis, Faculty of Vet. Sci. University Khartoum, Sudan. Connole, M.D. 1990. Review of animal mycosis in Australia. Mycopathologica. III (3): 133-164. Glawischnig, W. and D. Khaschabi. 1999. Generalisierte Aspergdlose bei einem juvenilen Alpaca (Lama pacos). Wen. Tiearztl. Mschr. 86: 317-319. Holmes, L.A., N.W. Frame, R.K. Frame, J.P. Duff and G.C. Lewis. 1999. Suspected tremorgenic mycotoxicosis (ryegrass staggers) in alpacas (Llama pacos) in the UK. Vet. Rec. 145 462-463.

Vaccination Programs

Vaccination Proarams 263

The methods of reducing infection of economically important animals include a wide range of management practices, such as testing and slaughter, hygiene and sanitation and immunization. Preventing and controlling a large number of animal diseases by immunization is probably the outstanding achievement of veterinary medicine in the last century. Although it is impossible to give exact schedules for each vaccine, certain principles are common to all methods of active immunization.As maternal antibodies may passively protect newborn animals, vaccination is usually not successful early in life. If immunity is necessary for newborn animals, the dam should be vaccinated during the latter stages of pregnancy. The vaccination should be timed so that peak antibody levels are reached at the time of colostrum production. Successful active vaccination is usually possible only after passive immunity has waned. As the exact

time of maternal immunity loss cannot be predicted, young animals must be vaccinated at least twice to ensure successful immunization. Very little is known about the efficacy of vaccines in camelids. In the United States of America for example no vaccines have been approved for use in camelids (Fowler, 1998). However, Fowler (1998) and Mayr (1998) recommend some vaccines in NWC. The following vaccine programs for viral, bacterial and fungal diseases are based on their recommendations and our own experience (Tables 45 and 4 ) 6. References Fowler, M.E. 1998. Medicine and surgery of South American Camelids. Iowa State University Press, Ames. Mayr, A. 1998.Nutzung des Immunsystems fur die Schutzimpfung und Paraimmunisierung von Neuweltkameliden. Lamas, Haltung und Zucht 6 (2):14-23.

Table 45 Vaccination reaime for Carnelidae against bacterial diseases Booster after 4 weeks after 4 weeks annual Particularities hyperimmunserum in suspected cases autovaccine with local strains hyperimmunserum 100 mL i.v. in endangered areas

Disease
1" vaccination at the aae of 2-3 m o n t h s

Vaccine Repeated vaccination 1-3 years

Tetanus (C/. tetani)

toxoid vaccine

Enterotoxemia (Cl. perfringens A,B,C,D)

toxoid and bacterial vaccine

1-2 months 1-2 months
after 4 weeks annual

Gas edema complex (Cl. chauvoei, septicurn, novyi)

toxoid and bacterial vaccine

Anthrax (C/. anthracis)

live attenuated

2-3 months
-

annual

in endemic areas autovaccine for young calves

E. coli diarrhea

inactivated oral application (doses > 1O"JCFU) 20-50 mL

for 1 days 0

annual

E. coli diarrhea

inactivated parturition oral application 20-50 mL for 1 days 0 parturition

6 weeks before

2 weeks before

autovaccine for pregnant camels

Salmonellosis

inactivated (doses > 10'0 CFU)

annual

autovaccine for young calves autovaccine for pregnant camels

Salmonellosis

inactivated parturition

6 weeks before
2 months

2 weeks before
parturition after 4 weeks

Leptospirosis

inactivated appropriate serovar

4 months

in endemic areas with appropriate strains

Table 46 Vaccination regime for Camelidae against viral and fungal diseases
1" vaccination at the age of

Disease 3 months after 3 weeks in endangered areas, Rabisin"

Vaccine

Booster

Rabies (Rhabdovirus)

inactivated cell culture virus

Repeated vaccination annual

Particularities

Camelpox (Orthopoxvirus) 1-2 weeks after 6 weeks
6-8 months

attenuated cell culture virus Turkey

6-9 months

after 4 weeks

life-long immunity?

commercial - South Africa, Ducapox

Ecthyma contagiosum (Parapoxvirus) for treatment 3timesevery 5 days with increased doses after 2 months annual

attenuated cell culture virus

Papillomatosis (Papovavirus)

inactivated Papilloma tissue

-

autovaccine

BVDIMD (FlavilPestivirus)

inactivated vaccine

2-4 weeks

in areas with MD abortions

Neonatal viral diarrhea (Rota, Corona) 8-12 weeks after 3-4 weeks

inactivated vaccine

4 and 2 weeks before delivery

annual

if required

Equine Herpes (E HV-1) 4 months also for treatment after 14 days

inactivated vaccine

annual

if required

Dermatophytoses (Ringworm)

Trichophyton verrucosum, attenuated

?

commercial - Camelvac Tricho, IDT, Dessau, Germany

Parasitic Diseases .

Schistosoma Oesophagostomum Chabertia Sktjabinema Thrichuris Trypanosoma Dipetalonema Trichostrongylus Nematodims Nematodirella Cameleostrongylus Bunostomum Moniezia Stilesia Avitellina Thysaniezia Eimeria Cryptosporidium Paramphistomum .Parasites of Old World Camels The organ localizationof parasites of the OWC is illustrated below.

Tnchostmngylus Oesophagostomum Chabertia Skjabinema Thrichuris Dictyocaulus Hydatid cysts Stmngyloides Cameleostrongylus 6unostomum Moniezia Thysaniezia Ticks (Argasidae & Ixodidae) Microthoracius (blood-sucking lice) Damalinia (biting lice) Paramphistomum Haemonchus .Parasites of New World Camels The organ localization of parasites of the NWC is illustrated below.

wool and fibers. Lima. Tom0 V.400 337.502. For example in the 1970s.7 11.0 Total 1. The economic losses due to parasitic infections can be substantial. meat.1 100.4 0. as well as transport.3 22.911 1.5 million (Table 47).Parasitic Diseases 271 Parasitic infections may significantly limit the productivityof camelids and other livestock by causing a substantial reduction in the provision of milk.555 296.489 % of total 46. Table 47 Estimation o f annual losses of meat due t o parasitic infections in alpacas in Peru Disease Parasitic pneumo-gastroenteritis Ectoparasites Sarcocystiosis Fasciolosis Hvdatidosis losses ($US) 695.02 million head of alpacas in Peru was more than $US 1. Cited by Leguia (1991) . Many conditions are of a subclinical nature.5 19. 1973.1 77 Source: Ministerio de Agricultura.822 170. Estudio de la Evaluacion de Problemas de Carnes en el Peru. the estimated annual loss in meat from 3.

(NWC. act as a source of protein for the host.1 ruduu Protozoal Infections Introduction The protozoal infections of camelids are listed in Table 48. the nuclear apparatus of protozoa is not separate from the cytoplasm. brucei (OWC) T. evansi (OWC) T.5. Balantidium coli Eimeria spp. Their genetic information is stored in chromosomes contained in a nucleus that is surrounded by two membranes containingseveral pores. Sarcocystis spp. Golgi apparatus and lysosomes. mitochondria. 5. The meta- bolic by-products are excreted by diffusion through the cell membrane. simiue (OWC) T. although the genus Typunosomu has a single flagellum. Additionally. Besnoitia spp. as does Buluntidium. As a means of locomotion.1 Classification of Protozoa Regnum Protozoa Phylum Sarcomastigophora Subphylum Mastigophora (Flagellates) Order Kinetoplastida Typanosoma spp. Entamoebu uses pseudopods that are prolongations of the cytoplasm. These pseudopodia also have phagocytic properties.1. brain Intestinal tract Multiple organs ? . T. Protozoa are eukaryotic organisms. for locomotion. Toxoplasma gondii Neospora caninum + + + + + + + + + + + + -I + Blood Genital tract Intestinal tract Intestinal tract Intestinal tract Intestinal tract Muscle. e. These are commensal or symbiotic organisms that assist in the digestion of cellulose and. e.g. other protozoa may have several. Cryptosporidium spp. congolense (OWC) T. Besides the nucleus. OWC) Table 48 Protozoa of camelids Disease Protozoa Occurrence OWC NWC Location Trypanosomosis Trichomonosis Giardiosis Balantidiosis Coccidiosis Cryptosporidiosis Sarcocystiosis Besnoitiosis Toxoplasmosis Neosporosis Trypanosoma evansi Tritrichomonas foetus Giardia spp. after having passed the abomasum. Among the protozoa are many species that are not parasitic. those found in the rumen. cruzi (NWC?) Order Trichomonadida Tritrichornonusfoetus (OWC) Order Diplomonadida Giurdiu sp.g. the protozoa possess certain other structures with distinct features and functions. Nutrition of the protozoa occurs mainly by pinocytosis or phagocytosis. In contrast with the prokaryotic cells of rickettsiae and certain algae. Movement occurs as some of the cytoplasm flows into the prolongation. vivux (OWC) T. they possess an endoplasmic reticulum. Some protozoa move by means of cilia.

cumeli (OWC) S. pellerdyi (OWC) E. Leese. T. tilopoidi (NWC) Family Toxoplasmatidae Besnoitiu sp.Protozoal Infections 273 Phylum Apicomplexa (Sporozoa) Class Sporozoea Subclass Coccidia Order Eucoccidiida Family Eimeriidae Eimeriu ulpucue (NWC) E. 1917. uucheniue (NWC) S. 1987. lumae (NWC) E. T. (OWC) Family Sarcocystidae Sarcocystis spp. vivux failed. and isolated from camels in Kenya (Roettcher et al. confirming the susceptibility of camels to this pathogen (Mihok et al. peruviunu (NWC) E.1979).2 Trypanosomosis Trypanosomosis is a disease of humans and animals caused by parasitic trypanosomes. punoensis (NWC) E. The trypanosomes of mammals are subdivided into two sections: the Stercoraria and the Salivaria. The response to infection with T. simiue was identified as the cause of an outbreak in dromedaries in a Kenyan national park. Their attempt to infect three camels intravenously with two different strains of T.. 1948). based on the mode of development in their insect vectors and vertebrae hosts.. vivux (Bennett. where camels may contract tsetse-transmitted trypanosomes. At necropsy. T. 1927. They are further divided into subgenera and species on the basis of morphological differences. (1985) experimentally confirmed that dromedaries were sensitive to T. buctriuni (OWC) E. 1994).. infections may also occur with T.This parasite described by Evans was the first recognized pathogenic mammalian trypanosome. congolense. in Africa. (OWC) Theileriu sp.1. T. simiue was also documented as a camel pathogen in Somalia (Pellegrini. rujusthuni (OWC) Family Cryptosporidiidae Cryptosporidium sp.NWC) S. However.(OWC. macusuniensis (NWC) E. brucei was milder.. However. Richard. The parasite is widespread throughout tropical and subtropical areas. cumeIi (OWC) E. congolense. auburnensis (NWC) E. parasitemia persisted throughout the three months of observation and the only changes seen were an ini- . NWC) Neosporu cuninum (OWC?) Hurnrnondiu heydomi (OWC) Sublass Pirosplasmia Order Piroplasmida Bubesiu sp. (OWC) Isospora cumeli (OWC) I. orlovi (OWC) Toxoplusma gondii (OWC. (OWC) Phylum Ciliophora Order Trichostomatida Buluntidium coIi (OWC) 5. Haerter et al. 1994). dromedurii (OWC) E. Dirie et al. brucei and particularly to T. The most important protozoal disease of camels is trypanosomosis (named surra). caused by Ttypanosomu evunsi (Cross. brucei. congolense resulted in an acute disease that led to death between days 22 and 37 with fever. simiue (Mihok et al. an experimental infection with T. progressive edema and general weakness. 1989). 1975. 1933)and T. serous fluid was found in the body cavities and hemorrhages on the serous membranes.

having a prominent undulating membrane and a long. It is hypothesized that T. evunsi infections in tigers. evunsi in 2000 camels was 48% (Olaho and Wilson. evunsi may affect many different species of mammals. 1983) and 79% in a smaller herd comprising 174 camels (Rutagwenda. and orangutans (Molyneux and Ashford. evunsi and T. T. and 7. pigs and Indian elephants as a mild or subclinical infection.2pm wide (Fig. 1992). donkeys. Occurrence ifti Surra is found within a wide range of climate and vegetation zones in Asia. evunsi originated from T. camels. 15-36 pm long (mean 24 pm) and 1. equiperdum based on biological. tapirs. biochemical and molecular studies. ences between the two species. equiperdum.274 Parasitic Diseases tial rise in fever and declining packed cell volume values. 58% of camels were found positive (Caille. foxes. Just north of this belt the prevalence of surra in camels is roughly estimated at between 15 and 20%. 1984). Central and South America and usually outside the tsetse belt in Africa. The disease was originally reported in India in 1880 and is most severe in horses. the Far East. In Kenya. the most prominent differences are the presence of maxi-circles in T. Morphologically it is indistinguishable from the long and slender form of T. In addition there have been reports of T. and the route of transmission. dogs and cats. 121). the prevalence of the infection was 2550% in 948 dromedaries (Bitter. However. Only few reliable data exist on the distribution and seasonal prevalence of the disease in endemic areas. deer. Occasionally it occurs in sheep. mules. evansi parasites in dromedary blood . 1987).2 to 56% depending on the diagnostic methods used (Baumann and Zessin. 1957). llamas. goats. (1998) in a review confirmed the many similarities between T. the prevalence of T. the Middle East.5-2. In Sudan. free flagellum and a small sub-terminal kinetoplast. 1986). In Somalia. which are missing in T. An epidemiological survey in Mo- T. brucei. evunsi is one of the salivarian trypanosomes. 1983). Brun et al. In the host's blood it most often occurs as monomorphic trypanomastigote. Electron microscopic investigation revealed no ultrastructural differ- Figure 121 Two T. evunsi. brucei by adaptation to a non-cyclical mode of transmission and loss of ability to undergo growth and differentiation in the fly vector (Hoare.

1998). subclinical infections and which often coexist with camels. Smears obtained from the larvae contained the epimastigote stage.. The main vectors involved are tabanids and Stomoxys (Molyneux and Ashford.. The shorter the interval between two feeds the greater the chance of successful transmission. 1967). on the interval between a fly feeding on an infected host and moving to a clean host. Eating parasitemic animal meat can infect carnivores. surra was diagnosed in Port Hedland. and 5 to 6 h in the gut of Muscidue flies (Rutter. Two endemic foci were identified in the south of the country affecting sedentary camels husbanded in small groups. The infected camels were destroyed and since then no further evidence of the disease has been seen in Australia. 1967).). transmitting the trypanosomes through its saliva. In Mauritania the prevalence varied between 1.As prevalence data are based on different tests which differ widely in sensitivity. Several biting or blood-sucking insects may serve as vectors. i. The aggressive feeding behavior of tabanids involves many attempts at feeding. 1998).2-25. might act as reservoirs. No cyclical development occurs in these flies in contrast to other salivarian trypanosome infecting tsetse flies. evunsi is transmitted mechanically by blood-sucking flies. In addition it may act as a reservoir. these figures should only be regarded as rough estimates (Butt et al. and 16.8% (Guitierrez et al. 2000). The infectivity of a fly is highest within minutes of feeding and decreases quickly with no transmission at all if the interval exceeds 8 hours (Losos.2% using different serological tests (Dia et al. 1947). O n the Canary Islands 7 out of 745 dromedaries yielded T. Other insects may also transmit the parasite. In South and Central America. the vampire bat (Desmodus rotundus). However. the vampire bat (Desmodus rotundus) can be infected from blood meals and then act as a vector. Experimentshave shown that the vomit from lapping flies that have fed on parasitemic blood and exudates caused by biting flies can be infective to laboratory rodents. The trypanosomes remain in the mouthparts of the fly. Transmission i84l T. evunsi in cattle and horses (ma1 de caderas) and in some wildlife species such as the capybara (Hydvochoerus).Protozoal Infections 275 rocco during 1996-1999 revealed a prevalence of 6. In 1907. Hilali and Fahmy (1993) reported large numbers of Cephalopinu titillator larvae in the nasal cavities of dromedaries in Egypt infected with two different sizes of epimastigote trypanosomes thought to be T. Huemutobiu and Hypoboscu (Rutter..3%employing blood smear examination. 1983). the ocelot (Felis purdulis) and deer (Odocoileus spp. Western Australia. evunsi. The para- . Trypanosomosis has not been reported in camelids in South America despite the presence of T. 2000).g. which was always observed in a dividing state. Mechanical transmission by contaminated hypodermic needles is also a potential means of transmission. al- though they are considered to be of less importance. 1983). In the 188Os.e. Lyperosiu. which have only mild. surra spread from Asia into European Russia. 1980). where it killed an estimated 70%of the camel population (Molyneux and Ashford. The trypanosomes remain alive in the mouthparts of some insects for not more than 15 seconds (Curasson. 1997). as the trypanosome has a restricted survival time in the vector. e. Other domesticated species like sheep and goats. trypanosomes have been demonstrated in llamas imported into the USA (Fowler. evunsi.. The efficacy of transmission depends on the interrupted feeding behavior of tabanids. Individual flies can therefore infect more than one host. but as long as 44 h in the gut of tabanids.6% (Atarorhouch et al. Mice and guinea pigs inoculated with the epimastigote form showed no parasites in their blood. while the seroprevalence was 4.

In chronic cases. Seiler et al. Calves may be weak at f l ul term. Death may take a few days or months. sheath and scrotum and on the legs up to the knees and hocks. Clinical Pathology 1% The anemia is macrocytic and hemolytic. the development of the biting fly populations after rain. It is assumed that parasites hide in the meninges where they might survive for a long time. chest wall. The chronic form of the disease leading to wasting and anemia is more common in camels. 1998). e. but are also observed in other causes of encephalitis (Salfelderet al. petechiae are seen on serous surfaces and within liver and kidney parenchyma. In most of the subacute and chronic cases. thus making animals more susceptible to other infections which may complicate the clinical picture. 1998). Surra has a marked seasonal pattern in some areas in association with wet conditions. mules and dogs was found to be pathogenic to sheep and goats (Mahmoud and Gray. However. 122). perivascular cuffs in the gray matter (Fig. An experimentally infected guanaco developed the subacute form of surra showing edema and wasting (Kinne and Wemery. Subacute infections occur with fever. SiEnilar structures are also found in the large infiltrates on the cauda equina. eventually ending in emaciation and death. premature birth and reduced milk production. It can cause abortion. emaciation and high mortality. Some camels may recover spontaneously. it is common to see severe hemorrhages on the cauda equina. 2000). 1980). In subacute cases in camelids. Edema and paralysis may also develop. Pathology iik Gross lesions in the camel are not very specific. Ascites and hydrothorax may be present and the lymph nodes are enlarged. Some other factors that may predispose to patent parasitemias are stressful climatic conditions and poor nutrition. mild to moderate nonsuppurative meningitis and focal meningoencephalitis are found.276 Parasitic Diseases site isolated from naturally infected camels. Acute cases often show signs of recurrent fever accompanied by progressive anemia and poor general condition. The edema varies from plaques on the neck and flanks to edema of the muzzle. this was shown not to be the case in Sudan where the infection was more prevalent during the dry rather than wet season (Elamin et al. In acute and subacute cases. More pathognomonic in camelids are the histological lesions in the central nervous system.These structures represent “Russel or Mott bodies” and are characteristic of human African trypanosomosis. There is a decrease in erythrocytes and an increase in lymphocytes. 123).In horses. subacute or chronic. 1992). Typical are broad. A few scattered petechiae are found in the edematous meninges of the cerebellum and brain stem. with a mortality of up to 90%. Clinical Signs + Surra may be acute. eosinophils and monocytes. horses. edema... (1981) described these structures as ”morular cells”.g. the disease can vary between individuals: some die within a few months following the infection while others develop chronic or subclinical conditions lasting two or more years. The infection is also accompanied by progressive .. Immunodeficiency may be a sequel to surra. In an infected herd. evading treatment. Eosinophilic. the carcass is anemic and often emaciated. PAS-positive ”corpuscular structures” in the meninges are often observed (Fig. Tabanid flies are more abundant early in the dry season in Sudan (Elamin et al. and camel herds congregate in larger numbers at the few available water holes facilitating efficient transmission of the trypanosomes by flies. Many infected camels have a mild and protracted infection that can persist for several years.

In acute trypanosomosis. a monocytosis of up to Figure 123 Eosinophilic PASpositive structures ("Russel bodies") caused by trypanosomosis . whereas the total white blood cell count was elevated. there are changes in some serum enzymes resulting in an increase in sorbitol-dehydrogenase and glutamate-pyruvate-transaminase as well as glutamate-oxalacetate-transaminase (Boid et al. a decrease in albumin.. In addition. an increase in y-globulins and a five-fold increase of IgM levels during the course of the infection (Boid et al. packed cell volume. 1980).Protozoal Infections Figure 122 Nonsuppurative meningoencephalitis caused by trypanosomosis. Hemoglobin. red blood cells and iron were sign&cantly decreased. Similar results were obtained from dromedaries with subacute trypanosomosis. Wernery (1995) compared blood parameters and iron of racing camels with chronic trypanosomosis with reference values (Table 49).. note the cuffing 277 changes in the serum protein concentrations. 1985).

These im- prove the chances of demonstrating trypanosomes in the blood of infected animals with fairly low parasitemia. particularly in the chronic and subclinical stages.08 17.0-13. This technique is easy to carry out in the field by a battery-poweredMHC. Other methods for detecting very low parasitemia include the miniature anion exchange centrifugation technique (Lumsden et al. A reliable diagnosis can be made on the basis of the demonstration and identification of trypanosomes in the blood. there are techniques for concentrating the blood samples.500 g in a microhematocrit centrifuge (MHC). Confirmation of a tentative diagnosis in the field is still largely carried out by relatively insensitive methods such as examining wet.2 WJdL 15% was observed during the first four weeks of the disease. Clinical signs such as emaciation and anemia (PCV < 25%) (Table 49) are often used as a provisional diagnosis. Trypanosomosis can be confused with any other chronic wasting disease. 1971).1981)and the silicone centrifugation technique (Ogbunde and Magaji. PW) Red Blood Cells (RBC) White Blood Cells WBC) Iron (Fe) * Wernery et al.5-12.54 17. The interface between the buffy coat and the plasma should be examined for motile trypanosomes under a microscope (Woo. It may be difficult or impossible to find trypanosomes in the blood of an infected animal.5 21 26-38 7. . There are no real pathognomonic clinical signs of infections with T..75 16.32 18. The latter technique was shown to be as sensitive as the above-mentioned concentrationmethods and has the advantage of being simple and rapid (Nessiem. 1969. 1983). thin and thick blood films. the buffy coat and the plasma. notably helminthosis and malnutrition.87 5. 1994).2 7. However. (1999) gldL % x 1 6 pL 0 x lo3 pL 1. although that may be difficult due to the often low and fluctuating parasitemia. The most applicable and commonly used in the field is the microhematocrit centrifugation technique (MHCT). The severity of an infection is not necessarily related to the number of parasites seen in the blood. The parasites in the blood of the vertebrate host are often scarce. but are unsatisfactory when considering successful measures of control. which can also be run by a car battery. 1982).278 Parasitic Diseases Table 49 Blood parameters and iron of racing dromedaries with subacute and chronic trypanosomosis Blood parameters Unit Reference values* Camels Camels with chronic with subacute trypanosomosistrypanosomosis Hemoglobin (Hb) Packed Cell Volume (Hematocrit.2 20. even when it is in the moribund state. Parasitological techniques applied for demonstrating trypanosomes in the blood are only successful in 50 to 60% of infected camels. evunsi. The buffy coat may also be examined as a wet preparation on a microscope slide. Microhematocrit tubes are filled with fresh blood and spun at 2. The MHCT can detect trypanosomes in camel blood 6 to 10 days earlier than in wet or thick blood films (Kelley and Schillinger.2 54.5 87-1 35 9. Trypanosome species can be identified in a fresh preparation or after Giemsa staining.0 6. Woo. 1979. The centrifugationseparates the blood into three different layers: the packed red blood cells.4 6.

brucei (Godfrey and KillickKendrick. evunsi in animals. Another agglutination test also available is the modified card agglutinationtest (CATT/ T. 1989). Even the improved indirect fluorescent antibody test (Luckins et al. Boid et al. One major reason for this is the constant antigen variations that occur in T. 1994). evunsi antibodies (an indirect hemagglutination test) was developed by Jaktar and Singh (1971). evansi (as in other salivarian trypanosomes) (Jones and M c h e l l . However. A simpler test established for use under field conditions was the latex agglutination technique (Suratex@) (Nantulya. evansi in a serological survey of Kenyan camels. The antigenic variation is also a major constraint for immunoprophylacticcontrol methods. evunsi (Schoening... expensive and inappropriate for use in large-scalesurveys. 1984. Kenya 1996). which was initially developed for T. non-specific antibodies. T.Evaluation of the performance: Proc. this method is time-consuming.. thereby complicating the interpretation of positive results when other salivarian trypanosomes are present. This test is not specific to T. Wuyts et al. the present ELISA has proven to be unsatisfactory in sensitivity as well as specificity (Antigen ELISAs for trypanosomosis . 1992. evunsi antibodies but can also detect antibodies to other salivarian trypanosomes. The development of enzyme immunoassays (ELISA)detecting circulating antigens in animal sera provides an opportunity for an early diagnosis of trypanosomosis. 1987). these tests are non-specific and have yielded many inconsistencies (Luckins et al.. Nantulya et al. 1984). 1994). while pastoralists still traditionally diagnose trypanosome infectionsby the smell of the infected animal's urine. evansi). 1976) measure an increase in the level of serum globulins. However... Nairobi. Schoening described a complement fixation test demonstrating antibodies to T. Despite improvements in parasitological techniques for the detection of trypanosomes. 1962). this assay also had difficulties with the standardization of antigens and the presence of interfering. In the diagnosis of surra. evansi (Boid et al. (1983) successfully used this assay to demonstrate antibodies to T. However. 1985) and T. .. a high proportion of infections are never detected. Wilson et al. 1978) had inherent drawbacks. However. Another promising assay for the diagnosis of T. antibody techniques like flocculation assays (including the formol gel and mercuric chloride tests) (Pegram and Scott. This phenomenon makes it difficult to detect circulating antigens and antibodies . wellequipped laboratories may more efficiently use DNA-amplification technologies in the diagnosis of T. brucei gumbiense (Dialli et al. evunsi antigen may also be detected in blood by the polymerase chain reaction (PCR) (Masiga and Gibson.a tremendous advantage for the parasite. and procedure standardizationis not possible.This test has never been routinely used as a diagnostic test because it is too difficult to perform. Development of patent parasitemia is 5 to 9 days in mice and 3 to 9 days in rats.As early as 1924. The development of an enzyme-linked immunosorbent antibody assay (ELISA) was a major breakthrough. 1979. The identification of circulating variable antigen types (VSG) would be of great value in developing more sensitive diagnostic tests. Mouse or rat inoculation increases the number of camels found positive by approximately 50% compared with blood film techniques (Molyneuxand Ashford. keeping it ahead of an attack by specific antibodies directed against the previous surface antigens. 1983). Workshop ILRI. 1924). In the near future.Protozoal Infections 279 Inoculation of laboratory rodents with blood from suspected infectious camels is a very sensitive method for detecting low parasitemia caused by T. This was an important breakthrough in the diagnosis of this disease (Rae and Luckins. 1980).

not all compounds effective against T. fers significantly among different species.280 Parasitic Diseases alone will not have a permanent effect on the cycle of the disease. Atadrugs..5%in 1990 to 2. 12mg/kg by slow intravenous injection is Monitoring for drug resistance is impor.5% in 1999) due to the treatment of positive cases (by the use of antibody ELISA) and the control of vectors (CVRL Annual Report. Treatment and Control Only a few 1992).. 1993.Antibody responses to T. The prevenbe employed when suspicion of resistance tive effect depends on the dosage used and arises. Also. 1978). Merial). Veriben@. where surra in dromedaries is endemic. 1979. This meant that only one is especially true for camelids due to their curative drug remained available for camunique physiological characteristics. 1989. Leverkusen. Triquin@(quinapyramine sulfate.Germany . Boid et al. AntrycideB and been approved by appropriate authorities Antrycide@ Pro-Salt. the degree of the trypanosome challenge Surra is endemic in most countries (Luckins.still used in the treatment of camels. Chemotherapy the tissues may cause phlebitis. munsi (Schillinger and Roettcher. The use of chemotherapy is often inadequate: e. however. and Sanofi@ (Rommel. the effectiveness of also applies to the use of vaccines.. the dependence on trypanocidal drugs for the control of surra is alarming. 1989).5mg/kg and should not be used in dromedaries. however. evunsi infections may vary and the levels may stay high for a considerable time after effective treatment (Luckins et al. at that time the comfor use in OWC or NWC. Antibodies to T. Leakage of the drug into where camels are reared. in use since 1925. there are only very limited pharmacoki.g. which is toxic to camels at doses of >3. 1984). This nearly 75 years of use. munsi infections in camels as demonstrated by ELISA do not differentiate between acute and chronic infections (Rae et al. evunsi are suitable for use in camels. diminazene aceturate (Berenil@. Imperial Chemical Inhardt Ltd.NaganoP (Bayer AG. As els . Hoechst AG production. The ELISA has been used with good results in the serodiagnosis of T. After should be used with great caution. It is known that monly used and successful trypanocides the pharmacokinetic behavior of drugs dif.production.. quinapyramine chloride. e. regionally or globally. 1989). Many of the drugs used for cattle are either not curative or too toxic for camels: e. underdosing is common. distributor WockIn the early 1970s.In the United Arab Emirates (UAE). Suramin (Nacies for safety and efficacy before they are ganol@) administered at a dose rate of 10used on camelids.Alternative drugs are Trypan@. 1980. was netic data available on camelids. 1996).) and Trypamidium-Samorin@ dustries Ltd (ICI)stopped their production (isometamidiurn chloride.to drug resistance.g. rosP. Merial) have of the quinapyramines. was stopped recently). 1999)..As a result of the limited number of drugs available for therapeutic or prophylactic use. it also (Kaminsky and Zweygarth. a decrease in the seroprevalence was achieved (from 12. This available today.against T. Berenil@has been successfully used in Bactrian camels with doses as high as 5 mg/kg bodyweight (Luckins. commun. However. 1992). B a n g et has a prophylactic effect for between 6 to al.. pers. Production of Antrycide@ has been Therefore it is important that drugs should resumed by a few drug companies and it is be studied carefully in every species. drugs stopped recently)..g. They NaganoP is decreasing in some areas due should undergo testing by regulatory agen. Brun and Lun. evunsi (Luckins et al. . Rae et al. 1994) that should 12 weeks (Kaufmann. Cymelaman@ (melarsomine.). Due to tant and there are techniques available its slow elimination from the body.

P = prophylactic.Merial. evunsi are resist. it is widely used in Bactrians in Asia ~ ~ . IM = intramuscular. 1989). Some farm managers midium.5-0. large losses in endemic areas. = administration Drug Trade Name Action Administ.7 mg/ challenge may be a factor to keep in mind.5 chloride4 Antrypol@ lsometamidium Trypamidiurn" IV 0.5 C IM 3.This drug is only curative when the mosis is difficult because of the developtrypanosomes are present intravascularly. p SC 5 6 sulfatekhloridel c. the degree of parasite be used but with great caution (0. Employing There is in vitro and in vivo evidence that frequent (monthly) PCV estimations on most isolates tested for T. France) with quinapyramine chloride at a ratio of was developed about 10 years ago (Ray3:2 (5-8. p IV 0. however. Table 50 Drugs for treatment o f Trypanosoma evansi infections in camels C = curative. ment of drug resistance. melarbe used curatively at 3-5 mg/kg together somine (CymelarsanB. However. administered subcutaneously..5-1 chloride Ve r id iu ma C IV 0. Administ. In cases of re.fully known.3 mg/kg).not advisable for use in camels 5 Not recommended for use in dromedaries. The lactic effect of 4 to 6 months. alt. Regular monside effects in camels such as tremors. kg intravenously administered as a 2% soControl and eradication of trypanosolution). Camels have subsequently mines (Zhang et al. Dose mglkg Melarsomine Cymelarsan" C deep IM 0.well-managed herds has proven useful in ant (innate) or non-responsive to isometa. SC = subcutaneous. treat any camel with a PCV of < 25%.itoring of infections is necessary to prevent vation and collapse leading to death. 1993).Lyons. Quinapyramine pros.naud et al. even more diffiOverdosing quinapyramines can cause cult is the control of vectors.keeping losses low. It is effective against T.residual effect in the dromedary is not yet sistance to suramin and the quinapyra. evunsi for chloride (Samorin@ Trypamidiurn@) or may 90 days. sali.5-5 Diminazene Berenil@ accturate5 1 Is called Pro-Salt Drug resistant t o T: evansi (reported in Sudan. (PI IV 5-1 O3 Suramin2 NaganoP lsometamidium Samorin" c.25 mg/kg. p sc 5 Quinapyramine Antrycide@ C sc 5 sulfate Trypacidem P sc Quinapyramine Trypacide" 5-8 sulfatekhloridel Quinapyramine Triquin" c. IV = intravenous.intramuscular injection at 0.25 c. India and the former USSR) 10 gkamel for treatment and 5 gkamel for prevention 4 Toxic effects when used in camels resistant t o Suramin and quinapyramine . may be evunsi when administered to camels by deep used prophylactically and has a prophy.Protozoal Infections 281 Quinapyramine methylsulfate may also The latest drug on the market.isometamidium apparently remained free of T..

thus making the parasites visible through a light microscope. Apart from animals exhibiting problems of infertility.1. diagnosis depends on finding the parasite in cervical and vaginal mucus and/or the preputial washings. Bovine trichomonosis is a venereal disease characterized by early fetal death in cows usually first seen as an infertility problem.282 Parasitic Diseases Table 50 lists the drugs that are used against T. The organism may be found in discharges from the uterus and in the aborted fetus (stomach). Tritrichomonasfoetus is pear-shaped. The diagnosis can be confirmed by PCR (Polymerase Chain Reaction) (Kaufmann. and possesses three free flagella arising from a basal body at the anterior end. 5. Tritrichomonasfoetus belongs to a group of organisms. exhibiting whitish-yellow. It is a common pathogen in bovines. Microscopic examination of fresh smears from the above specimens is easily performed. rolling movements are readily seen in fresh preparations. requiring several repeat examinations. but the organism may be only present intermittently and/or in minute numbers. clean samples may be cultured in special media for a few days allowing the organisms to multiply. is found extending throughout the cell. Subclinically infected bulls transmit the infection. 1991). A hyaline rod. often with a slight posterior projection (Fig. The parasite can be cultured in several different media and as it is motile the characteristic fast. 124). The pathogen was also isolated from one of four bulls in these herds. Sero- Figure 124 Tritrichomonas foetus from an endometrial smear of a dromedary with endometritis . commonly found in the digestive and reproductive tracts but also in other organs of a variety of animals. the axostyle. To enhance the chances of finding the organisms. 1996). A fourth flagella extends backwards to form the undulating membrane along the side of the organism continuing as a free flagellum. Trichomonadida. jerky. mucopurulent discharge (Wemery. The parasite was isolated from 24 out of 48 camel breeding herds with endometritis. particularly in developing countries.3 Tritrichomonosis Only one report of Tritrichomonasfoetus infection of camels has been published recently. evansi in camelids.

Iowa State University Press.surface water polluted with cyst-containly used because its effect is unreliable. Parasites have been observed in group. is a parasite of amphibians with long. 1987). The 5. have been isolated in a vari. diminazene aceturate.1. three different groups based mainly on the morphology of microtubular structures (median bodies) in the trophozoites. gested via contaminated water or by direct Many infections are latent. have been divided into (Tibary and Anouassi. USA) . occurs in rodents ed young llama with diarrhea (Kiorpes et as well as in birds and reptiles. 1985). 1997). preparations may have a positive effect Giurdiu spp. reptiles and mammals Giurdiu spp.4 Giardiosis first group.(including humans).Additionally. Veterinary Clinical Parasitology. G. public health authorities connidazole and metronidazole. ipro.ing animal feces in conjunction with inadpounds used against trichomonads are equate filtration are the primary sources. The Giurdia spp. G. Excystation ocsociated with acute or subacute to chronic curs in the small intestine where the cysts diarrhea due to enteritis of the small and release motile trophozoites that multiply (sometimes) large intestine. Some species or strains nucleated (2 or 4 nuclei) cysts may be inare considered pathogenic in humans.second group. narrow trophozoites. axostyle (A) and median bodies (MI. The cysts are sensitive to desicoutbreaks of giardiosis may result in sig. rnuris. is a OWC. but some are as. duodenuZis (G.Protozoal Infections 283 therefore one of the world's most common infectious intestinal parasites (Stevens. Kemp and Zajac. The oval. G. There includes two morphological forms: trohas been considerable discussion concern. dimetridazole. Rinsing the sider giardiosis a sexually transmitted disaffected organs with acridin and iodine ease (Stevens. logical tests are used for epidemiological surveys. ety of mammals. 1994.. 1985).phozoites (feeding stage) and cysts (infecing the significance of Giurdiu infections in tive stage). intestinulis). parasite in birds.cation but can survive for months in a nificant epidemics in humans and it is moist and cool environment.transmission from feces. The third al. have been found in a debilitat.Com. pear-shaped multimammalian hosts. ugilis. Giardia trophozoite (right) in an unstained fecal smear (courtesy of Professors Sloss. Waterborne asexually.. Contaminated food and untreated Chemotherapyis not regular. Figure 125 Giardia cyst (left) with nuclei (N). 6thed. They appear morphologThe life cycle (LC)of Giardia is direct and ically similar with small differences.

These diagnostic tests demonstrate Giurdiu-specific antigens derived from trophozoites. 1996). The cysts. recognized by their rapid "falling leaf" motion and concave ventral surface. 125). rolling form of movements. Infections in farm animals have been successfully treated with dimetridazole at a dose rate of 50 mg/kg daily for 5 days.5 Balantidiosis The ciliate (Ciliophora) Buluntidium coli is the only species associated with disease in mammals. Merifluorm from Meridian Diagnostics Inc. which may remain viable for days and weeks in moist feces. albendazole (20 mg/ kg) and fenbendazole (10mg/kg) daily for three days have proved effective in calves (Xiao et al. There are several fecal ELISAs that have been marketed for use in humans. In many countries this drug is forbidden for use in food animals. The pig is thought to be the primary host of B. 1 dogs and cats. lack of concave surface and the presence of only one nucleus. Large numbers of nonparasitic ciliates take part in the digestive process and occur in the rumen of ruminants and camelids as well as in the colon of equines. Occasionally it may invade the mucosa and cause ulceration associated with mild to severe enteritis. the efficacy of these drugs in camelids is unknown. Microscopic examination of fresh diarrheic feces mixed with some saline may reveal motile trophozoites. 126). The recommended method of cyst detection is by using the 33% zinc sulfate flotation technique with fresh feces. pigs. Some benzimidazoles.284 Parasitic Diseases Diagnosis of Giurdiu is based on the detection of pear shaped multi-nucleated cysts (Fig.1. USA is an in vitro-direct immunofluorescent test for the simultaneous detection of Giurdiu cysts and Cryptosporidium oocysts in fecal material (Fig. by the undulating membrane. 5. Trichomonads are also mobile organisms and of similar size and may be differentiated from Giurdiu spp. which is generally regarded as a commensal organism. coli.. monkeys and perhaps in other animals. The trophozoites may also initiate infection but they are much less re- Treatment ilil Metronidazole and fenbendazole are recommended for treating infected Figure 126 Giardia cysts in dromedary feces (irnrnunofluorescent test) . Occasionally the trophozoites may be seen. Repeated sampling and testing should be done because of the cyclical shedding of cysts.However.. It is a parasite of the colon in man. usually infect the host.

Trophozoites die within 15to 30 minutes in temperatures above 40°C. Fecal examination revealed only 300 cysts per gram feces. and the micronucleus lies in the notch of the macronucleus. but large numbers of trophozoites have been observed in fecal samples in diarrheic camels (Kayum et al.. The body surface is covered with slightly oblique longitudinal rows of cilia. 1969. Ali and Abdelaziz (1982) described a case of diarrhea in a dromedary in good condition (apart from having loose stools). The trophozoite averages 50 to 60 pn in length. Ovoid to spherical cysts are produced. Shommein and 0 s man. and the cytoplasm contains numerous food vacuoles. but larger forms up to 150pm are not uncommon. 1987. Symptomatic treatment with carbarsone (250 mg) . The authors reported large numbers of the organism in the feces of dromedaries. the peristome is subterminal and at the narrower end. One contractile vacuole occurs near the posterior end of the body. Ali and Abdelaziz. A limited number of cases of clinical balantidiosis in camels have been reported (Vosdingh and Vanniasingham. B. the macronucleus is kidney-shaped. another near the center. some with diarrhea for 3 months.Protozoal Infections 285 Figure 127 Balantidium coli trophozoite from a dromedary intestine (left) and B. 1992). 1982. They are faintly yellowish-green in color.. 1992). and the organism can be recognized within the cyst by the macronucleus. It is important to know that trophozoites are destroyed by flotation solutions but can be observed in direct fecal smears. Kayum et al. coli cysts are generally excreted. measuring 40 to 60pm. The organism is actively motile and moves quickly over the microscopic field (Fig. coli cyst (right) sistant to the microclimate than the cysts. 127).

128).. 1977. Egypt. and Somalia (Barnett. However. hemolytic anemia. are T. The camels did not show any signs and T. Baluntidium often plays a secondary role in the pathogenesis of intestinal disorders.286 Parasitic Diseases Figure 128 Balantidiosis in a young dromedary and kaolin (250mg) stopped the diarrhea after three days. have been found in NWC. Theileriosis Pathogenic protozoa belonging to the order Piroplusmidu. Neither Theileria nor Babesia spp.hemoglobinemia. e. 1994). very few reports have been published concerning tick-borne pathogens in camels. Boid et al. the above reports do not conclusively prove that B. The author did not describe any parasite in the blood cells of the animals. coli is a pathogenic organism in camels. 5. (1997) found Buluntidium cysts in apparently healthy camels. The latter T.1. the animals showed some signs seen in babesiosis of other animals.annulutu was not observed in blood samples taken over a period of one month. are common pathogens transmitted by ticks and are of significant importance in many domestic animals. and Theileria spp. 1988) and thought to be non-pathogenic. 1985). anisocytosis and polychromasia. Although ticks are often found on camels in large numbers. Reported Theileria spp. which include Babesiu spp. Nassar (1992) examined 200 apparently healthy camels and found 30% infected with Theileria spp.6 Tick-borne Diseases: Babesiosis. Only one unconvincing report of Bubesia infection in camels has been found (Egbe-Nwiyi. In central parts of Saudi Arabia. hemoglobinuria. In Egypt. however. no schizont stages were described. These few case reports are not considered reliable as they usually fail to give adequate taxonomic descriptions. dromedurii was reported in India (Rao et al. dromedurii. the former in Turkmenistan. Severe cases of balantidiosis have been observed in young dromedariesin the UAE.g. Magzoub et al.. However. Ten mL of bovine blood containinghigh numbers of T. annulata parasites were injected intravenously into five 2-year-old healthy dromedaries by the authors. The camels suffered from enteritis with loss of villi in the small intestine (Fig. camelensis and T. ..

are distinguished from those of Isospora spp. 1983). which have a two-host LC and which form tissue cysts in the intermediate hosts. Oocysts of Eimeria spp. The merozoites of the last schizont generation invade new cells and develop either to microgametocytes or macrogametocytes.Merozoitesform within the schizont and eventually rupture the invaded cell and invade other cells in turn a process that may be repeated two or three times. Diagnosis I!. becoming a schizont.7 Coccidiosis Another group of protozoa are the coccidia. The term coccidiosis is usually reserved for infections with Eimeria and Isospora spp.1. by the content of the sporulated oocyst. Young animals are particularly prone to infection of coccidiae. each containing two sporozoites. the oocyst. The oocyst is the resistant stage. which takes place outside the host. which are environmentally resistant forms that following sporulation may eventually infect susceptible new hosts. after or during the rains. The LC stages in both families ultimately result in the formation of oocysts. Coccidiosis occurs in all parts of the world that have substantial populations of Camelidae. four sporocystsare formed within the oocyst. Other species of importance to domestic animals are Cyptosporidium spp.. is ingested by a host following excystation the sporozoites are released usually penetrating the epithelial cells of the mucosa in the small intestine. Verification of suspected cases of coccidiosis depends on the demonstrationof unsporulated oocysts either in smears prepared from fresh feces or by concentrationmethods involving flotation in saturated salt solu- . They are important within the Eimeriidae and Sarcocystidae families (Table 51). They complete their life cycle (LC)in a single host. Each macrogametocyte finally forms one macrogamete and each microgametocyte several microgametes. Life Cycle of Eimeria Mi When the infective stage. pathogens which in mammals are parasites of the stomach and intestinal epithelium. or close to where animals are watered (Kawasmeh and Elbihari. able to survive outside the host for many months under suitable conditions (Fig. in contrast to the Sarcocystidae (tissue cyst-forming coccidia).Protozoal Infections 287 Table 51 Taxonomic classification of the coccidia of veterinary importance Family: Eimeriidae Cryptosporiidae Sarcocystidae Toxoplasmatidae sarcocystis Besnoitia Genus: Eimeria Cryptosporidium Hammondia Toxoplasma Neospora Isospora 5. The Eimeriidae are mainly intracellular gut-dwelling parasites (gut-dwelling coccidia) of the intestinal epithelium where they undergo both asexual (schizogony) and sexual (gametogony) multiplication. 129). The sporozoite develops to a trophozoite within the cell and grows quite large. Eimeria oocysts have four sporocysts with two sporozoites each and Isospora have two sporocystswith four sporozoites each. Zygotes result from the union o mif cro-(male) and macro-(female) gametes (fertilization). Disease outbreaks characterized by enteritis are mostly associated with young animals living in crowded and wet conditions. During sporogony.The zygotes become oocysts which are excreted with the feces. these organisms are intracellular and occur particularly in vertebrates.

H = microgametocyte. orlovi and 1.5 x 18. F. infecting both Bactrian and dromedary camels. There are five Eimeria spp. C1. I. cameli. 1987). It is often necessary to sporulate the oocysts for species differentiation. = first stage schizont. Fig. cameli. several schizont generations. merozoites give rise to male and female gametocytes. One isolation was from a calf which died from the infection.: 1.288 Parasitic Diseases Figure 129 Life cycle of Eimeria: A = feces. B = oocyst. F = schizogony. GI. from a dromedary calf showing abdominal pain and diarrhea. lesions in the intestine may be recognized and asexual stages may be seen in scrapings of the intestinal mucosa and on histological sections. D = initial infection. 1950) is thought by Pkllerdy (1965) to be an avian form accidentally ingested. Eimeria cameli and E. G2 = end of schizogony. At necropsy. The same probably applies to I. orlovi (Zigankoff. The calves exhibited profuse diarrhea. The main characteristics of the Eimeria species reported in camelids are listed in Table 52 a and b. Occurrence . 130 a-c shows the most important species found in dromedaries in the UAE. I = male (micro-) gamete fertilizes a female (macro-) gamete. Raisinghani et al. The sporulated oocysts were oval to ellipsoidal and measured 29. Each . Intestinal coccidia found to infect Camelidae are Eimeria and less so lsospora (Ouhelli and Dakkak. (1987) isolated Isospora spp. was isolated from 1-3-weekold calves in a dromedary herd in Kenya. dromedarii are the most wide- spread species of camelid Eimeria. E = invasion of intestinal mucosal cells by sporozoites. Recently lsospora sp. C2 = oocyst sporulation. Identification of the different species is usually conducted on the morphology of the oocysts. J = cyst wall forms around the fertilized macrogamete (zygote) developing to oocyst tions. found in camels (see Table 52a) and two lsopora spp. F2 = second stage schizont.4pm.

Iraq and Pakistan (Levine and Ivens. peruviana 28-37 x 18-22 ovoid ovoid E. cameli and E. but not in the colon. 1965). 1970) **** This species is common in the feces o f dromedaries in India (Dubey and Pande. Reichenow. Three different Eimeria species were identified: E. The animals were emaciated and developed watery diarrhea shortly before death. 1999) which is probably nonpathogenic. (1994) reported that 13out of 16 adult llamas died from coccidiosis in Germany. 1985) *** This species is apparently quite common in feces of dromedaries and Bactrian camels in India. a valid species while Pellerdy (1974) does ** This species is presumably common in the small intestine and t o a lesser extent in the cecum of the dromedary and Bactrian camel (Henry and Masson. reported in NWC by Guerrero et al. The parasite was believed to be Isospora orlovi. Histology revealed an extreme invasion of the intestinal mucosa with different stages and oocysts of the genus Eimeria. 1968). I t s prevalence and geographic distribution are unknown (Prasad. Haenichen et al. A limited number of severe outbreaks of coccidiosis of OWC and NWC. 1952. punoensis and E. 1964) ***** This species occurs in the feces of the Bactrian camel. dromedarii. most reports are . brown 2 layers present E. (1967) Shape 22-26 x 18-21 ellipsoidal ovoid-ellipsoidal E. 1974). 1. auburnensis 32-46 x 20-25 * Pathogenic according t o Rosadio and Ameghino (1994) E. Several researchers have identified a sixth Eimeria species: E. rajasthani**** 2 layers not visible ellipsoidal 34-39 x 25-27 oval 2 layers absent E. but Dubey and Pande (1964) do not recognize E bactrianias . E. (1987) also found E.. The parasites were only observed in the jejunum. punoensis 17-22 x 14-18 E.. Six Eimeria species have been described from NWC (Table 52 b). The species associated with disease are primarily E. Soulsby. orlovi and cameli is according to Kaufmann (1996) unknown. 1982. a similar Isospora was found in dromedary calves’ bloody diarrheic feces (Fig. 1960) 289 Table 52 b Oocyst morphology of Eimeria spp. have been reported (Gruvel and Graber. alpacae Species Size (pm) Wall thick thick smooth Micropyle present present present present absent Dresent oocyst contained 2 sporocysts with 4 sporozoites. 1985) Species Size (vm) Shape Wall Micropyle Eimeria bactriani* 22-34 x 25-27 spherical 1 layer present piriform thick present E. reported in OWC (after Levine. Hussein et al. spec. lamae 30-40 x 21-30 ovoid. rajasthani to be pathogenic in a survey conducted in Saudi Arabia. macusaniensis* 81-107 x 61-80 ellipsoidal-ovoid E. some with mortality rates up to 10% in young dromedaries in Chad. brown E. pellerdyi***** 22-24 x 12-14 * This species has been found in the small intestine of Bactrian and dromedary in Russia (Levine and Ivens. Levine. However. 130 d). dromedarii*** 23-33 x 21-25 ovoid.Recently in the UAE. 1932. cameli** 81-100 x 63-94 E.Protozoal Infections Table 52 a Oocyst morphology of Eimeria spp. 1970). macusaniensis. nolleri (Partani et al. The pathogenic role of two lsospora spp. (Minck. It is presumed that the parasite was accidentally ingested through avian droppings (Pellerdy.

Secondary bacterial infections may severely aggravate the disease and cause mortalities in young camels (Kinne and Wernery. A summary of the prevalence of Eimeria infections from different countries is shown in Table 53. . Anemia is often seen and respiration may be rapid. and progressive weight loss. 1997). 132 and 133). Their coat is rough and hair loss may occur. Histological sectionsshow destruction and & organization of the mucosa together with hemorrhages and infiltration of inflammatory cells (mainly eosinophils and macrophages) (Figs. dehydration.290 Parasitic Diseases Figure 130 a 4 Oocysts of Old World Camelids: (a) Eimeria dromedarii (b) Eimeria cameli based on fecal examination of healthy camelids. Animals with severe infections show signs of inappetence. Clinical Signs :L Young animals suffer from hemorrhagic enteritis (Fig. The feces may be stained with blood and mucus (Hussein et al.. Pathology ii:l Development stages of the parasites are found in the mucosa and lamina propria of the jejunum and ileum. 1987). 131) and diarrhea.

g. On the contrary. salt or sugar solutions by Fuellebom's method). Coccidial infections are generally self-limiting unless a re-infection takes place. Clinical coccidiosis must be treated. It is unknown whether the same principles can be referred to Camelidae. . are host-specific and immunity to any one species is only effective for that species. Both Eimeria spp. However. peracute and acute diseases may be exhibited before oocysts are excreted. which is thought to be a combination of cellular and humoral factors.Protozoal Infections 291 (c) Eimeria of probably goat origin often found in dromedary fecal samples in the UAE (d) lsospora orlovi oocysts with 2 sporocysts containing 4 sporozoites from a dromedary calf with bloody diarrhea Immunity *$I' In ruminant livestock immunity develops following infection. dysentery and often the demonstration of very large numbers of oocysts in the feces (microscopicexamination following flotation with e. Diagnosis is based on clinical signs of diarrhea. A direct smear of diarrheic feces examined under a microscope may reveal oocysts. therapy of non- clinical infection may defeat the animal's ability to mount an immune response. and lsospora spp. but finding oocysts in the feces is not a criterion for therapy.

that they have established an immune response. 1991 USA NWC Fowler 1998 USA NWC Jarvinen 1999 USA NWC Prevalence 22 40 86 24 14 14. Identification is done by the morpholo- gy of the freshly excreted oocysts as well as the sporulated oocysts. as is the case in some other anima1 species. 1999 India Dromedary Guerrero et al. is achieved by in- Figure 131 Hemorrhagic enteritis caused by E drom. 1967. 1971 South America NWC Schrey et al.292 Parasitic Diseases Table 53 Prevalence of Eimeria infections in camelids in different countries Authors Year Countrv Species 1934 Kazakhstan Yakimov Bactrian Bactrian 1956 Kazakhstan Pellerdy 1960 India Prasad Dromedary 1964 India Dubey and Pande Dromedary 1965 Gruvel and Graber Chad Dromedary 1976 Iraq Dromedary Mirza and A1 Rawas India Gill Dromedary 1976 Nigeria Chineme 1980 Dromedary Saudi Arabia Dromedary Kawasmeh and E l Bihari 1983 Levine Africa Dromedary 1985 Kasim et a 1 1985 Saudi Arabia Dromedary Saudi Arabia 1987 Hussein et al. edarii in a young dromedary . Dromedary Yagoub 1989 Sudan Dromedary Syria Daruish and Golemansky 1993 Dromedary UAE Dromedary 1997 Kinne and Wernery 1998 Saudi Arabia Dromedarv Mahmoud et al. Partani et al. Sporulation of the oocysts. usually employing a 2.5% potassium dichromate solution.5 13 25 ~- 28 Young animals may have had previous contact with the coccidia and there is a possibility.

Figure 133 Eosinophilic enteritis. masses of coccidial developmental stages (see Fig. depending on the species involved. 1997). The morphology of the sporocysts are helpful in the diagnosis of species. note the unsporulated oocyst of E.Protozoal Infections Figure 132 Severe eosinophilic enteritis in a 7-year-old dromedary caused by coccidiosis. cameli (right) . In many cases of necropsied dromedaries in the UAE. Several scrapings should be taken from different sites of the small intestine. At necropsy. The simple flotation method might not be adequate to isolate the large and heavy oocyst of E. but no oocysts were de- tected in feces. cameli (Kinne and Wernery. note the different developmental stages of the parasite 293 cubating the oocysts at 25°C for about 10 days. In these cases. coccidiosis was only confirmed during necropsy by histological investigations. 132) were seen histologically. mucosal scrapings may be directly examined as smears under the microscope and may often be diagnostic if oocysts and the different sexual stages are seen.

recovery is often spontaneous and occurs without any specific treatment. 100-200 mg/ kg given orally for 3 to 5 days. With regard to OWC. Camels seem to be very susceptible to poisoning by ionophorous antibiotics. the authors recommend formosulfathiazol (SocatyP).. Hussein et al.. There are numerous anticoccidials used in ruminants. Their use has been recommended in NWC with caution because there is species sensitivity to some of the drugs (Fowler. 1998. (1987) successfully treated infected animals with sulfadimidine. and in severe cases in combination with Theracanzan@. 50mg/kg i. 1998) and in a Bactrian (Miller et al. very little is known about the doses and efficacy of anticoccidial drugs in camelids.294 Parasitic Diseases Coccidiosis is a self-limiting disease. 1990). Haenichen et al.. (1994) used the following drugs in llamas: sulfadimethoxin (Theracanzan@. Another drug is toltrazuril (Baycox@) which is given orally: 15-20 mg/kg for 3 to 5 days. Chaudhry et al. Drugs recommended for treatment of coccidiosis in domestic ruminants are listed in Table 54. 1998). Following the multiplication stages in the intestine. Anticoccidials are used to control coccidiosis outbreaks in livestock. However. for 3 to 5 days.m. In young animals. and Table 54 Anticoccidial drugs recommended for domestic ruminants Drug Usage Amprolium therapeutic and DroDhvlactic Sulfonamides Sulfamethazine therapeutic Sulfaquinoxaline therapeutic Sulfaguanidine prophylactic (for sheep and swine) lonophorous antibiotics Monensin prophylactic Lasalocid DroDhvlactic Miscellaneous compounds Nitrof urazone therapeutic Decoquinate prophylactic (for cattle) Toltrazuril therapeutic (for sheep) Diclazuril therapeutic (for sheep and soats) overdosing with Salinomycin and Monensin has recently been reported in dromedaries (Wernery et al. Poisoning is characterized by skeletal and heart muscle degeneration and Figure 134 Degeneration of skeleton muscle in a dromedary caused by Salinomycin poisoning .

134). to Kaufmann (1996). epithelial hyperplasia with mucosal hypertrophy without any inflammation was seen (Anderson. 1994). 135).These changes were considered consistent with chronic gastric cryptosporidiosis in cattle (Anderson. reducing the risk of a buildup of infections. bial compounds have been tested for their 5. Feed and water troughs must be kept free of contamination from feces. were found in 15 dromedary camels in an epidemiological survey in Egypt (AbouEisha. 0 4 .1. C. Stockingrates should be kept to an acceptable level so as to avoid overcrowding. The control of clinical coccidiosis in young calves is essential and may be achieved by good management. Frequent rotation of pastures is a prerequisite for keeping most parasites at bay. emaciation. Fayer et al. 1987). resembling C. Oocysts are demonstrated in stained smears of fresh feces (Fig. An infection can lead to se.8 Cryptosporidiosis Figure 135 Cryptosporidium oocysts in the intestinal mucosa .Treatment and Control Although a large vere diarrhea. Oocysts of Cryptosporidium sp.. 5 ~ ) diagnostic enzyme immunoassays (EIAs) sporulate within the host and are infective and direct and indirect immunofluorescent when released in the feces. According czyk et al. muris.. dehydration number of chemotherapeutic antimicroand death.Neelsen stain (counter-stained with cargens of mammals that are usually confined bol-fuchsin). The Other Coccidia of importance to domestic most commonly used is a modified Ziehlanimals are Cryptosporidium spp. Several the host. The infective antibody tests have been developed (Graoocyst contains 4 sporozoites. Histologically. Isolates of this organism were found to colonize gastric glands in experimentally infected mice. (1991) reported a zoo Bactrian chronically infected with a Cryptosporidium sp.Protozoal Infections 295 splayed legs in conjunction with extremely elevated muscle enzymes (Fig. parvum may infect young camels. patho. The oocysts stain deep red to the microvilli of the intestinal mucosa of against a green-blue background. The small oocysts ( 4 . 1991). 1996). Transmission is via feces contaminating drinking water. Calving grounds should be well drained and kept as dry as possible.

2000). mediate host.. e.no really effective compound for therapy or prophylaxis has been found (Fayer et al. however. but less so for their final hosts (Dubey et al. Myocardial lesions have been attributed to Surcocystis spp. light infections give no clinical signs in NWC. Rehydration may help in mild to moderate cases. 1991). It revealed an eosinophilic myositis associated with macroscopic sarcocysts and aborted two hours before death. wool breakage. lameness. fulcutula (Fowler. showed promising anticryptosporidial effect both in in vitro and in vivo trials when employed at a low dosage (Castro Hermida et al. In the inter- Clinical Signs Usually the definitive hosts carry the infection without showing any signs of disease. Sarcocysfis spp. Etiology b. The sporozoites invade many organs via the blood stream.. 1970). Optimal management with well-drained calving grounds and the avoidance of overcrowding will prevent infection. Mason (1910) who found the cysts primarily in the myocardi- . Acute clinical disease may occur (referred to in cattle as Dalmeny disease) causing abortion. Some llamas have shown clinical signs similar to those in horses with protozoal myeloencephalitis caused by S. halofuginate lactate (Yvore and Naciri.Anvet other compound. Experimental studies have shown that even subclinical infections may have a negative effect on growth and blood parameters in young animals (Leek et al. 1989. suboptimal growth rate. However.9 Sarcocystiosis Species of Sarcocystidae have a two-host LC: an asexual stage in an intermediate host and a sexual in the final host. aucheniue. Oocysts are resistant to most disinfectants except formalin (5%) and ammonia..296 Parasitic Diseases efficacy against cryptosporidiosis. except that there is no asexual multiplication.. 1989).g. following ingestion of contaminated feces of the final host. are parasites using two hosts to complete their LC. the infective sporocysts. 1998).. Surcocystis spp. lasalocid. Most infections by Sarcocystis spp. some infections may cause losses (recordedin domestic animals).1. are mostly host-specificfor their intermediate hosts. release sporozoites into the intestine. The animal had been imported five years earlier to the USA from Peru. Peeters et al. 1993) in dairy calves.Recently. recently a few antiprotozoal drugs have been recognized as having some therapeutic and prophylacticproperties. La Perle et al. 1980). Also. 5. Carnivores commonly act as final hosts and herbivores as intermediate hosts. but in heavily infected animals the schizogony cycles in endothelial cells may give acute febrile disease.. It is not known whether these drugs are tolerated by camels.. 1993). resulting in abortion and death. Schizogony occurs in the endothelial cells of blood vessels of many organs before typical cysts in the striated muscles develop. According to Fowler (1998). Lasalocid is an ionophoric antibiotic produced by Streptomyces lasaliensis. in the intermediate hosts are subclinical. sporulation takes place in the intestinal wall and sporocysts are excreted for several weeks. Halofuginate lactate is commercially available as Halocur@ (Intervet). (1999) described Dalmeny disease in an alpaca caused by S. They can survive for months in the environment if kept cool and moist. mild myositis with myalgia may be seen interfering with muscular function. reduced milk production. in camels (El-Etreby. 1977. and paromomycin (Fayer and Ellis.The general developmental cycle in the final hosts in which sexual stages occur is similar to that of the Eimeria spp. Giles et al. and sometimes death in cases of heavy infection.

. 1999). Both types were microscopic. 1975. Both species produce macrocysts in the muscles. Leguia.Protozoal Infections 297 um and esophagus of camels. according to Hilali and Mohamed (1980) and Hilali et al. Kuraev.000 annually. 1975) in alpaca. 1982. Egypt. 1981. cameli. lama-canis (Leguia et al. The sporulated Sarcocystis sporocysts were only recovered in dog feces (Hilali et al. Sarcocystis aucheniae was demonstrated in Bolivia and Peru (Guerrero. Sudan and the former USSR (Dubey et al. 1984. Hilali et al.. Iran.. llama and vicufia and Sarcocycstis tilopoidi (syn. A third species... 1980.-infected camel meat to dogs and cats. are up to 12 mm long and 2 mm in diameter. The prevalence of infection with Sarcocystis in camel carcasses at slaughter varies from 4. described two different thin-walled and thick-walled cysts. guunicoe-canis) in guanacos (Gorman et al. 1987) to 88% in Saudi Arabia (Fatani et al. Since then S. (1996) found two morphologically distinct sarcocysts. Warrag and Hussein.The latter authors reviewing the previous studies on camel sarcocysts named the thick-walled cysts S. Fatani et al. (1995). 1989)is found as microcysts in alpacas in the myocardium and muscles. The final host of at least one of the species is the dog (Schnieder et al. 1983). heart and esophagus.The cysts. but the thick-walled cyst was only present in the esophagus.. 1995. Diagnosis Sarcocystis spp. The prevalence of Sarcocystis sp. 1984). Losses in alpacas are estimated to reach $US 300. 1999). 1967. Three Sarcocystis species have been reported in NWC (Leguia. Fatani et al. Fowler. S. 136). Dogs have been found to be the final host of at least one of the parasites (Hilali and Mohamed. 1989). Several scientists have fed Sarcocystis spp. may be identified by the typical ultrastructure of their Figure 136 Sarcocystis carneli in the heart muscle of a dromedary . The crescent-shaped bradyzoites that fill the cysts are 15-20 by 4-6 pm (Fig. and first reported Sarcocystis cameli.5% in Sudan (Ouhelli and Dakkak. 1996). 1998). Fernandez-Baca. in certain areas of Peru was estimated to be over 50% in animals above two to three years of age (Fernandez-Baca. and thought that they belonged to the same species. S. 1996). The infections are of economic significance..The *-walled cyst was found in all three indicator organs: diaphragm.The infection is of economic importance because part of or the entire carcass may be condemned at meat inspection. cameli has been reported in Afghanistan..

Sporulated oocysts contain two sporocysts each with four sporozoites. the organismsmay also be found in mucosal scrapings of the small intestine by a flotation-concentration technique (Dubey et al.. 1984). with few exceptions. Therefore. treatment and control are very seldom applied. including the myocardium. sucrose or zinc sulfate solutions. 1977).298 Parasitic Diseases cyst wall (Dubey et al.1. The sporocysts are released in the intestine before being shed through the feces. (1981) reported finding Besnoitia cysts at the base of the lamina propria in the intestine of a dromedary. However. Some infections may be subclinical and only detected after slaughter during meat inspection. Kharole et al. No inflammation was seen although the intestinal tissue was damaged by pressure from the large cysts.10 Besnoitiosis In India. species differentiation based on the morphology of the oocysts or sporocysts is not possible. There was no systemic or cutaneous involvement as was reported by Fazil and Hofmann (1981) as is often the case in other animal species.. Similar parasitic infections had been reported in buffalo calves. There are several serological tests that have been developed for the diagnosis of Sarcocystis infections in different intermediate hosts. at abattoirs it is important to keep offal away from predators. Fazil and Hofmann (1981) stated that besnoitiosis (which they called globidiosis) often occurred in camels with typical skin lesions on the distal part of the legs. Molecular techniques mostly based on PCR have proved to be useful in detecting infection and species identification. Microscopic cysts are often found accidentally in a histologic section of muscle. 1989). It is not possible to identify the particular species based only on the morphology of the bradyzoites. Bradyzoites are readily killed by freezing and by heating to approx. Histological examination is often used to demonstrate the presence of microscopic sarcocysts in the tissues of a host. The organisms may remain infective in uncooked or poorly cooked meat. Additionally. Macroscopic cysts are seen during meat inspection or at necropsy. ranging from 10pm to several 100 pm. are considered to be non-pathogenic. 5. lack a micropyle and they have a fine colorless wall...18°Cand cooking were effective for inactivating Sarcocystis in guanaco meat (Gorman et al.This method can also be used to extract the bradyzoites for further antigenic or molecular biological investigation (Lunde and Fayer. Giles et al. 1977.The oocysts of the Sarcocystis spp. Oocysts and sporocysts may be found during fecal examinations of the final host by using traditional flotation techniques based on saturated sodium chloride. Numerous different-sized cysts were found. Cysts or free bradyzoites may be demonstrated in squash preparations of small pieces of fresh meat samples followed by stereomicroscopy (magnification 10-60) (Gut. 1989). 65°C. Domestic dogs and cats should not receive uncooked meat or offal. 1980). The infection often became general- .. Although experimental studies have shown that subclinical infections may also have negative effects on the growth of young animals (Leek et al. Freezing to . Reported techniques so far are usually based on crude antigens that are not species specific (Uggla and Buxton.. The only way to control Sarcocystis infections is to break the LC of the parasite..Peptic digestion of minced muscular tissue followed by examination by a light microscope preferably equipped with phase contrast may be used to diagnose released bradyzoites (Dubey et al. 1990). cattle and sheep in the same area. Treatment and Control 311 Sarcocystis spp. 1982). 1989).

abortions and perinatal mortality are commonly attributed to the infection. Intracellular cysts.1 1 Toxoplasmosis Toxoplasmosis is caused by the cyst-forming coccidial parasite Toxoplusmu gondii. subcutaneous tissues and fascia as well as in the laryngeal.Protozoal Infections 299 ized with high fever and diarrhea indicating involvement of the intestines. but the mortality could reach 10% of clinically affected animals. T. 5. containingcysts of the organism. particularly cats. Small and large cysts of Besnoitiu was seen in the mucosa of the small intestine of six dromedaries in Iran (Tafti et al.The parasite in the intermediate hosts (which can be almost any mammalian species including man) may cause a severe disease. It is most likely that the cysts in the intestinal mucosa described as Besnoitiu are developmental stages of Eimeria species. besnoiti. Two separate stages of multiplication of T gondii may be recognized. however. Some of the cysts were surrounded by inflammatory reactions. mainly within fibroblasts. 2000). Cysts of several species of Besnoitiu infect different domestic animals and wildlife. Generally. Iowa State University Press. In sheep.1. characterize Besnoitiu. Toxoplusmu infections are subclinical. Morbidity was low. Kemp and Zajac. 1982). 1970). USA) .. nasal and other mucosa. The life cycle of the Besnoitiu species occurring in the skin is still unknown. excreted in cat feces (felids) (Fig. 137). although in pregnant individuals the infection may cause abortion or congenital disease in the offspring. an important worldwide zoonotic pathogen. which become infected by ingesting ToxopZusmu-infected animals.. . The final host is the cat and the intermediate hosts are mainly cattle. The best-known species of this genus is B. 6th ed. It is an intestinal coccidial parasite of FeZidue.This results in the development of oocysts. Veterinary Clinical Parasitology.. The nucleus of the host cell undergoes hyperplasia and hypertrophy (Soulsby. 1994. Figure 137 Oocyst of Toxoplasma gondii (T)next to an lsospora felis oocyst (F) from cat feces (courtesy of Professors Sloss. in which the parasites are found in the dermis. found particularly in Africa. A cyst wall is found around the infected cell with bradyzoites in a parasitophorous vacuole. The sexual cycle is only completed in the intestinal epithelium of felines (entero-epithelial phase) (Hutchisonet al. gondii is one of the most common cat zoonoses.

felis and C.confirmed this result. including the Sabin-Feldman dye test. insectivores. Howtract the infection by ingesting feed con. 1969). which contains large numbers of tachyzoites. rivoltu are coccidia of cats. However. The tissue cysts measuring up to 300 pm may be found in any tissue. New cells are invaded after rupture of the infected cell. It still needs to be C. the tachyzoites rapidly multiply within any nucleated cell. 1995).4% reactors in dromedavegetables) as well as the transplacental ries in the UAE. performed on the pleural fluid and the serum showed antibody titers to T.. Any type of cell may be invarq-dducing tachyzoites by endodyogjny. Cats given camel camels is indicative of past or present inmeat excreted oocysts of Cystoisosporafelis. Afzal and Zakkir zoites. This was attributed to a longer period of exposure to the parasite in older animals (Gill and Prakash. gondii. rivoltu and T. lagomorphs. gondii (Galuzo. 1965 cited by showing signs of mild dyspnea associated Gill and Prakash. Both in India and Saudi Arabia there was a higher prevalence of antibodies in adults than in younger animals similar to findings in other hosts. (1988) found an association between husbandry methods and the seroprevalence of T. but are most commonly found in the brain.g. Clinical toxoplasmosis-like signs were exOccurrence Only one case of acute toxo.ever. . an asexual multiplication (extra-intestinal phase). Other researchers usTransmission % Human infection may re. This may also occur in the final host . Switzerland).parallel to the entero-epithelial phase. Bommeli. 1972). cysts within cells are formed containing hundreds of organisms named bradyzoites. has any clinical significance in camels. gondii. In the acute infection.cance of the results from these surveys. the presence of antibodies shown in taminated with oocysts. spread of tachyzoites to the fetus during It is difficult to determine the signifiacute infection in pregnancy. 1951). primates and many birds species (Levine. Several seroepidemiological toxoplasmosis surveys in Camelidae have been reported (Table 55). 1985)). The oocysts are highly resistant when sporulated and can stay infective for a year or longer (Yilmaz and Hopkins.300 Parasitic Diseases ~~ cavity and Toxoplasma tachyzoites were found in macrophages and neutrophils in smears. have been recorded. carnivores. established whether the T. oocysts from cat feces (e. Several serological tests. marsupials. A seroprevalence of 38% in 521 racing dromedaries was detected. When the sporulated oocyst is ingested by a susceptible host (over 200 spp. 1990).the cat . gondii ELISA (Chekit Toxotest? Dr. gondii infections. The authors de. Housed camels had a much higher prevalence due to exposure to the final hosts (cats) than camels in the desert. gondii (Hilali et al. As the infection proceeds. earlier with pyothorax.. Twenty-four liters of tur. 1969).ing an indirect hemagglutination test also sult from ingestion of cysts with brady. gondii infection C. The camel had become anorectic a month earlier and aborted a near-term fetus.date from mice infected by a pathogenic scribed a six-year-old female dromedary strain of T.similar trials failed to produce the clinical bid fluid were drained from the pleural disease in camels (Blanc et al. This has been confirmed by a serological survey in the UAE (unpublished) using the recently established T. skeletal and heart muscle. on (1994) found 36..perimentally induced in three camels by plasmosis in camels has been reported subcutaneous injections of peritoneal exu(Hagemoser et al. including rodents. the sporozoites-emerge and enter tissues via the blobd and lymph. fections with T. Camels con. These cyst formations are characteristic of the chronic infection. Hussein et al.

experimentally infected orally with T. Afzal and Sakkir 1992 Sudan Latex Agglutination Test 1972 Turkmenistan Complement Fixation Test 1996 UAE 1994 UAE Indirect Latex Agglutination Test Direct Agglutination Test Indirect Hemagglutination Test Modified Agglutination Test ELISA Indirect Aaalutination Test Indirect Aaalutination Test 482 200 100 - 67 4.5 12 54 Micromethod Elamin et al. 1979 EavDt Sabin-Feldman Dve Test Michael et al. Johnson.3 26.3 24. 1992 USA 2000 UAE 1991 Peru 1984 Peru - This ubiquitous parasite has also been reported i NWC. 1999 Chile Indirect Hemagglutination Test El-Ridi et al.4 83. Unwblished Leauia et al. gondii (Cheney and Allen. Leauia et al.0 25 50 283 52 1 Dubey et al. 1981 Nigeria Indirect Hemagglutination Test Hussein et al. 1977 Egypt Sabin-Feldman Dye Test Rifaat et al. 1989.Two llamas. Abortions have been asn sociated with T.9 36. 1993) and seroprevalent studies have been undertaken.4 0 16 22.4 33. 1985 Sudan Indirect Hemagglutination Test ~ Kozojed et al. gon- . 1998 Egypt Direct Agglutination Test Okoh et al. 1987 Sudan Indirect Hemagglutination Test Eldin et al. 19 % aositive 73. 1977 Egypt Sabin-Feldman Dye Test Complement Fixation Test Rifaat et al.Protozoal Infections Table 55 The Drevalence o f I uondii in camelids in different countries Authors Year Country Test Camels/ Llamas 301 ~~~~ 1976 Afghanistan Micromodification of Indirect Hemagglutination Test Gorman et al.5 38.5 18 30.4 63 6 166 159 227 102 95 204 17.5 67. Berdyev Chaudhry et al.6 447 19 119 80 43 73 49 16. 1990 Egypt Indirect Hemagglutination Test Fahmv et al. 1978 Egypt Sabin-Feldman Dye Test Maronpot and 1972 Egypt Indirect Fluorescent Botros Antibody Test Egypt Indirect Hemagglutination Test Hilali et al. 1988 Saudi Arabia Indirect Hemagglutination Test Bornstein and Musa 1987 Sudan Sabin-Feldman Dye Test Abbas et al.7 2.

Urquhart et al. Demonstration and isolation of the parasite may be achieved by testing material from the intermediate hosts by histology. A live vaccine (Toxovac@. Cats should not be given raw meat. Neosporosis is severe in transplacental infected puppies. 1996). Consumption of undercooked camel meat may constitute a risk of infection to humans and Treatment and Control Effective treatment of toxoplasmosis is difficult to achieve. serology. In livestock. 1976) and almost completely inhibited in cats given 5 mg/kg toltrazuril daily (Daugschies. The antimalarial drug pyrimethamine (2. mice and insects cannot contaminate it. gondii organisms are present in the muscles and other organs (Work. indirect hemagglutination test. 1993). In addition the organism may be cultured in vitro. Boch and Neurohr. Experimental studies have recently been able to identify domestic dogs as the final host (Dubey and Lindsay. gondii cysts in their muscles and/or organs. 1972). The most characteristic signs are progressive ascending paralysis.20 "C) with subsequent thawing (Frenkel. gondii. gondii infection. immunohistology. 1975. 1996). However. 1998). The sexual stage occurs in a final host from which oocysts are excreted. Bradyzoites in the cysts do not survive heating to 65 "C nor freezing (.4-diamino-5-p-chlorophenyl-6-ethyl-pyrimidine) in combination with sulphadiazine is effective against tachyzoites (acute form of the disease) (Soulsby. 1982). Public Health Concern A Although. 1982). if the infection is diagnosed in a herd of camels. Sheffield and Melton. N. 1996). However. should therefore be of public health concern. but no specific antibodies were detected in precolostral sera obtained from the offspring suggesting that there was no fetal T.. shown in the two adult animals.. Detectable levels of the antibodies will not be found until the end of the short period of oocyst shedding in the final host (Dubey and Frenkel. 1982. caninurn was first recognized in dogs in 1988 and has since been reported worldwide (McAllister et al. animal inoculation and pepsin digestion. In abortion cases the parasite may be isolated from the placenta. control measures should be employed. direct agglutination test and ELISAs. In some intermediate hosts such as sheep and pigs. employing several tests. the antibodies may be demonstrated when the viable T. treatment of ovine toxoplasmosis with a combination of sulfamezathine and pyrimethamine proved successful (Buxton et al.302 Parasitic Diseases dii oocysts. it is a time-consuming and expensive test and has been replaced by a range of others such as: complement fixation test. molecular biological techniques (PCR).1 .Intervet) is available for use in sheep. Foodstuff should be stored so that cats. gondii..I Neosporosis 2 Neosporu caninurn is a protozoan parasite earlier confused with T. hitherto no pathological evidence of such infections has been reported. Oocyst shedding is reduced and partly inhibited in infected cats given this combination (Frenkel. Antibodies to T gondii were . there is great uncertainty whether camelids harbor T. The most commonly used serological test has been the classical dye test of Sabin and Feldman (1948) traditionally regarded as the definitive test.. 1967. i 5. particularly . indirect fluorescent antibody test. remained clinically normal and one delivered a healthy offspring (Jarvinen et al.:i Oocysts in the final host may be found in the feces. 1999). There is to the authors' knowledge no reported treatment of toxoplasmosis in camelids. Diagnosis . A large number of different serological methods have been used for the demonstration of antibodies to T.

Anderson. Two dogs fed 500g each of musculature from esophagus collected from 30 camels slaughtered at a Cairo abattoir started shedding H. 1997). and M. It is regarded as the most common cause of cattle abortions in the USA.. Protozool. Experimental infection in mice of Cyptosporidium muris isolated from a camel. B. Although the parasite is closely related to T. employing a direct agglutination test. 1994.1. References Abbas. Rec. Vet. 1995) also found that dogs experimentally fed dromedary camel meat shed H. 3 8 165-175. Balantidiasis in a camel. vkt.A. 1994. 40: Abou-Eisha A. United Arab Emirates. caninurn will infect or cause disease in humans (Fig.C. Pays TYOP. heydorni which has ruminants as intermediate and dogs as final hosts has now been also isolated from dromedaries. known. Cryptosporidial infection in man and farm animals in Ismailia Governorate. gondii there is no convincing evidence that N. Sci. J.. Mkd. A. Abomasal cryptosporidiosis in cattle. 1991. El Zubeir and T. unpublished).C. 42: 107-111. M. 5.E. H. heydorni oocysts from day 8 and 10 respectively for 5 and 7 days (Nassar et al. Antibodies to N. Sakkir. However. Yassin. reported finding antibodies to the parasite in a few of 161 camels in Egypt. 231-233. Hammondia hammondi with a rodent-cat cycle had been . Preliminary studies indicate that camels may become infected with the parasite (Naeslund. B. Polymyositis and hepatitis may also occur. 1987.Protozoal Infections 303 Figure 138 Neospora caninurn cyst in the brain of a mouse (courtesy of Prof. J. 138). caninum have been demonstrated employing an ELISA developed earlier for serology in dogs and cattle (Bjoerkman et al. Italy) of the hind limbs. B. 13: 787-92. Ali. Tech. 1983). Abdelaziz. Pathol.M. heydorni oocysts.H. Giza. (1998). Anderson. P Fioretti. Elev. Whether this parasite infects camels has not yet been properly documented. Vet. Warrag and Hussein (1983) and Hillali et al. B. 1987.13 Hammondiosis Previously only one species. Survey of antibodies against various infectious disease agents in racing camels in Abu Dhabi.M. Survey for certain zoonotic diseases in camels in Sudan. 2 4 235-238. There are at present no effective control measures to prevent disease or infection. Rev. Hilali et al. . (1992. Vet. Rev.. 110 506. Med. Afzal. 1982. Neosporosis also affects cattle (intermediate host) and is a relatively common cause of abortion and neurologically associated limb disorders in calves.T. and M.

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Pellerdy. Hodgin. Baker (eds.276. vol.. J.P. Toxoplasma. 44: 214-215. Toxoplasma infections in domestic animals and their importance in meat inspection. Coetzer. W. Jordan.O. Hyg. Connor. 1975. Munch. Blewaska. J. p.R. Academic Press Inc. Rome. Further studies in the use of monensin in the control of experimental toxoplasmosis. Proceedings of the 10th Conference of the World Association for the Advancement of Veterinary Parasitology.W. Morsy. 1964.W. Am.J. Abt. and O.Zur Chemopmphylaxeund Therapie der akuten Sarkosporidiose. S. p. Fleischwirtschaft 9: 971-973. Foreyt. 1988. Australia. and other tissue cyst-fonning coccidia of humans and animals. Zentralbl. and A. McColgan and C. B. Comp. T. Sudan. 9-30.. J. Tieriirztl. Vol. A. Mulligan (ed. Leptospirosis and coccidial infection in a guanaco.A. R. S. Med. Sci.): Parasitic Protozoa. 2. J.E..P. 1983. 78. 1984. Fayer and N. Trypanosomiasis in Eastern Africa.J. A. 6. 2 Orig. In: J. Trypanosomiasis Control and African RuraI Development. L. S. 98: 225-236. A. Publishing House of the Hungarian Academy of Sciences. 1967. Kreier and J. 1999. C. R.J. Budapest. In: J. Fayer. Jama. C. 1994. 1974. Blewett.M. African animal trypanosomiasis. Shillhorn van Veen. 784-786. Effect of amprolium on acute sarcocystosis in experimentally infected calves. Stephen.M. pp.D. 1442-1444.J. 4 7 1674-1676. 171. D. London. Neospora. 185: Hornby. Akademiai Kiado. H. In: J. pp. R. Richter.C. A. 1981.P. Dubey. Indian J. pp. In: H.): Tropical Parasitoses and Parasitic Zoonoses.R. Khalil and P. Pergamon Press. A note on the prevalence of Toxoplasma antibodies among camels and pigs in Hissar. Clinical manifestation of the trypanosomiasis in livestock and other domestic animals. Johnson. Finlayson. USA. London and New York. M. A. Sharma. G. Unwin.. Feline toxoplasmosis. Garnham.A. Trees. Heydorn. lasalocid and monensin against experimentally induced sarcocystosis in calves.. M. Anim.C.M. Thomson and R.): Proceedings of the 1st International Congress of Parasitology. Bornstein. 167-205. Pathol. 1981. Integrated control of protozoan diseases of livestock. 61: 932-936. Buxton. M. Rifaat. Rommel. 1986. (Chemoprophylaxis and therapy of acute sarcosporidiosis). 1988. Musa and EM.P. Berl.): The African Trypanosomiasis. Perth. 510-516. Cape Town. Lappin. In: The International Symposium on the Development of Animal Resources in the Sudan. p. Coccidia and Coccidiosis.C. 1947. The Sarcocystis murk infection as a model for research on the chemotherapy of acute sarcocystosis of domestic animals.): Infectious Diseases of Livestock with Special Reference to Southern Africa.. D. 250 268. A. H. Rommel. Italy. Gautam. India. Khartoum. Matuschka. Dunsmore (ed. ASSOC. Corradetti (ed. Oxford University Press. Vet. H.W. Am. San Diego. California. .Protozoal infections 31 1 Further reading Boch. Sarcocystis. M. 1965. T.E. pp.A.E. Georg Allen. 1965.P. Tustin (eds. Bakteriol. J. In:A. Wochenschr. Longman. 28-34.A. Parasitol. L.Vet. 1993. Salem Shafia.9 4 229-234. Schwerdtfeger and S. Res.R. Evaluation of decoquinate. 1986. In Practice 21: 578-587. J. Stationary Office. Comparison of seroepidemiological findings of antibodies to some infectious pathogens of cattle in camels of Sudan and Somalia with reference to findings in other countries of Africa. 1970. Haralambidis and F..

NWC) Occurrence OWC NWC Location Sarcoptic mange Psoroptic mange Chorioptic mange Demodectic manae Tick infestation Spinose ear tick Sucking lice Biting lice Fleas Flies Sarcoptes scabiei Psoroptes sp. the Table 56 Arthropods of camelids Disease Species Arachnea and the Insectea. Ambylomma spp. the latter especially in Peru. pharynx Skin Skin Skin Lymph nodes . both within the phylum Arthropoda. Hyalomma spp. which may directly or indirectly cause a great diversity of health problems.2 Infestations with EctoDarasites I . which has the largest NWC population (Alvarado et al. orif ices Skin. Some ectoparasitesplay a significant role in many disorders. 5. . 1966). Demodex SD. Sarcophagidae Calliphoridae Oestridae Glossinidae Tabanidae Culicoides Linguatula serrata + + + + + + + + + ~ ~~ + + + + + + + + + + + + + + + + + + Biting midges Tongue worm Skin Skin Skin Skin ~____________ Skin Skin Skin Skin Ear canal Skin Skin Skin Wound. I . some biting insects are vectors of disease agents such as T. NWC) Choriopfes (OWC. For example.1 Classification of Arachnea Phylum Arthropoda Class Arachnea Subclass Acaria Order Astigmata (Mites) Family Sarcoptidae Sarcoptes (OWC. Both are regarded as the two most economically important diseases in camelids. I Camelids like other livestock are exposed to and affected by a range of ectoparasites (Table 56). The ectoparasites of camelids can be classified into two zoological classes. Rhiphicephalus spp. and the mite Sarcoptes scabiei is the cause of sarcoptic mange. evansi. perineum Nose.5.. Damalinia breviceps Vermimvlla SDD. lxodes spp.2. Chorioptes sp. NWC) Family Psoroptidae Psoroptes (OWC. Otobius megnini Microthoracius spp.

decoloratus (OWC) Rhipicephalus spp. gemma (OWC) A. (OWC. pulchellus (OWC) R. The sarcoptic mites differ from most other mange mites. asiaticum (OWC) H. infection occurs when the mites become dislodged by their host scratching or rolling on the ground. NWC) Order Metastigmata (Ticks) Family Argasidae (Soft ticks) Ornithodoros savigny (OWC) 0. protonymphal and tritonymphal stages. franchini (OWC) H.2. The mites are rarely found beneath the stratum germinativum. The causative mite is Sarcoptes scabiei.tholozani (OWC) Otobius megnini (NWC) Family Ixodidae (Hard ticks) Hyalomma spp.2 Sarcoptic Mange Sarcoptic mange occurs in more than 100 species of mammals including humans. detritum (OWC) H.It has an oval. H. scabiei consists of egg. Her lifespan is about four weeks and the development time from egg to adult is about 12 to 16 days. All three developmental stages (including the adults) are capable of migrating on the skin surface. R. Fomites also play an important part in the transmission of the mites.lahorensis (OWC) 0. The eggs are produced at a rate of three to four daily. impressum (OWC) number of subspecies or variants. The fertilized female lays her eggs in tunnels. ~ O Z O C ~ ~(owc) ZUS 5.Infestations with Ectooarasites 313 Order Prostigmata Family Demodicidae Demodex (OWC. Due to the continual outgrowth of the epidermis the burrows containing the mites and eggs are mostly found in the comeum. The mite is thought to have a . scabiei var cameli. whereby infection may take place indirectly. S. scabiei var. anatolicum (OWC) H. hominis. The different isolates or subspecies are morphologically indistinguishable. they inhabit the epidermis of the skin excavating tunnels in the outer cell layers. Sarcoptic I Amblyomma spp. lepidum (OWC) A. rufpes (OWC) H. S. variegaturn (OWC) Boophilus spp. Epidemiology and Transmission Mection is mainly through direct contact. The eggs hatch in 3-5 days and larvae with three pairs of legs emerge (Fig. The mites burrow in the stratum corneum through the dead cell layers until they reach living cells in the stratum granulosum and stratum spinosum. each designated according to which host it has been isolated from S. scupense (OWC) H. The disease in humans is generally referred to as scabies. the host-specificity is not complete and transmission from one host species to another may occur. Life Cycle The developmental cycle of S. 1978). Morphology Sarcoptes scabiei belongs to the burrowing mites (Fain. However. ventrally flattened and dorsally convex tortoise-like body (Fig. 139). 140). larval. r. sanguineus (OWC) Dermacentor spp. B. However. A. dromedarii (OWC) H. aucheniae etc. NWC) lxodes spp. scabiei var. appendiculatus (OWC) R.

Nayel and Abu-Samra (1986 a) found that S. 1989). scubiei of camels remained viable away from their host for 4 days. However. Alvarado et al.. scubiei var. During the dry season in the tropics. horses and humans has been reported (Mellanby. indirect transmission may occur. sheep and goats. scabiei mite (left) mites can survive outside their host for several days and remain infective (Arlian. 1989) if the microclimate is sufficiently moist and cool. The disease also occurs worldwide in a wide range of wildlife species (Bornstein. The infection is endemic in some areas with epizootics occasionally resulting in high mortality in wildlife. aucheniu to sheep. S. The infection is regarded as highly contagious and common among many animal species. and a close-up of a female 5. scubiei isolated from naturally infected sheep and goats have been successfully transferred to dromedaries (Nayel and Abu-Samra. dogs and camelids. the mites most likely do not survive for long o f the host. 1966). 1966. It is particularly prevalent in swine. most probably during the cool and moist part of the night and early morning hours. in f crowded wet places such as waterholes. 1995). 1986a. and less so in cattle. It is often . Transmission of S. scubiei mites may remain infective between one half and two-thirds of their survival time (Arlian. Observations indicate that when dislodged from their host. Sarcoptic Mange i Camelids n Sarcoptic mange is regarded as one of the most prevalent and serious camel diseases (Lodha. b). 1946. S. 1983). equines. Higgins.314 Parasitic Diseases Figure 139 Sarcopres scabiei with eggs from the skin of a dromedary (right).

It is often cited that animals in poor condition are more prone to infection (Lodha. Nayel and chuk. Most authors report tica" was previously widespread in North that the humps and dorsal aspects of the American captive camelids where it ap.companied by intense pruritus with excotion is still highly prevalent among the riation and secondary infections. 1973. The disease "sarna sarcop. udder. 1545.However. These lesions are often acturies (Alvarado et al. some reports state that the infection is more prevalent in younger animals (Rathore and Lodha. 1966. and 1826 killing twothirds of the animal population.sions on the dorsum (including the hump) ans and farmers considered sarna the most both in naturally and experimentally inimportant disease affecting NWC for cen. routine deworming with ivermectin (Rosy.fected camels. Abu-Samra (1986 a. The in.body may be affected. and shoulder fection is also common among NWC (Fig. It can generally be regarded ing on the medial aspect of the thighs or inas a chronic deb'ilitating condition with guinal region. Nayel and Abu-Samra. 1966). 1983.According to an old monograph by Cardozo (Alvarado et al. 1998). 1986.1984). 1983. this is controversial as others report that animals in very good condition can also become infected (Nayel and Abu Samra. found a higher prevalence in Saudi Arabia during the hot summer months. There are conflicting opinions regarding the seasonality of the disease. scabiei (Nayel and Abu-Samra. c) found mangy leA few decades ago Peruvian veterinari.. b. 1986~). 1992). medial high morbidity and low mortality. .Infestationswith EctoDarasites 315 Figure 140 Larvated Sarcoptes scabiei eggs from the skin of a dromedary to be the main cause of financial losses (Guerrero and Alva. 141). Any camelid regardless of sex and age may be affected by S. the head and neck.. Some authors describe a quiescent phase usually coinciding with winter (Pegram and Higgins. Rathore and Lodha.Higgins. However. The itchherds of the campesinos and is considered ing and rubbing causes alopecia. cited by Windsor et al. others finding a higher incidence in the winter (Lodha. In severe cases any part of the (Fowler. 1966. 1966) there were outbreaks of this disease in 1544. 1992). Rathore and Lodha..areas of the flanks. The infesta. 1548. 1 9 8 6 ~ )Higgins (1984) on the other hand . ranked second in importance to all the disorders in dromedary camels (Pegram and The first signs of infection Higgins. However. 1973. and second only to try. 1973). probably through (Lodha. 1984).neck are usually free of any signs of mange pears to be decreasing. 1966. 1992). Higgins. 1986 c). 1989).are small hyperemic papules often appearpanosomosis.

1991. and crusting. The latter may be rubbed away revealing a "red raw surface". The lesions spread and aggravate excoriation. Figure 142 Severe chronic camel mange . If untreated. 142). bite and scratch trying to alleviate the extreme pruritus. Within a few weeks. camels with severe acute sarcoptic mange decondition. The incubation period is believed to be around 2 to 3 weeks (Lodha. Bomstein and Zakrisson. the acute disease may develop to the chronic stage (Fig. (1994. 1993). resulting in more scabs. 1981). in experimentallyinfected dogs and rabbits Arlian et al. Hyperkeratosis and proliferation of the dermis leads to the skin becoming thicker. seriously disturbing the animals. However. Grazing and even milk production may show a rapid decrease. 1966. Experimental transmission studies in dogs and pigs showed that the incubation period is dependent on the number and condition of the mites transmitted (Bomstein. The incubation period is greatly reduced if the animal is reinfested after clinical recovery from a previous infection.31 6 Parasitic Diseases Figure 141 First signs of camel mange Hairless areas with serous exudation forming scabs follow the first acute signs and itching may increase. Camels with generalized mange may eventually die from extreme wasting caused by the reduction in normal feed intake due to intense irritation and pruritus (Abu-Samra and Imbabi. Localized or generalized acute exudative dermatitis develops. which is the stage most often encountered in the field. Immunity Absolute protective immunity following recovery after treatment is not known. 1996) demonstrated partial immunity or protection against challenge infections. alopecia. erosions and wounds. The camels desperately rub. fissured. and corrugated-appearing like a dried cracked field of clay. Higgins. 1983).

keratinous and epidermal mate. The chances of making a correct diagnosis by skin biopsies are less likely because S. 1995. 1999). macrophages. The scrapings should first be examined scrapings from the individual mangy animal. pigs and guinea pigs have been demonstrated 2 to 5 weeks following infection (Bornstein and Zakrisson. In mange.In naturally infected dromedaries Bornstein et al. varying degrees of superficial dermatitis. The when applying multiple skin scrapings. demonstration of the tive tissue and infiltration with lymphomite is possible by taking deep skin scrap. 143).Infestations with Ectoparasites 317 It was shown by Alvarado et al. scubiei mites are rarely seen in biopsies.and macrophages. which are placed into a ni rial are collected and placed into a broad water bath of 37°C for a few hours u t l the mouthed centrifuge tube. 1993. This similarly applies to to the sediment. hyperplasia and para. recommends adding 20mL of KOH soluFinding S. 1995). scubiei by an ELISA. However. (1966) that some animals in alpaca herds were more susceptible. Antibodies to S. Apart from the char. 1984). scubiei. Also.done by mildly heating the material to ings should be done by parallel strokes of stimulate the mites into migrating from the a sharp scalpel blade at the margins of the skin-scabs and debris to the surface. disease. Higgins giant cells (Abu-Samra. Eosinophils and mast cells are be caused by S. (1997) also demonstrated antibodies to S. epidermal spongiosis. This is "valley" areas (Higgins.glass to search for living mites that are stimsions where the skin is thickened and cor. 1966. In chronic le. 1984).ulated into movement when the environrugated. Bornstein et al. which is then examined camels (Higgins. Stud. some eosinophils and ings from several affected areas. The earliest lesions sometimes intermingled with neutrophils are often unnoticed. red foxes. Care should be taken to scrape at least with a stereomicroscope or a magnifying 1cm2 area of the mangy skin. lesions of acute sarcoptic mange often suggest a S. 1993). The supernatant is discarded sarcoptic mange is less than 50% (Hill and and one to two drops of glycerin are added Steinberg. alopecia dermis often show proliferation of connecand hyperkeratosis.tion to the skin material and placing the ies of infected dogs have shown that even tube into boiling water for 30 minutes. Bornstein. there is a quiescent period during which one may mistakenly think that the animals have been spontaneously cured. If no mites are obing deeper scrapings utl capillary oozing served.ing them easier to see. Higgins (1984) four scrapings should be taken per animal. according to under a low power light microscope in Higgins (1984) due to the seasonality of the search of the mites and their eggs. All three died of sarcoptic mange. loo%potassium hydroxide (KOH) ni occurs on the whole scraped surface. these findings alone are not conclusive because other conditions may cause similar skin lesions (Lodha. scrapings should be made in the mental temperature is above 18°C. 1981).. sample is then centrifuged at 1500 rpm for the probability of vedying a diagnosis of 5 minutes. scubiei in naturally and experimentally infected dogs. The scrap. scabiei infection due to hypersensitivity reactions seen in the skin. This is to be followed by tak. All solution is added to each tube containing scrapings.cytes. Epidermal (1984) stressed the importance of taking erosions and crusting are often seen due to proper and adequate numbers of skin self-trauma (Fig. Abu-Samra and Imbabi. makmange lesions. The papillary layer and acteristic clinical signs of pruritus. Lesions in three naturally infected alpacas in the above-mentioned study were left unchecked. At least three to material has disintegrated.the skin scrapings.and hyperkeratosis may be obDiagnosis Any pruritic skin disease may served. scubiei is often difficult. Histologically. .

1966). 1966. and handling of animals (Basu Differential Diagnosis Several skin dis. riding.scabies: pronounced intensive itching durtact with abrasive surfaces when lying ing the night. irritant dermatitis associated with con. scabiei in naturally infected camels (Bornsteinet al. 1927. idiopathic hyperkeratosis (associated with zinc responsive dermatoses recognized in NWC). 1990).~ Figure 143 5. goat. Only a few sarcoptic mites burrowing into the skin of the animal can provoke a generalized hypersensitivityreaction leading to the typical acute signs of mange in the host. infected by the itch mite S. Bornstein and Wallgren. scabiei var horninis). Zoonotic Potential iin Humans occasionally become infected with S. infestations with other ectoparasites mals to humans are called pseudo-scabies. Delafond and Bouguinon in eases may mimic sarcopticmange. These are: 1895 were the first scientists to discover 1. 1991. 1987. Schillinger. as has been shown in sarcoptic mange of humans and pigs (Davies and Moon. 1996. fox and llama (Leese. Fain. scabiei from ani3. Direct transmission between the herders and their animals is most likely during milking. Basu et al.. sheep. 8. particularly the papule and scab formation stages. 1995. ringworm. scabiei in llamas at the MusCum National d’Histoire Naturelle in Paris.et al.. Raisinghani and Kumar. fections by s. 2. horse. Alvarado et al. Ckorioptes sp. ferret. scabiei from camels exhibit signs similar to those of classical 1989). 1997). An indirect diagnostic ELISA has been developed for dogs and pigs to detect antibodies to s. distinguished from true human scabies (in4. note that mixed infection S. camelpox.... 6. scabiei (Bornstein et al. inhalant or food allergies (Rosychuk. Two stumay occur. 1989). skin necrosis). (incl. scabiei from camel. scabiei mites from skin biopsies (HE stain) The lesions of mange are most probably caused by hypersensitivity reactions. Humans 5. 1996) and alpacas (Alvarado et al. Preliminary studies also show that a similar ELISA detects antibodiesto S. 1966).).318 Parasitic Diseases _. 7. endocrinal dermatopathy. Staphylococcus aureus dermatitis. Erythema and papule formation are seen mainly in the interdigital down (Rosychuk. 9. 1996). pig. Demzatopkilus congolensis (contagious dents were accidentally infected by the affected llamas (Alvarado et al. .. 1997). chamois. 1978. Cross-infections by S.

e. Pseudo-scabies is usually self-limiting.Infestationswith Ectoparasites 319 spaces of the hands. The first red spots were detected on the right forearm 24 h later.3g) or PriodermB (malathion 0. it is essential that the whole animal be covered with the solution. organophosphorous compounds and synthetic pyrethrins. 1986c). More recent drugs are applied parenterally as well as topically. the forearms. It is believed that the mites had crawled over the lead rope onto the arm. is recommended (Nayel and Abu-Samra. the application of a 15% solution of salicylic acid.. 142) was walked for 6 h to a different location. the lesions receded within 72 h. The clinical signs will gradually wane and disappear within about two weeks when contact with the infected animal/s is interrupted or the animals are treated. Figure 144 Erythema with papules on a human leg caused by Sarcoptes scabiei from a dromedary Treatment and Control a1 effective acaricides available today. Before acaricides are applied. scabiei identified. Some are conventional preparations for skin application: organochlorines. Additional hand-dressing of chronic. Skin scrapings were taken from the leg and s. Secondary infections can occur leading to pyoderma. elbows and axillary folds (of milkers) and between the thighs (in riders). The salicylic acid solution is applied a few times at an interval of 2-3 days followed a day or two later by washing with soap and water. a keratolytic agent. such areas should preferably be washed with lukewarm water and soap to soften the scabs and keratinized material.5% w/v) for 3 consecutive days and StromectoF 6mg (ivermectin) orally. the ayurvedio preparation "Charmil" gel (Pathak et al.Also effective against nematode infections are endectocides or macrocyclic lactones (avermectins and milbemycins). After treatment with JacutinB emulsion (lindane 0. cameli when a mangy camel (see Fig. As long as there is continuous contact with mangy animals. preventing a reinfection. Local topical application of the acaricide only over visible lesions is an incorrect procedure. 1995).In addition. Scales and detritus may be removed with a firm brush. hyperkeratotic areas is often necessary. old remedies have been recently reported to be affective against sarcoptic mange in dromedaries. There were no lesions on the head and very few papules on the body. Eight days later severe erythema and papules were observed on both legs (Fig.g. the clinical signs will continue in the contact person. the flexor surface of the wrists. One of the authors accidentally became infected with S. 144) and both arms with severe itching. In addition. scabiei var. When using acaricides as dipwash or sprays. Extra local hand-dressing with the acaricide solution employing a hard brush may also be applied on the parts of the skin .

scabby and corrugated (Higgins. clinical improvement is gradual. but sometimes 4 or more applications are needed until a cure is reached.1%hexachlorocyclohexane(Gammatox@) on chronically infected camels found that 3 days following the first wash with GammatoxB. but may more easily be applied in sedentary herds. moxidectin.. Abu-Samra (1999) reported even better results with 0. Raisinghani et al. Boyce et al. 1991. New endectocides have recently reached the market. Pruritus completely ceases after one week to 10 days following the second injection.. Unfortunately. They . 1996). 1981. doramectin was applied intramuscularly at a dose of 200 pg/kg. Depending on the severity of lesions. Another promising form of endectocides is the pour-ons. and the edema on the legs had subsided. following thorough application of 15% salicylic acid solution. pers.3 Psoroptic Mange Psoroptic mange mites spend their entire life on the skin.. Oukessou et al.g. The injectible modem endectocides or macrocyclic lactones (like ivermectin. The animals should be treated 3 times within an interval of 7 to 10 days. Only two of the severe cases had to be treated twice.. a combination of topical and injectible treatments is necessary. most of the treated camels (75%)became calm with reduced signs of pruritus. 1986. Four weeks after the second injection all previously alopectic areas are covered with growing hair (Hashim and Wasfi. If the same applies to camelids. Ivermectin@ has been shown to be effective and safe in Camelidae and cattle when the same dose and regime is employed (Ibrahim et al.. 1989. doramectin) may cure sarcoptic mange in pigs and cattle. these drugs would be of great advantage to nomadic camel owners. 1993. Camelids need to be well-restrained in the couched position. Kuntze and Kuntze. which are poured onto the skin of the dorsal part of the body.320 Parasitic Diseases particularly thickened. Both ivermectin and moxidectin are marketed for use as pour-ons for cattle with very good acaricidal as well as nematodicidal properties.. The recommended dose is 200 mg/kg given subcutaneously and repeated after 15 days. After treatment. In a trial on 15 camels (9 juveniles. All 15 camels were cured (Mumin. Complete healing of skin lesions was reached on day 145 (Raisinghani et al. this treatment protocol is not always successful. 1983). doramectin) have made the treatment of sarcoptic mange much easier. Six days after the second wash. feeding superficially. 1989). 1999). Some have a longer period of bioavailability in the animal than the ivermectins.. Nayel and Abu-Samra (1986 c) using the acaricide 0. Kumar and Yadav. 1989). 6 adults) showing mild to severe sarcoptic mange. There are indications that one injection of these new drugs (e. The subcutaneous injection is painful to camelids and some diffuse swelling at the injection site may appear after 24 h. comm. Two days after the second wash most of the scales had been shed. resulting in complete recovery from chronic mange after 3 weeks.2.. 1998). 1984. Bayer) applied topically three times. The drug is absorbed through the skin.C. USA) was enough to successfully eradicate sarcoptic mange in a herd of mangy pigs (Jacobsson et al. The topical application of acaricides is very laborious and difficult to carry out under nomadic conditions.. Raisinghani et al.1% solution of phoxim (Seb a d @E. One intramuscular injection of doramectin (Dectomax@. NY. one week apart. there was no pruritus and the restless animals behaved normal. 5. Pfizer. the cracks and fissures started to heal. Hair began to grow 5 days after the third wash.

1966. This stimulates a local inflammatory reaction that exudes serous exudate. A mite may be found in the center of the first papules seen. 1992. It was recently shown that Psoroptes sp. about 0. with a moist surface. see sarcoptic mange.Infestations with EctoDarasites Figure 145 Psoroptes sp. is larger than S.. a characteristic scab will form. Common lesions consist of dry flakes in the ears. Guerrero and La Rosa. flanks and base of the tail. hosts and geographic origins are conspecific (Zahler et al. nares. 1966). The exudate coagulates forming a crust or scab.75 mm long and is oval shaped with all four legs projecting beyond the body. For laboratory procedure. Mites were also found in the perineum. Diagnosis . the male’s rounded abdominal tubercles. but are less commonly found on camelids than S. The dermatitis causes intense pruritus and fiber loss. 1965.. mites are usually found at the edges of the lesions.. (1989) in Bactrians in Mongolia. Gabaj et al. uucheniue) has been isolated from the ears of alpacas in South America (Chavez and Guerrero. (originally named P. Early lesions are small papules about 5mm in diameter. axillae. scubiei. . Foreyt et al.. 8 Clinical Signs Psoroptes sp. 1962). isolates of different phenotypes. The ears may occasionally be filled with purulent discharge reicat sponsible for head shaking and poor coordination. 145). In many countries sarcoptic and psoroptic mange are reportable diseases. scabiei. The dermatitis does not become hyperkeratotic to the extent seen in sarcoptic mange. Some of the features that distinguish Psoroptes from the other common non-burrowing mite Chorioptes are the pointed mouthparts. groin. Fowler. (1992) recorded the only documented case of psoroptic mange in dromedaries and Werner et al. from the skin of a dromedary 321 reportedly infest camelids. 1998) and therefore only one species is mentioned in the text. ’ Skin scrapings reveal the mites. Within 5 days.The female’s third pair of legs end in bristles instead of suckers. Morphology Psoroptes sp. neck and legs (Alverado et al. yellowish. and the three jointed pedicels bearing funnel-shaped suckers on most of the legs (Fig. Lesions are generally found around the shoulder and along the back. communis var. 1998) and found in the ears and necks of llamas (Alverado et al. However. The piercing and chewing mouthparts of the mite can severely damage the skin.

goats and equines and... ly has one species been recognized (Essig et al. It includes eggs (70-90pm x 19-25pm). was also responsible for mange in a herd of alpacas from Chile recently imported into France (Petrowski. Iowa State University Press.5 Demodectic Mange The preferred site of the burrowing mite of the genus Demodex is at the hair follicles and sebaceous glands of the skin.2. Pour-on 1% (flumethrin). Bayticol. It has been shown that pourons may be used. but has rounder mouthparts and tarsal cup-shaped suckers on short unsegmented pedicels.51. elongated 0. The mite is most probably transmitted from the dam to the offspring during nursing. lives on the skin. closely resembles Psoroptes sp. udder and legs in cattle and on horses’ legs below the knees and hocks. Veterinary Clinical Parasitology.An infestation of Chorioptes sp. The thorax has four pairs of short stumpy legs. three alpacas and two camels. 1998).4 Chorioptic Mange The mange mite Chorioptes commonly infests cattle. 146) is found in all domestic mammals and hu- Figure 146 Demodex mite from the skin of a dromedary (courtesy of Professors Sloss. unlike S. Five days after the single topical treatment was applied. Unlike Psoroptes sp. (Fig. Kemp and Zajac.5 to 4 0 mm in length. Infestation with Chorioptes is most probably rare in camels. no more living mites were found and the healing process of the skin lesions began a few days later. and lasts 3 weeks.2. Only recent. one larval stage and two nymphal stages. 1999). its mouthparts allow the mite to feed on scales and other skin debris. It is usually regarded as a mild condition.2 mm long mite.. Demodex sp. Chorioptes sp.322 Parasitic Diseases 5. However. USA) . lesions may resemble those caused by Psoroptes sp. 1994.. 1mL/10 kg applied on Bactrian camels with psoroptic mange proved to be effective. sheep.5 mm thick. 1984). causes pruritic mange mostly seen on the neck. The abdominal tubercles of the male are clearly truncate. scubiei. Chorioptes sp. having hyperemic skin covered by scabs 0. All the acaricides used topically are effective against the Psoroptes and Chorioptes. 1984)and in the Netherlands on one llama. It is a cigar-shaped. The LC is only partially known. It has been reported on a Bactrian camel (Higgins. 6th ed. tail. one of which had ”foot mange” (Cremers. 5. Adult mites are about 3.

and 60 species according to Hoogstraal (1985) and Gothe and Neitz (1991). which drops off mia” (Rutagwenda. the host after engorging and then moults Lesions. viral and rickettsia1 diseases in they attach during their parasitic life cycle many animal species. some ticks also cause paralysis in camels as well as in other livestock 43 species of 10 different genera have been incriminated in causing toxic reactions according to Fowler (1998). has been reported on dromedaries in Iran where the eyelids of 15%of the camels were infested (Rak and Rahgozar. i. the soft ticks. Infested camels are often irritated and exhibit pruritus.). The one-host ticks: All the three instars enThere is a significant loss of blood: about 1 gorge (take their blood meals) on the same to 3 mL for every tick completing its blood host. the Ixodidae. Demodex sp. canis. 1956). these mites may cause mange.ent host for every instar.e. The former have a rigid chitinous scutum that covers the entire dorsal surface of the adult male. commonly occurs in llamas and alpacas in Bolivia (Sqire. The attachment sites of ticks commonly show dried blood with scabs (inflammatory reaction) and frequently these sites. Being lifecycle. R. mans worldwide.pers. In some animals. In general. the most significant sequela to infestation is the damage to the hide. The nymph after camel (Steward.2. 1972). A Hyalomma sp. some Rhipicephalus spp. the larvae and nymph allowing the abdomen to swell after feeding. 1984). the hard ticks and the Argasidae.bovis etc. The number of hosts to which bacterial. Thousands of ticks may be found on the same animal: e. D. was isolated from camels exhibiting mange on a ranch in Kenya (Bornstein. The two-host ticks: The larva engorges the same infested animal. . The two ecdyses also take place on meal. some Ixodes (e.varies from one to three. ricitick’s mouthparts and may attract flies. of particular severity in dogs.The high calf mortality rate of host: e.6 Infestations with The soft ticks lack a scutum.There was no evidence of any secondarybacterial infection in the investigated camels.g.g.g. Most of the species are named after their hosts. are made by the on the ground: e.tus) spp. commun. The mite most probably also infests other NWC in other countries. nus) and Rhipicephalus (e.5cm2 moults and the imago then seeks a new skin surface. Boophilus spp. According to the tor role appears to be much less important number of hosts they require to fulfill their in camelids than in other livestock. develop into large ulcerations (sores) (Hoogstraal. ticks are classified into the folblood-feeders. I . However.infestationswith EctoDarasites 323 ways to secondary bacterial infections. tick infestations may cause local and generalized disease causing damaged hides and mortalities. Demodex sp. Metastigmata (Ticks) Ixodids spend a relatively short period Ticks are important vectors of protozoal. was said to have caused the death of a and moults on the host. Ticks belong to two families. D.feeding drops onto the ground where it ed by 100 nymphs and adults per 2. following infestationsby Amblyomma lepidum. 1950) that had been infest. This chitinous scutum covers only a small area in the adult female. 5. Allegedly. nor were there any significant histological changes other than distention of the hair follicles. Demodex sp. appendiculasome causing myiasis y d are also gate.g.g. causing economic loss. although small. In bovines. their vec. These follicular mites mainly live as commensals in the skin. ticks may cause debility lowing three groups: and anemia in camels and other animals. on the host. 1975). 20% encountered in some camel herds in The three-host ticks: These need a differKenya has been attributed on ”tick-ane.

Dolan et al. During January and July in the Yemen Arab Republic’s hot arid lowlands the tick seems to produce two generations per year. prevalence. Yemen Arab Republic and Kenya have been published by Pegram et al. There are few reports that list particular species of hard ticks found on NWC. and the numbers may be very high. the sand tampan. Comprehensive checklists of ticks found on camels in Ethiopia. is a common soft tick on camels in hot and arid deserts. Ornithodoros savignyi. Some species of ticks may adapt to different climates by adjusting their LCs accordingly. 1998).2. However. 1999). lahorensis and 0. dromedarii to be the most common followed by H. 1992). Masses of these ticks may be seen on the sand in places where large numbers of animals congregate. but only one generation per year in the cooler highlands. This species sometimes uses three hosts for better survival (Hoogstraal et al. this tick uses three hosts for completing its LC (Hoogstraal et al. Other genera of hard ticks found on camels are Amblyomma. 1984). excavatum is also often found in large numbers wherever domestic stock is plentiful in the Middle East and northern Africa. Large . Jonsson and Rozmanec. There are three genera of veterinary sigruficance in the family Argasidae: the bird ticks. 147 a-e). 1993) and in India (Singh and Chahbra. particularly on llamas in the western USA. during treks (Fowler. in cracks and crevices seeking shade. although they can infest other mammals (Higgins. and Ixodes holocyclus caused tick toxicosis in a llama (Vogel. andtolicum. H. It is reported that it may employ either a two-host or a three-host LC (Higgins. 1987). such as holding grounds and marketplaces. Egypt. there are only a few tick species (adults) that are camel host-specific. 1997). (1981. which is classified as a two-host tick infesting a wide range of domestic animals.1 Ticks Found on Camelids A large number of tick species may infest OWC. Three camel soft tick spe- cies are recorded: the most important is Ornithodoros savignyi. The subspecies H. (1981) is recommended. particularly camels and cattle. Van Straten and Jongejan (1993) recently reported on camel ticks in Sinai.6. 1981). asiaticum. Hard ticks are reported to be a problem. (1983) and Pegram and Higgins (1992). anatolicum anatolicurn. 1995. The cattle tick Boophilus microplus has been reported attacking dromedaries in Australia (Kennedy and Green. The latter genera Ornithodoroslive in sandy soils. and Singh and Chhabra (1999) on ticks in Haryana in India. the ear ticks and the sand tampans. even in very hot areas. followed by 0. On cattle. It is thought that these species only survive where camels are present. Singh and Chhabra (1999) found H. the soft tick lacks a scutum and its integument is leather-like. H. Amblyomma parvitarsum Neumann was found parasitizing vicuiias in Peru (Dale and Venero.324 Parasitic Diseases As the name implies. the excellent study on ticks of Saudi Arabia by Hoogstraal et al. biology and epidemiological significance in camels in the Middle East and North African regions. It can also attack humans and other livestock. dromedarii. and is found on camels in large numbers. Dermacentor sp. scupense (Pegram and Higgins.. The tick is found to be active throughout the year. 1984). dromedarii is a desert-adapted two-host tick widely found in arid lands wherever camels are reared. The most important tick genus infesting camels is Hyalomma with the species H.. The immature stages are found in rodent burrows. 1977). tholozani (Fig. Another example of an extremely adaptive tick is H.. For comprehensive information regarding tick distribution.franchini and H. H. 1981). Rhipicephalus and Dermacentor. 5. with an adult peak in June and July (McCartan et al. 1982). particularly goats.

infestations with Ectoparasites 325 Figure 147important hard and soft camelid ticks (courtesy of Mr. K. Dubai Municipality. Valsan. UAE) Hard ticks: (a) Hyalomma dromedarii (male and female from dorsal and ventral) . Pest Control.

326 Parasitic Diseases (b) Amblyomma lepidum (male dorsal and ventral) (c) Rhipicephalus pulchellus (male dorsal and ventral) .

Infestations with Ectoparasites 327 (d) Dermacentor variabilis (male and female dorsal) Soft tick: (el Ornithodoros savignyi (dorsal and ventral) .

inguinal. The adults do not feed and may hide for several months in crevices of buildings and feeding troughs where the females lay their eggs. Ticks are easily seen on their predilection places. On longhaired animals. which may infest other hosts. in a herd of dromedaries from Kenya (Younan and Bornstein. The skin may get rough and thickened with scar tissue. in/on the ears. Pathology and Pathogenesis Camels may be infested with ticks throughout the year. com. one species mentioned causing disease in llamas is the spinose ear tick (Otobius megnini). Among the soft ticks (Argasidae). sheds. around the eyes. suvignyi may be painful. thereby interfering with the well-being of the host. 2000).. which may attack a host within 10 days seeking out the ears. the nostrils and in the nose. anemia and deconditioning will develop. including humans. It is only the larvae and the nymphs which are parasitic. These hatch to larvae.328 Parasitic Diseases Figure 148 Hyalomma dromedarii between the front legs of a young dromedary J numbers of this tick may be seen crawling on the sand where large numbers of animals are kept. lips. especially during the cold months of the year. numbers may fluctuate with the climate. and axillary regions. often relatively deeply imbedded in the skin. The larvae may survive up to 4 months without finding a suitable host. The nymph moults twice within the infested ear and drops to the ground. Wounds may become secondarily infected. The soft ticks may cause problems in llamas and alpacas in certain localities in the western USA. Streptococcus uguluctiue was isolated from wounds caused by Hyulomma sp. wooden fences and trees with rough bark. The parasitic stages may remain on the same host for several months. causing irritation and direct injury to the skin. causing excess production of waxy substances and severe inflammation in the outer ear canals. When infestation is heavy. . pers. The ticks on camels are mostly found in the perineal. 148). ticks may go unnoticed. A preferred tick habitat is around buildings. The bites of 0. However. whereafter it moults to the adult stage. leading to pyoderma. but it is not considered to be a significant vector of disease to either humans or livestock. Numbers may be high. between the toes and on the mammary glands (Fig. Animals that are kept on open pastures and ranges are less likely to encounter the spinose ear tick.

8 . More than 60 of 869 known tick species are capable of causing paralysis (Hoogstraal.2 Tick Paralysis Many species of ticks have been incriminated in causing tick paralysis. A bite from a single tick.. A llama in Australia exhibiting typical signs of tick paralysis thought to be caused by lxodes holocyclus did not survive in spite of intensive treatment and removal of the ticks (Jonssonand Rozmanec. 1981). In OWC. Epidemics of suspected tick paralysis incriminating both Hyalomma spp. Sizable numbers of ticks may lead to anemia. have also been reported in Sudan (Musa and Osman. Clinical Signs In NWC.2. It is suggested that heavy tick loads contribute to reduced growth rates and calf mortality (Dolan et al. Table 57 Zoonosis associated with carnelinfesting ticks (Pegrarn and Higgins. praetextatus Thogoto virus 5. anatolicum Thogoto virus H.Infestationswith EctoDarasites 329 Sores are often seen at dermato-mucosal borders on the nose. Gothe and Neitz. 1996). dromedarii that is thought to be the main cause of paralysis. 1998). may kill an animal. dromedarii is the vector of Theileria camelensis (Hoogstraalet al. generalized hyperemia and a severe moist eczema primarily caused by Hyalomma spp. which was reported in the former USSR. Toxicosis is characterized by sweating.2. 1992) Vector Agent H. They recovered following treatment including removal of the ticks.. 1995) and also in seven llamas and one alpaca in the USA (Cebra et al. Tick paralysis occurs in OWC as well as NWC.This virus has also been isolated from the ticks commonly found on camels. Camel ticks are also vectors of viruses infecting humans: Hyalomma anatolicum is an important vector of Crimean-Congo hemorrhagic fever (CCHF) virus. 1990).. excavatum Rickettsia prowazeki H. Dermacentor spp. It caused high mortality (above 24%) in calves in the Sudan (Agab and Abbas.. Seven of the diseased animals showed generalized muscle flaccidity. truncatum CCHF virus ? virus (Paralysis) R. H. it is the larva of H. were identified as causing tick paralysis in two young llamas in the USA (Barrington and Parish. scupense ? virus (Paralysis) H. It is not known whether ticks play any part in introducing secondary bacterial infections to the mammary glands. pigs and avians through toxins from adult ticks.. 1985. 1979). and Rhicephalus spp. Studies of other animal species have shown that there is variable host susceptibility and most probably also a seasonal or annual variability. Dermacentor spp. individual females of several species of hard ticks. 1996). 1963) and that H. The latter occurs in susceptible ruminants. impeltaturn (see also under 2. 1997). (Urquhart et al. The female llama recovered after 3 days after being clipped to remove all the ticks.. marginatum CCHF virus H. gemma may transmit Cowdria ruminantium (Heartwater) to cattle (Karrar et al. under certain unknown circumstances. e. pulchellus Rickettsia prowazeki R. 1983). dromedarii and H. as distinct from tick toxicosis. Vectors of Disease Pathogens I The importance of camel ticks as vectors of disease pathogens for livestock has been described. Tick bites may predispose to myiasis.g. impeltatum Wanowrie virus CCHF virus H. dromedarii Dhori virus Khadam virus CCHF virus Q-fever (Coxiella burnetii) H.6. Pakistan and Nigeria (Hoogstraal. There is evidence that Amblyomma lepidum or A. 1991). lips and vulva. produce neurotoxins which are injected by the tick when it ingests a blood meal.10 Unusual Arboviruses) (Table 57).

preventing acetylcholine release into the synapses of the neuromuscular junctions (Gothe et al. . 1979). synthetic pyrethroids or the macrocyclic lactones). The signs may develop rapidly within a few hours or may take 24 to 48 hours until the victim dies of respiratory arrest from involvement of the respiratory centers in the brain.serum was used without success in tick es. the pathogenesis and clinical manifestation of the disease in NWC is similar to that in other animal species. Reinfestation can occur because of the difficulty of eradicating the ticks from the environment. carbamates. es that react with tissues and saliva of the parasite.2.of Dermacentor variabilis were resistant to ommended. The recently available endectocides possess an extended period of bioavailability but their pharmacokinetics are unknown in camelids. 1982. 1997) curing fluid may help in distinguishing tick paral. Analysis of cerebrospinal kg (Jonsson and Rozmanec. impair physiological responses and/ Chemical Control '13Routine prophylactic or kill the arthropod (Wikel. However. preceded by ataxia.1996). The ability to rise is lost in 12 to 36 hours. 1998). organophosphates. the clinical signs may appear earlier and the first deaths may already occur 3 days following the tick invasion. which is thought to act on the end plates of the motor neurons..330 Parasitic Diseases appropriate acaricides to the predilection sites (chlorinated hydrocarbons. numerous inAccording to Fowler (1998). This can be done by applying the challenge of the larvae. and they progressively increase in severity as they move toward the cranium. control of significant pigs immunized with whole larval extract numbers of ticks attacking camels is rec. dromedarii infestations on camels. Signs are usually not apparent until 5 to 7 days after the tick has begun to feed.6. Ixodes hoZocyclus canine hyperimmune Diagnosis $9 Diagnosis is based on clinical serum is used in affected small animals signs and the finding of ticks known to and calves (cattle)at a dose rate of 0. There is a strong indication that the di. Regular inspection of the outer ear canals followed by treatment is recommended to avoid a build-up of infestation.The tick paralysis in North America is most likely due to a salivary neurotoxin. Loss of all motor functions occurs. Since Trager (1939) showed that guinea tick control is not practiced in camelids as in cattle.3 Tick Control sition. Most cases of tick paralysis in NWC have been reported from non-indigenous regions (Barrington and Parish. However. The first signs of paresis and paralysis are seen in the hindquarters.paralysis of a llama caused by I. holocycZus.about 75% of cases. There is no effective treatment that can neutralize the tick paralysis toxin.1996) in controlling H. Stretch reflexes are also impaired and pain perception remains.5 mL/ cause paralysis. as used for cattle. This can disrupt blood meal acqui5. Subcutaneous injections of ivermectin (10mg/50 kg) are effective in controlling both larvae and nymphs of the spinose ear tick (Fowler. agnosis of tick paralysis is correct if the patient recovers rapidly (within a few days) Vaccination ii?lThe hosts of hematophagous arthropods may stimulate immune defensfollowing removal of the ticks. 1995). According to Musa and Osman (1990). The ear canals may be cleaned manually and solutions of insecticides or acaricides instilled. This hyperimmune ysis from other causes of paralytic diseas. A 1% flumethrin (BayticoP Bayer) pour-on formulation was successfullyused (El-Azazy. It should be noted whether the ticks in the area have developed resistance to a particular acaricide. The drug (1 to 2mL/10kg) was poured from the shoulder along the middle of the back over the hump to the tail.

A certain percentage of the ticks die and the fertility of those remaining may be reduced by up to 70% (Willadsenet al.2.7. NWC) Order Dipterida (Flies) Suborder Brachycerina Family Sarcophagidae (Flesh flies) Wohlfuhrtiu mugnificu (OWC) Wohlfuhrtiu nubu (OWC) Sarcophugu dux (OWC) .2. and the Dipterida (flies). Llamas may suffer from both biting and sucking lice and both may be found on the same individual. autumnalis (OWC. Antibodies produced in the host destroy the cells lining the tick's gut and blood escapes into the hemocele.2 Infestation with Lice There are two orders: the Anoplurida..7. Family Calliphoridae (Blowflies) Luciliu cuprinu (OWC) Chrysomyu bezziunu (OWC) Culliphoru spp. the Siphonapterida (fleas).1 Classification of Insects Among the class Insectea there are several orders of particular veterinary interest: the Anoplurida (suckinglice). NWC) Cephenomyiu spp. The latter have not yet been reported on OWC. the sucking lice.(OWC) Suborder Nematocera Family Ceratopogonidae (Midges) Culicoides spp.7 Insects Found on Camelids 5. the biting lice. Recombinantvaccines have also been developed and are commercially available. The fertility of males is also affected. and Mallophagida. (OWC) Chrysops spp. (OWC) Huemutopotu spp. 149). 1989). Family Glossinidae (Tsetseflies) Glossinu spp. Today there are two types of tick vaccines available for cattle. muzzui (NWC) M . (NWC) Family Oestridae (Bot flies) Cephulopinu titillator (OWC) Oestrus ovis (OWC. the Mallophagida (biting lice).Infestations with EctoDarasites 331 vestigators have been trying to develop anti-tick vaccines.2. Phylum Pentastomida Linguutulu serrata 5. NWC) Hydrotea spp. One crude vaccine is made from extracts of the partly engorged adult female B. Huemutobiu spp. minor (NWC) M . NWC) Phormia spp. NWC) Stomoxys culcitruns (OWC. these vaccines have a limited application and have not yet been developed for Cumelidue. Family Tabanidae (Horse flies) Tubanus spp. (NWC) CochZiomyia hominivorux (OWC. microplus. NWC) M . pruelongiceps (NWC) Order Mallophagida (Biting lice) Dumuliniu breviceps (NWC) Order Siphonapterida (Fleas) Vermipsyllu spp. (NWC) Family Muscidae (Flies) Muscu domesticu (OWC. However. (OWC. Phylum Arthropoda Class Insectea Order Anoplurida (Sucking lice) Microthorucius cumeli (OWC) M . Biting lice have a blunt broad head that is distinctly different from the elongated mouthparts of the sucking lice (Fig. 5.

Llama wool infested with biting lice lacks luster and the coat is ragged. The transmission of the parasite is either by direct or close contact between the hosts or indirectly by grooming equipment. Kemp and Zajac. g i . the back along the vertebral column and the sides of the neck and body. Iowa State University Press. blankets. Sucking lice are usually found around the head. USA) and sucking louse (right) Anoplurida (Sucking Lice) The only blood-sucking lice reported to occur both on Bactrians and dromedaries in Asia as well as in Africa is Microthoracius cameli (Soulsby. Infestation may result in damaged hides. 1986). taking a blood meal. being smaller than the biting lice (two-thirds their size) and often hidden in the fiber. praelongiceps.332 Parasitic Diseases Figure 149 Biting louse (left) (courtesyof Professors Sloss. minor. The same clinical signs of camel lice infection are also seen on NWC. scratching and rubbing. They may be quite difficult to see with the naked eye. Veterinary Clinical Parasitology. resulting in self-trauma. scratching posts. neck and withers.. 1994. Anemia may follow heavy infestations. or dust bath areas. mazzai and M . 6thed. Camel lice are generally only a problem in temperate regions where the animals have long winter hair. The predilection sites are at the base of the tail. Treatment Table 58 lists the drugs used against lice.M . Heavy infestation may result in matted wool and alopecia. The host experiences pruritus. saddles. Mallophagida (Biting Lice) The biting louse Damalinia breviceps is a common llama parasite (Fowler. The llama and the alpaca may be infested with M . Lice infestation is characterized by licking. The coat becomes rough and secondary bacterial infections may follow the pruritus. particularly in young animals. 1982).

There are larvae of 1976). southern Russia. and Mongolia (Yasuda.7. the Far East (James. dead or living tissue.4 Infestation with Flies Some Dipteridu as adults are external parasites. As an obligate parasite. or somatic (e. Spain (Ruiz-Martinez et al. Ivornec@* lverrnectin Inj. Reports are available for sucking lice and endoparasites. 1965. 1986). no in. 1998). like lice.5 rna/ka lverrnectin Pour on * Internationally registration approval for lvornec injectable exists for Sarcoptes scabiei var. Five of these belong to the blowHiggins. and as an interme. during a certain period of their life. Myiasis may be cutarickettsia. Al. Turkey. flies (CalZiphoridae) and one to the Oestridae In addition. Surcophugu dux 5. nasal diate host for filarids and cestodes. Many members of this order are also important vectors of pathogens. Withdrawal period is 28 days for meat...(e. 0.7. feed on infest camelids in cooler countries (Zedev. Camels producing milk for human consumption should not be treated. V ioffi). such as Typhus-like also cause myiasis.2.tative parasites such as Lucilia cuprina may though fleas are important vectors of in.C. causing myiasis. 150). Trade Name AsuntoP Generic Name Cournaphos Formulation 50% wettable powder Myiasis is defined as the invasion of living mammalian tissue by larvae of dipterous Vermipsyllidae flies (Urquhart et al. while some parasitize the tissues of the hosts as larvae. 1940.Obligateparatack camelids.sites such as Chrysomya bezziunu and faculIides felis fezis (Yeruham et al. 1947).They have also been reported affect.g.3 Infestation with Siphonapterida (Fleas) Myiasis 5.). lvornex Pour-on is used in carnelids (as field reports say successfully) without market authorization. 1996) that. 1997). 1947. 1971).also cause myiasis.(Zumpt. Iran. at least Fleas (Vermipsylla alacurt. Higgins.. Yersiniu pestis. Musca domestica can fectious pathogens. Hadani et al. It occurs in the Mediterranean basin (James.05% (500 pprn) directly onto skin. Nematocerina (Table 59). Valentin et al.). caused by Lucilia spp.g.. wet hair coat thoroughly Methoxychlor Dusting powder 50% directly onto skin Severin@ Severin Dusting powder As above S. insects have been reported in camelids. The order is divided into two suborders: Brachycerina. stances of pathogen transmission by these caused by Hypodermu spp. caused by Oestrus). WohZjiuhrtiu magnifica is the most important fly causing myiasis in camels. 1987).Infestations with EctoDarasites 333 Table 58 Treatment against lice in carnelids Application Apply at a concentration of 0.2 rng/kg Ivornec@* 0. The female fly deposits larvae near any skin .six fly species known to cause myiasis in ing Bactrian camels in zoos (Pegram and camels. lice. cameli only.g. 1992) and llamas (Fowler. several other species may at. Wohlfahrtiu nuba.2. 1997) (Fig. as is the case of Ctenocephu.. Sarcophagidae Producing Myiasis Treatment Treatment is the same as for (Flesh Flies) Wohlfahrtiu magnifica.neous (e.

There have been several reports of the larvae of W.334 Parasitic Diseases Table 59 The Dipterida associated with myiasis or "nuisance" in camels (after Pegram and Higgins.(Camel louse fly) Himobosca maculata Glossinidae .. Haematopota coronata Stomoxys calcitrans .(Sheep head fly) Hippoboscidae .Valentin et al.(House fly) Musca autumnalis .(Horn fly) Haematobia exigua .(Camel nasal bot fly) Oestrus ovis .(New World screwworm fly) Chrysomya bezziana .. and Hadani et al. Culicoides spp. the eyes and the nose may be attacked without pre-existing wounds (Zumpt.(Blow flies) Cochliomyia hominivorax .(Sheep nasal bot fly) Cephenemyia sp..(Face fly) Hydrotaea irritans . 1976. 1965). .(Midges) Aedes spp. (1989) reported a prevalence of 10% in dromedary camels in the Sinai. mugnifcu causing severe vaginal myiasis in the Bactrian camels in Mongolia (Schumann et al. Tabanus sp. Dipetalonema evansi Onchocerca fasciata wound.(Green bottle fly) Sarcophaga dux Wohlfahrtia magnifica . 1979. Ribbeck and Beulig. Ribbeck et al. (1997) found an infestation rate of 8 to 15%among female camels in Mongolia. The fly seems to prefer camels.(Louse flies) Hippobosca camelina .(Old World screwworm fly) Lucilia cuprina .(Tsetse flies) Glossina spp. 1976).(Muscid flies) T: evansi Bacteria and viruses Salmonella Thelazia leesei T: evansi ~ Trypanosoma spp. although other domestic animals and humans are infested (Zumpt. Nematocerina Culicidae . The prevalence of Wohlfahrtian myiasis in thirteen Mongolian Bactrian camel herds ranged between 6. Valentin et al.5 to 19%(Schumanet al. A case of preputial myiasis was also reported in a camel.(Bot flies) Tabanidae . mucous membrane or tick bite as well as in the nasal and aural cavities. Mucous membranes of the female geni- tal organs. 1965). 1992) Family (common names) Species Vector Capacity Brachycerina Calliphoridae . 1997).(Horse flies) T: evansi Muscidae .(Buffalo fly) Musca domestica .(Mosquitoes) Ceratapogindae .(Stable fly) Haematobia irritans .(Old World flesh fly) Wohlfahrtia nuba Cephalopina titillator .. Chrysops sp.(Flesh flies) Oestridae . Sarcophagidae . 1977.

Wohlfahrtia nuba causes myiasis in humans and animals particularly in camels in Sudan (Higgins. The vulval region is usually swollen and the hind legs encrusted with blood. may be seen on the vagina and vulval labia. Some may even be emaciated. occur simultaneously with various stages of cicatrization. 1986). . 1958). 1986). Numerous larvae may be seen in the inflamed wounds. fly (flesh fly) from vaginal myiasis of a Bactrian camel from Mongolia (courtesy of Prof. Ethiopia and "eastwards to Karachi" (Soulsby. Al three instars may be found concurl rently in the wounds suggesting that superinfestations. cows and bullocks in India (Alwar and Seshia. acute as well as chronic stages. 1997). 1997).Infestations with EctoDarasites 335 Figure 150 Wohlfahrtia spp.The genital area may become fibrotic and deformed. (1997) counted an average of 105 larvae per affected Bactrian in Mongolia... Valentin et al. blood-oozing lesions. Affected animals often show nervous behavior. tripping with their hind legs and bending their backs (Valentin et al. 1982). These camels often are in bad condition. with a history of chronically recurring genital myiasis (Valentin et al. Ribbeck. deeply embedded in the sensitive dermis. Germany) Figure 151 Lucilia cuprina Ulcerous. R. Dr. sometimes the size of a tennis ball. The larva was reported to be the only facultative parasite in wounds of camels and humans in Sudan (Higgins. The larvae of Sarcophaga dux have been found in skin lesions of camels.

Clinical Signs -/i The maggots penetrate and often liquefy the tissue considerably extending the lesions. and any necrotic tissue should be removed. which may develop a foul odor and ooze a foul-smelling liquid.336 Parasitic Diseases Calliphoridae Producing Myiasis (Blowflies) Luciliu cuprinu The most important blowflies belong to the genus Luciliu. Wounds resulting from accidents. 1986). in the perineal area where urine and feces attract the ovipositing fly. It may lay eggs on the skin of both humans and domestic animals. It is an obligate parasite. causing perineal myiasis (Higgins.e. including camels (Soulsby. Hydrogen peroxide. castration. Clinical Signs -‘ Preferential sites for a fly strike are folds of skin. from which second and third instars were collected. Severe infections are common and many cause death. the sheep and goat nasal bot. lymph and necrotic tissue. cuprinu. cuprinu have long been known to infest camels (Higgins. the fly of the “old world screwworm”. Treatment and Control Insecticides kill the larvae. and some species of nasopharyngeal deer bot fly found in North America. 1986). The infestation was most severe on the legs and umbilical cord. 1986). as well as any discharge from natural orifices will attract the female fly. 1992). host. the larvae of L. Once they are destroyed the wound should be cleaned and dressed. ether or chloroform may cause hidden larvae to crawl out from crevices and cavities. The “new world screwworm” (Cochliomyiu horninivorax) infested 17 out of 500 dromedaries near Tripoli. Chysornyu bezziunu Chrysornyu bezziunu. it takes between 8 hours to 3 days for the first stage larvae to hatch. care should be taken to use as little insecticide as possible to avoid further irritation of the lesions. e. cuprinu is greenish to bronze and is therefore also called the green-bottle fly (Fig. The latter two species are important in NWC imported into the USA. infected wounds and soiled and matted fur around infected sores and discharges. Infested wounds may be 10 to 15 cm in diameter (Higgins. The larvae of L. The green-bottle fly is widely distributed around the world. the new world screwworm has been eradicated from Libya. A green-bottle female may lay about 1. such as tick bites and injection sites. However. Cattle and camels are often attacked around the ears and under the tail.The fly deposits clusters of 150 to 500 eggs at the edge of a wound of a living . 1986). The larvae feed on epidermal cells.g. branding. and are the main cause of blowfly strike in sheep in Australia and South Africa.. 1982). The camel bot. Attracted by the smell. Since this finding.L. The female fly lays clusters of light yellow eggs in carcasses. Depending on the temperature. Even small wounds. found not only in Australia but also in the Middle East. 151). Oestrus ovis. Cephulopinu titillator (OWC). Libya (Husni and Elowni. Oestridae Infestations (Bot flies) Three species of bot flies are found in camelids.000 eggs altogether during her lifespan. and scalding by dips may also attract the fly (Fig. which may be seen rubbing and biting the infested parts. Its face is orange-yellow. India and Africa (Higgins. 152). occurs in Africa and in Southern Asia wherever camels are found. i. it even lays eggs onto rotting vegetation. The larvae may cause considerable stress to the infested camel. The fly is bluish-green with four black stripes on the prescutum. Ivermectin may also be used.

hominivorax in a Libyan camel . (c) Lesions caused by C.Infestationswith EctoDarasites 337 Figure 152a-c (a) Chrysomya bezziana fly. (b) Cochliomyia hominivorax fly.

OWC are commonly infected with C. Higgins. belonging to the family Oestridae. 155). Higgins. The larvae moult twice. spending up to 1 months in the host before leav1 ing to pupate on the ground (Fig. 1965). dark brown thorax and the head is orange (Fig. One generation per year occurs in the former USSR (Zumpt. 0. the camel nasal b o t f l y (courtesy of Dr. A. The fly deposits its larvae in the nostrils from which the small. 1965. Figure 155 Different larval stages o f C titi/. 1986). UK) Cephalopina titillator The camel nasal bot fly Cephalopina titillator. two generations have been reported (Zumpt. titillator larvae. In other regions. The fly has a reddish.338 Parasitic Diseases Figure 153 Cephalopina titillator.7mm-long first Figure 154 Larvae of Cephalopina titillator in the nasopharynx of a racing dromedary near the Eustachian tube stage larvae migrate to the nasopharynx and nasal sinuses and attach to the mucosa (Fig. is an obligate parasite of camels. 154). lator collected from the nasopharynx of a racing dromedary . 153).

ulcer-like erosions. titillator hook into the mucous membranes with their two black hooks. Hemortween 47 and 100%(Hussein et al. from the lesions indicates the risk Sudan were infested (Musa et al. The tissue surrounding the larvae was fiOften infested camels do not show any brotic and calcified. titillator larvae per animal. 1991). lymphocytic infiltration and thickenthe camels were infested..7% infestation rate was found in 1250 containing pus and areas of fibrosis were camels in Iraq (Higgins.243 C. local inflammation of the * I . In addition.. In a review of reports from Africa and Asia. Cephalopina flies usually do not make larvae in the lungs of 4 camels out of 40 in the camels panic. the lowest in quamation. Fatani and Hilali (1994) examined submucosa. of secondary infections (Hussein et al.7%). thought to be caused by larvae penetrating the ethmoturbinates leading to meningitis (Burgemeister et al. Inflammation of the nasopharyngeal mucosa occurs when the larvae of C. around the nostrils of the camels. (1989) found 8 to dle East. 52% of um.9%)and the lower nasal meatus (6. desquamation of their lining epitheliAl-Asha abattoir in Saudi Arabia. the infestation rates varied be. titillator at phy. Large numbers of flies Iran. Klebsiella ozaenae. may cause both respiratory and neurological disorders. hydropic degeneration and hyNovember.infestationswith Ectoparasites 339 According to Zayed (1998) the most common sites of the larvae are the pharyngeal cavity (95. 1989). peaking in Feb. The gross pathology in these cases may be seen resting on the heads and was heavy congestion and hemorrhages. Mortalities have reportedly also been associated with heavy infestations. The isolation of pathogenic bacteria such In one study. Similar findings were reported perplasia of the epithelial cells of the muby Patton (1920) cited by Higgins (1986). Epidemiology 1% The prevalence of C. Clinical Signs Unlike many other oesOryan et al. nodules 46..ing of the interacinar connective tissue. 1983). 1965) and Diplococcus pneumoniae and Coynebacteriall 44 dromedaries examined in western urn spp. pharynx and congestion of the nasal cavity (Hussein et al..A rhagic areas. (1991) found larvae deep in the turbinate bones and ethmoid area. followed by the labyrinth of the ethmoidal bone (71. titillator is very high. 1982).. incidence of larval infestation during the Histopathologic examinations revealed desyear was in January to March. Infiltration of lymphocytes.cells.The infestation larvae.The first molt of the larvae were only found in the labyrinth of the ethmoidal bone and the second was found to occur in both the labyrinth of the ethmoidal bone and the pharyngeal cavity.The highest seen in the mucosa of the nasopharynx.1y0). 1982. nulomas were seen in the upper part of the 1982). reticusurvey in Saudi Arabia revealed that 32 out loendothelial cells and fibroblasts and graof 35 camels were infested (Hussein et al. eosinophils and plasma emergence of mature larvae from the nos. 1996). titillator trids. Inflammatory reaction clinical signs.. including the Mid. from Sudan was 74% ( S w a n .A cosa. ruary and September.6%). 1975). particularly during the of lymphocytes. Al-Ani et al.. 1986). Al-Ani et al. but they may be restless or infiltration of mononuclear cells was seen off their feed and may sneeze and snort in the interstitial lung tissue as well as foci when infested..the turbinates (28. the prevalence in camels as Pasteurella haemolytica. the pharyngeal 923 dromedaries for infestation with the mucus glands showed degenerative atrosecond and third instars of C. (1993) reported C.Pathology Musa et al. Necrosis was also seen around the trils (Urquhart et al.

evansi soft tissue mass occluding the nasophar. fected with Cephenernyia spp.sponsible for livestock “fly-worry”and are ing to Fowler (1998). causes fly-worry to cattle were common co-habitants of livestock and horses on pasture. Thelazia spp.. brucellosis. The NWC are aberrant par.e.Camelids infested with gins. “pink eye” or infectious bovine keratoconthree Cephenemyia bots were found in the junctivitis in bovines. It was shown in India that the Oestrus ovis and Cephenemyia spp. 1997).c. The affected animal may be short of breath and consequently fail to keep up with the others when used as a pack animal. Treatment Ivermectin (0. without nasal discharge.biting and non-biting flies. the face fly. findings are seldom re. a very 1985). Rafoxanide (7.340 Parasitic Diseases Oestrus ovis Oestrus ovis has been observed in camels in Egypt (Kaufmann.stock. .2 mg/kg. fly species that irritate other domestic liveCephenernyia spp. In a %month.A large Stomoxys calcitrans is a vector of T. llama breeders in the vectors of significant bacterial. Musca auturnnalis. The adult fly only lives for about 2 weeks. White-tailed deer tropical areas. whether the LC is completed in lesser house fly). 1996). leptospirosisand vesicular stomatitis (HigClinical Signs . causing old llama exhibiting inspiratory dyspnea.) has been used with some success (about 85% effective against C. grazing. It is the intermedipastures where the three llamas had been ate host of several pathogenic parasites.The animals showed sneezing. the fly and its larvae are sheep and goat parasites. such as restlessness. Several Cephene. 1998). Granulomatous swellings may develop in the nasopharynx and nasal cavities. The most immyia spp. Pestered camels shaking. The Muscidae family includes many ported in the literature. If it becomes obstructive. and these deer are commonly in. per 0s) as a drench have been shown to be effective. were reported in three (see Table 59). StoAmerica where cervids and camelids co. head horses (Higgins.5-10 mg/kg per 0s) as a drench or bolus and trichlorfon (75 mg/kg. helminth USA consider these parasites important. The female fly produces live larvae that it places around the nostrils. s. and protozoal pathogens causing disease Cephenemyia spp.fly). The larvae migrate into the nasal passages where they remain from 2 weeks to 9 months. and Paraflaria bovicola. sneezing and coughing with or may have significant milk reduction. Muscidae Infestation (House and Stable Flies) OWC and NWC are pestered by the same Cephenemyia spp. nasal common fly in some temperate and subdischarge and coughing. However. Haematobia (horn fly) and Fannia (the asite hosts. llamas in California (Fowler and Murphy. Then the larvae move into the frontal sinuses where they develop into second and third stage larvae. the animal may be forced to breathe through an open mouth.g.and several other pathogens causing seynx was observed radiographically. vere diseases such as anthrax. Commonly found worldwide. Hydrotaea (sheep-head habit pastures. are found in areas of North portant genera are Musca (house fly). 1986). 1996) and in llamas (Fowler.moxys (stable fly). Many of these are rethe llamas is not known. The mature larvae are evacuated by sneezing onto the ground where they pupate for 3 to 9 weeks. eliminating the larvae (Kaufmann. nasopharynx (Mattoonet al. titillator).and may transmit Moraxella bovis. show fly preferred to feed on camels rather than similar signs. accord. 1986). Llamas attacked by flies try to avoid them by pressing their muzzles close to the ground or against other animals.

7. The irritation and distress caused by the flies may distract the host from feeding and may be so severe that it leads to decreased productivity. The flies then become infective to other hosts during subsequent feeding (Fig. (biting midges) may transmit Onchocerca fasciafa. The coloration of the wings together with the characteristics of their short.Infestations with Ectoparasites 341 the flies to move onto another animal in order to complete their blood meals. 156).6 Ceratopogonidae Infestation (Midges) This family consists of very small flies that are commonly known as biting midges. This is of epidemiological significance as several blood meals increase the risk of transmission of pathogens. . Figure 156 Glossina fly (courtesy of Fotoarchiv. only causing Figure 157 Tabanusfly 5. These ferocious biting flies feed on a variety of animals and humans. Chrysops and Haematopota (Fig.157). They belong to the suborder Nematocerina. the flies become infected with salivarian trypanosomes that undergo multiplication. The Tabanidae are large robust flies with powerful wings (wing span of up to 6.5 Tabanidae Infestation (Horse Flies) There are several species of horse flies or tabanids that are important vectors of T. El Bihari (1985) suggested that Culicoides spp.2. When taking a blood meal. attacking anywhere on the body. 5.5 cm). three-segmented antennae is useful in differentiatingthe important genera: Tabanus. Some horse flies are also known to transmit anthrax and other pathogenic bacteria. Calliphoridae. Two genera particularly: the Tabanus and Haematopota. the drops of blood the biting fly leaves at the feeding sites may attract other flies.2. legs and inguinal regions. Germany) Glossinidae Infestation (Tsetse Flies) The genus Glossina comprises approximately 30 species and subspecies confined to a large belt of TropicalAfrica. Camels may become infected by some Tsetse-transmitted trypanosomes. stout. i.e. protozoa and helminths. Tsetse flies are the common intermediate hosts for Trypanosoma of mammals in Central Africa. Afflicted animals usually try to escape from the feeding flies. a filarid worm of camels. Hanover. In addition. Institute for Parasitology. Their predilection sites are the ventral abdomen.7. The females feed on man and animals and are known to transmit various viruses. evansi in camels.

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1997. Sudan J. Efficacy of closantel plus albendazole against natural infection of gastrointestinal parasites in camels. Further reading Al-Qudah. T. (Siphonaptera. In: Thompson. Alpacas. Zedev. Life-cycle of Sarcoptes scubiei var. Ann. 1997. Appl. J. Ann. Myiasis in Man and Animals in the Old World. 8 0 65-70. Zeyhle and D.K. P.K. R. Seham Elias. An outbreak of cameline filariosis in the Sudan. Trager. Med. Incidence and intensity of Onchocercafusciutu Railliet and Henry. 1989.Comp. Edinburgh. S. J. Parusitol. Vogel. Etude de variabilite de Sarcoptes scabiei avec une r6vision des Sarcoptidae. 1968. Genital myiasis (Wohlfahrtiosis) in camel herds in Mongolia. Dunn and F. M.M. Teran and R. Localization and migration route of Cephlopinu titillutor (Diptera: Oestridae) larvae in the head of infested camels (Camelus dmmedurius). R. Mohammed. McKenna. Suppl. Zahler.A. Vet. Tick paralysis. G.S. Butterworth and Co. Rev. K. J.346 Parasitic Diseases Urquhart.W. J. and D.L. M. and A. 1996. Armour.C.P. Parasitol. 28: 1713-1719. 24: 57-62. 1999. F. Zayed. Immunol. A. Purasitol. Vyszenski-Moher. Parasitol.H.. Willadsen. Duncan. 1995. (Siphanaptera.L. 1999.and intra-specific variation within the genus Psoroptes (Acari: Psoroptidae). Anim. Vet. A. cunis.A.M. Rinder. A.F. Gothe and H. W.A. Inter. 61: 77-80... E. 9. Cobon and J.Parusitol. Fadl. Trop. J. 1988.h i . Hiepe. Ticks (Acari: Ixodidae) infesting the Arabian camel (Cumelus dromedarius) in the Sinai. Purasitol. 1989. Thompson. Immunologic control of a parasitic arthropod. E. A. J. Nielsen. Untersuchungen uber Biologie. 1993. Vet. Monatsh. Essig. Med. J. Lymbery (eds. F.S. 1 7 605-616. Wikel. UK.M. Vermipsyllidae) in farm and wild animals in the Mongolian People's Republic]. Husb. Elbashir. 7 1-196. 60: 40-42. . London..L.G. L. Assoc. Br. McManus. S. Oxford. 2nded. Acquired immunity to ticks.J. On the morphology of the larva of Wohlfahrtiu mugnifica (Schiner) found in the wound of camel in Inner Mongolia. Rosen and S. Perl. Elamin. Porsch. 31: 788-791. Ann. Puthol. Vet. 73: 335-346. Vet. Nasher. Immune responses to arthropods and their products. O. Ilchmann and Th. Riding. J. Hlth. Trop.M.O. Part 11: 328-334.A. Anim. Antwerp. Entomol. Med. Veterinary Parasitology. 48: 473-479. 1995.S. Karrar. I. 1968.7 27-36. London. Entomol. Jennings. M. Baumann. 83: 201-217.. R. Vet. Lahnstein.A.. Valentin. Hyg. 143: 1346-1351. Vermipsyllidae) bei Nutzund Wildtieren in der Mongolischen Volksrepublik [Studies into biology. Acurol. Wachia.P.K. Blackwell Science. G. J. Zumpt. Host immunity to ticks. cattle and camels in the People's Republic of Mongolia. Genetic evidence suggests that Psoroptes isolates of different phenotypes. 1939. J. Med. Gough.L. Int. and distribution of Vermipsyllu spp. Egypt with a note on the acaricidal efficacy of Ivermectin.A. Bowles. Vet. 2 7 2148. 1993. Purasitol. Exploratory studies on the efficacy of Bayticol Pour-on in sheep. A l .. 149: 195-200. Rev. Fain. pp. 41: 1-21. Wikel.H. B.O. 1992. 1. and F.M. 1982..V. G. Bates. Windsor. Kemp. 1940. D. L. J. 1986. host and geographic origins are conspecific. Yasuda.E. Yeruham. R. 25: 57-81. 1996. Effects of parasitic infestation on the productivity of alpacas (Lamu pucos). Identification of a protective antigen from Boophilus microplus. J. 1998. Van Straten.S. Sci. 1998. Biology and systematics of Echinococcus.. G. Windsor. 1993. G. 82: 173-178. M. Sharif. R. M. Molecular examination of the sympatry and distribution of sheep and camel strains of Echinococcus granulosus in Kenya. S. M. 4 :391-397. P. Hum. 1976. Tellam. Bajanbileg. Rev. An apparent flea allergy dermatitis in kids and 4 lambs. Exp. J. Epizootiological studies on heartwater disease in the Sudan.A. Wallingford CAB Intemational. 3349. 1910 in local camels in Saudi-Arabia. Saleem and M.G. Summer: 21-22. Purasitol.Actu Zool.): Echinococcus and Hydatid disease. Vorkommen und Verbreitung von Vermipsyllu spp. Al-Rawashdeh and EK. M. G. A. Schein and S.. G. Chosen Natural History SOC. Vet. A. R. Vet. 1965. Am. 7 4 427-430. Werner.C. Arlian. G. Prod. occurrence. Jongejan.

Cooperia spp. and usually refers to both parasitic and nonparasitic worms belonging to the phylum Platyhelmintha (flukes and tapeworms) and Nemathelmintha (nematodesor roundworms). primarily domestic ruminants and Table 60 Nematodes of Old World and New World Camels Disease Trichostrongylidosis (Gastrointestinal worms) Species Haemonchus contortus Ostertagia ostertagi Marshallagia manhalli Camelostrongylus mentulatus Spiculopteragia peruviana Lamanema chavezi Trichostrongylus spp. Nematodirus spp.5. but some are also common to other hosts. Sub-cutaneous tissue + + + + + + + + + + ~ + .3 Infection with Nematodes WWIt Introduction The word helminth is derived from the Greek helrnins or helrninfhesmeaning worm. large intestine Small intestine EsoDhaaus c3 Eve Blood Aorta. A number of helminths are camelid-specific. Graphinema aucheniae Dictyocaulus viviparous Dictyocaulus filaria Parelaphostrongylus tenuis Anuiostronuvlus cantonensis Oesophagostomum columbianum Chabertia ovina Bunostomum spp. Strongyloides papillosus Skrjabinema ovis Trichuris spp. Parabronema skriabini Thelazia SDD. Capillaria spp. Gonavlonema SDD. Dipetalonema evansi Onchocerca spp. Occurrence OWC NWC location c3 c3 c3 c3 c3 Intestine c3 Small intestine Small intestine c3 Bronchi Bronchi Subdural space Luns Intestine Intestine Small intestine ~~ + + + + + + + + Dictyocaulosis (Lungworm) Parelaphostrongylosis (Meninseal worm) Ansiostronclvlosis Oesophagostomosis (Nodular worm) Chabertiosis Ancylostomatosis (Hookworm) Strongyloidosis Oxyuridosis (Pinworm) Trichuriosis (Whipworm) Capillariosis Gonavlonemosis Habronematidosis Thelaziosis Onchocercidosis + + + + + + + + + + + + + + + + + + + + + ~ Small intestine Colon Cecum.

Some reports are case histories. OWC) Huemonchus longistipes (OWC) Ostertugia ostertagi (NWC.falculatus (OWC) T affinus (OWC) Cooperia spp. dromedary Impalaiu nudicollis (OWC) only host. Their LC is direct and the L3 is the infective stage. The predominant gastrointestinal nematode species in llamas in North America are different from those found in alpacas in South America (Rickard. pectinata (OWC) C. There has been recent interest in defining the parasitic fauna in NWC outside their countries of origin. OWC) T. OWC) T.g. The species composition of nematodes investigated in these surveys seems to differ between continents.only host N. OWC) Ostertugiu spp.3. OWC) Nematodirella dromedurii (OWC) only host Nematodirella cumeli (OWC) only host. columbiformis (NWC.3. OWC) MurshaZlagia mongolicu (OWC) Camelostronmlus mentulutus (NWC.only host N. dromedurii (OWC) . Most investigations of helminthosis in camelids have been surveys of the prevalence of worm eggs in fecal samples or parasites in the intestinal tract of slaughtered camels. battus (NWC. helvetiunus (OWC) N. Bactrian Lamunema chuvezi (NWC) only host 5. Investigations of camelid parasites are fairly recent and veterinarians and parasitologists studying these worms are often not cognizant that the LC of the parasite under study is the same as or similar to that in other animals. (OWC) C. OWC) Trichostrongylusuxei (NWC. lamae (NWC) . OWC) 5. Zunceolutus (NWC) N. Trichostrongylus spp. surnabada (NWC. (NWC) Teladorsagiu circumcinctu (OWC) Ostertugia trzfurcatu (OWC) Murshallugia murshalli (NWC. 1994). filicollis (NWC) N .2 Trichostrongylidosis (Gastrointestinal Worm Infection) These parasites are relatively small and parasitize the gastrointestinal tract (GI). probolurus (OWC) T.1 Classification of Nematodes Phylum Nemathelmintha Class Nematoda Order Strongylida Family Trichostrongylidae (Gastrointestinal worms) Huemonchus contortus (NWC. OWC) C. (NWC. dromedary Impalaia aegyptiuca (OWC) only host Family Molineidae Nematodirus spathiger (NWC. vitrinus (OWC) T. OWC) Spiculopteragiu peruviana (NWC) only host Graphinemu aucheniae (NWC) only host Impalaiu tuberculuta (OWC) only host. mauritunicus (OWC) N. Dakkak and Ouhelli (1987) have compiled a comprehensive list of helminths found in dromedaries and Fowler (1998) wrote a review of those parasites infecting NWC (Table 60). . ubnormulis (OWC) N. oncophora (NWC.348 Parasitic Diseases wild animals. but only a few are profound studies of the pathogenesis of particular camelid parasites. OWC) N. in North America and Europe. e.

. Institute for Parasitology. (right). (c) Nematodirus spp (d) Trichostrongy/us spp.Infection with Nematodes 349 Figure 158a-d Common Trichostrongylidae eggs of camelids: (a) Haemonchus longistipes (left) and Trichostrongy/us spp. (Figs.. (e) Cooperia spp. b and e: courtesy of Fotoarchiv. (b) Ostertagia spp. Germany) . Hanover.

B = development of L1 to infective L3 on pasture. Haernonchus. D = L3 develops to L4. one group of very few that have been studied to some extent and known without doubt to be pathogenic are Haernonchus spp. The most important genera affecting the GI tract are Haemonchus. Cooperiu and Nernatodirus (Fig. Marshallagia. A B Figure 159 The direct life cycle of Trichostrongylidae (e. Among the common nematodes.g. Trichostrongylus): A = egg discharged with the feces. C = camel ingests L3 while grazing. Of these. L5 and to adult parasites . Haemonchus (The Large Stomach Worm or Wire Worm of Ruminants) Bihari (1985) convenientlygrouped helminthic infections of the camelids’ GI tract into two categories: common and occasional. 158). Trichostrongylus.350 Parasitic Diseases The widely spread trichostrongylid parasites are known to cause considerable morbidity and mortality in ruminants and camelids. Ostertugia. Haemonchus spp. are blood-sucking pathogenic parasites of compartment 3 (C3) of camelids. Ostertagia.

1962). a piercing lancet. After ingestion. Huernonchus Zongistipes is considered to be a species adapted solely to camels. the infective larvae (L3)develop within 4 to 6 days. Haemonchosis in camelids is similar to that described in sheep (Arzoun et al.. Both stages suck blood (Fig. develops. In sheep. and the female has a red and white spiral appearance because the uterus winds around the intestine. Zongistipes has been studied by Richard (1989). considering the number of L4 and adult worms harbored by the host. enabling the parasite to draw blood from the mucosal vessels. The eggs and infective larvae are sensitive to desiccation and low temperatures. Adult worms are morphologically relatively easy to differentiate from other trichostrongylids such as Ostertugia spp. The parasites ingest blood and are motile. Life Cycle P: The prepatent period of Huernonchus is unknown in camelids. the LC may be delayed for many weeks or even months in cooler conditions. The LC is direct in most of the trichostrongylids as shown in Fig. 1995). However. Substantial blood loss may occur. leaving wounds that hemorrhage into the stomach lumen. are found most often in dromedaries and H. In the pasture. This was shown to be apparent for H.05 mL per day by ingestion and seepage from the wounds (Clark et al. but may also infect small stock (Kumar and Yadev. 159.. contortus may cause a blood loss of 0. (1984a) observed a prevalence of 89% during the rainy season and 64% during the dry season. (1995) and Jacquiet et al. the larva moults twice close to the gastric glands and just before the last moult the "tooth". In heavily infected ani- Figure 160 Haemonchus longistipes in a dromedary's C3 . or Trichostrongylus spp. Zongistipes (Jacquiet et al. 1984a. Haemonchosis The most important feature of Huemonchus infection is anemia.. 1993).b). Jacquiet et al. particularly during the rainy season. A high prevalence of H. giving it the appearance of a barber's pole. The adult female parasites are prolific egg layers. (1996). where the disease is well studied. Arzoun et al. each H. They are one of the largest nematodes of the C3. 160).Infection with Nematodes 351 Huemonchus spp. The infection is often accompanied by diarrhea. The adult male is often homogeneously red (after a blood meal). Zongistipes in dromedaries has been reported from Sudan.

Arzoun et al. In temperate regions. The larvae in the host’s glands stimulate the formation of grayish white nodules. particularly in animals sharing grazing with sheep (Dakkak and Ouhelli. the larvae become arrested (hypobiosis)in early autumn and development starts again in spring. 1987). The parasite has limited distribution. as well as leucocytosis. lyrutu were first found in llamas in Peru (Vasques and Marchinares. 1997). It occurs in llamas in the western USA. each containing two to three larvae that mature in 15 to 18 days. are highly adapted to cattle. The prepatent period is usually about 3 weeks.g. ostertugiu and 0. 1971). such as 0. Ostertugiu lyrutu and Huemonchus contortus were first found in alpacas. which was first described in alpacas. However. M . The chronic form may be difficult to differentiate from other chronic camel diseases. and has also been reported in camels in India and Russia (Dakkak and Ouhelli. which in turn create severe clinical signs. 1967. phosphate. The parasite also infects sheep. magnesium and copper levels were also diagnosed by Kaufmann (1996). 1967). Low PCV. 1967. progressive deteriorationoccurs with marked anemia seen in 10 to 45% of cases (Faye. calcium. Haemonchosis in the camel is often associated with hypoproteinemia. which are readily seen in the mucosa of C3 at necropsy. trifurcutu. 1989). 198413). 1995). These are most evident when the larvae emerge from the glands. anorexia.. 0. Richard 1979 and 1989. Acute haemonchosis in experimentally infected camels induced clinical signs of mucoid diarrhea. The LC varies according to climate and host species.352 Parasitic Diseases mals. A few years later. The affected animals died despite treatment with ivermectin. 1998). small stock and wild ruminants. Cumelostrongylus mentulutus is a common camelid stomach worm. anemia. 1984b. 1987). Different climates produce differencesin the epidemiology of the parasite. edema of the lower limbs. loss of body weight. Other Common Trichostrongylids The common stomach worms of Ostertugiu spp. At the same time. ostertugi.. llamas and vicufias from Titicaca in Peru (Guerrero and Chavez.. including neutrophilia and eosinophilia (Graber et al. goats. the larvae may survive the hot unfavorable environmental conditions during the summer in hypobiosis. Teludorsugiu sp. but arrested development may occur (Fowler. Jacquiet et al. 1987).eventually leading to emaciation and death. including hypoalbuminemia and hypoglubulinemia. and unidentified Murshullugiu sp. Queval et al. e.. lyrutu. and Spiculopterugiu peruviunu. There are some other parasites found in the abomasum or C3 of camelids closely resembling Ostertagia: Murshullugiu murshulli. Significant numbers of the parasites in the C3 may give rise to extensive pathological and biochemical changes. 0.. Windsor (1997) reported three cases of ostertagiosis in llamas in northern Scotland south and southwestern England. antelope and lla- . The L3 of Murshullugiu marshalli penetrate the gastric glands of C3 and are eventually surrounded by a 2 to 4 mm diameter large nodule. In other areas of the world where the summers are hot. trypanosomosis. general malaise and death after 8 to 10 weeks (Arzoun et al. in guanacos in Argentina (Navone and Merino. It is a common parasite in sheep in the Mediterranean./ Cumelostrongylus mentulutus. mongolicu.. eggs. together with two other species: Trichostrongylus longispiculuris and Cumelostrongylus mentulutus. Teludorsugru circumcinctu.The eggs may easily be confused with Nemutodirus spp. they are also found in camelids with an LC similar to Huemonchus spp. Murshullugiu mongolicu has only been reported in Mongolia (Dakkak and Ouhelli. and 0.

lmpalaia tuberculata and 1. probolurus. cameli is reported in the Bactrian camel of the former USSR. C. the carcass is dehydrated and enteritis is often evident in the ileum. Trichostrongylus axei is found in the abomasum of ruminants.It was found in the districts of Bikaner and Jodhpur in Raiasthan with a Prevalence of over 42%. particularly in temperate zones. are found parasitizing dromedaries: Nematodirella dromedarii. are considered to be one of the most important causes of parasitic gastroenteritis in ruminants. Graphinema aucheniae This parasite is only found in C3 in NWC. are small and thin. Gibbons et al. oncophora and C. about 7mm long and difficult to see with the naked eye. N. It was first described in llamas in Argentina (Led and Boero. oncophora and C. Severe damage to the villi and erosion of the mucosa resulting in villous atrophy. coincide with the parasitic phases of the larvae while in the mucosa. colubriformis. lamae. abnormalis. Cooperia Cooperia spp. N. The latter two species are parasites of the C3. are found mainly in the small ruminants’ intestines but also frequently in camelids. N. 1972). C. are small nematodes similar in size to Ostertagia. battus. Young animals may exhibit rapid progressive dehydration following diarrhea. C.Infection with Nematodes 353 mas (Soulsby. filicollis and N. mentulatus may cause significant disease in camels. The following species are reported in OWC: N. and relatively easy to differentiate from other trichostrongyles. N. dromedarii and N. The eggs are large and twice the size of other trichostrongyle eggs (see Fig. N. They are parasites of the small intestines of ruminants and camelids throughout the world. nudicollis. leading to death. lanceolatus are species found in NWC (Fowler. At necropsy. N. mentulatus is commonly found in the Middle East and in areas north of the African continent (Kaufmann. aflnus have been recorded in camelids. N.Nematodirus battus is the most pathogenic species in temperate areas. . The Trichostrongylus spp. T. mauritanicus. The adults are slender. zurnabada in NWC. such as T. Occasionally T. Trichostrongylus Trichostrongylus spp. spathiger. Its LC and epidemiology is similar to trichostrongvles. falculatus and T. vitrinus.. (1977) discussed the classification of these seldom-mentioned species.3. pectinata are found in OWC and C. 5.3 Infections with Molineidae Nematodirus These parasites are found worldwide. 1987). T. in C3 in camelids and in the stomach of horses. spathiger. about 2mm long. donkeys. pigs and humans. species closely related to Nematodirus spp. N. Nematodirella dromedarii was first reported in India and described by Lodha and Raisinghani (1979). Other Trichostrongylus spp. 1982). but less commonly in South America and the USA. occasionally of the small intestine (Kaufmann. 1998).According to Kaufmann (1996).and are mostly found in camels in Africa (Dakkak and Ouhelli. 1996). 158a-e). 1996). In addition. It seldom occurs in single infections. They are small intestinal parasites. helvetianus.

laying eggs containing fully developed larvae L1. Heavy infection causes hepatic and respiratory failure and death may follow.. The infective larvae develop within the eggs.354 Parasitic Diseases Lamanema chavezi One of the most important NWC nematode pathogens is Lamanema chuvezi. The migration of the larvae causes catarrhal and hemorrhagic enteritis with areas of mucosal necrosis. the ingested L3 penetrate the intestinal mucosa of the host and pass into the mesenteric lymph nodes where they moult into L4.3. chavezi larvae showed increased levels of glutamate-oxalacetate-transaminase 14 days later. The parasites are found worldwide. filuriu (NWC. Their LC is direct. The eggs are coughed up and swallowed. Approximately 4 days following the infection. showing multiple small foci of coagulative necrosis and petechial hemorrhages. The prepatent period is about 30 days (Guerrero et al. which actively feed on microorganisms in the environment.000 larvae orally died after 20 days. 1998) showing a characteristic mottled appearance (Leguia. The adult parasite is long and slender. 5. but usually occurs while the eggs pass through the gut of the host. Five young alpaca given 10. Areas of lung congestion are also seen. The liver is often condemned. particularly in temperate climates. 1973). llama aberrant host) Family Angiostrongylidae Angiostrongylus cuntonensis (NWC. the liver lesions become fibrotic and may calcify (Fowler. the liver is congested. Ingested larvae penetrate the intestinal wall and pass to the liver and lungs. The L3 stage is reached in 5 to 7 days. about 8cm long. The . and is found in the trachea and bronchi. giving them excellent resistance to adverse climatic conditions (Leguia. This was shown experimentally: a $-month old alpaca given 200. 1973).000 L. unlike those of other trichostrongyle larvae. 1973). Hatching may already begin in the lungs. alpaca aberrant host) Dictyocaulus The parasite belonging to the family Dictyocaulidae occurs in the respiratory passages of the lungs and is the major cause of parasitic bronchitis in domestic animal species. In acute infections. When maturation is completed the parasites migrate back to the small intestine via the trachea. 1991).. exhibiting severe anemia (Guerrero et al. OWC) Family Protostrongylidae Pureluphostrongylus tenuis (NWC. Particularly vulnerable are recently weaned NWC. Life Cycle I The preparasitic (free) stages feed on food reserves stored in their intestinal cells. 1991).. in which the infection may be very severe. The LC is poorly understood. indicating liver damage (Guerrero et al. The L4 reach the lungs via the blood and lymph within a week of infection. Llamas and alpacas are believed to be aberrant hosts.4 Dictyocaulosis (Lungworm Infection) Parelaphostrongylosis (Meningeal Worm Infection) Ang iostrongylosis Family Dictyocaulidae DictyocuuIus vivipurus (NWC) D. It is thought to be a parasite of the mountain viscacha Lagidium viscuciu boxi. The females are ovo-viviparous. Some eggs may be expelled via nasal discharges. When the larvae have returned to the intestine.

1982). filaria are commonly found parasitizing Camelidae in South America (Fowler. In deer.viviparus (Soulsby. Many animals gradually recover. hindering recovery. Life Cycle The llama is an aberrant host and it is not known whether the LC of this parasite is the same in the llama as in its natural host.infection with Nematodes 355 last molt occurs in the bronchioles and the L5 move up the bronchi and mature into the adult form. It is a small. ending up in the feces. but this may take months. they penetrate the wall. 1998). where they embryonate and hatch (Soulsby.Heavily infected animals may die due to respiratory failure following the development of interstitial emphysema and pulmonary edema. the L3 may hibernate (over winter) on pasture in sufficient numbers to initiate infection the following spring. Furthermore. The parasite may also infect and cause neurological disease in several other Cervidae and domestic livestock such as sheep. viviparus and D. Both D. 1952) has been described in camels in Asia and Europe. Parelaphostrongylustenuis Adult P. reaching the spinal cord in 10 days. Larvae require a moist environment to survive. i. It is usually a /I herd problem. Intermediatehosts such as terrestrial snails and slugs eat the larvae. D. Epidemiology In endemic areas with temperate climates.e. Dictyocaulus filaria in OWC has been reported in several African and Asian countries as well as in Europe. goats and llamas. Affected animals may cough. tenuis are found in the cranial venous sinuses and subdural spaces of the white-tailed deer (Odocoileus virginianus) in which the infection is sub-clinical. Body temperature is usually normal unless secondary pneumonia develops.The larvae then reach the bronchi and trachea and are coughed up and swallowed. . The prepatent period in cattle is about 3-4 weeks. hair-like nematode. The larvae are then carried via the circulation to the lungs. The disease is mostly seen in young animals. Demonstration of larvae in feces using the Baemann method is an important diagnostic tool. Several young animals may simultaneously show signs of the infection. An infection may also persist from year to year by carrier animals. In Europe generally only calves in their first grazing season show clinical disease. but it can affect any age group. They then migrate to the spinal subdural space and further on to the brain where they enter their final location. Clinical Signs There are usually no clinical signs of disease but fatal neurological disease may occur in the aberrant hosts. The final host ingests the infected snails and after the larvae are released into the stomach.1982). high rainfall and permanent pastures. Coughing may be evident during the prepatent period when no eggs are yet laid. particularly in areas with a mild climate. Clinical Signs ~1 Parasitic bronchitis is a problem. cameli (Boev. In endemic situations. the venous sinuses. thus infections are not considered a problem in hot and dry climates. eggs are laid and eventually hatch on the meninges. Superimposed bacterial infections might occur. by penetrating the dura mater. Some authors consider it to be synonymous with D. specific antibody tests are commercially available for the diagnosis in cattle. However. Eggs may also be deposited in the venous circulation and then carried to the lungs. older animals acquire a strong immunity. small numbers of adult parasites may survive in the bronchi of affected animals. with dyspnea and nasal discharge. Diagnosis is based on clinical signs of respiratory distress.

1994).3. 1989). Thin-walled eggs are passed in the feces. stiffness. Angiostrongylus cantonensis. The 5.venulosum (OWC) 0. The nodules formed are visible to the naked eye. The infection may cause death in llamas. found in the large intestine of ruminants. However. the development occurs within the nodules. The L3 of 0. and is less pathogenic. 1994). However.5 Oesophagostomosis and Chabertiosis (Nodular Worm Infection) Family Chabertiidae Oesophagostomurnspp. the L3. Chabertia ovina. are often called nodular parasites because many cause nodules in the wall of the intestine. Other ungulates may be aberrant hosts. identification of the larvae to species is not possible. as well as sheep and goats. 1998). The parasites are distributed worldwide. 0. In some species. The development and bionomics of the preparasitic stages are similar to those of the Strongylus spp. The alpaca died and the nematodes were found in the lungs at necropsy (Fowler. None of the nodular worms in NWC have been identified as to species (Fowler. but are more important in tropical and subtropical regions. alpacas and guanacos (Rickard.Local hemorrhages in the spinal cord often lead to death (Cheney and Allen. Angiostrongylus cantonensis A lungworm. paralysis and abnormal position of the head (Fowler. columbianum (OWC. ataxia. are stout roundworms 1-2cm long.356 Parasitic Diseases such as the llama. 1998). venulosum.g. The two species. columbianum and 0. also called the ”largemouthed bowel worm” is found in domestic and wild ruminants and in camelids throughout the world. circling. 1998). caribou (Rangifertarandus) and red deer (Cervus elaphus). 0. hypermetria. camelids. but rarely causes clinical disease.vigintimembrum (OWC) Chabertia ovina (OWC. columbianum and 0. inflammation in the wall of the intestine. Diagnosis k a At necropsy the thin. A recently developed ELISA has shown promising results in demonstrating meningeal worm infestations in domestic goats (Rickard. Oesophagostomum spp. i. elk (Cervus canadensis). It is particularly common in sheep and goats. manifested as lameness. However. Migration of the larvae in the spinal cord produces lesions like encephalomalacia. Epidemiology Llamas cohabiting with white-tailed deer are at risk. essentially sheep and goat parasites. e. normally a parasite of rats in the Pacific Basin. (NWC) 0. was found in an alpaca during quarantine. blindness. venulosum can cause severe enteritis. These nematodes. will penetrate the intestinal mucosa where the third ecdysis takes place. columbianum may migrate deep into the intestinal mucosa. NWC) 0. Life Cycle ’ The LC of these nematodes has not been established in camelids. provoking inflammation. NWC) . have also been reported in camels in Africa and Asia (Kaufmann.moose (Alces alces). pigs and primates. paraplegia. slender parasites are difficult to find. the latter species has fewer tendencies to cause nodules. Larvae may be found in the feces by the Baermann technique. Chabertia ovina Another parasite of the cecum and colon.e. 1996). The worm is rarely reported in dromedaries and NWC. The infective stage. it is assumed that the LC in Camelidae is similar to that in ruminants.

3. Diagnosis Diagnosis is made by demonstrating the eggs (Fig. because the pathogenic ef8 fect of infection often occurs before the end of the prepatent period.6 Bunostomosis (Hookworm Infection) Family Ancylostomatidae Bunostomum spp.5 to 2. the larvae migrate to the lungs where the third ecdyces occur. The immature adult then passes to the colon. the presence of 250-300 worms is considered pathogenic. However. The larvae are then coughed up and swal3 .5 to 2cm length and enlarged anterior end. The parasites are seldom reported in camelids.5cm long parasites of the small intestine of ruminants belong to the larger nematodes of the ruminants’ small intestine. The L3 enters the mucosa of the small intestine but seldom the cecum or colon. 161) in the feces and by identification of the L3 in larval cultures. 1989). The infection is per 0s. The 1. 1998). which is ventrally curved with a marked buccal capsule. The oral aperture is surrounded by a double leafcrown. In sheep. They are mainly found in NWC living in warm tropical climates (Fowler.Infection with Nematodes 357 Figure 161 Chabertia ovina egg in dromedary feces first finding of the worm in guanacos was in 1989 (Navone and Merino. the number of eggs might be low. are blood sucking hookworms occurring in small ruminant intestines in many parts of the world. After about a week. The L3 Life Cycle infection of the host occurs either orally or through the skin. This may cause local hemorrhage and loss of proteins. ( W C ) Bunostomum trigonocephalum(OWC) Bunostomum spp. Clinical signs in heavily infected animals include diarrhea tinged with blood and mucus. The anterior end of the worm is bent dorsally. Life Cycle The LC is direct. The LC is direct. Clinical Signs The L5 and adults feed on the intestinal mucosa. the L4 emerges onto the surface of the gut and migrates to the cecum where it develops into the W. The adult worm is easily recognized by its 1. If the route is through the skin. 5.

5. The infective larvae are not resistant to desiccation and therefore can only survive on moist pastures in fairly hot climates. Germany) Order Rhabtitida Family Strongyloididae Strongyloides papillosus Figure 163 Egg of Strongyloidespapillosus from a dromedary .358 Parasitic Diseases lowed. Hanover. egg from dromedary feces (courtesy of Fotoarchiv. Infection usually occurs together with other gastrointestinal strongyles and thus the hookworms may contribute to the general effect of the parasitism. reaching the intestine after about 1 days. weight loss and sometimes diarrhea with dark feces. Progressive edema may clinically manifest with the characteristic "bottlejaw" (edema of the intermandibular region) that is seen quite often in affected camels.7 Strongyloidosis Figure 162 Bunostornurn spp. hypoalbuminemia. 162. The egg is shown in Fig.3. The prepatent period is between 1 1 and 2 months. Significantinfections in sheep with more than 100 to 500 worms may produce anemia. Institute for Parasitology.

Prenatal infections have also been experimentally shown to occur in pigs and cattle. 164. The LC is shown in Fig. The epidemiology of S. A B Figure 164 Life cycle of Strongyloides sp. C1 = transcutaneous infection by L3. 163). D = final hosts with adult partenogenic female parasites in the gut. common in very young animals of severalhost species. particularly in African countries (Dakkak and Ouhelli.: A = egg. The species is reported to be common in dromedaries. B = free-living life cycle (right) and infective L3 (left). 1987). Such larvae stimu- lated by parturition are mobilized and excreted in the dam’s milk. Although these worms are generally of little pathogenic significance.Infection with Nematodes 359 Strongyloides papillosus Strongyloides is the only important species of the Rhabtitida and belongs to a group of parasites of the small intestine. Neonatal animals acquire the infestation shortly after birth from arrested larvae in the tissues of the dam. papillosus is unknown in camelids. Strongyloides eggs are oval with a thin shell. Cz = oral infection on pasture. In camels it is the larvated egg that is passed out in the feces (Fig. infection of calves while suckling . they may cause severe enteritis and death.

ovis is considered to be the species affecting NWC in South America (Fowler. ruoi. globulosu is the most prevalent in dromedaries in Africa and Asia (Kaufmann. 1996). 1996). The latter worm was suggested to be the typical whipworm of the llamas (Rickard and Bishop. T. as the different species of Trichuris are difficult to distinguish. The L3 hatch in the small intestine and the larvae migrate to the large intestine where the parasites mature within 25 days (Schad. Trichuris spp.360 Parasitic Diseases 5. Adults live in the colon and migrate to the rectum from where the female traverses the anal sphincter to deposit her fully embryonated eggs around the anus. significant parasites in these animal species (Boyce et al. ufinus (Kaufmann. skrjubini and T. (NWC) Nematodes belonging to the genus Trichuris are common parasites of several mammals. It is considered a benign parasite. The eggs are flattened on one side. Epidemiology The worm has also been found in goats and antelopes. Diagnosis The eggs are usually not seen in the regular fecal flotation analysis. ruoi (OWC) Life Cycle The LC is direct. Several species are found in camelids and some authors consider Trichuris spp. Hayat et al. tenuis has been more frequently reported in animals in the northwest Pacific regions (Rickard and Bishop.3.. T. Partani et al. T. 1998) while T.It is a small parasite measuring between 3 to 8 mm. T. On pasture. most authors do not identify the particular species. b). although it might cause irritation and pruritus in and around the anus. tenuis is closely associated with camelids (Cafrune et al. the eggs may reach the infective stage after 3 weeks (Soulsby.. are between 3 to 8cm long and are easily identified by the long and much thinner anterior body portion that becomes shorter and thicker posteriorly..9 Trichuriosis (Whipworm Infection) Capillariosis Order Enoplida Family Trichuridae Trichuris tenuis (NWC) T. 1999). However. 1991a. The authors were convinced that T. Whipworm eggs were found in over 50% of the animals surveyed and T. 1984. 1999). ufinus (OWC) T.. 1998). T.3.. 1959).8 Oxyuridosis (Pinworm Infection) Order Oxyurida Family Oxyuridae Skrjubinm ovis (NWC) The sheep pinworm. curneli (OWC) Family Capillariidae Cupillaria spp. OWC) T. particularly ruminants. tenuis was demonstrated during necropsy of one llama and one vicuiia in each of the herds. Recently T. Life Cycle I The LC is direct. 1982). 1994). T. Skrjubinemu ovis. have occasionally been reported to occur in camels: T. has been found in the guanaco in Argentina (Fowler. 1998). The eggs drop off and are ingested with water and food. devel- . Scotch tape applied around the anus and then applied to a glass slide is the recommended diagnostic method. Rickard. ovis (NWC. 1998. ovis. globulosu (OWC) T. 5. curneli. 1991b. Other Trichuris spp. However. tenuis was found during a survey in llamas and vicuiias in northwestern Argentina (Cafrune et al. skrjabini (OWC) T.

but are small and t i .Infection with Nematodes 361 Figure 165 Trichuris spp. Clinical Signs h i 1 Trichuris infections may be benign but high numbers of W and adults may cause irritation and inflammation of the cecum and colon.3. Capillaria The capillaridsare closely related to Trichuris.The genus conhn tains numerous species found in a variety of hosts. Clinical signs may occasionally be similar to haemonchosis.The parasites traumatize vessels in the mucosa. Gongylonemapulchrum. leesei (OWC) T. Treatment ilii Modern anthelmintics are effective against adult Trichuris spp. The prepatent period varies between species from 50 to 80 days. have been found in NWC (Fowler.1 0 Gongylonemosis Parabronemosis Thelaziosis Order Spirurida Family Gongylonematidae Gongylonernupulchrum (NWC. The ingested eggs hatch and the larvae penetrate the wall of the anterior small intestine of the host and migrate after 2 to 10 days of maturation to the cecum and large intestine. but may be confused with those of Cupillaria spp. and can cause hemorrhage. which can result in malfunction of water absorption and dehydration. verrucosum (OWC) Family Habronematidae Purubronemu skrjabini (OWC) Family Thelaziidae Theluziu culiforniensis (NWC) T. where they develop into adults. but less so against larval stages. depending on the soil moisture and temperature. egg in drome- dary feces opment may be prolonged. 165). 1998). rhodesi (OWC) Gongylonemosis The cattle "gullet worm". Eggs identified as Cupillaria spp. (Fig. producing catarrhal enteritis. Diagnosis Barrel-shaped doubly operculated eggs are characteristic. OWC) G. has been reported in alpacas in Peru . 5.

166) l i t The development of larval stages to maturity takes place in the conjunctival sac. Zeesei in dromedaries penetrates the conjunctival sac and from there migrates into the lacrimal duct. it may also inhabit the rumen wall. 1996). The TheZuzia spp. usually in the lacrimal duct. which are taken up by the feeding intermediate host: mainly different species of Musca flies. pulchrum OCCUTS more often in sheep. and T. rhodesi. Occasionally the infection may cause irritation. Ivermectin drops or diethylcarbamazine (2 mg/L) may also be instilled into the conjunctival sac (Kaufmann. Thelazia californiensis has been found in llamas’ conjunctival sac (Fowler. In ruminants. has occasionally been found in camels. The infection is usually subclinical and diagnosis is made by chance during necropsy. Also T. goats and cattle in the abomasum and C3. Parabronemosis Parabronema skrjabini is rarely found in dromedaries. sheep. 1974). 1974. Thelaziosis TheZazia spp. The adult parasite is found in the esophagus within the mucosa or submucosa in a zigzag pattern. Zeesi is reported to occur in Africa and Asia. including cockroaches. The larvae are liberated in the stomach of the final host and migrate to the esophagus. T. It may also infect humans in the oral epithelium or sometimes subcutaneously. where the final development to adult worm occurs (Dobrynin. This occurs when the intermediate host takes a meal from secretions of the eye of the host. In severe cases the whole cornea may be opaque.362 Parasitic Diseases (Fowler. wild boars and camelids.Adult worms may also be found on the cornea. resulting in lacrimation with mild conjunctivitis. are 1 to 2cm long thin parasites mainly found in or around the eyes of numerous animals (as well as humans). Flies may often be seen clustering around affected eyes. cattle. which in turn ingests it. 1996). The infective larvae then migrate to the mouthparts of the fly from which they are transmitted to a new host. donkeys. Life Cycle (Fig. which may progress to keratitis. usually found in cattle. G. Eggs or L1 may be found in lacrimal secretions. 1998) as well as in dromedaries. i One or both eyes may often be infected without clinical signs. 1998). one of 70 different species of beetles. goats. 1% The parasites may be physically removed using topical anesthetic drops. 1996). Eggs are passed in the feces and hatch when ingested by an intermediate host. . The L3 of T. zlerrucosum (Kaufmann. Zeesei is considered to be the dromedary eye worm (Drobynin. a species Diagnosis Y’!~ Diagnosis is based on finding the parasites in the eye. are ovoviviparous. Life Cycle itit Stomyoxys and Haematobia flies are intermediate hosts that deposit the infective L3 on the final host. Local anesthetics are a useful help in demonstrating the worm. Kaufmann. The adult female parasite deposits eggs containing L1 into the host’s lachrymal secretions. Development to L3 occurs in the ovaries of various flies within a month. pigs and buffaloes than in horses. which are rarely infected also with the rumen gullet worm G.

C =the infected fly ingests eye secretions and simultaneously infects the animal with L3. . B = development of larvae L1 to L3. In the intermediate host. NWC) Onchocercidae have an indirect LC depending on insect vectors as intermediate hosts. Microfilariae of some species only appear in the final host’s circulation or tissues at certain periods during either the day or the night.: A = a fly ingests eye secretions together with eggs and/or L1 of Thelazia.Infection with Nematodes 363 ---- Figure 166 Life cycle of Thelazia spp. This phenomenon is important in reaching a proper diagnosis. connective tissues or body cavities of their hosts. The microfilariae reach the blood or tissue lymph spaces from where the intermediate hosts (mosquitoes and other arthropods)feed and become infected. They are diurnal or nocturnal.1 1 Onchocercidosis Order Filariida Family Onchocercidae Dipetalonema evansi (OWC) Onchocerca armillata (OWC) Onchocerca fasciatu (OWC) Onchocercu gutturosa (OWC. The L1 are called microfilariae.3. the L1 develops to L3 and migrates to the proboscis of the arthropod vector from where the L3 may be transmitted to the final host. The parasites are long and relatively t i and live in blood or hn lymph vessels. a flexible eggshell. D = development of the larvae to adults in the infected host 5. the infective L3 in the vector fly. Some are enclosed in a thin membrane.

strating the microfilariae in blood smears or finding the adult parasites during surgery or necropsy confirms diagnosis. Onchocerca The Onchocerca spp.. Figure 167 The microfilarian Dipeta- lonema evansi in dromedary blood . t i and slender.. Most of the parasites are relatively harmless. and Butt et al.DemonDipetalonema evansi is a filarid nematode only found in camels. The intermediate hosts are insects belonging to the families Simuliidae and Ceratopogonidae (Culicoides spp. The prevalence of infection may reach 80% in certain areas of Russia and is reported to be approximately 15% in dromedaries of Rajasthan in India (Pathak et al. 167).364 Parasitic Diseases Dipetalonema evansi Trypanosomosis may be confused with D. According to Kaufmann (1996). the parasites are also found in other parts of North and East Africa and in Pakistan and India (Butt et al. 1998). apathy and sometimes orchitis and aneurysms in the spermatic cord as well as arteriosclerosis and heart insufficiency. usually cause the formation of nodules in the connective tissue of their final hosts.). 1982). For diagnosis. blood samples should only be taken around midnight.They only appear in the blood stream around midnight (Michael and Saleh. evansi in camels.The vectors are Aedes spp. It occurs in the pulmonary and spermaticarteries as well as in the lymph nodes and lymph vessels. Diagnosis Lf Light infections are often clinically not apparent. but heavy infections may cause emaciation. The number of microfilariae in circulation is often too small for easy detection and therefore concentration techniques may be used for diagnosis.evansi infection(Kaufmann. and lie tightly hn coiled in nodules. 1998). 1977). The parasites have been reported in dromedaries in Egypt. and about the same prevalence in Pakistan when direct diagnostic methods are employed (Butt et al. 1996). 1998). considering the nocturnal periodicity of the microfilariae (Fig. Michael and Saleh (1977) described a slide agglutination test for D. The parasites are 2 to 6 cm long.. the Far East and eastern parts of the former USSR (Soulsby. (1998) recommended a formol gel test as being the most reliable of the indirect tests.

1996). 1996). The former is only found in dromedaries and has been reported in Sudan.fusciutu and 0.Infection with Nematodes 365 Figure 168 Onchocerca fasciata nodules in a dromedary camel Figure 169 Histological preparation of 0. Ethiopia. The infection is difficult to diagnose and usually does not cause any clinical signs. Kenya and Mauritania (Kaufmann. 168 and 169). This filariid develops in the aorta particularly in cattle. media and adventitia of the aorta. sheep and goats. although its prevalence in cattle may reach 90%. buffalo. . flies. During slaughter. It occurs in subcutaneous tissue and the nuchal ligament (Figs. the worms are often found in nodules in the intima. Other Onchocercu species found in camels are 0. fasciata in a dromedary (HE stain) Onchocercu armillutu has been found in the aorta of dromedaries in Nigeria (Kaufmann. Vectors are SimuIium spp.gutturosu. It has been reported in donkeys in Africa and Asia (Soulsby. 1982).

The pathogenesis of experimental Haemonchus longistipes infection in camels.5 5.C. one is surprised when studying the extensive list of parasites. M. Boyce. Parasitol.m. Athar.A single host may be infected by several species of parasites. 1984. 1 day orally. from camelids (Lama glama and Vicugna vicugna) in Argentina. Allen and E. H. Muhammed..T.2 0.M. Butt. 1-3 davs orally.3. D. Camel Prac. Pathol. 1-3 days orally. camelids are the least likely to regularly suffer from outbreaks of clinical helminthosis due to their natural arid environment. J.5 5 100-1 50 5 7. There are broad-spectrum antihelmintics that have high efficacy against both larvae and adult nematodes..S.F. Comp. 1 day orally. Evaluation of different tests for the diagnosis of trypanosomiasis and depetalonemiasis. Pract.4 0.C. References Arzoun. Hussein. G. 1999. 94: 169-174..5 18 0. G. M.H.4 0.C. Assoc.5 12. 1989. 1 day spot on 25 0. However.5 0. spot on orally. W. M.M. A.366 Parasitic Diseases Table 61 Nematocidal anthelmintics for OWC and NWC Anthelmintic Fenbendazole Febantel Netobimin A bendazole 1 Oxfendazole Thiabendazole Mebendazole Levamisole Administration OWC Dose rnglkg NWC orallv. Recovery of Trichuris tenuis Chandler. 5-7. or i.S. 1 day orally. 185: 13071308.12 Treatment of Nematode Infections It is believed that of all the domesticated species. Courtney. Parasitol. Vet. H. H.. 1984a.2 0.5 0. 85: 961-962.Z. Anwar.2 0. Hussein.2 0. J. Med. not all of which have the same sensitivity to the particular anthelminticdrug used. This applies particularly to breeding herds. Aguirre and L. Vet. H. Kollias. 1984b. Chamers. Rickard. I. vigilance in the form of regular monitoring should be maintained. . Larvae or immature stages are generally not as sensitive to the drug as adults. Vet.G.5 5-7.5 5 10 5-8 5-8 8 5-8 5 50-1 00 22 5-8 5-8 - Pyrantel pamoate lvermectin Doramectin Moxidectin mot on S. 1998. 14: 43-53. I. 1 day S.. 1 day orally.F. Food Anim. Efficacy of ivermectin against gastrointestinalnematodes in dromedary camels. 1930. The prevalence and pathogenesis of naturally occurring Haemonchus longistipes infection in Sudanese camels. and Res. Clin. Allen. C. Hussein. A. Khan and M. orally. 5 217-225.5 5-7. and M.2 0. 1-3 days orally. 1 day orally. and G. Cheney. J. Parasitism in llama.A.2 0.. Hussein and M. 1 day S. Cafrune. North Amer.H. Arzoun. 5: 261-266. Nematocidal anthelminticsare listed in Table 61. Therefore. J.

J. Sci. L. Camel Prac. Helminth parasites of llamas (Lama glama) in the Pacific Northwest.E. Merino. 42: 45-53. M. El-Bihari. N. Bibliogr. Orlov. 20: 227-254. 141: 315-326.M. J. Cheikh. 20: 437-449. Cabaret.A. Humbert. 1998. Daynes. D. Berlin. G. Clinical manifestation of natural infection with gastrointestinal nematodes in camel. Hum.. USA. Jacquiet.F.A Diagnostic Manual. lzvestiya Aka- demii Nauk Turkmeneskoi SSR. France. B. The epidemiology and economic impact of llama parasites..R. Sudan. Elev. Rojas. A. L.R. 1998. A. 9: 241-244. . Goby. Pays Trop. S. First report from the Republic of Argentina and of a new host Lama glama Cuvier. Leguia. Yadav. and C.. 1998. C.A.A. Camelostrongylus mentulatus (Railliet and Henry. Cheikh and E. 1979. Bhan. Vet J.M.L. Rev. Tech. 58: 110-115. Common gastrointestinal helminths of camels of Pakistan. and Res.. Boero. Iowa State University Press. Int. Parasitology 110: 483-492. Kumar.A. Proceedings of the Khartoum Workshop on Camels. 1909). Amer. 1967. Epiz. G. 1977. Thiam and D. J. Guerrero. Rev. 1991. vtt. Anim.L. P. 8: 113-118. Comes. 1923 (Nematoda: Trichostrongyloidea). 1989. S. H e m h d e z and M. P. 1979.A. Kaufmann. Cockrill (ed. S.Hlth. Jacquiet. SOC. C. Michael. Adaptation to arid environment: Haemonckus longistipes in dromedaries of Saharo-Sahelian areas of Mauritania. Gibbons. 22: 147-150.K.H. Faye. J. and J. C. Rickard. 1993.L. Establishment and pathogenesis of gastrointestinal nematodes of camel and sheep. Gaceta Veterinaria 34: 187-190. Parasitol.K.J. Mid.I. Fowler. and M. Manohar and A. Argentina. Ouhelli.447-461. Dia. Br. Boston. M i d .G.S.An All-purpose Animal. Richard.. and H. 6: 423-445. J. Birkhauser Verlag. I. 1962. D. from the Mitre Peninsula. 1991a. Anim. Led. 1974. Guide de l'elkvage du dromadaire. Kiesel and C. Contribution to the knowledge of the endoparasitic fauna of Lama guanicoe Muller. Report of Nematodirella dromedarii (Nematoda: Trichostrongylidae) on the Indian camel (Camelus dromedarius) with remarks on the genus Nematodirella Yorke and Maplestone. Brunet. Queval. parasites of domestic ruminants in Mauritania. Pays Trop. M. Today. Durette-Desset and P. 1926. 7 54-56. Anim. Vet. 1997. Vicuiia.K. The development of Tkelazia leesei Railliet and Henry.T. in the body of the intermediate host. K. J. 1776. J.K.E. M. J. 2: 29-42. Medicine and Surgery of South American Camelids: Llama. Cabaret. Thiam 1996. Hashmi and I.C.): The Camelid . 66: 193-204. In: W. G. 5: 251-254. 1933. Hussein. Etude des strongyloses gastro-intestinales et de l'haemonchose 2 Haemoncus longistipes. 1985. 1989. 1967. Dec. 1967. J. Khartoum. 1977. Navone. and C. Parasitol. 1973. Trop. Cedex. C.. Bishop. and Res.Wash. The slide agglutination test for the diagnosis of filariasis in camels. 1972. Elev. Tab0 and J. and M. 5: 39-45. Dakkak. J. Alpaca. Res. Enqu6te sur les helminthes du dromadaire tchadien. New parasitic nematodes reported in alpacas (lama pacos) from Peru. vtt. Prod. Service. Biologcheskikk Nauk. 1996. J. Helminths and helminthoses of the dromedary. Vega. 4 Partani. Comp. Helminthol. 1910. Kumar. 1995. Raisinghani. and S. Bol. Ckileno Parasitol. Guanaco. A. Helminths of the camel: A Review. A review of the literature. A. 1979. Camel Prac. Revista de Investigaciones Pecuarias IVITA Universidad Nacional Mayor de San Marcos. R. (Nematoda-Trichostrongylidae). Badar. J. A review of the genus Impalaia Monnig. vet. Basel. Vet. Chavez. Lodha.. 1987. Sanofi Sante Nutrition Animale. Indian J. Richard. Parasitol.. Mtd. 5: 255-256. Saleh. Maqbool.Infection with Nematodes 367 Clark. Rev. M. Measurements of blood loss caused by Haemonckus contortus infection in sheep. 2nd ed. Graber. with description of Spiculopteragia peruvianus n. Graber and M. Biological and pathological features of Lamanema chavezi in alpacas (Lama pacos). Ofice Int. Serum proteins and haematological values in camels in relation to helminth infection. Elev. Ann. Parasitic Infections of Domestic Animals . Eco- logical morphological and genetic characterization of Haemonchus spp. D. and J. R. Tierra del fuego. D. Sci. 49: 817-822. Rev..S. L'haemonchose du dromadaire. Aha. Ckileno Parasitol. Ames. G. M. H. M.M. Dromedary pathology and productions. Hayat. sp. Pays Trop. Guerrero. 4 :46-51. Bol. 23: 977-980. 52: 435-446. Dobrynin. Rev.H. A. Sci.

Textbook of Veterinary Clinical Parasitology.A. I. Izvestiya Akademii Nauk Turkmeneskoi SSR. leur evolution dans l'annke .Redescription of Trichuris tenuis Chandler. Further reading Chakraborty. 1965. Dobrynin. J.K. 1972. J. A. SOC. Acute and subacute fasciolosis of alpacas (Lama pacos) and treatment with triclabendazole. Fac. El-Bihari. N. Adaptations des Haemonchinae des ruminants domestiques au milieu subdesertique (Mauritanie). Helminths. Clin. Sharma. Pays Trop. 16-17 131-137.A. Urquhart. Hlth. 1982. Bailli6re Tindall. Helminths. from llamas (Lama glama) in Oregon with a key to the species of Trichuris present in North American ruminants..M. 1994. Blackwell Science.I.Wash.L. 3 7 19-25. 1959. Anim. 1910.J. G. Schad. Parasitol.M. Proc. Haemonchus longistipes.S. K. The slide agglutination test for the diagnosis of filariasis in camels. Sci. D. Thesis. Michael. and C. Ve't. Vet. P. London. G. Tager-Kagan. 1991b. 1 0 239-247. Vasques.H. Peru.368 Parasitic Diseases Rickard. Resultats d'enquetes sur les helminthiases du dromadaire dam le departement de Zinder (Rep. Jacquiet. Occurrence and pathology of Gongylonema infection in captive herbivores. Dunn and F. J. J. Oxyuroidea). Znd ed. M. Biologcheskikh Nauk. Trop. R. and J. 1993. L. Parasitol. Mkd. Int. 1997.. Establishment and pathogenesis of gastrointestinal nematodes of camel and sheep. Vet. Lima. Amer. 1930. Food. UK.L. 1984. Rev.K. 5 2 163-167.. Anim.M.G.J. J. Rev. 9: 241-244. Hlth. Duncan. Saleh. Kawasmeh. Marchinares. Z. Type I1 ostertagiasis in llamas. Soulsby. Blackwell Scientific. 7* ed. The discovery of the intermediate host of Thelazia leesei Railliet and Henry. 1994. Vet.W. 1977. Experimental infection of sheep by camel stomach worm. 3: 73-77. E.L. Jennings. 8 113-118. 1991.S.G. 141: 608. Vet. 1984. A.C. Ashour and A. S. Rickard. du Niger). S.L. Oxford. and S. Windsor.A revision of the North American species of the genus Skrjabinema (Nematoda. 1971. N . Prod. D. Sudesh. Lima. P. Parasitol. Trop. Yadav. Vet. C.moyens de lutte.A. 26: 138-147. Armour. G. and A.A. 15: 257-261. Bishop. Helminthol. 1997. Pract. Elnaiem. 1995.. Soulsby. Acade'mie de Monfpellier. Parasites. Oxford. Vet. Anim.E. Revista del Instituto de Zoonosis e Investigation Pecuaria. Veterinary Parasitology. 1961-62.A. Leguia. Cooperia mcmasteri in alpacas and vicuiia (Cooperia mcmasteri en alpacas y vicuiia). Rec. 77: 70-75. Anim. 1996. France. Diaz. Ind.M. 68: 1069-1072. Parasitologicalsurvey in sheep and other animal species in the Pun0 Department. Arthropods and Protozoa of Domesticated Animals. Efficacy of some anthelmintics against gastrointestinal nematodes in camels (Camelus dromedarius). . 1:25-109. Elev. I. 29: 51-52. L. Med. Prod.

- + + + + + + + + + + + + + + + . Avitellina woodlandii Echinococcus hydatidosus Coenurus cerebralis Cysticercus tenuicollis Cysticercus bovis Cysticercus dromedarii - + + - Intestine carnivores Intestine carnivores Intestine carnivores Intestine humans Intestine carnivores Small intestine Small intestine Small intestine Small intestine Small intestine + + Bile ducts Bile ducts Bile ducts Bile ducts Forestomachs Portal vein in liver. liver Small intestine Heart. benedeni Avitellinidae Stilesia spp. Liver Muscle Muscle. Fasciola hepatica Fasciolidae E gigantica (Liver fluke) Fascioloidesmagna Dicrocoelium dendriticum Paramphistomatidae Paramphistomum sp. Schistomatidae Schistosoma sp. mesenteric vein Small intestine Small intestine Small intestine Peritoneum. Liver Small intestine - + + Taeniidae Anoplocephalidae (Tape worm) Echinococcus granulosus Taenia multiceps Taenia hydatigena Taenia saginata Taenia hyaenae Moniezia expansa M.Table 62 Cestodes and trematodes of Old World and New World Camelids Larval stage Adult parasite Location of Immature parasite Occurrence OWC NWC Family Species + + Lung. lung Thyzaniezia sp. Liver Brain Spinal cord Abdominal cavity.

370

Parasitic Diseases

5.4.1 Classification of Cestodes
Phylum Platyhelmintha (Flatworms) Class Cestodea Subclass Eucestodia Order Cyclophyllida Family Taeniidae Hydatids of Echinococcus grunulosus (OWC) Coenurus cerebralis, cysts of Tueniu multiceps (OWC) Cysticercus tenuicollis, cysts of Tueniu hydutigenu (OWC, NWC) Larval stage of T. helicometru (NWC) Cysticercus bovis, larval stage of T. suginutu (OWC, NWC) Cysticercus dromedurii, larval stage of T. hyuenue (OWC)
Family Anoplocephalidae Monieziu expunsu (OWC, NWC) Monieziu benedeni (OWC, NWC) Family Avitellinidae Stilesiu centripunctutu (OWC) S. globipunctutu (OWC) S. vittutu (OWC) Avitellinu woodlundi (OWC) Thyzunieziu sp. (NWC) T. ovillu (OWC)

containing one intermediate host. Adult tapeworms are found in the small intestine of the final host, in which the prepatent period lasts between 40 to 50 days. Once the egg is ingested by the intermediate host, it finds its way to its predilection site where it develops to a larval stage named metacestode. The metacestodes have different forms depending on the species. Some of these larval stages are characterized as:

Cysticercus - A fluid-filled cyst containing one invaginated scolex. Coenurus - A metacestode larva similar to cysticercus, but containing numerous invaginated scolices. Hydatid cyst - Another metacestode larva consisting of a large cyst filled with fluid. The germinal epithelium lining the cyst produces invaginated scolices, brood capsules.
When the final host ingests the intermediate host containing the metacestode, the scolex attaches to the mucosa of the small intestine. Proglottids start to grow from the base of the scolex. The main families found parasitizing camelids are the Taeniidae and Anoplocephalidae.
5.4.2.1 Cestode Larvae in Internal Organs

5.4.2 Tapeworm Infection
Tapeworms have an elongated flat body without alimentary canal o r body cavity. They are hermaphroditic and the body is segmented. Each segment or proglottid contains one or two sets of male and female reproductive organs, which are formed at the neck - the growth region of the worm. These proglottids mature as they are pushed further away from the head or scolex, and the fully gravid proglottid eventually contains a residual of branched uterus packed with eggs. The typical LC of the cestodesbelonging to the order Cyclophyllidea is indirect,

Taeniidae Hydatid disease Hydatids, caused by the tapeworms belonging to the genus Echinococcus, are found worldwide in numerous mammalian species, including humans. Echinococcosis is recognized as one of the world’s most important zoonoses. Hydatid cysts are frequently found in OWC as well as in NWC, particularly in lungs and liver. Hydatido-

Infection with Cestodes (TaDeworms)

371

sis is reported to be common in North and East Africa with a prevalence of 31% in Egypt (Hallawani, 1956), 45.4% in Sudan (Saad et al., 1983), 14.8% in Somalia (Macchioni et al., 1987) and 48% in Libya (Ibrahem and Craig, 1998).A lesser prevalence was reported in Central Africa (Dakkak and Ouhelli, 1987). In Nigeria, a prevalence of >57% was found (Dada, 1978). The infection is also common in Asia (Dakkak and Ouhelli, 1987), in Iraq and Iran with a prevalence of 49.1% and 42.8%,

respectively (Barber0et al., 1963; Afshar et a. 1971). l, The genus Echinococcus contains four species: E. granulosus, E. rnultilocularis, E. oligarthrus and E. vogeli.
Life Cycle (Fig. 170) E. granulosus lives in the small intestine of wild and domestic canids. It is a small, 6mm-long parasite with a scolex and three to four proglottids. The terminal gravid proglottid occupies nearly half of the adult worm and often

D

Figure 170 Life cycle of Echinococcus granulosus: A = eggs voided in feces; B = intermediate hosts ingest eggs; larval development in the host t o hydatid cysts in the lungs and/or liver; C = carcass at slaughter; D = dog becomes infected by eating parasitized offal; E = final host, the dog infected with Echinococcus granulosus

b -

372 Parasitic Diseases
Figure 171 Two hydatid cysts in the liver of a breeding dromedary

disintegrates while still in the gut of the fi- protoscolices and brood capsules may denal host, releasing the eggs into the feces. velop into new external cysts. In the canid, adult tapeworms may live up The parasite infection in the final host is not pathogenic. In domestic animals, the to two years. The oncospheres within the eggs can hydatid cysts in/on the liver and lungs survive outside the host for nearly two usually cause no clinical signs of disease. years. Ingested eggs are immediately in- Most infections are only revealed during fective and hatch in the intestine, releas- meat inspection at slaughter. However, a ing the oncospheres that penetrate into variety of clinical signs may occur if cysts venules or lymphatics of the gut wall and have developed at other sites, such as the migrate to the predilection sites, the liver brain, heart, and kidney. Affected lungs and lungs. Occasionally oncospheres are may cause respiratory signs and if one found in other organs where they may de- large cyst or several smaller hydatids are velop into hydatids. present in the liver, abdominal distention The cyst, developing slowly and in the may occur. Rupture of hydatid cysts may lung and liver, may take 6 to 12 months to cause death from anaphylaxis.Additionalmature to a diameter of up to 20 cm. In the ly, released daughter cysts may spread and abdominal cavity, cysts may become very develop in other parts of the body. Howlarge, sometimes containing several liters ever, some cysts are sterile, depending on of fluid. the age of the host (Soulsby, 1982). In camels, the lung is the organ most ofThe wall of the cyst consists of an outer, relatively thick, concentrically laminated ten affected with hydatids, followed by the membrane and an inner germinal layer, liver (Dada and Belino, 1978). Multiple from which brood capsules each contain- cysts are seen particularly in the lungs. Hying a number of scolices or protoscolices datid cysts are occasionally found in the (larvae)are budded off. Some of the brood spleen and are usually solitary (Saad et al., capsules are regularly found floating in the 1983).The number of fertile cysts found is cyst fluid. Complete daughter cysts are usually higher in the lungs than in other sometimes formed and if a cyst ruptures, organs. Cysts are often calcified (Fig. 171).

Infection with Cestodes (Tapeworms)

373

Pathology 1 Gross and histological char9 acteristics of echinococcus cysts in Cumelidue are similar to those described in other animals (Barker et al., 1993). Some variations in the arrangement of cyst layers were observed histologically by Saad et al. (1983),who found that the cellular infiltration was mainly by lymphocytes, plasma cells and eosinophils (Fig. 172).
i There are a number of different strains of E. grunulosus. They differ in important biological characteristics, including infectivity to humans (Bowles and McManus, 1993).E. grunulosus of camel origin raised experimentally in dogs was successfully transmitted to goats and sheep, but cattle and donkeys were not susceptible to the infection (Dada et al., 1981). Various cycles exist between the intermediate and canid final host. These are divided into the pastoral and sylvatic cycles. The dog is always involved in the pastoral cycle, but the domestic intermediate host species may vary: sheep/dog, cattle/dog, OWC/dog, NWC/dog etc. The pastoral cycle is the primary source of hydatid disease in humans. Such infections are caused by accidental ingestion of oncospheres

from dog coats or foodstuffs contaminated by dog feces. In the sylvatic cycle, wild canids are involved: deer/coyote, moose/wolf, wallaby/dingo, NWC/fox and hare/fox. This cycle is less important as a human source of infection. However, in hunting communities the infection may be introduced to domestic dogs by feeding them contaminated viscera from wild animals. The cycle in NWC follows the pattern NWC/dog and NWC/fox (Fowler, 1998). Public health workers are concerned about the zoonotic risk of hydatidosis in OWC for camel pastoralists. Epidemiological studies have recorded the highest incidence of human hydatid disease in pastoralists in Kenya. However, it has been shown that the E . grunulosus strain affecting camels in Kenya is different from the sheep and cattle E. grunulosus strains, and that humans appear resistant to infections by the camel strain (MacPherson and McManus, 1982). However, opinions differ concerning the infectivity of E. grunulosus from camels to humans (Shaafie et al., 1999).
1 Hydatids are frequently found during slaughter or necropsy. Infect-

Figure 172 Histology picture (HE staining) of the layers of a hydatid cyst and cut-surface of scolices from a breeding camel

374 Parasitic Diseases

ed dogs pass eggs in their feces that cannot morphologically be distinguished from eggs of Tueniu spp. The tapeworm may be demonstrated microscopically in the mucous portion of purged material. Immunodiagnostic tests using ELISA are used in human medicine. In addition, radiographic diagnosis is used. Recently, PCR techniques have been available which may identify antigenic material in feces. Treatment of domestic animals (intermediate host) is rarely employed in hydatidosis. In endemic areas, anthelmintic treatment of dogs may be used to break the cycle of infection. Praziquantel(5-10mg/kg per os), bunamidine hydrochloride (25-50 mg/kg per 0s) and some recent formulations of combinations consisting of both cestocidal and nematocidal components, e.g. febantel/praziquantel/pyrantel, are effective against the adult tapeworms in the dog.

Taenia multiceps Coenurus cerebralis The adult tapeworm of Tueniu multiceps is up to 1m long and is found in the small Taenia helicometra intestines of dogs and wild canids. Its Infections with larval stages of Tueniu helilarval stage, Coenurus cerebralis, is found cometru of canids have been reported in alin the brain or spinal cord of such inter- pacas and vicuiias from South America mediate hosts as sheep, goats and other (Fowler, 1998). ruminants. Occasionally it has been reported in dromedaries (Kaufmann, 1996). 5.4.2.2 Cestode Larvae The coenurus cysts, measuring 5 to 6 cm Found in Muscles in diameter, cause increased pressure intra-cranially, giving rise to CNS clinical Taenia saginata - Cysticercus bovis signs such as "gid and staggers". A cyst Cysticercus bovis, the larval form of the T. contains hundreds of invaginated proto- suginutu tapeworm in the small intestine scolices. of humans, is rarely found in camels. The metacestode is commonly found in the Diagnosis iliii Clinical signs are nonspecific muscles of cattle worldwide, particularly and diagnosis is usually made during in Africa and South America. Other ruminecropsy. nants and Cumelidue may occasionally serve as intermediate hosts. It has been Treatment The treatment of T. multiceps found that the predilection sites for this is the same as described for hydatid infec- parasite are the heart, masseter, tongue tions. and muscles of the diaphragm, but the cys-

Taenia hydatigena Cysticercus tenuicollis Tueniu hydutigenu, a large tapeworm that may reach 5 m, is found in the small intestine of dogs, wild canids and occasionally other carnivores. The intermediate hosts are ruminants, particularly sheep, but also pigs, alpacas, vicufias (Fowler, 1998) and dromedaries (Kaufmann, 1996). The oncospheres are carried hematogenously via the blood to the liver. They migrate in the liver parenchyma for about 4 weeks before they emerge to the liver surface and then attach to the peritoneum. Within a further 4 weeks, each larva may develop into a cyst, Cysticercus tenuicollis, measuring 6 to 8 cm in diameter. Each cyst contains one invaginated scolex. During migration in the liver, the larvae cause hemorrhagic tracts that may become fibrotic. If the infection is heavy, the developing cysticerci may cause severe liver damage, with fatal consequences. However, the infection is often asymptomatic. The cysts are occasionally found at slaughter.

Infection with Cestodes (Tapeworms)

375

ticerci may be observed throughout the musculature (Soulsby,1982).

Life Cycle (in Cattle) The mobile proglottids are shed in the feces. The eggs may stay viable for weeks or months in sewage, in rivers and on pasture. Eggs survive on dry sunny pastures over 14 weeks. When ingested, the eggs release the oncosphere into the small intestine. The oncosphere penetrates the mucosa, reaching the blood circulation, and is disseminated throughout the body into skeletal and heart muscles as well as fat tissue and oth'2.

er organs. The cysticercus C. bovis develops and becomes infective in approximately 10 weeks, and will be viable after between 4 and 9 months. Some cysts might stay viable throughout the intermediate host's life, depending upon the degree of infection and the age of the infected animal (Soulsby, 1982). The cyst is 0.5 cm in size and surrounded by a tissue capsule. Humans, the final hosts, are infected by the ingestion of raw or undercooked infected meat. After approximately 100 days, gravid proglottids will be passed in the stool.

Figure 173 Life cycle of Taenia hyaenae: A = eggs voided in feces; B = the intermediate host, the dromedary, has ingested the eggs, which has developed into a Cysticercus dromedarii; C = the hyena, the final host, preying on the intermediate host, the dromedary; D = hyena, the final host

376 Parasitic Diseases
Muscle cysticerci infections are usually not associated with clinical disease.
I

5.4.2.3 Cestodes of the Intestine

Anoplocephalidae, Avitellinidae
Seven cestode species are parasites of the small intestine of Camelidae. Moniezia expansa and M. benedeni, both reported in camelids, are common tapeworms in ruminants found worldwide. Both are significant NWC parasites in some areas of South America. M . expansa has been found in NWC in the USA and often in OWC in Africa and Asia. M . benedeni has only been reported in dromedaries in Africa. The Moniezia spp. are long tapeworms reaching up to 6 m. The heads (scolex) are unarmed with no rostellum, or hooks, but with 4 prominent suckers. The proglottids are broader than they are long. Mature protoglottids release eggs into the feces. The eggs are triangular (Fig. 174). Oribatid mites ingest the oncospheres on the pasture, which develop into cysticercoidswithin 1to 4 months. The final host becomes infected by ingestion of the infected mites that contaminate the forage.

Only prevention can break the LC. Rigorous meat inspection should be implemented and the consumption of raw meat should be avoided. In addition, proper disposal of abattoir waste and offal should take place to avoid infestation of carnivores.

Taenia hyaenae Cysticercus dromedarii There are a large number of taeniid cestodes with an unknown LC in wild carnivores’ small intestine. Cysficercus dromedarii, the larvae of T. hyaenae (in various species of hyena in Africa), are often found in the muscles of dromedaries, cattle and goats (Kaufmann, 1996). The natural and common intermediate hosts are several species of antelopes. C. dromedarii cysts are twice as large as C. bovis, 12 to 18mm in length. Although infected meat is not pathogenic to humans, meat with large numbers of cysts should be destroyed. Life Cycle !hi The LC is shown in Fig. 173.

Pathogenesis !ii0 Moniezia spp. infections are generally considered to be of little path-

Figure 174 Moniezia expansa eggs in dromedary feces

Infection with Cestodes (TaDeworms)

377

ules are formed with proliferate inflammation and epithelial desquamation (Arnjadi, 1971). The head and the anterior part of the parasite are embedded in the nodule and the posterior proglottids of the worm move freely in the intestinal lumen. The infection may lead to death. Stilesia Other tapeworms belonging to AvitelThree Stilesiu spp. are found in dromeda- linidae have been reported in camelids. ries. S. globipunctutu and S. centripunctutu Avitellinu woodlundi has been found in camare widely reported in Africa and Asia, els in Africa (Dakkak and Ouhelli, 1987), whereas S. vittutu has only occasionally and according to Kaufmann (1996) Avitellibeen observed (Dakkak and Ouhelli, 1987). na centripunctutu is widespread in these anS. globipunctutu occurs primarily in the imals in Africa and Asia. Thyzunieziu spesmall intestine of ruminants in southern cies are reported in llamas and T. ovillu in camels in Chad (Graber, 1966; Graber et al., Europe, Africa and Asia. 1967).Little is known of the LC and epideLife Cycle Little is known about the LC miology of the latter species. They seem to of Stilesia parasites. Oribatid mites may have no pathogenic significance. play an important role, as shown by SoulsTreatment Praziquantel has been shown by (1982) in Chad and India. The immature worms penetrate the mu- to be effective (15mg/kg in sheep and cosa of the duodenum and jejunum. Nod- goats). ogenic importance. However, there are indications that heavy infections may impair nutrition and cause diarrhea, debility, and sometimes obstruction of the intestine.
1 1

Four species are found in OWC and two are reported in NWC. NWC) F. within the egg.. Eurytremu puncreuticum. The parasites have suckers for attachment.1 Trematodes of the Liver Most of the helminths parasitizing the liver are trematodes. iary ducts. As juvenile flukes. An immature fluke of FascioZoides mugnu. is rarely found in dromedaries. the miracidium develops to a sporocyst. The adult flukes of the Digenea are oviparous. in- . the large American fluke. is also found in camels in Africa and Asia.2.5.2 Trematode Infections 5. 1991.Trematodes parasitizing in OWC and NWC and their organ localization are listed in Table 62 (p. D. is found as adults in the bile ducts of a number of mammals. (OWC) Family Schistosomatidae Schisfosomu bovis (OWC) S. the common large liver fluke. They are hermaphroditic except for some species of Schistosomatidae. In the snail. liver flukes. Encysted metacercariae survive for months and. but is less frequent than E hepuficu. which develops to the cercariae. and many are leaf-like. mutfheei (OWC) 5. dendriticum is rarely reported in NWC. the ciliated larva develops (miracidium). the small liver fluke. 1996). a deer parasite in North America. Fusciolu gigunficu. they then penetrate the gut wall and migrate to the predilection sites of the host. is frequently found in dromedaries in Africa and Asia and in Bactrians in Europe (Dakkak and Ouhelli.5. once ingested by a final host. the common liver fluke. Fasciola hepatica Fusciolu heputicu. The bodies of the flukes are generally dorsoventrally flattened and unsegmented. 1987) as well as in NWC (Leguia. The former is found in temperate and cool areas of high altitude in the tropics and subtropics. the fluke that occurs in the pancreas and rarely in the bil- The two most important ruminant liver flukes are Fasciola hepatica and E giguntica. 1988). NWC) Family Paramphistomatidae Purumphisfomum spp. but also in several other domestic and wild species. the giant liver fluke.5. gigunficu (OWC) Fuscioloides mugna (NWC) Eu ytremu puncreuticum (OWC) Dicrocoelium dendrificum (OWC. cattle and other ruminants. Fasciola hepuficu. 369).. particularly sheep. Dicrocoelium dendriticum. will hatch in the intestine. Fasciola hepatica and E gzgantica The Large and Giant Liver Fluke 5. C a h e et al. They emerge in large numbers from the snail and attach themselves to vegetation and encyst to metacercaria.1 Classification of Trematodes Superclass Trematoda Class Digenea Family Fasciolidae FuscioZu heputica (OWC. The miracidium must find a suitable snail host within a few hours. They lay eggs with a lid (operculum) at one pole and. has been found in hepatic cysts of one llama (Conboy et al. is reported in dromedaries in Africa. The latter predominates in tropical regions.

E = redia. Spillage from water troughs may also be a suitable habitat for the snail. B = water snail. Another impor- Figure 175 Life cycle of Fasciola sp. the 1to 2 cm-long. D = sporocyst. The fluke is distributed worldwide and causes fasciolosis or liver fluke disease. which may be easily transmitted via wet pastures shared with sheep and cattle. When fully matured in the bile duct of its final host. When young. Lymnaea sp. The disease is characterized by weight loss. G = metacercaria. I = final host with adult parasite in liver . The There are several factors necessary for outbreaks of fasciolosis. This host requires a wet environment. anemia and hypoproteinemia. Camelids are sensitive to infections with E hepatica. 175. encysted on grass and partly immersed in water. the snail. including mud or open waters. H = final host accidentally ingesting metacercariae. C = miracidium.: A = egg. particularly along banks and edges of small ponds. low-lying swampy areas and continuously irrigated pastures.Infection with Trematodes (Flukes) 379 cluding humans and camelids. F = cercaria. One is the availability of a suitable habitat for the intermediate host. Its tegument is armed with backwardly projected sharp spines. An oral and ventral sucker may clearly be seen under a microscope.. lancetlike fluke enters the liver. it is leaf-shaped and grayish brown in color. Life Cycle I LC is shown in Fig.

The prevalence of E hepatica and infections in OWC is relatively low and the infection is benign. but a dot-ELISA detected antibodies to F.380 Parasitic Diseases Figure 176 Fasciola hepatica infesta- tion in a Bactrian liver (courtesy of Dr. Weber. 1991). The prevalence of fasciolosis in vicuiias was 10 to 18. This unexpectedly high prevalence was attributed to either high rainfall or areas with irrigated agriculture. There is a direct correlation between development time and the temperature. Pathology ilki Both the acute and the chronic forms of fasciolosis have been observed in camelids. hepatica in 16% of the tested llamas (Rickard. 1995). Leakage of plasma proteins due to cholangitis causes hypoproteinemia. Several researchers have diagnosed fasciolosis in NWC. a prevalence of 1 to 6%was recorded (Rickard and Bishop. Germany) tant requirement for the development of the fluke is the optimal temperature. but it is rare in OWC. The acute disease is associated with liver damage and hemorrhages caused by the parasite’s migration to the liver parenchyma.. 1996).. while in alpacas from Bolivia it was over 51% (Cafrune et al. In Saudi Arabia.6% in Argentina (Cafrune et al.. Thickening of the bile ducts may occur. 1992). Magzoub and Kassim (1978) found a relatively high prevalence of 10. 1991).particularly in the Eastern Province.43%. It is known that llamas and sheep have a low resistance to E hepatica (Rickard and Foreyt. A miniium mean temperature of 10°C is necessary for the snail to breed. resulting in partial or total condemnation of affected livers at meat inspection. Magzoub (1988) reported a fasciolosis prevalence of 92%in camels in Sudan. Continuous stasis of the bile results in hepatic fibrosis. USA. (Al-Khalidi et al. which eventually leads to the elevation of the intrahepatic blood pressure. 1996) and 8% in alpacas and llamas in Peru (Leguia. 176). as well as for the development of the eggs. In the chronic disease. M. Leguia (1991) has described acute infections in NWC with mortalities reaching 100%. 1990). In llamas in Oregon. The . the fluke living in the bile ducts damages the mucosa of the ducts with its cuticular spines (Fig. for the development of the fluke inside the snail. Examination of the feces from 283 dromedaries in Iraq employing a sedimentation method also revealed a relatively high infection rate of Fasciola spp.

Diarrhea and/or constipation may occur. 1995). For the treat. seasonal occurrence and cli.Fasciola gigantica ease the chosen compound should be effective against adult flukes.Nitroxynil has good effect against adult ter slaughter.available in combination with levamizole.7mg/kg per 0s) is effective against adult not be diagnosed during the period prior and 12 to 14-week-old immature flukes in to fluke maturation. 1991). 1996). The infection is often first recognized at meat inspection af. Depression and emaciation follow. ment of acute fasciolosis it is important to The dosage is 15mg/kg per 0 s in sheep use a product that is particularly effective and 17mglkg in cattle. particularly in the submandibularregions. is the drugs may be tried against trematodes in common liver fluke of African domestic stock. Clorsulon (2 mg/kg S. the Pacamelids: . The assay detected specificantibodies during the second week Oxyclozanide is used in cattle. ciolosis on the premises and/or identification of the snail or snail habitat are helpful. Acute fasciolosis is less frequent than the chronic manifestation and is associated with liver insufficiency. 1991)and llamas (Duff et al. infections can.against adult flukes. It is effective against all stages of fluke infection. Netobimin is metabolized into albendazole and has a similar activity against E hepatica. which lasts for 8 to 12 cattle.c. It is also ovicidal and kills the eggs present in the bile ducts and in the gut.C. and the wool becomes brittle and breaks easily.Serologicaltests are employed flukes at a dose of 10mg/kg. The compound is also tically or prophylactically. Albendazole has a broad-spectrum activit .. It is effective against adult E hepatica y in sheep (7. but the in research.5mg/kg per 0s) and in cattle (10mg/kg per 0s). Edema may be seen. at a dosage of 5 mg/kg.Infection with Trematodes (Flukes) 381 compromised fluke-infected liver also may be susceptibleto secondary bacterial infections. It can also be matic conditions. The following The giant liver fluke. A dot-ELISAwas developed to dose must be increased by 50% in acute detect antibodies to E hepatica antigens in disease. or is also important. Animals with the chronic form become anemic and anorectic. 1999). Fasciolosis is a zoonotic disease and is becoming increasingly important in humans: the Peruvian Sierras have infection rates of 15 to 25% (Leguia.administered S. For the chronic dis. weeks following infection. It has a shorter milk withholding time than most following experimental infections. Clinical Signs ?Kt Fasciolosis in camelids is generally subclinical. The milk yield is reduced. gigantica. other flukicides and is only effective Flukicides are used therapeu. F. However. The dosage for sheep and cattle is 20mg/kg per 0s. It is also effectivein alpacas (Leguia. Diagnosis GI& Diagnosis is mainly based on Closantel kills most of E heputica in sheep clinical signs.C. against the juvenile parasites that damage the liver parenchyma. llamas (Rickard. Triclabendazole is the drug of choice for outbreaks of acute disease (Roberts and Suhardono. Clorsulon is available in combination with Examination of feces for egg identification ivermectin. It is frequently found in Asia. the dose is 10mg/kg for sheep and 12mg/kg for cattle given orally. as is the case in some ruminants..A previous history of fas.at a dose of 10mg/kg per 0s. s.

= sporocyst. hepati