P. 1
62159343 Poultry Diseases and Their Treatment

62159343 Poultry Diseases and Their Treatment

|Views: 568|Likes:
Published by wojewoda

More info:

Published by: wojewoda on Oct 17, 2011
Copyright:Attribution Non-commercial

Availability:

Read on Scribd mobile: iPhone, iPad and Android.
download as PDF, TXT or read online from Scribd
See more
See less

12/04/2012

pdf

text

original

Sections

  • By
  • Paul McMullin
  • M.Abubakar.Tahir
  • M.Sc.(Hons) Animal Nutrition
  • University of Agriculture Faisalabad
  • Amyloidosis
  • Anatipestifer Disease, New Duck Syndrome, Duck Sepicaemia
  • Arizona infection, Arizonosis
  • Ascites
  • Aspergillosis
  • Avian Encephalomyelitis Egg Drop
  • Avian Encephalomyelitis, Epidemic Tremors
  • AvianInfluenza-Highly Pathogenic (HPAI), Fowl Plague
  • Avian Leukosis (Serotype J), Myelocytomatosis
  • Avian Leukosis, Lymphoid Leukosis, Leukosis/Sarkoma Group
  • Avian Rhinotracheitis 'Swollen Head Syndrome'
  • Beak Necrosis
  • Bedbug Infestation
  • Big Liver and Spleen Disease
  • Biotin Deficiency, Including Fatty Liver and Kidney Syndrome
  • Biting Lice
  • Blackfly Infestation
  • Botulism
  • Breast Blister
  • Caecal Worm
  • Calcium Tetany
  • Campylobacter Infection
  • Candidiasis, Moniliasis, Thrush
  • Cannibalism, Feather pecking
  • Capillariasis-Hairworm Infection
  • Cellulitis
  • Chicken Anaemia
  • Chlamydiosis, Psittacosis, Ornithosis
  • Chondrodystrophy, Slipped Tendon or Perosis
  • Coccidiosis of Turkeys
  • Coccidiosis, Caecal, E tenella
  • Coccidiosis, E mitis
  • Coccidiosis, Ileorectal, E brunetti
  • Coccidiosis, Intestinal, of Ducks and Geese
  • Coccidiosis, Kidney
  • Coccidiosis, Mid-intestinal, E maxima
  • Coccidiosis, Mid-intestinal, E necatrix
  • Coccidiosis, Upper Intestinal, E acervulina
  • Colibacillosis, Colisepticemia
  • Contact Dermatitis, Hock Burn, Pododermatitis
  • Cropworms
  • Cryptosporidiosis
  • Dactylariosis
  • Degenerative Joint Disease
  • Depluming and Scaly Leg Mites
  • Dissecting Aneurysm, Aortic Rupture
  • Duck Viral Hepatitis
  • Duck Virus Enteritis, Duck Plague
  • Dysbacteriosis, Non-specific Bacterial Enteritis
  • Egg Drop Syndrome 76
  • Endocarditis
  • Epiphysiolysis
  • Equine Encephalitis (EEE, WEE, VEE)
  • Erysipelas
  • Fatty Liver Haemorrhagic Syndrome
  • Favus
  • FemoralHead Necrosis-FHN
  • Fowl Cholera, Pasteurellosis
  • Fowl Pox, Pox, Avian Pox
  • Gangrenous Dermatitis, Necrotic Dermatitis
  • Gape
  • Gizzard worms-Chickens
  • Gizzard worms-Geese
  • Goose Parvovirus (Derzsy's Disease)
  • Haemorrhagic Disease, Aplastic Anaemia, Haemorrhagic Anaemia
  • Haemorrhagic Enteritis
  • Heat Stress
  • Hexamitiasis
  • Histamonosis, Histomoniasis, Blackhead
  • Hydropericardium-Hepatitis Syndrome, Angara Disease
  • Impaction and Foreign Bodies of Gizzard
  • Inclusion Body Hepatitis
  • Infectious Bronchitis, IB
  • Infectious Bronchitis, IB-793b Variant Sudden Death Syndrome in Broiler Parents
  • Infectious Bronchitis, IB Egg-layers
  • Infectious Bursal Disease, IBD, Gumboro
  • Infectious Coryza
  • Infectious Laryngotracheitis, ILT
  • Intussusception
  • Leukocytozoonosis
  • Lymphoproliferative Disease (LPD)
  • Malabsorption Syndrome, Runting/Stunting
  • Marek's disease
  • Mycoplasma gallisepticum infection, M.g., Chronic Respiratory Disease-Chicken
  • Mycoplasma gallisepticum infection, M.g., Infectious Sinusitis-Turkeys
  • Mycoplasma immitans infection
  • Mycoplasma iowae infection, M.i
  • Mycoplasma meleagridis infection, M.m
  • Mycoplasma synoviaeinfection, M.s. Infectious Synovitis
  • Mycotoxicosis
  • Necrotic Enteritis
  • Newcastle Disease (Paramyxovirus 1)
  • Non-starter and 'Starve-out's
  • Oregon Disease-Deep Pectoral Myopathy
  • Ornithobacterium Infection, ORT
  • Osteomyelitis Complex, Turkey
  • Osteoporosis, Cage Fatigue
  • Paramyxovirus 2-Yucaipa Disease
  • Paramyxovirus-3
  • Paramyxovirus-6
  • PEMS and Spiking Mortality of Turkeys
  • Pendulous Crop
  • Proventricular Worms
  • Pseudotuberculosis
  • Pullet disease, Bluecomb, Avian Monocytosis
  • Red Mite and Northern Fowl Mite
  • Respiratory Adenovirus Infection, 'Mild Respiratory Disease'
  • Respiratory Disease Complex
  • Reticuloendotheliosis, Lympoid Tumour Disease
  • Rickets (hypocalcaemic)
  • Rickets (hypophosphataemic)
  • Rotavirus Infection
  • Roundworm, large-Ascaridia
  • Ruptured Gastrocnemius Tendon
  • Salmonella Gallinarum, Fowl Typhoid
  • Salmonella Pullorum, Pullorum Disease, 'Bacillary White Diarrhoea'
  • Salmonellosis, Paratyphoid Infections
  • Salmonellosis, S. Enteritidis and S. Typhimurium infections
  • Salpingitis
  • Shaky Leg Syndrome
  • Spiking Mortality of Chickens
  • Spirochaetosis
  • Spondylolisthesis, Kinky-back
  • Spraddle Legs or Splay Leg
  • Staphylococcosis, Staphylococcal Arthritis, Bumble Foot
  • Streptococcus bovis Septicaemia
  • Sudden Death Syndrome, 'Flipover'
  • Tapeworms, Cestodes
  • Tibial Dyschondroplasia, TD
  • Ticks
  • Transmissible Enteritis, Bluecomb
  • Trichomoniasis, Canker, Frounce
  • Tuberculosis
  • Turkey Coryza
  • Turkey Rhinotracheitis (Adult)
  • Turkey Rhinotracheitis (in rear)
  • Turkey Viral Hepatitis
  • Twisted leg
  • Ulcerative Enteritis, Quail disease
  • Vibrionic Hepatitis, Avian Infectious Hepatitis
  • Viral Arthritis
  • Visceral Gout, Nephrosis, Baby Chick Nephropathy
  • Vitamin A Deficiency, Nutritional Roup
  • Vitamin B Deficiencies
  • Yolk Sac Infection, Omphallitis

Poultry Diseases and Their Treatment

By Paul McMullin

M.Abubakar.Tahir

M.Sc.(Hons) Animal Nutrition

University of Agriculture Faisalabad
1

M.Abubakar.Tahir

Amyloidosis
Introduction
A Coronavirus infection of chickens with a morbidity of 50-100% and a mortality 0-25%, depending on secondary infections. Infection is via the conjunctiva or upper respiratory tract with an incubation period of 18-36 hours. The infection spreads rapidly by contact, fomites or aerosol. Some birds/viral strains can be carriers for up to 1 year. The virus, which may survive 4 weeks in premises, is sensitive to solvents, heat (56°C for 15 mins), alkalis, disinfectants (Formal 1% for 3 mins). Poor ventilation and high density are predisposing factors.

Signs
   Sudden death. Muscular shivering. Otherwise as for standard IB.

Post-mortem lesions
   Oedema of pectoral muscles and subcutaneously on abdomen, lesions progress to necrosis and scarring of deep pectorals in convalescence. In layers the ovules may be intensely congested. Other lesions of 'classical' IB may be encountered.

Diagnosis
3-5 passages in CE allantoic cavity, HA-, typical lesions, FA, ciliostatic in tracheal organ culture, cell culture (Vero, CK) only after adaptation Serology: HI, Elisa (both group specific), SN (type specific), DID (poor sensitivity, short duration, group specific).

Treatment
Sodium salicylate 1gm/litre (acute phase) where permitted - antibiotics to control secondary colibacillosis (q.v.).

Prevention
Live vaccines of appropriate sero-type and attenuation, possible reactions depending on virulence and particle size.

2

Anatipestifer Disease, New Duck Syndrome, Duck Sepicaemia
Introduction
An acute or chronic septicaemic disease caused by Riemerella anatipestifer, syn Pasteurella, or Moraxella a. It affects ducks of any age, sometimes turkeys, and may also be isolated from chickens, game birds and wild waterfowl. Mortality is 2-75% in young ducks. Transmission is mainly direct, bird-to-bird, via toenail scratches, especially of the duckling foot, or through respiratory epithelium during respiratory disease. It can also be by faecal contamination of feed, water or the environment where survival of the infectious agent may be prolonged. Adverse environmental conditions and pre-existing disease are predisposing factors.

Signs
         Weakness. Neck tucked in. Head/neck tremor. Ataxia. Disinclined to walk. Incoordination. Dyspnoea. Ocular and/or nasal discharge. Hyperexcitability

Post-mortem lesions
        Perihepatitis without much smell or liver damage. Pericarditis. Airsacculitis. Enlarged liver and spleen. Occasionally fibrinous meningitis. Salpingitis Purulent synovitis. Chronic arthritis, sometimes with erosions of the joint cartilage.

Diagnosis
Lesions, isolation and identification of organism - blood or chocolate agar in candle jar or 5% CO2. Differentiate from duck viral enteritis, duck viral hepatitis, fowl cholera, colibacillosis, coccidiosis, chlamydiosis.

Treatment
Sulphonamides and potentiated sulphonamides are the products most commonly recommended for drinking water application. Subcutaneous injections of penicillin + dihydrostreptomycin, or streptomycin + dihydrostreptomycin are also highly effective.

3

Paralysis. feed etc. Arizonosis Introduction Caused by the bacterium Arizona hinshawii. Erosions of the cartilage of the hock joint in a duck with chronic Riemerella anatipestifer infection. Transmission is vertical. Autogenous bacterins sometimes used. Congestion of duodenum. Figure 40. from long-term intestinal carriers. Blindness. correct house relative humidity. Cheesy plugs in intestine or caecum. Vent-pasting. rodents. Post-mortem lesions      Enlarged mottled liver. renamed Salmonella Arizonae. Nervous signs. cloudiness in eye. mainly in North America. Inappetance. 4 . Mortality is 10-50% in young birds. older birds are asymptomatic carriers. Huddling near heat. Unabsorbed yolk sac. Inactivated and attenuated vaccines available in some countries. transovarian. It affects turkeys. Diarrhoea. adequate protection. and is not present in the UK turkey population. rigid depopulation and disinfection.Prevention Good husbandry and hygiene. sulphonamides in feed. Signs         Dejection. Foci in lungs. and also horizontal. Arizona infection. reptiles. 'hardening off'. through faecal contamination of environment.

Thickening of atrioventricular valve.    Salpingitis. fumigation of hatching eggs. Poor development. Severe muscle congestion. Post-mortem lesions       Thickening of right-side myocardium. The disease has a complex aetiology and is predisposed by reduced ventilation. Diagnosis Isolation and identification. or gentamycin at the hatchery is used in some countries. inject eggs or poults with antibiotics. Perihepatitis. Prevention Eradicate from breeder population. Recumbency. salmonellosis. Pericarditis. Ascites Introduction Associated with inadequate supplies of oxygen. Lungs and intestines congested. spectinomycin. coli-septicaemia. 5 . Ascites is a disease of broiler chickens occurring worldwide but especially at high altitude. Pulmonary arterial vasoconstriction appears to be the main mechanism of the condition. Differentiate from Treatment Injection of streptomycin. Ophthalmitis. poor ventilation and physiology (oxygen demand. Possibly cyanosis. Progressive weakness and abdominal distension. mortality 1-2% but can be 30% at high altitude. General venous congestion. and respiratory disease. Formerly in-feed medication with nitrofurans was also used. may be related to type of stock and strain). Signs       Sudden deaths in rapidly developing birds. monitor sensitivity. methods as per Salmonella spp. Morbidity is usually 1-5%. Dilation of the ventricle. good nest and hatchery hygiene. high altitude. Dyspnoea.

Differentiate from broiler Sudden Death Syndrome and bacterial endocarditis. Vitamin C (500 ppm) has been reported to be of benefit in South America. control respiratory disease. Weakness. but may be as high as 12%. etc. turkeys. ducks. Silent gasping.cartilage nodules increased in lung. worldwide. Morbidity is usually low. Ascites. Diagnosis Gross pathology is characteristic. Signs  Acute        form: Inappetance. Transmission is by inhalation exposure to an environment with a high spore count. Pericardial effusion. penguins. waterfowl. Occasionally similar lesions are produced by other species ofAspergillus or even other fungi such as Penicillium. Aspergillosis Introduction A fungal infectious disease. A cardiac specific protein (Troponin T) may be measured in the blood. in which the typical sign is gasping for breath. It affects chickens. This may offer the ability to identify genetic predisposition. there is usually little bird-to-bird transmission. avoid any genetic tendency. Spores are highly resistant to disinfectants. Spleen small. Mortality among young affected birds is 5-50%. 6 . Absidia etc. especially in young chicks. Sometimes the same organism causes eye lesions or chronic lesions in older birds.     Liver enlargement. The infection has an incubation period of 2-5 days. Microscopic . Thirst. game birds. caused by Aspergillus fumigatus. Prevention Good ventilation (including in incubation and chick transport). The fungus can infect plant material and many species of animals including birds and man. Drowsiness. Nervous signs (rare). Treatment Improve ventilation. Rapid breathing.

It may be confirmed by isolation of the fungus. The powdery surface is dark green in colour. Post-mortem lesions    Yellow to grey nodules or plaques in lungs. It affects chickens. Growth occurs in 24-48 hours and colonies are powdery green/blue in appearance. Environmental spraying with effective antifungal antiseptic may help reduce challenge. Figure 8. quail. mortality none. Treatment Usually none. Diagnosis This is usually based on the signs and lesions and microscopic examination for the fungus. may have greenish surface. Epidemic tremors for its effect in young birds. Avian Encephalomyelitis Egg Drop Introduction Avian encephalomyelitis virus infection in laying bird causes inapparent infection or drops in egg production. turkeys. Amphotericin B and Nystatin have been used in high-value birds. Differentiate from excessive exposure to formalin or vaccinal reactions in day olds and from heat stress in older birds. Prevention Dry.M. Thiabendazole or Nystatin has been used in feed.Abubakar.  Wasting. The means of transmission is unknown but 7 .Tahir 2  Chronic Forms:  Ocular discharge (ocular form only). plaques in peritoneal cavity. typically by putting small pieces of affected tissue on Sabouraud agar. 'Furry' airsacculitis in aspergillosis of an adult duck. See Avian Encephalomyelitis. Morbidity 5-60%. good quality litter and feed. trachea. pheasants and occurs in most poultry-producing countries. Conjunctivitis/keratitis. Brain lesions may be seen in some birds with nervous signs. air sacs. preferably after digestion in 10% potassium hydroxide. hygiene.

Paralysis. Prevention Vaccination of breeders/layers at 9-15 weeks. Predisposed by immunosuppression. Treatment None. The route of infection is transovarian with an incubation period of 1-7 days. rising titre to AE virus. subsequent disease in progeny if breeders.probably by faecal contamination of environment. It has a worldwide distribution. and there is serious disease in the progeny (see next section). Avian Encephalomyelitis. EDS76. Epidemic Tremors Introduction Avian encephalomyelitis is a viral disease of the central nervous system of chickens. some lateral. Post-mortem lesions  None. feed. Virus in faeces may survive 4 weeks or more. 8 . Signs      Nervous signs. water etc. Signs   Drop in egg production. turkeys. In breeders there may be a drop in hatchability of about 5%.The embryo protection test has been used in the past. Vertical transmission is very important. Immunity is usually long lasting. and quail. mortality high. with an oral infection route. lentogenic Newcastle disease. small (5-10%) and lasting no more than 2 weeks. incubation >10 days. Differentiate from Infectious Bronchitis. pheasants. Diagnosis History. now Elisa is used more commonly. Virus in faeces may survive 4 weeks or more. lateral transmission is probably by the oral route. Dull expression. Morbidity 5-60% depending on the immune status of the majority of parents. Imbalance. Serology . Ataxia and sitting on hocks. transmission occurs over about 1-2 weeks. attenuated or not.

ducks. Highly pathogenic forms are usually of the H groups 5 and 7 and may now be identified (if H5 or H7) by the presence of a sequence at the haemagglutinin cleavage site that codes for multiple basic amino acids. Mycotic Encephalitis. and isolates are designated sero-type/ species/location/reference number/year/subtype designation(H/N). Avian Influenza-Highly Plague Introduction Pathogenic (HPAI). Post-mortem lesions     Gross lesions are mild or absent. its pathogenicity is variable. now Elisa is used more commonly. Brain abscess. pigeons. Diagnosis A presumptive diagnosis is based on the history. The higher the proportion of the chickens dying or showing signs the higher the IVPI. especially in turkeys. The definitive classification of high pathogenicity is an intravenous pathogenicity test (IVPI) in 6-week-old chickens result of greater than 1. Prevention Vaccination of breeders at 9-15 weeks. Tremor may be inapparent but is accentuated if chicks are held inverted in the hand. Effectively all 9 . This viral disease can cause exceptionally high mortality. vitamin deficiency (E. Microscopic . The cause is a virus. Fowl One of only two 'Class A' diseases of poultry targeted for emergency disease control measures by OIE. and lack of significant lesions. In addition official control measures disrupt trade in poultry products from affected areas. toxicities. quail. Marek's disease. attenuated or not.2 . and/or viral isolation may be carried out if required. Enterococcus hirae infection. There may be focal white areas in gizzard muscle (inconstant). The embryo protection test has been used in the past. signs. Treatment None. neck and wings. A few recovered birds may develop cataracts weeks after infection. the equivalent of the World Health Organisation for animal diseases. turkeys. EE (especially in pheasant in the Americas). A. Histopathology is usually diagnostic and IFA. riboflavin).nonpurulent diffuse encephalomyelitis with perivascular cuffing. Immunity is long lasting. Differentiate from Newcastle disease. This is a test in which the virus is inoculated into susceptible chickens that are then kept under observation. pheasants. Tremor of head. partridges. Orthomyxovirus type A. The virus infects chickens. and ostriches.

Pasteurella) may increase mortality. Avirulent in one species may be virulent in others. It can result in inapparent infection. It is inactivated by a temperature of 56°C in 3 hours and 60°Cin 30 min. A serious outbreak occurred in The Netherlands in 2003 with a few linked cases in Belgium and one in Germany. in the years 1983-84. conjunctivitis or severe pneumonia. over 30 days at 0°C.g. Marked loss of appetite. from December 1999. Nasal and ocular discharge. Coughing. See current OIE records for up to date information on distribution of HPAI. in northern Italy. Cessation of normal flock vocalisation. Broken contaminated eggs may infect chicks in the incubator simulating vertical transmission. The virus is moderately resistant. Avian Influenza is a potential zoonosis. The small number of human deaths associated with HPAI appear to have resulted from direct exposure to infected birds on farm or in markets. can survive 4 days in water at 22°C. 550%. Nervous signs such as paralysis. reduced feed consumption. and the high mortality that 'low-path' AI can cause in turkeys. 10 . clothing. Infections with other pathogens (e. equipment. waterfowl. but possibly by the conjunctival or respiratory route and the incubation period is 3-5 days. Apathogenic and mildly pathogenic influenza A viruses occur worldwide. Drops in egg production. More recently outbreaks have occurred in Australia. Cyanosis of comb/wattles. The virus replicates mainly in respiratory tissues of chickens and turkeys but in the intestinal tract of clinically normal waterfowl. Ovarian regression or haemorrhage. Signs            Sudden death. H5 viruses of low pathogenicity may become highly pathogenic usually after circulating in poultry flocks for a time (Pennsylvania. even with 'low pathogenicity' strains. Because of this. air sacs and conjunctiva. trachea. The route of infection is probably oral initially. Transmission is by direct contact with secretions from infected birds. drinking water. Diarrhoea (often green). Morbidity is high but mortality usually relatively low. especially faeces. Outbreaks due to HPAI were recorded in the Pennsylvania area. OIE and other bodies are currently examining ways to improve control of LPAI. by acid pH. It can remain viable for long periods in tissues. Depression. Mexico and. Italy). Highly pathogenic avian influenza A (HPAI) viruses of the H5 and H7 HA subtypes have been isolated occasionally from free-living birds.birds are considered to be at risk of infection. Post-mortem lesions   Inflammation of sinuses. by oxidising agent and by formalin and iodine compounds. USA. Pakistan. Swollen face.

etc. while ducks may be symptomless. Dehydration. It has occured in Europe. bacterial sinusitis in ducks. cleaning. isolation. although it may reduce losses initially. Muscles congested. Vaccination is not normally recommended because. correct disposal of carcases. as with many such tests occasional false positive reactions can occur. bleeding and vaccination needles. NDV-. 21-day interval to re-stocking should be followed. Diagnosis A presumptive diagnosis may be made on history and postmortem lesions. vaccinated birds may remain carriers if exposed to the infection. lateral transmission by faecal-oral route (this declines as the bird ages). To be effective inactivated vaccines must be the right subtype for the particular situation (H5 will not protect against H7 and vice versa). controlled marketing of recovered birds. Prevention Hygiene. Confirmation is by viral isolation in chick embryo. Vaccines have been used in recent outbreaks in Mexico and Pakistan. DID+. Commercial Elisa test kits are now available. though there is high mortality of affected birds. This condition has until now been seen only in meat-type chickens. In outbreaks a regime of slaughter. North and South America. Eradication by slaughter is usual in chickens and turkeys. However. lesionless carriers of highly pathogenic virus. Differentiate from Newcastle disease. The agar gel precipitation test is non-group-specific and is used to confirm any positives. all-in/all-out production. Haemorrhage in proventricular and gizzard mucosae and lymphoid tissue of intestinal tract. Treatment None. Transmission is by congenital infection from antibody-negative females. Minimise contact with wild birds. with considerable strain-to-strain variation. disinfection. Morbidity is low. other respiratory infections. fowl cholera.      Necrosis of skin of comb and wattles. Subcutaneous oedema of head and neck. The incubation period is 10-20 weeks. nutrition and antibiotics may reduce losses. quarantine. but good husbandry. Myelocytomatosis Introduction Caused by an avian retrovirus. Avian Leukosis (Serotype J). Congenitally infected birds tend to remain 11 . infectious laryngotracheitis. Survivors can be expected to have a high degree of immunity but may harbour virulent virus. HA+. Turkey lesions tend to be less marked than those of chickens.

age. Enlargement of abdomen. Lymphoid Leukosis. Minimise stress. Many are asymptomatic. 'nonshedders' . Critical hatchery practices:     Separate infected and uninfected lines. Treatment None. Separation in vaccination. Handle clean lines before infected lines.tumours usually contain well-differentiated myelocytes. preferably on separate hatch days and in separate machines.an Elisa test is aviailable to identify antibody positive birds. Prevention Checking of antigen in the albumen is a basis for eradication . Loss of weight. lesions. Prevent/ reduce cross-infection in hatchery and on farm. Two cell types may be found in the same tumour. liver. shed virus and develop tumours. Microscopic . sacral joint. birds with egg antigen will be antibody negative. 'Shedders' . There is also evidence that it is slightly more sensitive than conventional testing. Differentiate from Marek's disease. particularly of the sternum. Most characteristically are chalky white tumours in the bone marrow. PCR testing of embryonally infected chicks using DNA testing is uniformly positive for blood and faecal samples.most but not all.antibody negative.only 3% produced infected chicks. Post-mortem lesions     Liver enlargement. Signs       Depression. Serology . often with tumour foci. ribs. ultimately identification of virus by isolation and/or PCR. Diagnosis History. Virus survival is poor but sufficient to allow cross contamination in hatcheries and on farm in rear.80% produce infected chicks. histology. Splenomegaly and enlarged kidneys also occur. Persistent low mortality. Emaciation. 12 .

It affects chickens worldwide with susceptibility varying considerably among different strains and types of stock . There may be increased susceptibility to other infectious diseases due to damage to the immune system. Mortality tends to be chronically higher than normal for a prolonged period. osteopetrosis. Signs       Depression. fibrosarcomas. Leukosis/Sarkoma Group Introduction Lymphoid Leukosis. Loss of weight. The causative viruses are rapidly inactivated at ambient temperature and on exposure to most disinfectants. coligranuloma. initially in the bursa. Morbidity is low but mortality high. age. especially in young birds. Liver may be very large. spleen. it may be as short as 6 weeks for some of the other manifestations. 13 . Delay live vaccine challenges. Enlargement of abdomen. erythroblastosis. myxosarcomas. kidney etc. Microscopic . In lymphoid leukosis the incubation period is about 4-6 months. Emaciation. Egg production is somewhat reduced. Avian Leukosis. other tumours. Many are asymptomatic. Avoid migration errors (birds unintentionally moving between pens). lateral transmission is poor but infection may occur by the faecal-oral route. Minimise group sizes. cytology. then liver.cells lymphoplastic Diagnosis History. Post-mortem lesions   Focal grey to white tumours. myeloblastosis (see Sero-type J).egg layers are generally more susceptible to lymphoid leukosis. Persistent low mortality. Differentiate from Marek's disease. lesions. liver or bursa.Farm practices:     Brood and rear lines separately and maintain separate for as long as possible. Vertical transmission is most important by infection of the egg white in infected breeders (who are long-term carriers). A complex of viral diseases with various manifestations such as lymphoid leukosis.

Conjunctivitis. Figure 9. 14 . guinea fowl and possibly pheasants seen in Europe. Diffuse lymphoid tumours in an enlarged liver from a mature broiler parent hen. eradication . There is rapid lateral transmission with infection by aerosol through the respiratory route. The incubation period is 5-7 days. As for many infections. Signs        Decreased appetite. morbidity is 10-100% and mortality can be 110%. South America and North America. first isolated from poults in South Africa in 1978. Avian Rhinotracheitis 'Swollen Head Syndrome' Introduction A viral disease of chickens. Facial and head swelling (though this can occur in other conditions). Ocular and nasal discharge. Snick. Two subgroups have been identified on the basis of the G-protein sequence: A (original UK isolates) and B (original southern Europe isolates). fomites can be important in moving infection between farms.Treatment None. turkeys (see separate summary). control arthropods. Africa. This was a case of Myelocytoma Avian Leukosis (Sero-type J). Prevention Good hygiene. weight gain and feed efficiency. Dyspnoea. vertical transmission is uncertain. It is caused by a pneumovirus of the Paramyxoviridae family. all-in/all-out production. Loss of voice.checking of antigen in the albumen is a basis for eradication (see Sero-type J for details).

Sinusitis.

Post-mortem lesions
  Serous rhinitis and tracheitis, sometimes pus in bronchi. If secondary invasion byE. coli then pneumonia, airsacculitis and perihepatitis. Congestion, oedema and pus in the air space of the skull occurs in a proportion of affected birds due to secondary bacterial infections.

Diagnosis
Clinical signs, serology, isolation of ciliostatic agent. Differentiate from Infectious Bronchitis, Lentogenic Newcastle disease, low virulence avian influenza,Ornithobacterium rhinotracheale. Serology - Elisa normally used, not all commercial kits are equally sensitive to response to both A and B challenge viruses.

Treatment
Antibiotic not very effective. Control respiratory stressors, chlorination of drinking water, multivitamins.

Prevention
All-in/all-out production, vaccination (degree of cross protection between A and B types remains to be established). Live vaccines can reduce clinical signs and adverse effects, inactivated vaccines may be used in breeders prior to lay.

Figure 10. Pus in skull bones. This is a common sequel to avian pneumovirus infection in both chickens and turkeys.

15

Beak Necrosis
Introduction
A condition seen in chickens and turkeys caused by excessively fine mashed feeds.

Signs
   Feed accumulates along edges of lower beak leading to distortion and necrosis of horny tissue. Has been associated with curled tongue in turkeys in the past. This may also be associated with ulcers in the roof of the mouth (palate) which can be confused with some forms of mycotoxicosis.

Post-mortem lesions
 See signs.

Diagnosis
Clinical signs, exclusion of other causes of similar signs.

Treatment
Not usually sufficiently severe to justify medication. Mild water sanitation may help control secondary infections in the affected tissues.

Prevention
Check feed particle size by granulometry, grind less finely.

Bedbug Infestation
Introduction
A condition of poultry, pigeons (and mammals) caused by infestation with the external parasite Cimex lectularius. The parasites are up to 5 mm long and feed at night. It occurs mainly in subtropical and some temperate areas. Adult parasites can survive for 1?12 months in the environment without feeding. Eggs laid by the adult parasites hatch in 4?20 days, there are five nymphal stages each of which feed on birds. Growth to adult parasite takes 1?3 months, depending on temperature.

Signs
   Lack of thrift. Anaemia. Reduced production when infestation is serious.

16

Post-mortem lesions
 Anaemia.

Diagnosis
Identification of the parasite. Differentiate from other blood sucking parasites.

Treatment
Appropriate insecticide treatment of the environment, in particular the cracks and crevices where the parasites hide during the daytime.

Prevention
Thorough treatment of the empty building at turn-around with an appropriate insecticide. Fumigation is also helpful.

Big Liver and Spleen Disease
Introduction
This condition was first seen in Australia in 1980. It is now known to be caused by an Avian Hepevirus. Related viruses have been reported to cause a hepatitis/splenomegaly syndrome in the USA, sub-clinical infection in pigs and Type E Hepatitis in man. The pig origin virus can cause disease in man, but avian hepeviruses are believed not to be zoonotic. The lesions are associated with deposition of antigen/antibody complexes in tissues. Only chickens are known to be naturally affected, most commonly broiler parents in lay. Natural infections have only been demonstrated in chickens over 24 weeks of age though it is possible that vertical transmission and/or infection in rear occurs with a subsequent period of latency. Transmission is usually by the faecal/oral route. Faecal contamination of drinking water is likely to be an efficient means of spread of this infection. Embryos inoculated intravenously become persistently antigen positive.

Signs
    Chronic under production or egg drops of up to 20%. Mortality of up to 1% per week for 3-4 weeks. Anaemia. Premature moulting.

Post-mortem lesions
  Enlarged spleen (over 1gm/kg bodyweight, often with pale foci). Liver usually enlarged, sometimes with subcapsular Affected birds may also have: haemorrhage.

17

Serological tests (agar gel immunodiffusion) may be used to detect either the specific antigen (which is likely to be positive first) or the antibody response to it. 18 . Biotin Deficiency. Reduced feed intake and blood sugar can precipitate fatty liver and kidney syndrome. Must be confirmed by laboratory tests. Signs       Poor growth. Diagnosis Typical signs and lesions. A RT-PCR test may be used to detect viral RNA in tissues. Elisa tests have been developed experimentally. webbing between toes. Histopathology may also be used but the findings are not specific to this condition. It may be helpful to control other conditions which may be occurring at the same time. Including Fatty Liver and Kidney Syndrome Introduction Biotin deficiency has occured in turkeys and chickens in many countries but is now rare in birds consuming properly formulated feeds. Pale livers and kidneys in fatty liver and kidney syndrome. Scabs around eyes and beak. Sudden deaths in fatty liver and kidney syndrome. Good biosecurity. in embryos. Chondrodystrophy. Drinking water which is well chlorinated should be helpful in reducing challenge by this route. Post-mortem lesions   See signs.    Lung congestion Ovarian regression Yolk peritonitis Pale foci and haemorrhages in pancreas. Leg weakness. Viral particles may be demonstrated in bile. Thickened skin under foot pad. Prevention Thorough cleaning and disinfection after depletion of an affected flock. Allin/all-out production. Treatment No specific treatment known.

Differentiate from mites. Parasites on birds. Scabs around vent. Diagnosis Identification of the parasites. Check flocks regulary for rapidly moving insects at the base of the feathers on the abdomen or around the vent. Signs         Lack of thrift in young birds. Menocanthus stramineus is the most pathogenic and is said to be capable of causing anaemia in heavy infestations. They are spread by direct contact between birds and by litter etc. especially around vent. Biting Lice Introduction Various species of lice are common external parasites of poultry worldwide. lesions. response to treatment/prevention. Differentiate from pantothenic acid deficiency (skin lesions). Lice eggs stuck to feathers. bedbugs. 19 . has very low bioavailability. may be some feather damage and crustiness of skin. Irritation. Drop in egg production. Loss of vent feathers. Loss of condition. Crusty clumps of eggs ('nits') may be visible at the base of feathers. Prevention Supplementation of diets with biotin .naturally present in many raw materials. Away from birds adults survive about 4-5 days. Treatment Addition of biotin in feed or water. The parasites are 1-6 mm in size and their life cycle takes about 3 weeks. Treatment Malathion powders and pyrethroid sprays where approved for bird application.Diagnosis Signs. Post-mortem lesions  Usually none.

Biological control using a strain of Bacillus thuringensis has had some success and is preferable to insecticides. as the larvae within eggs are not killed by most products. Swarms of flies. Signs   Anaemia in young birds. Treatment Treatment is difficult. The flies transmit leucocytozoonosis and also a filarial parasite in ducks. especially in autumn and winter and treat if required. Prevention Similar measures as for mosquito control. The condition tends to occur near to rapidly flowing streams. Diagnosis Anaemia. Eggs and larvae survive through the winter to cause new infestations in the following year. 5 mm long and found in North and South America that are external parasites of birds and mammals. season. local history. Weekly treatments are required. It is usually necessary to treat twice at a 7-10 day interval to fully control the condition.Prevention Avoid direct contact with wild and backyard poultry. Examine for lice regularly. 20 . Blackfly Infestation Introduction Grey-black hump-backed flies. Post-mortem lesions  Anaemia. although these insects can travel up to 15 miles. Effective removal of all organic material at flock depletion should be practised in all-in/all-out production systems.

because it rests on the litter. The single most important measure is careful pick-up and removal of all dead birds on a daily basis. mouse toxicology on serum or extract of intestinal contents. weakness. Treatment Remove source of toxin. and toxin-containing material (pond-mud.Botulism Introduction A condition of chickens. supportive treatment if justifiable. Prevention Preventing access to toxin. The toxin and bacterial spores are relatively stable and may survive for some time in the environment. Signs    Nervous signs. selenium. signs. The toxin is produced in decaying animal (usually carcases) and plant waste. Diagnosis History. Post-mortem lesions     Possibly no significant lesions. 21 . A soiled beak. Differentiate from acute Marek's disease ('Floppy Broiler Syndrome') by histology of the brain. maggots) is consumed by the birds. wings then neck. Maggots or putrid ingesta may be found in the crop. progressive flaccid paralysis of legs. then sudden death. especially in hot weather. carcases. ducks and other waterfowl occurring worldwide and caused by a bacterial toxin produced byClostridium botulinum mainly types A / C. Toxin may also be produced by the bacteria in the caecum. antibiotics. Morbidity is usually low but mortality is high. It has also been suggested that poultry carcases lost in litter can be a cause of botulism in cattle grazing land or consuming silage where poultry litter has been spread. Affected broilers tend to settle with eyes closed when not disturbed. Mild enteritis if has been affected for some time. Feathers may be easily pulled (chicken only). turkeys. suspect food and stagnant ponds. is also quite typical. This will reduce the risk of botulism both in the poultry and in any grazing animals on land where poultry litter is spread.

leg weakness. are small whitish worms with a pointed tail. nematode parasites of poultry and game birds. Infection is by the oral route. Poor feather cover and caked or wet litter are predisposing factors.Breast Blister Introduction A complex condition of chickens and turkeys occurring worldwide associated with trauma. The meaning of the technical terms relating to parasite life cycle are defined in the glossary. the cause of Blackhead. Heterakis gallinaeeggs and larvae are a transport hosts for Histomonas. Treatment Not usually appropriate. 22 . give way to scar tissue. and infection withStaphylococcus spp. bacteria. up to 1. Diagnosis Based on lesions. Signs  None. Morbidity may reach more than 50% but the condition is not fatal. control of leg problems. Post-mortem lesions  Inflammation of sternal bursa along the keel bone which may. Prevention Good litter management and handling. and a four-week prepatent period.5 cm in length that occur in the caecum. Earthworms may be transport hosts for eggs. They are found worldwide. Caecal Worm Introduction Heterakis gallinae. Morbidity is high but it is not associated with mortality. There is an incubation period of 2 weeks for eggs to embryonate. in chronic cases. or paratenic hosts with partially developed (L2) larvae. Signs  Swelling over the keel bone with bruising and discolouration.

Levamisole.Post-mortem lesions  Inflammation of caecum. Routine anthelmintic treatment. an undeveloped egg as found in fresh faeces. Prevention Avoiding access to earth and earthworms. The life cycle ofHeterakis showing the location of adults. are effective. Death from respiratory and cardiac failure. Predisposing factors include heat stress with reduced feed intake and panting. possibly with nodule formation. Signs   Paralysis. and the embryonated egg. The egg may be ingested directly by a chicken. Calcium Tetany Introduction A metabolic disease of chickens. 23 . especially broiler parents. or by an earthworm which is in turn ingested by a chicken. Diagnosis Adults can be seen in caecal contents at post-mortem examination. Treatment Flubendazole. Figure 11.

principally in the caecae. lack of other significant lesions. other acute infections and other causes of sudden death. Congested lungs. It may be that management that favours dry litter reduces the risk of infection and/or transmission within the flock. 24 . Diagnosis This is made on signs. Campylobacter jejuni infection is not currently considered to be pathogenic in poultry though a Campylobacter-like organism is considered to be the cause of 'Vibrionic Hepatitis'. All campylobacters are delicate organisms that survive for relatively short periods outside the host unless protected by organic material. biofilm or engulfed by protozoa. Campylobacter jejuni is the commonest species found in poultry. pets and wild animals. Infected poultry are a potential reservoir of this zoonosis. managing birds for maximum uniformity.Post-mortem lesions    Cyanosis. Campylobacters are a significant cause of enteritis in man. Prevention Keep pullet flocks on low calcium diet until 5% production hen/day. Treatment Provide 5 gm of oyster shell per hen on 3 successive days along with vitamin D in drinking water. lesions. In poultry they tend to multiply in large numbers in the hindgut. are bacteria that commonly infect a broad range of livestock species. There is an annual cycle with increased risk of infection in the summer months in some countries. The reason for this is unclear. Active ovary with egg in oviduct. Campylobacter Infection Introduction Campylobacter spp. There are indications that plantar pododermatitis. Differentiate from IB 793b. and response to treatment. carcase quality and litter quality are better on farms which tend to have Campylobacter-negative stock.

In practice the success of this will also depend upon the degree of environmental contamination by the organism. as well as processing plant technologies to reduce carcase contamination. Samples should be tested as quickly as possible after collection. sourcing of water from high quality supplies. Many infections are introduced during thinning or other forms of partial depopulation. Key aspects of this include effective sanitation of drinking water. housed poultry can be maintained free of Campylobacter infection by consistent application of excellent biosecurity. Diagnosis Isolation of the organism from caecal contents. cloacal swabs or composite faeces. The organism is sensitive to air so swabs should be collected into transport medium and other samples placed in airtight containers with minimal airspace. Prevention In principle. 25 . and changing of overalls and boots on entering bird areas. Research is ongoing on the development of vaccines. For this reason it may be difficult to stop the spread of infection between houses once it becomes established in one house. good hand hygiene by stockmen. Insects and rodents may act as a means of transfer of the infection from the general environment into the poultry buildings. Post-mortem lesions  None. Treatment Not required on clinical grounds. avoidance of contact with pets and other farmed species.Signs  None. phage treatments and competitive exclusion approaches.

or copper sulphate 1gm/2 litre water for 3 days if approved locally. A finely divided powder of copper sulphate (where approved) at 200gm/tonne continually or to 14-16 weeks in replacement pullets. Morbidity and mortality are usually low. Slow growth. copper sulphate (1 kg/tonne feed) for 5 days. Control of Candida through drinking water is sometimes practised with chlorination (e. oesophagus.g. The cause is a fungal yeast. characterised by thickening and white plaques on the mucosa. turkeys. possibly confused or masked by signs of the primary disease. crop. Poor appetite. Colonies of this fungus appear as white to ivory colour. especially in the crop but sometimes in the proventriculus. Diarrhoea. Treatment Nystatin (100 ppm in feed) for 7-10 days. and sometimes other birds and mammals. The route of infection is normally oral and the organism is often present in healthy animals with disease occurring secondary to stress and poor hygiene. histopathology. smooth and with a yeasty smell.Candidiasis. and associated with gizzard erosion. sodium or calcium proprionate at 1 kg per tonne continually. Thrush Introduction A disease of the alimentary tract of chickens. Diagnosis Lesions. microscopic examination of a digested smear (heat in 10% potassium hydroxide) to demonstrate the hyphal forms of the yeast in the tissues. The fungus is resistant to many disinfectants. occasionally proventriculus and intestine. Signs     Dejection. Moniliasis. Ensure good hygiene. intestine and cloaca. 26 . Raised focal lesions may slough into lumen as caseous material. proprionic acid. Prevention Avoid excessive use of antibiotics and other stressors. Post-mortem lesions   White plaques in mouth. Candida albicans and the condition is seen worldwide.

Beak trimming may be necessary. Take care to provide fresh clean feed and water. through shafts of light in the house). high temperatures. Soluble multivitamins and/ or methionine may be of some benefit in some circumstances.Chlorox. tenosynovitis and other diseases affecting mobility. complying with local regulations and any relevant codes of practice. nutritional deficiencies. If so it should be carried out carefully by trained operators. Cannibalism. Treatment Correct any husbandry problems. Feather-pulling. It should be repeated periodically. distribution of lesions. Feather pecking Introduction A complex multifactorial behavioural problem of poultry and game birds seen worldwide. control ectoparasites. Predisposing factors include overcrowding. This is economical and effective. Generalised anaemia. low light level.g. 27 . Prevention Proper density and temperature. uncontaminated by fungi. face. Post-mortem lesions   Skin wounding related to particular signs exhibited. head. Morbidity is usually low but mortality is high among affected birds. feed form (mash takes longer to consume than pellets). and strain of bird. wings. anaemia. Differentiate from bacterial dermatitis. Diagnosis Age. sodium hypochlorite) at 5 ppm. boredom. post-mortem cannibalism. excessive light intensity or variation (e. Signs   Pecking at feet (especially young chicks) and vents (adult layers and turkey poults 812 days old). Provision of a diet that closely matches the nutritional requirements of the stock concerned.

Wasting Poor growth.Capillariasis .Hairworm Infection Introduction Nematode parasitic worms of poultry. Morbidity and mortality are usually low. about 0. Dejection.other approved benzimidazoles can be expected also to have activity. prepatent period about 21-25 days according to species. Treatment Coumphos has been licensed in some markets. Worm eggs in the environment are resistant. game birds and pigeons ofCapillaria species. contorta in the crop and oesophagus. C.05 mm wide and hair-like in appearance. Hairworms in mucosa of crop. small intestine or caecum. Diagnosis This may be by a combination of macroscopic examination. 28 . Signs     Diarrhoea. Fenbendazole has been shown to have high efficacy . The worms are 7-18 mm long. some are transmitted direct from bird to bird. or characteristic worm eggs in faeces in patent infections. C. Differentiate from other causes of enteritis. Prevention Separation of birds from possible transport and intermediate hosts. effective cleaning of houses. Levamisole. Infection is by the oral route. obsignata in the small intestine. Some species have earthworms as intermediate hosts. Worm eggs take about 20 days to embryonate with an L1 larvae. Post-mortem lesions   Enteritis. seiving intestinal contents.

often minor. Signs  Affected flocks tend to have poorer than average productivity and uniformity. coli. which can replicate in the tissues. Post-mortem lesions  Typically it presents as exudate ranging from liquid and pale cream pus to yellowish solid plaques of caseous material under the skin of the abdomen and/or in the leg. Many meat inspectors become skilled at detecting subtle differences in skin colour in the affected birds. Treatment Treatment would not be possible if the problem is identified at a final depletion.Cellulitis Introduction Cellulitis is literally an inflammation of connective tissues. but the affected birds are not readily detectable prior to slaughter. However its main importance is as a cause of condemnation in meat poultry. Prevention Toe scrapes at 15-25 days of age when feather cover is poor are the most likely predisposing factors. It typically occurs between skin and muscles and between muscles and may be an incidental finding in a range of conditions. skin wounds by particular strains of E. Many affected birds have no other lesions and are reasonably well grown. particularly broiler chickens. In the USA it is called 'Inflammatory Process'. Careful flock management with a view to reducing toe wounds has the greatest impact in controlling cellulitis. If identified at a thinning there may be time for antibacterial treatment to have some benefit for those birds in the early stages of the problem. Diagnosis Typical lesions. The condition is caused by infection of. though most of the birds showing toe scrapes will not go on to develop cellulitis. 29 . Routine monitoring of skin damage at about 25 days of age may be helpful in fostering good practices.

80°C for 5 minutes) and many disinfectants even for 2 hours at 37°C. The virus is resistant to pH 2. Transmission is usually vertical during sero-conversion of a flock in lay. ether. heat (70°C for 1 hour. Inclusion body heptatitis etc. legs wings or neck. virus may be isolated in lymphoblastoid cell line (MDCC-MSB1). Gangrenous dermatitis on feet. chloroform. No clinical signs or effect on egg production or fertility in parent flock during seroconversion. lateral transmission may result in poor productivity in broilers. Sudden rise in mortality (usually at 13-16 days of age). Signs     Poor growth. Mortality is typically 5-10% but may be up to 60% if there are predisposing factors present such as intercurrent disease (Aspergillosis. poor litter quality). Acute mycotic pneumonia. PCV of 5-15% (normal 27-36%). and control of other diseases as appropriate.g. 30 . Post-mortem lesions       Pale bone marrow. demonstration of ongoing sero-conversion in parent flock.) or poor management (e. may be beneficial. Gumboro. Treatment Good hygiene and management.Chicken Anaemia Introduction A viral disease of chickens caused by Chicken Anaemia Virus or CAV. Pale birds. Atrophy of thymus and bursa. Discoloured liver and kidney. Hypochlorite appears most effective in vitro. If gangrenous dermatitis is a problem then periodic medication may be required. Prior to confirmation that it is in fact a virus it was known as Chicken Anaemia Agent or CAA. Diagnosis Gross lesions.

Intercurrent salmonellosis and. especially pigeons and robins. their degree of attenuation is variable. Egg transmission does not occur. Psittacosis. Immunity: there is a good response to field challenge (in birds over 4 weeks of age) and to attenuated live vaccines. It is transmitted by contact. Elisa. psittacines. Conjunctivitis. Depression. Morbidity is 50-80%. or IFA. mortality 5-40%. They should be used at least 6 weeks prior to collecting eggs for incubation. Weakness. 15 weeks. Fibrinous pericarditis. It is a 'Scheduled Disease' rarely diagnosed in UK. Occasional transient ataxia in pigeons. Weight loss. say. but occurring probably worldwide. perhaps. man. Greenish-yellow diarrhoea. Wasting. rarely chickens. a bacterium of highly variable pathogenicity. pigeons. Elementary bodies are highly resistant and can survive in dried faeces for many months. Chlamydiosis. Serology: antibodies develop 3-6 weeks after infection. faecal dust and wild bird carriers. Ornithosis Introduction An infection of turkeys. Airsacculitis. Nasal discharge. Their use may be restricted to those flocks that have not sero-converted by. Production drops in naive laying flocks Post-mortem lesions     Vascular congestion. Iodophores and formaldehyde are effective disinfecting agents. Inappetance. and may be detected by SN. caused by Chlamydia psittaci. other infections may be predisposing factors. 31 . Signs           Respiratory signs. ducks.Prevention Live vaccines are available for parents. phenolics are less so.

Slipping of Achilles tendon (or perosis). Distortion of hock. exclusion of wild birds. either singly or in combination (although deficiencies of pyridoxine. Duck septicaemia.     Perihepatitis. Intracytoplasmic inclusions are helpful but confirmation requires demonstration of causal organisms (Giemsa stain. Slipped Tendon or Perosis Introduction Caused by deficiency of manganese. zinc. biotin. lesions. Chondrodystrophy. Signs       Short legs. Differentiate from Duck viral hepatitis. Live and inactivated vaccines are protective although the former result in carriers and the latter require several applications. This condition is seen in chickens. Lameness. IFA). Treatment Tetracycline (200-800 ppm in feed for 3-4 weeks) and/or quinolone medication and supervised slaughter. In turkeys it may be an inherited deficiency of galactosamine. niacin may also be involved). In embryos parrot beak. Congested lungs and air sacs in the turkey. Malposition of leg distal to hock. shortened bones. choline. Fibrinous pneumonia. Prevention Biosecurity. ducks and turkeys. 32 . folic acid. Necrotic foci in liver. may rupture in pigeons. Spleen enlarged and congested. Serology: complement fixation. Elisa and gel diffusion. signs. Diagnosis History.

while E. This disease is not very common in commercially reared turkeys though most turkey growers receive preventative medication for at least part of their lives. Tucked appearance. analysis of feed. The contents may be haemorrhagic or be watery with white material shed from the mucosa. Five species of Eimeria have been identified that cause lesions in turkeys. correct mineral balance. rickets. infectious arthritis. Prevention Addition of manganese. meleagridis affect the lower small intestine rectum and caecae. Treatment For flock proceed as for prevention. meleagrimitis affects the upper small intestine. choline. while E. vitamins. Differentiate from twisted leg. adenoides affects the caecae and rectum. E. Signs      Huddling. 33 . Weight loss. gallopavonis and E. ruptured ligaments. E. Diagnosis Lesions. infectious synovitis. of which two are associated with significant disease effects. Post-mortem lesions  The affected area of intestine shows thickening of the wall and dilation. Coccidiosis of Turkeys Introduction Infection of turkeys with Eimeria spp. ruffled feathers. Watery diarrhoea that may occasionally be blood stained or contain clumps of mucus or shed mucosa.Post-mortem lesions     Shortening and thickening of long bones. Shallow trochlea. Depression. no value to affected bird. Lateral slipping of tendon. dispersa is found in the small intestine. Tibia and metatarsus bowed.

Prevention The ionophore coccidiostats lasalocid and monensin are routinely used in turkey growers. Sulphaquinoxaline). Diclazuril is also used for this purpose. The intestines are dilated. Exposure of previously unmedicated birds to these compounds can cause toxicity. Treatment Toltrazuril. typically to 12 weeks of age. Turkey coccidiosis of the upper small intestine caused by E.g. Dosage levels of ionophores may be critical to efficacy and safety. lesions. show some spotty congestion and have abnormal contents due to the sloughed epithelium. meleagrimitis. Figure 37. Sulphonamides (e. Avoid use of tiamulin in ionophore treated birds. gamonts). The exudate can range from semi-liquid to solid white cores. 34 . Differentiate from necrotic enteritis.Diagnosis Signs. Salinomycin is toxic for turkeys even at very low doses. Turkey caecal coccidiosis caused by E. adenoides. Amprolium. microscopic exam of scrapings (oocysts. Figure 38.

histomonosis. Shuttle programmes with chemicals in the starter diet usually improve control. Differentiate from ulcerative enteritis. Inappetance.Coccidiosis. microscopic examination of scrapings. Caecal. Closed eyes. Diarrhoea. Morbidity is 10-40% and mortality up to 50%. E tenella Introduction This was at one time the commonest type of coccidiosis and is certainly the most easily diagnosed. tenella is more common when 'straight' ionophore programmes are used. Diagnosis Signs. Ruffled feathers. Recovered birds have good immunity to the same parasite. 35 . Signs       Depression. of caecal mucosa. Vaccines are used mainly in breeders but increasingly in broilers. Post-mortem lesions    Petechiae. Sulphonamides. lesions. blood in faeces. In some markets the organic arsenical compound 3-Nitro is used as an aid in the control of caecal coccidiosis. Treatment Toltrazuril. Vitamins A and K in feed or water. It is caused by Eimeria tenella and results in lesions in the caecum of chickens worldwide. Thickening. Amprolium. hygiene. Prevention Coccidiostats in feed. E. Production less affected than in some of the other forms of coccidiosis. ecchymoses. Accumulation of varying quantities of blood and caseous necrotic material in the caecum. Transmission as for E. vaccination by controlled exposure. mitis (see above).

identification of typical small round oocysts and other stages in fresh scrapings from the small intestine. E mitis Introduction This condition of chickens. Signs  Reduced feed conversion efficiency and weight gain.Figure 15. 36 . Treatment Not usually treated but susceptible to the products used for other forms of intestinal coccidiosis. Predisposing factors include exposure to faeces and litter conditions that favour development of the parasite (temperature. secondary bacterial enteritis. Post-mortem lesions  The lesions are minimal and located in the lower small intestine (ileum) which tends to be pale and flaccid with scattered petechiae. The disease occurring is proportional to the amount of infective agent ingested. Coccidiosis. The caecal walls are thickened and haemorrhagic and there is a mass of blood in the caecal lumen. faeces and on fomites and birds are infected by the oral route with an incubation period of 2-5 days. seen worldwide. is caused by the protozoan parasite Eimeria mitis. which colonises the small intestine. May predispose to wet litter. Diagnosis Mild lesions. The parasite is moderately resistant in the environment and highly resistant to conventional disinfectants. The infective agent is found in litter. humidity). Moderate Eimeria tenella infection in the caecae of a chicken (Score 3).

Sulphonamides. E brunetti Introduction A relatively rare form of coccidiosis affecting chickens worldwide caused by Eimeria brunetti. Poor production. Signs       Depression. Closed eyes.Prevention Normally controlled by anticoccidials in feed. This species is not usually included in vaccines for broilers. Diarrhoea. Morbidity and mortality are variable. caecum and rectum. Of moderate to high pathogenicity. There is good immunity to the same parasite in recovered birds. Severe necrotising enteritis. Post-mortem lesions    Petechiae and thickening of the distal third or more of intestine. 37 . it is found in the terminal ileum. vaccination by controlled exposure. lesions. Coccidiosis. May be included in vaccines. Amprolium. Treatment Toltrazuril. Oocysts in caecum and rectum. Vitamins A and K in feed or water. Ruffled feathers. hygiene. Differentiate from ulcerative enteritis. caecal coccidiosis. extending into caecal tonsils. Diagnosis Signs. blood in faeces. microscopic examination of scrapings. Prevention Coccidiostats in feed. Inappetance. Ileorectal.

2 days off. 38 . Vitamins A and K in feed or water. 3 days on). Signs     Sudden death. In the goose E. Coccidiosis occurs only very rarely in commercially reared ducks in the UK. There is thickening of the intestinal mucosa and there are lines of haemorrhagic spots in the mucosa. compared to four per oocyst forEimeria. 3 days on. Tyzerria has eight sporocysts in each oocyst. Amprolium.g. Post-mortem lesions  Massive haemorrhage in upper small intestine. Diagnosis Signs. Intestinal. lesions. anatipestifer. of Ducks and Geese Introduction Young ducks and geese may suffer from Eimeria spp infection.Figure 16. Treatment Sulphonamides (e. Sulphadimidine 30-600gm/100 birds/day. while in ducksTyzzeria perniciosa is most pathogenic. Coccidiosis. Tucked appearance. Duck viral enteritis. Differentiate from Duck viral hepatitis. large number of merozoites). Depression. Blood-stained vent. anseris is the most important. Moderate Eimeria brunettiinfection in the terminal ileum and rectum of a chicken. microscopic examination of scrapings (usually few or no oocysts.

Treatment Controlled trials of treatments have not been published. Reduced feed intake. Tiny white foci and petechiae in the kidneys. Kidney Introduction A disease of geese caused by Eimeria truncata that can cause high mortality in geese of 312 weeks of age. Hygiene. Prevention Good Hygiene. Kidneys light grey to greyish pink. Weakness. however this is not routinely practised. 39 . presence of coccidial stages in fresh scrapings of kidney lesions.Prevention If required coccidiostats could be used in feed. Diagnosis Lesions. Post-mortem lesions    Enlarged kidneys. Diarrhoea .faeces tend to be whitish. Coccidiosis. Signs     Depression. it can also infect Barbary ducks and swans.

Blood or pigment in the faeces. Caused by Eimeria maxima. Because of the area of intestine affected it tends to have a significant effect on productivity and susceptibility to necrotic enteritis. vaccination. Diagnosis Signs. Poor absorption of nutrients/pigments. Signs        Depression. acervulina coccidiosis and there may be large numbers of characteristic oocysts in smears. Ruffled feathers. hygiene. E maxima Introduction One of the more common forms of coccidiosis in commercial broilers. Depigmentation of skin and plasma is especially evident in this form of cocccidiosis and this is commercially important in some markets. contents often orange in colour. Amprolium. Mid-intestinal. commercial vaccines commonly contain more than one strain of E. of moderate to high pathogenicity it is seen worldwide. lesions. mucosa tends to be pinker than normal. 40 . Vitamins A and K in feed or water. Poor production. Mild to severe enteritis. microscopic examination of scrapings. Inappetance. Differentiate from necrotic enteritis. This infection is often associated with E. This is one of the less immunogenic species. Prevention Coccidiostats in feed. Closed eyes. Treatment Sulphonamides. Post-mortem lesions     Petechiae and thickening of middle third of intestine. non-specific enteritis.Coccidiosis. maxima. Morbidity and mortality are variable.

Deep scrapings necessary to show large schizonts. Inappetance. Poor production. Diagnosis Signs. microscopic examination of scrapings Differentiate from necrotic enteritis.Figure 13. Diarrhoea. of middle to posterior third or more of small intestine. blood in faeces. Coccidiosis. 'Sausage-like' intestine. Signs        Reduced feed consumption. Mid-intestinal. E necatrix Introduction A highly pathogenic form of coccidiosis. Post-mortem lesions     Petechiae and thickening. lesions. Oocyts in caecal scrapings. other types of coccidiosis. Closed eyes. The lesions are subtle compared to other forms of coccidiosis. Ruffled feathers. Schizonts seen as white spots through the serosa interspersed with petechiae. caused by Eimeria necatrix. 41 . Depression. The intestine is slightly thickened and there are scattered haemorrhages in the mucosa when seen from the inside. It occurs in chickens worldwide and has variable morbidity but mortality is high in severely affected birds. Severe necrotising enteritis. in which the parasite is present in the small intestine and in the caecum. Moderate Eimeria maxima infection in the jejunum of a chicken (Score 2).

hygiene. In this case the intestine is thickened and can become ballooned and sausage-like. Signs        Depression. Figure 14. commercial vaccines commonly contain more than one strain of E. Depigmentation. vaccination.Treatment Toltrazuril. which is moderately pathogenic. Ruffled feathers. Moderate Eimeria necatrix infection in the jejunum of a chicken (Score 3). Coccidiosis. It is seen in layers and in broilers. acervulina. Sulphonamides. This is one of the less immunogenic species. Prevention Coccidiostats in feed. Morbidity is variable and mortality low or absent. Poor production. maxima. Upper Intestinal. Amprolium. Diarrhoea. E acervulina Introduction This is probably the commonest cause of coccidiosis in chickens and occurs worldwide. Eimeria mivatiis currently considered not to be a valid species distinct from E. Closed eyes. Post-mortem lesions 42 . Vitamins A and K in feed or water. Haemorrhages and white spots are visible from the outside of the intestine. Inappetance. both alone and in association with other species of coccidia and is caused by Eimeria acervulina.

43 . Immunity is quite short lived (about 30 days) in the absence of continued challenge. Prevention Coccidiostats in feed. Moderate Eimeria acervulinainfection (score 2) in chicken duodenum. In milder infections there may be scattered white spots. Petechiae. A detailed description is beyond the scope of this book. Various publications provide a photographic key to severity of lesion. White spots or bands in the mucosa. Poor absorption of nutrients/pigments. Amprolium.the duodenum and part of the ileum. Differentiate from necrotic and non-specific enteritis. lesions. restricted to upper third of small intestine . Figure 12. hygiene. A system of assessing the severity of coccidial challenge by attributing a 'score' is often used. Sulphonamides. microscopic exam of scrapings. Treatment Toltrazuril. vaccination by controlled exposure. Diagnosis Signs. In general terms a score of 0 indicates no lesions and a score of 4 indicates maximal severity of lesion or death.     Thickening. and other lesions. in severe the entire surface is pale or denuded of epithelium. In severe infections they become confluent and cause sloughing of the mucosa. in feed or water.

turkeys.most strains are rapidly lactose-fermenting producing 44 . Reduced appetite. Dejection. mucosal damage due to viral infections and immunosuppression are predisposing factors. Post-mortem lesions              Airsacculitis. Pericarditis. sero-typing. Diagnosis Isolation. Infection is by the oral or inhalation routes. It is most commonly seen following upper respiratory disease (such as Infectious Bronchitis) or Mycoplasmosis. Arthritis. but is susceptible to disinfectants and to temperatures of 80°C. Morbidity varies. Cellulitis over the abdomen or in the leg. The infectious agent is moderately resistant in the environment. coughing. Omphalitis. with an incubation period of 3-5 days. Synovitis. fomites. Enteritis. Signs       Respiratory signs. water. sneezing. Omphalitis. Colisepticemia Introduction Coli-septicaemia is the commonest infectious disease of farmed poultry. and via shell membranes/yolk/navel. Perihepatitis. mortality is 5-20%. Poor navel healing. Granulomata in liver and spleen. Aerobic culture yields colonies of 2-5mm on both blood and McConkey agar after 18 hours . Swollen liver and spleen. or in young birds that are immunologically immature. It is frequently associated with immunosuppressive diseases such as Infectious Bursal Disease Virus (Gumboro Disease) in chickens or Haemorrhagic Enteritis in turkeys. Poor growth. pathology. Lesions vary from acute to chronic in the various forms of the disease. etc.Colibacillosis. It is caused by the bacteriumEscherichia coli and is seen worldwide in chickens. Peritonitis. Snick. Salpingitis.

and in broiler parents. neomycin (intestinal activity only). Treatment Amoxycillin. flouroquinolones. feed and water. tetracyclines. potentiated sulphonamide. Figure 17. other enterobacteria such as Proteus. Contact dermatitis is commonly monitored at processing as a means of measuring 'welfare status'. Hock Burn. whereas others progress to deep ulcers so the size. Contact Dermatitis. Immunity is not well documented though both autogenous and commercial vaccines have been used. as well as Pseudomonas. Staphylococcus spp. Pododermatitis Introduction Contact dermatitis affects skin surfaces which have prolonged contact with litter. the breast area. gentamycin or ceftiofur (where hatchery borne). Differentiate from acute and chronic infections with Salmonella spp. Prevention Good hygiene in handling of hatching eggs. etc. good sanitation of house.brick-red colonies on McConkey agar. stage of resolution and severity of lesion is likely to affect the degree of discomfort or pain suffered. Well-nourished embryo and optimal incubation to maximise day-old viability. Some lesions are superficial. The liver is almost entirely covered by a substantial layer of fibrin and pus. the foot pad. It is seen in growing broiler chickens and turkeys. Control of predisposing factors and infections (usually by vaccination). 45 . when severe. rear surface of the hock and. hatchery hygiene. Severe perihepatitis in colibacillosis in a broiler parent chicken.

Figure 18. and. 46 . Prevention This condition is closely linked to intestinal function as this is the prime determinent of faecal consistency and stickiness. drinker management. Diagnosis Signs and lesions. See the discussion in the section on Dysbacteriosis. level of soya bean meal in feed (according to some authors. stickiness of droppings). and adequate ventilation to remove moisture are all important. at the back of the hocks. most importantly.Pododermatitis is often related to high droppings pH. Choice of drinker type (nipple as opposed to bell). If severe the foot and hock lesions may contribute to lameness or serve as a portal of entry for secondary infections. Moderate pododermatitis on a foot pad. proper insulation in cold climates. It can be reproduced by adding water to the litter. and sometimes in the breast area. Post-mortem lesions  As described under signs. Signs  Blackened skin progressing to erosions and fibrosis on the lower surface of the foot pad. litter moisture. Treatment Not applicable.

Treatment Levamisole. Emaciation. although bird strains do not infect mammals very well. The same species causes infections of the hindgut and cloacal bursa in chickens. A further species causes respiratory disease in quail. Prevention Effective cleaning of housing. Diagnosis Microscopic examination of mucosal scraping. Some have beetle or earthworms as intermediate hosts. Post-mortem lesions   Inflammation and thickening of mucosa of crop and oesophagus. Cryptosporidium baileyi can cause respiratory disease in chickens and turkeys. The oocysts are excreted ready sporulated in the faeces and infection occurs by inhalation and ingestion. Routine worming.Cropworms Introduction The nematode worms Capillaria spp and Gongylonema ingluvicolainfect the mucosa of the crop and oesophagous of poultry and game birds. and ducks. turkeys.C. Coumaphos. They replicate in the brush border on the surface of epithelial cells. meleagridis also infects both species. Cryptosporidiosis Introduction Cryptosporidia are related to the coccidia. White convoluted tracks in the mucosa. 47 . and vice versa. acervulinaoocyst). Avoidance of access to intermediate hosts. but much smaller (typically oocysts are less than ¼ of the size of an E. They also differ from coccidia in being poorly host specific. Signs   Anaemia.

Signs     Incoordination. Circling. Swollen sinuses. 48 . Steam cleaning is effective in reducing infection as oocysts are inactivated above about 65°C Dactylariosis Introduction A rare fungal disease of chickens and turkeys caused byDactylaria gallopava. Torticollis. Low weight gain. Prevention The oocysts of cryptosporidia are extremely resistant to chemical disinfection. Post-mortem lesions    Sinusitis. Tremors. Diagnosis Identification of the parasites attached to the epithelium by microscopic examination (smears histopathology acid-fast staining).Signs      Snick. Pneumonia. coli-septicaemia) there may be benefit in medicating for these. Airsacculitis.g. It is becoming increasingly common for water companies to screen water supplies for cryptosporidia because of the human health implications of mammalian strains. recumbency. Diarrhoea. Treatment Unfortunately there is currently no known effective treatment in poultry. If other disease processes are complicating the situation (e. Cough. There are no effective preventative medicines or feed additives.

and cartilage flaps. especially of femoral anti-trochanter but also other leg joints.Post-mortem lesions   Necrotic lesions with associated congestion in cerebrum. Signs   Lameness. Morbidity and mortality are low but affected birds are more likely to be 'picked upon' and may end up suffering damage and needing to be culled. Microscopically there is necrosis and there may be fissures of articular cartilage and associated osteochondritis. Mycotic lesions in lungs. Treatment None. Diagnosis Gross and microscopic lesions. Diagnosis Lesions. or developmental defects. Prevention Use fresh dry litter (avoid old sawdust). The cause remains to be confirmed. isolation of the fungus. Degenerative Joint Disease Introduction A condition of chickens and turkeys seen worldwide. Treatment 49 . but it may result from physical damage. air sacs etc. Rapid growth is a possible predisposing factor. Post-mortem lesions   Damaged epiphyseal articular cartilage. Reduced breeding performance. resulting in erosions.

Unthriftiness. especially during period of rapid growth. Application of mineral or vegetable oil is also beneficial. up to 0. Raised thickened scales. Mange lesions on legs and unfeathered parts. 50 . Depluming and Scaly Leg Mites Introduction External parasites of adult chickens. The adult females are short legged. For small flocks dipping the affected parts in a solution of acaricide may be beneficial.5mm in diameter. Post-mortem lesions  As described under signs. Signs     Cause irritation and the bird pulls feathers. It may be best to cull affected birds from small flocks. Prevention Avoidance of physical sources of injury to bones and joints.Knemidocoptes spp.None available. microscopic examination for mites in scrapings. pheasants. Appropriate management of a segregation pen and early marketing of mildly affected birds may limit losses and improve flock welfare. Treatment Not usually required in commercial poultry. There may be a place for growth-control programmes. Prevention Careful cleaning of buildings during down-time will help reduce the risk of these infections. Exclusion of wild birds from chicken areas is advised as far as possible. round. pigeons etc. Diagnosis Signs.

birds found on breast or side. pericardial sac. Reserpine in diet of birds of 4+ weeks (no longer licensed in the UK). presumably due to a sudden increase in blood pressure. Abdominal cavity full of blood. genetic condition of turkeys linked to male sex and high growth rate. kidneys. Morbidity is around 100% and mortality 0-95%. Signs    Sudden death with no warning signs. recovered birds carrying the virus for 8 weeks. A longtitudinal split of the abdominal aorta is the most common lesion. Prevention Limit feed in birds of 16+ weeks. It has been suggested that degenerative changes in the wall of the artery and copper deficiency may be factors. Haemorrhages in lungs. Duck Viral Hepatitis Introduction A viral disease of ducks occurring worldwide and previously a scheduled disease in UK. a tranquilizer. A sudden noise or other cause of excitement can lead to an 'outbreak'. Skin pale. Aortic Rupture Introduction A complex. leg muscles. a picornavirus may also 51 . Aspirin at 250 ppm in feed or water may be of benefit. Diagnosis History and lesions. was included in feed at 1 ppm for 3-5 days to reduce blood pressure. Treatment None currently licensed. The infective agent. The disease is transmitted by infected ducks and other waterfowl and spreads rapidly. Post-mortem lesions      Carcase anaemic. Possibly blood in the mouth. Reserpine.Dissecting Aneurysm. Rupture of major blood vessel at base of heart or by the kidneys.

Duck Virus Enteritis. rapid deterioration and death. Recovered birds may carry the virus for a year. Punctate/diffuse haemorrhages. Microscopically . Live. lesions. coccidiosis. 52 . mostly in ornamental collections. arching of back. also the Netherlands and other countries. paddling of legs. Newcastle disease. Post-mortem lesions     Liver swollen. in USA since 1967. Death in good condition. fomites and arthropods. Diagnosis History. All waterfowl are susceptible and the Barbary duck is more susceptible than the Pekin. Fall on side. Depression. Treatment Antiserum. only slightly attenuated vaccine is applied at day old by foot web stab and may be repeated in breeding birds to provide maternal immunity.5 ml serum of recovered birds given intramuscularly. Prevention Vaccination and/or antiserum. often in opisthotonus. breeder vaccination. Differentiate from Duck plague (viral enteritis). The disease follows a very acute course with a morbidity of 5-100% and mortality of 5-100%. Kidneys and spleen swollen. Duck septicaemia (anatipestifer). Signs     Sudden death. A different picornavirus causes a similar condition in North America. Duck Plague Introduction A herpesvirus infection of ducks and geese diagnosed in the UK in 1972. SN serology. 0. Transmission is by infected birds.survive for ten weeks in brooders and five weeks in faeces.focal necrosis. isolation in CE (causes stunting of 9 day embryo). bile duct proliferation and inflammation. Influenza and a 'Type II Variant' hepatitis caused by Astrovirus.

Dehydration. heart. Thirst. The condition is seen mainly in rapidly growing broiler chickens with good food intake. coccidiosis. Haemorrhage in intestine. intranuclear inclusions Differentiate from Duck hepatitis.Signs              Sudden deaths. 53 . Non-specific Bacterial Enteritis Introduction Inflammation of the small intestine associated with wet litter. body cavities. Crusty plaques from oesophagus to bursa (covered by yellowish plaques in later stages). Dysbacteriosis. Occasionally cyanosis of the bill in the young. vaccination if approved by authorities (CE adapted live virus). spleen. Post-mortem lesions     Severe enteritis. Ataxia. Severe diarrhoea. Photophobia. Diagnosis Isolation: Duck CAMs 12 day embryos die in 4 days. Young ducks may show thymic and bursal lesions. Treatment None. HA-. is common in countries with restrictions on the use of antimicrobial growth promoters and pressure to reduce therapeutic antimicrobial usage. Rapidly spreading disease. Paresis. probably through interference. Drop egg production. pasteurellosis. Closed eyes. but vaccination in face of outbreak is of value. excess caecal volume and fermentation. Occasionally penile prolapse in the penis in drakes. liver. Tremor. sometimes dysentery. pericardium. vent gleet. oesophagitis (birds on restricted feed). Prevention Isolation from waterfowl.

France. Treatment should coincide with good relittering and it is important to provide fresh sanitary drinking water. Spain. Argentina. Water intake may be increased or irregular. Holland. rather we are dealing with a disruption in the normal flora of the gut. Post-mortem lesions    Excessive fluid content throughout the small intestine. Good control of coccidiosis. Apparently a similar disease had been seen over a 4-year period in broiler parents in Holland. especially where treatment is initiated early. Feed acidification may be helpful in some circumstances. In the autumn of 1976 a distinct egg drop syndrome was first identified in Northern Ireland. The cause has been identified as Adenovirus BC14. often with gas bubbles.Dietary changes. England. Germany. Egg Drop Syndrome 76 Introduction Egg drop may be defined as a sudden drop in egg production or a failure to achieve a normal peak in production. No single bacterium appears to be responsible. first isolated in Northern Ireland in 1976. Peru. lesions. 127. Uruguay. Treatment Amoxycillin and tylosin treatment appear to be beneficial. microscopic examination of scrapings from the wall of the small intestine (to exclude coccidiosis and perhaps to assess the bacterial flora). Diagnosis Signs. Careful choice of any feed enzymes and their matching with local raw materials can have an impact on substrates made available to intestinal bacteria. feed interruptions and subclinical coccidiosis may be contributory factors. Voluminous caecae. Mortality is usually negligible. Prophylactic antimicrobial medication may be necessary in some circumstances. Wet faeces in the rectum. Prevention Competitive exclusion ('normal adult flora') use in day-old chicks reduces the risk of this condition. Circumstantial evidence suggests that the main route of transmission is through the eggs (vertical transmission) 54 . It affects chickens and has occurred in Ireland. Signs   Diarrhoea. Brazil.

Poor internal quality. Newcastle disease. specifically vitamins E. Isolation of haemagglutinatin agent in duck eggs or cell culture. which can be caused by a large number of factors acting individually or in combination. oviduct). Signs      Egg drop at peak or failure to peak. Lack of signs in the birds themselves. The infection is commonly present in ducks and geese but does not cause disease. extremes of temperature. It is important to rule out other possible reasons for egg drop. may be infectious or metabolic. Lateral transmission from bird to bird is slow and may be prevented or slowed for weeks by netting divisions. Post-mortem lesions   No specific lesion . Spread from house to house may take 5-10 weeks. Elisa. DID. Management problems may be involved: inadequate water supply. selenium. signs/lesions (mainly lack of). SN. Histopathology .it may be possible to demonstrate degenerative changes in the epithelial cells of the magnum of the oviduct. Avian Encephalomyelitis. sudden changes of feed. Rough. thin or soft-shelled eggs and shell-less eggs. Contamination of egg trays at packing stations may play a part in transmission. Parasites. Diphtheritic Fowl Pox). group antigen distinct from classical adenoviruses (white cells. insecticides or nicarbazin. B 12. Serology: HI. and D as well as calcium. Drops may be of 5 to 50% and last for 3-4 weeks. as may wildfowl and biting insects. Coryza. Nutritional deficiency should be considered. throat swabs. Diseases in which egg drop occurs. inadequate lighting programme. Marek's disease/Leukosis or any infectious disease causing a significant systemic disturbance (CRD. phosporus.followed by latent infection during rear with viral excretion starting shortly before sexual maturity. Cholera. Metabolic diseases include Fatty Liver Syndrome. Infectious Laryngotracheitis. intoxication by sulphonamides. Loss of shell pigment. Infectious diseases include Infectious Bronchitis. Unvaccinated flocks with antibodies before lay do not peak normally.only a slight atrophy of ovary and oviduct. Diagnosis History. 55 . Clinical disease occurs during sexual maturity.

Peripheral vessels congested.Treatment None. streptococci. If successive flocks are affected on the same site prophylactic medication ahead of the anticipated problem may be of benefit. The choice should depend on sensitivity testing of an isolate. Endocarditis Introduction A condition of chickens associated with several bacterial infections such as staphylococci. Post-mortem lesions   Right ventricular failure and ascites. rickets. growth plate disease. Erysipelothrixetc. bacterial infection. Soluble multivitamins may be recommended as a nonspecific measure. Signs   Fluid-distended abdomen. Culture of lesions to confirm the bacterium involved. Prevention Vaccination with inactivated vaccine prior to lay. Prevention Good hygiene at turn-around. and /or trauma. Vegetative lesions usually on the right atrioventricular valve. Epiphysiolysis Introduction A complex condition of chickens that may be associated with trauma. osteomyelitis. 56 . Diagnosis Differentiate from broiler ascites syndrome by examination of the interior of the heart. Treatment Medication is only likely to be of value in reducing deterioration in birds that are starting to develop lesions.

chickens. The natural hosts are wild birds and rodents. Prevention Control of predisposing factors. ducks and pigeons having a high morbidity and high mortality. WEE. Paralysis. These conditions currently only occur from northern South America to North America. turkeys. Flaccid neck. Microscopic lesions not pathognomonic. Horses are also seriously affected. It is transmitted between birds by pecking and by mosquitoes. partridges. Diagnosis Gross inspection. 57 . Post-mortem lesions  Separation of epiphyses at the growth plate. wild birds. Tremors. Signs         Nervous symptoms. Ataxia. Post-mortem lesions   No gross lesions. VEE) Introduction A viral disease of pheasants. Paresis. Treatment Not applicable. often occurs or is identified in the processed carcase. May also be asymptomatic.Signs  Apparent dislocation at extremities of long bones. sometimes seen in vivo. histology may be helpful in identifying underlying problems such as rickets or 'FHN'. Circling. Equine Encephalitis (EEE.

rhusiopathiae) seen in turkeys and increasingly in free-range chickens. It is also seen in some mammals. Signs         Inappetance. and CE. water. Sudden death. Haemorrhages in fat. May be diarrhoea and respiratory signs. Perineal congestion. Post-mortem lesions       Carcase congestion. TC. pheasants. Sleepiness. rarely in geese. control cannibalism.Diagnosis Isolation in mice. Liver. especially snood. fishmeal and semen and by cannibalism. Prevention Protection from mosquitoes. in soil. Vaccinate at 5-6 week. Depression. ID by VN. 58 . Endocarditis. The bacterium is fairly resistant to environmental effects or disinfectants and may persist in alkaline soil for years. It may be transmitted by faecal carriers for 41 days. kidney. epicardium. ducks. There is likely to be an increased risk if housing or land has been previously used by pigs or sheep. Joint lesions. Erysipelas Introduction A sudden onset infection with the bacterium Erysipelothrix insidiosa (E. Chronic scabby skin. Treatment None. Marked catarrhal enteritis. COFAL. spleen swollen. muscle. Swollen snood.

Sudden drop in egg production. Tetracyclines in feed may also be helpful. history. and acute Newcastle disease. mycotoxins. vaccine at 16-20 weeks if the condition is enzootic. synoviae plate tests for a few weeks.a combination of the procaine and benzathine salts may be injected. Death by internal exsanguination after rupture of haematocyst. Differentiate from pasteurellosis. Some birds with pale comb and wattles. greasy and soft with numerous haemorrhages. salmonellosis. Diagnosis Lesions. Prevention Good biosecurity to prevent spread from other susceptible species. Sudden death. Vaccination or natural infection may cause false positive reactions in the Mycoplasma gallisepticum and M. Treatment Penicillin . Headparts pale. especially caged layers and with a complex set of causes including excessive calories. deficiency and stress. Signs     Overweight typically by 25%. 59 . colibacillosis.Diagnosis Isolation on blood agar. Post-mortem lesions     Obesity. often along with bacterin. and identification. Liver yellow. Fatty Liver Haemorrhagic Syndrome Introduction A condition occurring worldwide in chickens. the demonstration of the organism in stained impression smears from tissues.

B 12 and inositol. vitamin E.Treatment Reduce energy intake. isolation. 60 . Loss of condition. Prevention Feed to avoid obesity. Signs      White. 'Honeycomb' skin. Prevention Good hygiene of facilities. Diagnosis Lesions. It is very rare in commercial poultry production. powdery spots and wrinkled crusts and scab on comb and wattles. avoid mycotoxins and stress. Post-mortem lesions  See signs (above). Trichophyton gallinae. Favus Introduction A fungal infection. of chickens and turkeys. Feather loss. supplement with choline. culling affected birds. Thick crusty skin. Treatment Formalin in petroleum jelly.

turkeys.75% of all male broilers placed had lesions in the hip bone. FHN is the commonest infectious cause of lameness in broilers in the UK. Diagnosis Base on post-mortem lesions and isolation of a causative organism.Femoral Head Necrosis . rickets. Treatment Antibiotic therapy in accordance with sensitivity is likely to be beneficial only for birds in the early stage of this process and may not be economically justifiable.FHN Introduction A condition of chickens and turkeys that may be associated with several different bacterial infections e. Signs   Lameness. staphylococci. Prevention Exclusion of floor eggs and dirty eggs from the hatchery. streptococci. Differentiate from synovitis. highly contagious disease caused by the bacterium Pasteurella multocida in a range of avian species including chickens. Fowl Cholera. Pasteurellosis Introduction Fowl Cholera is a serious. especially hypophosphataemic. coli. Careful attention to mineral and Vitamin D nutrition to avoid subclinical. and water fowl. indicated that 0. arthritis. Predisposing factors include immunosuppresive viruses such as Infectious Bursal Disease Virus and Chicken Anaemia Virus and non-infectious bone pathologies such as hypophosphaetamic rickets.g. Use of a wing for support during walking and hip flexion. Post-mortem lesions  Degeneration of the epiphyses of long bones with thinning of the cortex and tendency to break when force is applied. E. Post-mortem studies of birds culled due to lameness and of birds found dead. It is seen worldwide and was one of the first infectious 61 . (increasing order of susceptibility). spondylolisthesis.

by Louis Pasteur in 1880. Diarrhoea. streptomycin. The disease can range from acute septicaemia to chronic and localised infections and the morbidity and mortality may be up to 100%. erythromycin. Lungs with a consolidated pink 'cooked' appearance in turkeys. Enteritis. penicillin. Purulent arthritis. Coughing. Yolk peritonitis. Signs           Dejection. Diagnosis Impression smears. confirmed with biochemical tests. Sudden death. Focal hepatitis. Swollen and cyanotic wattles and face. Lameness. ocular and oral discharge. Nasal. Post-mortem lesions         Sometimes none. The incubation period is usually 5-8 days. The disease often recurs after medication is stopped. equipment. Treatment Sulphonamides. Purulent pneumonia (especially turkeys). Differentiate from Erysipelas. Reservoirs of infection may be present in other species such as rodents. Ruffled feathers. The route of infection is oral or nasal with transmission via nasal exudate. necessitating long-term or periodic medication. 62 . but may persist for prolonged periods in soil. Swollen joints.no growth on McConkey). isolation (aerobic culture on trypticase soy or blood agar yields colonies up to 3mm in 24 hours . septicaemic viral and other bacterial diseases.diseases to be recognised. Predisposing factors include high density and concurrent infections such as respiratory viruses. The bacterium is easily destroyed by environmental factors and disinfectants. and people. contaminated soil. tetracyclines. faeces. Cellulitis of face and wattles. Loss of appetite. or limited to haemorrhages at few sites. and possibly pigs. cats.

bacterins at 8 and 12 weeks. and where there are biting insects. Poor growth. The virus persists in the environment for months. pigeons and canaries worldwide. Figure 19. hygiene. Caseous deposits in mouth. 0-50%.Prevention Biosecurity. Avian Pox Introduction A relatively slow-spreading viral disease characterised by skin lesions and/or plaques in the pharynx and affecting chickens. Morbidity is 1095% and mortality usually low to moderate. The swelling is made up of oedema and purulent exudates (pus). throat and sometimes trachea. spreading eruptions and scabs on comb and wattles. It is more common in males because of their tendency to fight and cause skin damage. and mosquitoes (infected for 6 weeks). live oral vaccine at 6 weeks. 63 . Depression. fomites. Pox. good rodent control. Severe localised Pasteurella infection in the swollen wattle of a 30-week-old male broiler parent chicken. Infection occurs through skin abrasions and bites. It is transmitted by birds. or by the respiratory route. Inappetance. The duration of the disease is about 14 days on an individual bird basis. Poor egg production. Fowl Pox. Signs       Warty. turkeys.

It is confirmed by IC inclusions in sections/ scrapings. pharynx. Less commonly there may. in the diptheritic form. Turkeys by thigh-stick at 2-3 months. Diagnosis A presumptive diagnosis may be made on history.Post-mortem lesions    Papules progressing to vesicles then pustules and scabs with distribution described above. isolation (pocks on CE CAM) with IC inclusions. Microscopically . DNA probes. Differentiate from Trichomoniasis or physical damage to skin. usually with chicken strain by wing web puncture.intra-cytoplasmic inclusions (Bollinger bodies) with elementary bodies (Borrel bodies). signs and post-mortem lesions. be caseous plaques in mouth. Chickens well before production. There is good cross-immunity among the different viral strains. reproduction in susceptible birds. Flocks and individuals still unaffected may be vaccinated. check take at 7-10 days post vaccination. 64 . trachea and/or nasal cavities. Figure 20. Prevention By vaccination (except canary). If there is evidence of secondary bacterial infection broad-spectrum antibiotics may be of some benefit. Fowl pox lesions on the wattle of an adult broiler parent chicken. Treatment None.

Swelling and infarction of the liver. usually over wings and breast. Post-mortem lesions    Patches of gangrenous skin with underlying emphysematous and/or sanguinous cellulitis. occasionally Staphylococcus aureus. Necrotic Dermatitis Introduction A bacterial condition seen in chickens and usually caused byClostridium septicum. Sudden mortality. It occurs due to invasion of 'normal' wounds by 'normal' bacteria in immunosuppressed birds. 65 . wattles. Foci in liver. wings. sometimes thighs and other parts. early Infectious Bursal Disease Virus infection). especially following congenital Chick Anaemia Virus infection or early Infectious Bursal Disease Virus infection (Gumboro Disease). Signs      Occasionally dejection. Morbidity may be up to 50% and mortality is high. Avoid skin trauma and immunosuppression (congenital CAV infection. The spores of Clostridial bacteria are highly resistant in the environment. penicillin or amoxycillin. Recovery of an abundant growth of causative organism in recently dead birds. Gangrenous skin.Gangrenous Dermatitis. spleen. Prevention Good hygiene and management. rarely Clostridium noyvi / oedematiens. Loss of appetite. Treatment Sulphaquinoxaline. Diagnosis Clinical signs and/or lesions. Immunosuppression is therefore a predisposing factor. Severe cellulitis especially of thighs.

Figure 21. Dyspnoea. slugs and snails acting as transfer hosts but the life cycle may also be direct. confirmation of presence of the parasite. Signs     Gasping. Diagnosis Signs and lesions. turkeys. and other game and ornamental birds occurring worldwide.g. There is an 18-20 day prepatent period. by ingestion of embryonated egg or L3. from rookeries. Head shaking. Prevention Flubendazole. Presence of worms. The condition is seen more commonly in poultry on free range where ground may be contaminated by wild birds e. a nematode worm parasite of chickens. pheasants. paired parasites up to 2 cm long. levamisole. Loss of appetite and condition. Post-mortem lesions   Tracheitis. Treatment Flubendazole in feed. Infection is by the oral route with earthworms. Severe gangrenous dermatitis on the upper surface of the wing of a broiler chicken. 66 . Gape Introduction Syngamus trachea.

Amidostomum anseris. necrosis and partial sloughing of gizzard lining.Geese Introduction A nematode worm parasite. Loss in condition and weight. Worms develop to L3 in eggs and infection is by the oral route direct from environment. Signs    Depression. and Histiocephalus are nematode worm parasites of chickens. Treatment Levamisole. Gizzard worms . Slow growth. Post-mortem lesions   Ulceration. Diagnosis Lesions. Cheilospirura and Streptocara are seen worldwide but Histiocephalus is restricted to Europe. Prevention Prevention of access to intermediate hosts. Signs    Depression.Chickens Introduction Cheilospirura. Loss in condition and weight. Slow growth. confirmation of presence of the worms.Gizzard worms . routine worming. beetles etc act as intermediate hosts. 67 . Streptocara. weevils. affecting geese and ducks. They are more common in free-range birds because of their increased access to intermediate hosts. benzimidazoles such as flubendazole. Adults are 2-4 cm long and usually bright red. muscular wall may be sacculated or ruptured. Grasshoppers.

visualisation of worms. Membrane covering tongue. muscular wall may be sacculated or ruptured. Swollen eyelids and eye and nasal discharge. necrosis and partial sloughing of gizzard lining. 68 . The younger the bird affected the more acute the condition and the higher the mortality. Diagnosis Lesions. spleen and pancreas. Swelling and congestion of liver. Loss of down. Excessive water intake. benzimidazoles. Vertical transmission resulting in congenital infection may occur. Goose Parvovirus (Derzsy's Disease) Introduction Goose Parvovirus is a highly contagious condition of geese and young Muscovy ducks. Adults are 2-4 cm long and usually bright red. Prevention Rotation of ground on annual basis.Post-mortem lesions   Ulceration. Reddening of skin. Post-mortem lesions   Pale myocardium. Signs         Prostration and death in acutely affected goslings. Treatment Levamisole. Profuse white diarrhoea. Reduced feed intake. Losses are negligible in birds over 5 weeks of age. Derzsy's Disease is caused by a parvovirus distinct from chicken and mammalian parvoviruses. The amount of maternal antibody passed from the breeding birds will affect the severity and timing and severity of the condition in the young birds.

The preferred approach is to immunise breeding birds with an attenuated live vaccine. mycotoxins and viral infections and usually following a course of approximately 3 weeks. Pale comb and wattles. Aplastic Anaemia. Carcase anaemia. 69 . Ideally flocks that have suffered the disease should not be used for breeding as they may become persistent excreters of the infection. Bone marrow pale with fatty change. Antimicrobials may be of value in reducing the effects of secondary bacterial infections. Signs      Dejection. Haemorrhagic Disease. Ascites. Liver yellow. Prevention Hatching and brooding geese from different parent flocks together should be avoided. mortality is 5-50%. serosa and mucosae. Morbidity varies. Post-mortem lesions     Haemorrhages in one or more sites: skin. Poor growth. muscles. Administration of immune serum has been shown to be effective but may require two doses (day old and around 3 weeks). Treatment No specific treatment. Diagnosis Signs and lesions in birds of the appropriate age and species. Fibrinous perihepatitis. liver. Loss of appetite. Blood in droppings. Haemorrhagic Anaemia Introduction A complex condition of chickens associated with drug toxicities.   Fibrinous pericarditis. heart.

spleen shows lymphoid hyperplasia. Treatment Vitamin K. Post-mortem lesions     Petechiae in various tissues. Microscopic . The source of virus is unknown but there is easy lateral spread within flocks. Signs       Sudden deaths. The virulence of the virus varies but morbidity may be 100% and mortality 10-60%. Diagnosis Typical lesions. caused by Type II Adenovirus distinct from classical fowl adenovirus and occurring in most turkey-producing areas. The route of infection is usually oral. May induce immunosupression and precipitate respiratory disease or coccidiosis. Blood from vent of moribund birds. add liver solubles to feed. Course 10-21 days. 70 . Prevention Avoid causative factors. Spleen mottled and enlarged.sero-conversion frequently occurs in absence of clinical disease. Haemorrhagic Enteritis Introduction A viral disease of turkeys. Drop in feed and water consumption. Diarrhoea. lesions. Elisa . Serology: DID. reproduction with filtered contents. Intestine distended with blood. reticulo-endothelial hyperplasia and intranuclear inclusions. signs. double-immuno-diffusion of splenic extract. and weeks in litter. the virus surviving in frozen faeces for months. similar to pheasant Marble Spleen disease. remove sulphonamides.Diagnosis History.

Immunity: there is an early age resistance irrespective of maternal antibody status. some in turkey B-lymphoblastoid cell lines. convalescent serum. Live vaccines are commonly used in many countries at 4-5 weeks of age. Immunity to the disease is long lasting. Prevention All-in/all-out production. Ducks are relatively resistant to heat stress. In this case a loop of intestine has been opened to show the blood.and T-line lymphocytes for up to 5 weeks following exposure. oral tetraycline. Turkeys dying with haemorrhagic enteritis commonly have the small intestine distended with blood. Signs    Panting. good hygiene and biosecurity.Treatment Warmth and good management. especially associated with high relative humidity and low air speed. Heat Stress Introduction A condition seen in chickens. Reduced feed consumption. Increased thirst. Maternal antibody may interfere with vaccination. 71 . Disinfect and 3-4 weeks house rest. Pathogenic strains can depress both B. good management. feather cover. and turkeys caused by high environmental temperature. nicarbazin in feed. high stocking density. drinking water temperature and availability. acclimation. Figure 39. Predisposing factors include genetics. Some are produced in live turkeys.

fomites. Intestine flabby with some bulbous dilation. pigeons. Hexamitiasis Introduction Hexamita meleagridis (pigeons H.   Reduced egg production. Post-mortem lesions   Dehydration. Mucoid exudate in nostrils and mouth. signs. pheasants. Inter-species transmission may occur. maximise airflow. Feeding during cooler hours may be beneficial. 72 . watery diarrhoea. if relative humidity is low then wet the roof and fog. Diagnosis Temperature records. Loss in weight. contains excessive mucus and gas. carriers. Terminal coma and convulsions. Prevention Houses of optimal height and insulation. chirping. Prostration. Post-mortem lesions   Carcases congested. lesions. Treatment Cool water. Legs and wings outstretched. It is transmitted by faeces. Later depression. columbae) is a protozoan parasite of turkeys. In commercial ducks a related parasiteTetratrichomonas can cause poor growth and drops in egg production. evaporative coolers. pattern of losses. and some game birds. Inappetance. exclusion of other conditions. feed with a reduced protein:energy ratio. Frothy. Signs       Initially birds nervous. painted white to reflect heat. Reductions in stocking density of meat poultry may be quickly achieved by partial depletion ('thinning').

increase ambient temperature. This condition has high morbidity and mortality in turkeys. Sulphur-yellow diarrhoea. Diagnosis Lesions. Poor growth. and also. Cyanosis of head. Furazolidone. Signs        Depression. and occasionally chickens. gallinae the parasite is easily destroyed. trichomoniasis. 73 .  First half of intestine inflamed. Progressive depression and emaciation. pheasants and game birds that acts together with facultative bacteria to produce the condition of Blackhead. Inappetance. Caecal tonsils congested. Outwith earth worms orH. Blood in faeces (chickens). The effect of antibiotic may be related to the control of secondary bacterial enteritis. paratyphoid. Histamonosis. hygiene. dimetridazole. avoid interspecies mixing. and mixing groups of different ages. histomonosis. significant disease has been seen in breeding chickens and free-range layers. The problem is seen in high-biosecurity facilities. Within a turkey shed transmission is rapid in spite of the fact that it is difficult to infect birds orally with unprotected parasites. Blackhead Introduction Histomonas melagridis is a protozoan parasite of turkeys. if possible. Prevention Depopulation. scrapings from fresh material. It has recently been demonstrated that infection occurs readily via the cloaca when birds are on contaminated litter. presumably introduced with worm eggs. all-in/all-out production. Differentiate from transmissible enteritis. The parasite is ingested in the ova ofHeterakis worms or as larvae in earthworms or faeces and there is an incubation period of 15-20 days. Treatment Tetracycline. Histomoniasis. dimetridazole and ipronidazole have been used in the past. Although chickens are relatively resistant to the condition.

scrapings from fresh material. however they may not be present in the early stages. nitrofurans (e.g. concrete floors. Prevention Good sanitation. given recent new knowledge on the mechanism of transmission. usually grey in colour. Ulcers. Some herbal products based on the essential oils (e. avoid mixing species. 74 .M. especially in chickens. Treatment Historically nitro-imidazoles (e.g. It is a condition caused by an adenovirus.Abubakar. It affects mainly broilers and broiler parents in rear and has also been seen in pigeons. Having both chickens and turkeys on the same property is likely to increase the risk of this disease in turkeys. Intensive relittering may help reduce the level of infection. 'Herban)' have been used with some apparent success though controlled trials and formal approval for this purpose are not recorded. dimetridazole). Angara Disease Introduction This condition was first identified in broilers in Pakistan in 1987.g. Liver may have irregular-round depressed lesions. It spread rapidly in broiler producing areas in that country and the same or a very similar condition has been seen in North and South America. Diagnosis Lesions. and only nitarsone is approved in the USA. caseous cores with yellow. nifursol) and arsenicals (e. At the time of writing no products of these groups are approved for use in the European Union. Arsenicals are less effective in treatment than they are in prevention. Hydropericardium-Hepatitis Syndrome. possibly in combination with an RNA virus and immunosuppression caused by Chick Anaemia Virus or Infectious Bursal Disease.Tahir Post-mortem lesions    Enlargement of caeca. Regular worming to help control the intermediate hosts.nitarsone) have been used to treat this important disease of poultry. Use of an anti-histomonas product in feed where such products are approved but due care with respect to residue avoidance would be required.g. furazolidone. The disease is readily reproduced by inoculating birds with a bacteria-free filtrate of a liver extract from an affected bird. grey or green areas. Mortality may reach 60% but more typically 10-30%.

Grit would not be classed as a foreign body. Congestion of the carcase. virology. Older birds ingest grit to facilitate the grinding activity in the gizzard. Impacted gizzards are then found in 'non-starter' type chicks or poults. treatment of drinking water with 0. Yellow mucoid droppings. Formalin-inactivated oil adjuvant vaccines are reported to be highly effective and are used in areas where the condition is endemic. Impaction and Foreign Bodies of Gizzard Introduction The gizzard or crop may become impacted with litter. This condition usually affects only a small number of birds.g. pale friable liver and kidney. Prevention The condition typically occurs in areas of high poultry density where multi-age operation is traditional.1% of a 2. Most young commercial poultry consume feeds that have a small particle size. grass. Gizzard activity also acts as a pacemaker of intestinal activity and controls the speed at which food is passed to the small intestine. however if young chicks to do not begin to eat feed properly they often consume litter instead. Huddling with ruffled feathers. Good water sanitation (e. to reduce their particle size to aid digestion. however sometimes free-range poultry consume large stones.5% iodophor solution) appears to be beneficial. The normal function of the gizzard is to aid in the physical grinding of food materials. histopathology. Diagnosis Lesions. Lungs oedematous. Control of predisposing immunosuppressive diseases may help limit losses. Post-mortem lesions     Excessive straw-coloured fluid distending the pericardium (up to 10 mls). string etc. Enlarged.Signs     Sudden increase in mortality. and birds of any age can 75 . Treatment None. Lethargy.

Signs   Reduced feed intake. A number of different sero-types have been isolated from disease outbreaks but they may also be isolated from healthy chickens. Daily monitoring of the crop-fill is a useful procedure. It allows us to confirm the proportion of chicks consuming feed and can give inexperienced poultry keepers feedback on the effectiveness of their brooding management. A foreign body may be found in the interior of the gizzard. 76 . and on opening is found to contain a mass of fibrous material. Italy. Post-mortem lesions    The gizzard is more firm than normal and.15 days with a morbidity of 1-10% and a mortality of 1-10%. Sweep floors after maintenance activities to remove nails and other potentially dangerous foreign bodies. Prevention Good brooding management to encourage early adaptation to the diet and adequate consumption of feed and water. The disease was first described in the USA in 1963 and has also been reported in Canada. This may extend into the proventriculus and on into the duodeunum. Infected birds remain carriers for a few weeks. This usually happens after maintenance activities have been carred out in the housing.consume nails. France and Ireland. Treatment None effective in young birds. Reduced weight gain. staples etc. and may penetrate the body wall. Inclusion Body Hepatitis Introduction A disease of chickens characterised by acute mortality. the UK. caused by an adenovirus. Australia. Obvious non-starters should be culled in this situation. Diagnosis Lesions. It has a course of 9. often with severe anaemia. Nails commonly penetrate the lining of the gizzard.

Signs     Depression. Microscopically . yellow. for instance due to early IBD challenge or congenital CAV infection. Post-mortem lesions      Liver swollen. Bursa and spleen small. Progeny of high health status breeding flocks appear to be at greater risk. 77 . Formaldehyde and iodides work better. Serology: DID for group antigen. but on the other hand many field cases show eosinophilic inclusions that do not appear to have adenovirus particles. Diagnosis A presumptive diagnosis may be made on history and lesions. Differentiate from Chick anaemia syndrome. Pallor of comb and wattles. Confirmation is made on finding inclusions in the liver. chloroform. vibrionic hepatitis. pH). and deficiency of vitamin B12. Blood thin. Ruffled feathers. Treatment None. Soluble multivitamins may help with the recovery process. A form of the disease affecting birds under 3 weeks of age in Australia has been reproduced with serotype 8 adenovirus.Transmission may be vertical or lateral and may involve fomites. Immunosuppression. Since adenoviruses are commonly found in healthy poultry. The virus grows well in tissue culture (CEK. isolation alone does not confirm that they are the cause of a particular problem. may be important. and high temperatures. The virus is generally resistant to disinfectants (ether. SN for individual sero-types. Curiously. fatty liver syndrome. Kidneys and bone marrow pale. perhaps because they have lower levels of maternal antibody.basophilic intranuclear inclusions. Infectious Bursal Disease. CEL). sulphonamide intoxication. Inappetance. many different sero-types have been isolated from different cases. mottled with petechiae and ecchymoses.

The cause is a Coronavirus that is antigenically highly variable. E. Typing by haemagglutination-inhibition is also used. and complicating infections (Mycoplasma. Wet litter. which may survive 4 weeks in premises. Signs        Depression. Some birds/viral strains can be carriers to 1 year. maternal immunity (young birds). coli. 1931).Prevention Quarantine and good sanitary precautions. Loss of appetite. About eight sero-groups are recognised by sero-neutralization. the age of the bird. Huddling. Caseous plugs in bronchi. 78 . Morbidity may vary 50-100% and mortality 0-25%. fomites or aerosol. disinfectants (Formal 1% for 3 mins). Newcastle disease). Tracheal oedema. Infectious Bronchitis. alkalis. Post-mortem lesions       Mild to moderate respiratory tract inflammation. probably the commonest respiratory disease of chickens. gasping. Airsacculitis. Tracheitis. depending on secondary infections. These differences are due to structural differences in the spike proteins (S1 fraction). new sero-types continue to emerge. is sensitive to solvents. was first described in the USA (N. Poor ventilation and high density are predisposing factors. Diuresis. The virus. Dakota. heat (56°C for 15 mins). Coughing. prior vaccination. prevention of immunosuppression. Its affects vary with: the virulence of the virus. Diarrhoea. dyspnoea. Kidneys and bronchi may be swollen and they and the ureters may have urates. IB Introduction This infection. Infection is via the conjunctiva or upper respiratory tract with an incubation period of 18-36 hours. The infection is highly contagious and spreads rapidly by contact.

fomites or aerosol. Maternal immunity provides protection for 2-3 weeks.antibiotics to control secondary colibacillosis (q. with typical lesions. Definitive diagnosis is based on viral isolation after 3-5 passages in chick embryo.v. DID (poor sensitivity. Cellmediated immunity may also be important. Humoral immunity appears 10-14 days post vaccination. lesions and serology. depending on secondary infections. Muscular shivering. 79 . alkalis. The infection spreads rapidly by contact. possible reactions depending on virulence and particle size. heat (56°C for 15 mins). Poor ventilation and high density are predisposing factors. flourescent antibody positive and ciliostasis in tracheal organ culture. Elisa (both group specific). short duration. Otherwise as for standard IB. Some birds/viral strains can be carriers for up to 1 year. disinfectants (Formal 1% for 3 mins).). SN (type specific). Treatment Sodium salicylate 1gm/litre (acute phase) where permitted . IB . group specific). is sensitive to solvents. Avian Influenza and Laryngotracheitis.Diagnosis Tentative diagnosis is based on clinical sgns. Infection is via the conjunctiva or upper respiratory tract with an incubation period of 18-36 hours.793b Variant Sudden Death Syndrome in Broiler Parents Introduction A Coronavirus infection of chickens with a morbidity of 50-100% and a mortality 0-25%. Infectious Bronchitis. Serology: HI. Signs    Sudden death. Prevention Live vaccines of appropriate sero-type and attenuation. mycoplasmosis. Local immunity is first line of defence. The virus. HA negative. which may survive 4 weeks in premises. Differentiate from Newcastle disease (lentogenic and mesogenic forms). vaccinal reactions.

Other lesions of 'classical' IB may be encountered. fomites or aerosol. Rales may or may not be present. A few birds are carriers up to 49 days post infection. short duration. Prevention Live vaccines of appropriate sero-type and attenuation.Post-mortem lesions    Oedema of pectoral muscles and subcutaneously on abdomen. CK) only after adaptation Serology: HI. Rough shells.antibiotics to control secondary colibacillosis (q. There is rapid spread by contact. The condition has a morbidity of 10-100% and mortality of 0-1%. Diagnosis 3-5 passages in CE allantoic cavity. Coughing. Signs       Drop in egg production (20-50%).). ciliostatic in tracheal organ culture. FA. sneezing. HA-. possible reactions depending on virulence and particle size. typical lesions. Infectious Bronchitis. DID (poor sensitivity. with much antigenic variation. 80 . Elisa (both group specific). group specific). Infection is via the conjunctiva or upper respiratory tract. Soft-shelled eggs. Poor ventilation and high density are predisposing factors. Loss of internal egg quality. lesions progress to necrosis and scarring of deep pectorals in convalescence. In layers the ovules may be intensely congested. cell culture (Vero. The virus is moderately resistant and may survive 4 weeks in premises.v. IB Egg-layers Introduction A Coronavirus infection of chickens. Treatment Sodium salicylate 1gm/litre (acute phase) where permitted . SN (type specific).

particle size (if sprayed) and general health status. Local immunity is the first line of defence. Flaccid ovarian follicles in a broiler parent chicken undergoing challenge with Infectious Bronchitis virus. SN. Prevention Live vaccines of appropriate sero-type and attenuation. EDS76. Differentiate from Egg Drop Syndrome. Serology: HI.Post-mortem lesions   Follicles flaccid. Diagnosis 3-5 passages in CE. typical lesions. FA.antibiotics to control secondary colibacillosis (q. Treatment Sodium salicylate 1gm/litre (acute phase) where permitted . HA-.v. Humoral immunity appears 10-14 days post vaccination. DID. Yolk in peritoneal cavity (non-specific). Maternal immunity provides protection for 2-3 weeks.). virulence. Figure 22. although reactions can occur depending on prior immunity. Cell-mediated immunity may also be important. 81 . Elisa.

Differentiate from Egg Drop Syndrome.antibiotics to control secondary colibacillosis (q. Poor ventilation and high density are predisposing factors. Treatment Sodium salicylate 1gm/litre (acute phase) where permitted . The condition has a morbidity of 10-100% and mortality of 0-1%. Signs       Drop in egg production (20-50%). Diagnosis 3-5 passages in CE. Local immunity is the first line of defence. HA-. SN. particle size (if sprayed) and general health status. IB Egg-layers Introduction A Coronavirus infection of chickens. with much antigenic variation. typical lesions. FA. Coughing. 82 .Infectious Bronchitis. although reactions can occur depending on prior immunity. Rough shells. A few birds are carriers up to 49 days post infection. Elisa. The virus is moderately resistant and may survive 4 weeks in premises. Loss of internal egg quality. Serology: HI. Humoral immunity appears 10-14 days post vaccination. EDS76.). sneezing.v. Prevention Live vaccines of appropriate sero-type and attenuation. Soft-shelled eggs. Maternal immunity provides protection for 2-3 weeks. DID. Rales may or may not be present. virulence. Yolk in peritoneal cavity (non-specific). There is rapid spread by contact. fomites or aerosol. Post-mortem lesions   Follicles flaccid. Cell-mediated immunity may also be important. Infection is via the conjunctiva or upper respiratory tract.

The route of infection is usually oral. There is no vertical transmission. first identified in the USA in 1962. but may be via the conjunctiva or respiratory tract. and affected birds excrete large amounts of virus for about 2 weeks post infection. faeces etc. Subclinical infection in young chicks results in: deficient immunological response to Newcastle disease. Signs are most pronounced in birds of 4-6 weeks and White Leghorns are more susceptible than broilers and brown-egg layers. susceptibility to Inclusion Body Hepatitis and gangrenous dermatitis and increased susceptibility to CRD. 83 . The infective agent is a Birnavirus (Birnaviridae). Morbidity is high with a mortality usually 0. persisting for months in houses. The age up to which infection can cause serious immunosuppression varies between 14 and 28 days according to the antigen in question. In addition to the direct economic effects of the clinical disease. which targets the bursal component of the immune system of chickens. Marek's disease and Infectious Bronchitis. seen worldwide. IBD. Sero-type 1 only. The virus is very resistant. the damage caused to the immune system interacts with other pathogens to cause significant effects. Flaccid ovarian follicles in a broiler parent chicken undergoing challenge with Infectious Bronchitis virus. especially with sero-type 2). Infectious Bursal Disease. Generally speaking the earlier the damage occurs the more severe the effects. Gumboro Introduction A viral disease. with an incubation period of 2-3 days. Mealworms and litter mites may harbour the virus for 8 weeks.20% but sometimes up to 60%. (Turkeys and ducks show infection only.Figure 22. The disease is highly contagious.

A history of chicks with very low levels of maternal antibody (Fewer than 80% positive in the immunodifusion test at day old. especially in the Delmarva Peninsula in the USA. Subclinical disease . subsequent diagnosis of 'immunosuppression diseases' (especially inclusion body hepatitis and gangrenous dermatitis) is highly suggestive. Diarrhoea with urates in mucus. The normal weight of the bursa in broilers is about 0. Unsteady gait. Inappetance. 84 .History. weights below 0. Half-life of maternally derived antibodies is 3. Vaccination date prediction uses sera taken at day old and a mathematical formula to estimate the age when a target titre appropriate to vaccination will occur. Coccidiosis. Vent pecking. Dehydration. lesions. Other possible causes of early immunosuppression are severe mycotoxicosis and managment problems leading to severe stress. (previously SN and DID). Haemorrhages in skeletal muscle (especially on thighs). Tests used are mainly Elisa. histopathology. This may be confirmed by demonstrating severe atrophy of the bursa. Serology: antibodies can be detected as early as 4-7 days after infection and these last for life. Treatment No specific treatment is available.1% are highly suggestive.4 days. Cryptosporidiosis of the bursa (rare). Haemorrhagic syndrome. Huddling under equipment. Variants: There have been serious problems with early Gumboro disease in chicks with maternal immunity. They are all serotype 1. Use of a multivitamin supplement and facilitating access to water may help. Elisa vaccination date prediction < 7 days).3% of bodyweight. IBD viruses have been isolated and shown to have significant but not complete cross-protection.Signs       Depression. Antibiotic medication may be indicated if secondary bacterial infection occurs. Post-mortem lesions     Oedematous bursa (may be slightly enlarged. may have haemorrhages. normal size or reduced in size depending on the stage). Diagnosis Clinical disease .5. Swollen kidneys with urates. especially if present prior to 20 days of age. rapidly proceeds to atrophy. Differentiate clinical disease from: Infectious bronchitis (renal).

biosecurity measures may be helpful in limiting the spread between sites. Infectious Coryza Introduction A usually acute. Infectious Coryza is caused by the bacterium Haemophilus paragallinarum and is seen in many countries especially in multi-age farms that are never depopulated.Prevention Vaccination. Morbidity is high but mortality low if uncomplicated although it may be up to 20%. turgid and oedematous. Carriers are important with transmission via exudates and by direct contact. It is not egg transmitted. It is enlarged. When outbreaks do occur. highly infectious disease of chickens. vaccination of progeny depending on virulence and age of challenge. and tracing of contacts may indicate sites on which a more rebust vaccination programme is indicated. This bursa is from an acutely affected broiler. 85 . the rectum and the vent. The route of infection is conjunctival or nasal with an incubation period of 1-3 days followed by rapid onset of disease over a 2-3 day period with the whole flock affected within 10 days. A strong immunity follows field challenge. occasionally pheasants and guinea-fowl. including passive protection via breeders. characterised by catarrhal inflammation of the upper respiratory tract. especially nasal and sinus mucosae. sometimes chronic. resulting in increased culling. Figure 23. Immunity after a live vaccine can be poor if maternal antibody was still high at the time of vaccination. This shows the anatomical relationship between the bursa. In most countries breeders are immunised with a live vaccine at 6-8 weeks of age and then re-vaccinated with an oil-based inactivated vaccine at 18 weeks.

chronic or localised pasteurellosis and vitamin A deficiency.The bacterium survives 2-3 days outside the bird but is easily killed by heat. drying and disinfectants. agglutination and IF have all been used but are not routine. erythromycin. DID. tylosin. Flouroquinolones are bactericidal and might prevent carriers. Sneezing. Signs         Facial swelling. Dyspnoea. Caseous material in conjunctiva/sinus.requires X (Haematin) and V (NAD) factors. Tracheitis. preferably in raised CO 2 such as a candle jar. Dihydrostreptomycin. Swollen wattles. Conjunctivitis. respiratory viruses. Post-mortem lesions      Catarrhal inflammation of nasal passages and sinuses. Serology: HI. identification of the bacteria in a Gram-stained smear from sinus. Prevention Stock coryza-free birds on an all-in/all-out production policy. sulphonamides. Controlled exposure has also been practised. Drop in egg production of 10-40%. while bacterins only protect against homologous strains. Commercial bacterins may not fully protect against all field strains but reduce the severity of reactions. Birds recovered from challenge of one serotype are resistant to others. Live attenutated strains have been used but are more risky. 86 . Treatment Streptomycin. Intercurrent respiratory viral and bacterial infections are predisposing factors. at least two doses are required. Eye-lid adherence. Diagnosis A presumptive diagnosis may be made on signs. Vaccines are used in areas of high incidence. Bacterin at intervals if history justifies or if multi-age. Differentiate from Mycoplasmosis. Confirmation is by isolation and identification . Purulent ocular and nasal discharge. lesions. Loss in condition. Inappetance.

ILT Introduction A herpesvirus (pathogenicity can vary) infection of chickens. in severe form may be enough. Apply strict biosecurity in moving equipment or materials between these these categories of stock. IFA. Gasping. caseous plugs may be present. PCR. after 4 weeks of age. pheasants. Movement and mixing of stock and reaching point of lay are predisposing factors. 87 . Nasal discharge (low pathogenicity strains).Infectious Laryngotracheitis. histology. peafowl and turkeys with a morbidity of 50-100% and a mortality usually 10-20% but sometimes up to 70%. Keep susceptible stock separate from vaccinated or recovered birds. Sera may be examined by VN or Elisa. vaccination. Sinusitis. Differentiate from Newcastle disease. severe bronchitis. Coughing of mucus and blood. Prevention Quarantine. Drop in egg production. Fairly slow lateral spread occurs in houses. Ocular discharge. Diagnosis Signs. lesions. Treatment None. if enzootic or epizootic in an area. The route of infection is via upper respiratory tract and conjunctiva or possibly oral and the course of the disease is up to 6 weeks. Isolation in CE CAMs. often with blood in lumen. Post-mortem lesions   Severe laryngotracheitis. Transmission between farms can occur by airborne particles or fomites.intranuclear inclusions in tracheal epithelium. All-in/allout operation. antibiotics to control secondary bacterial infection if this is marked. Signs        Dyspnoea. Microscopically . The virus is highly resistant outside host but is susceptible to disinfectants. Recovered and vaccinated birds are long-term carriers.

rarely chickens. The disease has a short course and morbidity and mortality are high. Different species of this parasite have been reported from North America. Diagnosis Typical post-mortem lesions Treatment As appropriate for the underlying disease condition.Intussusception Introduction A condition of chickens associated with increased intestinal motility. Anorexia. Survivors may carry infection. Post-mortem lesions  Telescoping of the bowel. Thirst. Leukocytozoonosis Introduction Caused by Leucocytozoon species. ducks. Prevention Control of coccidiosis and other causes of intestinal inflammation. Signs      Sudden onset of depression. protozoan parasites of turkeys. Coccidiosis. it may actually protrude at the vent and be cannibalised. Loss of equilibrium. usually in the lower small intestine. Simulid flies or culicoid midges are intermediate hosts. Rapid breathing. Asia and Africa. worms and other forms of enteritis are predisposing factors. 88 . guinea fowl. Signs  Mainly sudden deaths. Careful attention to feeding practices to avoid anticipation of feed arrival if on restricted feeding.

Treatment None known. disposal of recovered birds. gametes in erythrocytes. Persistent low mortality. Loss of weight. lesions. Hepatomegaly. Lymphoproliferative Disease (LPD) Introduction A Type C retrovirus infection of turkeys with low morbidity and high mortality. Differentiate from Reticuloendotheliosis. Microscopically .megaschizonts in brains of birds with nervous signs. Diagnosis History. Prevention Separation from intermediate hosts. age. histology and blood smears. cytology. Diagnosis Lesions. Anaemia. Enlargement of abdomen. Emaciation. liver or bursa. Post-mortem lesions     Splenomegaly. schizonts in liver. especially in enlarged spleen. Post-mortem lesions  Focal tumours. May be asymptomatic. Signs       Depression. Treatment 89 . Anaemia.

Runting/Stunting Introduction A condition of chickens and turkeys that may be associated with several different viruses. Diarrhoea. control arthropods. Runting (permanent). for example enteroviruses. in future eradication. The condition has been seen in Europe. Abnormal feathers ('helicopter wings' 'yellow-heads'). Treatment Daily cull of affected birds between 14 and 28 days.M. Malabsorption Syndrome.Tahir None. Diagnosis Pathology. Signs         Uneven growth. Post-mortem lesions     Enteritis. Eating faeces. It is suspected that these viruses can be vertically transmitted and the most severe signs in young birds are associated with this. reoviruses. Pale shanks in corn.Abubakar. Poor management may contribute to the problem. Pancreatic atrophy/fibrosis and pancreatic atrophy (rather variable). Diarrhoea in older birds may be an effect of on-farm infection. all-in/all-out production. Prevention Good hygiene. Poor early management (feed and water supply. 90 . North and South America and Australia. Stunting (temporary). Poor feathering. rotavirus etc. temperature control) may lead to a similar picture in the absence of specific infection. Pot-bellied appearance. enterovirus-like particles. direct electron microscope examination of intestinal contents.(maize-) fed birds (often associated with orange intestinal contents and/or faeces). Sometimes osteomyelitis and/or rickets.

Vertical transmission is not considered to be important. ovary. Intestines of a young broiler chick suffering from malabsorption syndrome. good parent nutrition and egg selection and santitation. Figure 24. lungs. muscles. b) Visceral . etc. seen worldwide.Prevention Good broiler farm hygiene.poorly digested food enclosed in mucus. fomites. c) Cutaneous . Mortality in an affected flock typically continues at a moderate or high rate for quite a few weeks. as well as more longstanding paralysis of legs or wings and eye lesions. The route of infection is usually respiratory and the disease is highly contagious being spread by infective feather-follicle dander.Tumours of feather follicles. Morbidity is 10-50% and mortality up to 100%. In 'late' Marek's the mortality can extend to 40 weeks of age. avoidance of intercurrent disease and management problems (such as chilling). and rarely turkeys in close association with chickens. both parasitic and bacterial. A sample of the faeces produced is shown at the bottom of the picture . Affected birds are more susceptible to other diseases.Acute infiltration of the CNS and nerves resulting in 'floppy broiler syndrome' and transient paralysis. The disease has various manifestations: a) Neurological . The virus survives at ambient temperature for a long time (65 weeks) when cell associated 91 . They are distended with poorly digested feed. tests. Infected birds remain viraemic for life.Tumours in heart. Marek's disease Introduction Marek's disease is a Herpes virus infection of chickens. From the 1980s and 1990s highly virulent strains have become a problem in North America and Europe.

lung. wings and neck. Vision impairment. Loss of weight. Mycoplasma gallisepticum infection. all-in/all-out production. vaccination generally with 1500 PFU of HVT at day old (but increasingly by in-ovo application at transfer). age affected. It is inactivated rapidly when frozen and thawed. M. kidney.lymphoid infiltration is polymorphic. and skeletal muscle. chronic respiratory disease in chickens. deficiency of thiamine. association with other strains (SB1 Sero-type 2) and Rispen's. game birds. clinical signs. Genetics can help by increasing the frequency of the B21 gene that confers increased resistance to Marek's disease challenge. Skin around feather follicles raised and roughened. resistant strains. Ducks and geese can 92 . distribution of lesions. Grey iris or irregular pupil. pigeons and other wild birds.and is resistant to some disinfectants (quaternary ammonium and phenol). histopathology. Signs      Paralysis of legs. It is common practice to use combinations of the different vaccine types in an effort to broaden the protection achieved. Differentiate from Lymphoid leukosis.. Thickening of nerve trunks and loss of striation. Prevention Hygiene.g. especially at the start of lay. gonads. deficiency of Ca/Phosphorus/Vitamin D. Post-mortem lesions    Grey-white foci of neoplastic tissue in liver. spleen. heart. Treatment None.Chicken Introduction Infection with Mycoplasma gallisepticum is associated with slow onset. botulism. Microscopically . Chronic Respiratory Disease . turkeys. Diagnosis History.

Occasionally arthritis. and to a lesser extent fomites. Haemophilus. Survival seems to be improved on hair and feathers. Pasteurella spp. Intercurrent infection with respiratory viruses (IB. virulent E. In turkeys it is most associated with severe sinusitis (see separate description in the turkey section). Slow growth. Post-mortem lesions      Airsacculitis. Poor productivity. ART). airborne dust and feathers. Reduced hatchability and chick viability. Occasional encephalopathy and abnormal feathers. Inappetance. The route of infection is via the conjunctiva or upper respiratory tract with an incubation period of 6-10 days. serology. coli. Culture requires inoculation in mycoplasma-free embryos or. and inadequate environmental conditions are predisposing factors for clinical disease. In adult birds. Perihepatitis (especially with secondary E. though infection rates are high. more commonly in Mycoplasma Broth followed by plating out on Mycoplasma Agar. aerosols. Catarrhal inflammation of nasal passages. ND. demonstration of specific DNA (commercial PCR kit available). Suspect colonies may be identified by immuno-flourescence. In others it is actually increasing because of more birds in extensive production systems that expose them more to wild birds. and in lyophilised material. morbidity may be minimal and mortality varies. Stunting. coli infection). Leg problems. sinuses. though in some countries this infection is now rare in commercial poultry. The condition occurs worldwide. or by direct contact with birds. isolation and identification of organism. Diagnosis Lesions. Fomites appear to a significant factor in transmission between farms. Spread is slow between houses and pens suggesting that aerosols are not normally a major route of transmission. Pericarditis. trachea and bronchi. 93 . Signs          Coughing. Transmission may be transovarian.become infected when held with infected chickens. Nasal and ocular discharge. tenosynovitis and salpingitis in chickens. subsequent stress may cause recurrence of disease. exudates. Recovered birds remain infected for life. The infectious agent survives for only a matter of days outwith birds although prolonged survival has been reported in egg yolk and allantoic fluid.

Aspergillosis. tetracyclines. hatchingeggs and chicks. tylosin. biosecurity. aerosols. Effort should be made to reduce dust and secondary infections. Suspect flocks should be re-sampled after 2-3 weeks. and fomites. exudates. Elisa is accepted as the primary screening test in some countries. all-in/all-out production. Morbidity is low to moderate and mortality low. other Mycoplasma infections such as M. meleagridis(turkeys). generally as a confirmatory test. or by direct contact with birds. 94 . Productivity in challenged and vaccinated birds is not as good as in M. In some circumstances preventative medication of known infected flocks may be of benefit. subsequent stress may cause recurrence of disease. HI may be used.Serology: serum agglutination is the standard screening test.-free stock. therefore M. PCR is possible if it is urgent to determine the flock status. though in many countries this infection is now rare in commercial poultry. It is seen worldwide. suspect reactions are examined further by heat inactivation and/or dilution. Some inactivated vaccines for other diseases induce 'false positives' in serological testing for 3-8 weeks. Recovered birds remain infected for life. Infectious Sinusitis . Transmission may be transovarian. Differentiate from Infectious Coryza.g. vitamin A deficiency.Turkeys Introduction A slow onset chronic respiratory disease of turkeys often with severe sinusitis and associated with Mycoplasma gallisepticuminfection. Treatment Tilmicosin. fluoroquinolones. M. viral respiratory diseases. Mycoplasma gallisepticum infection.g.g. spiramycin. Prevention Eradication of this infection has been the central objective of official poultry health programmes in most countries. and routine serological monitoring. Live attenuated or naturally mild strains are used in some countries and may be helpful in gradually displacing field strains on multi-age sites. synoviae and M. The route of infection is via the conjunctiva or upper respiratory tract with an incubation period of 6-10 days. These programmes are based on purchase of uninfected chicks.. infection status is important for trade in birds.

isolation and identification of organism. PCR is possible if it is urgent to determine the flock status. Differentiate from viral respiratory disease. and biosecurity. Effort should be made to reduce dust and secondary infections. more commonly in Mycoplasma Broth followed by plating out on Mycoplasma Agar. although prolonged survival has been reported in egg yolk and allantoic fluid. serology. especially Turkey Rhinotracheitis. Perihepatitis. Stress. In some circumstances preventative medication of known infected flocks may be of benefit. Culture. Inappetance. Survival seems to be improved on hair and feathers. malnutrition. requires inoculation in mycoplasma-free embryos or. intercurrent viral disease such as Newcastle disease (even lentogenic) and Turkey Rhinotracheitis are predisposing factors. and in lyophilised material.The infectious agent survives for only a matter of days outwith birds. suspect reactions are examined further by heat inactivation and/or dilution. Some inactivated vaccines induce 'false positives' in serological testing. fluoroquinolones. often with inspissated pus. 95 . Swollen sinuses. of swabs taken from the trachea or lesions. Nasal and ocular discharge. Leg problems. spiramycin. all-in/allout production. Suspect colonies may be identified by immunofluorescence. These are based on purchase of uninfected poults. Pericarditis. tetracyclines. tylosin. Slow growth. Airsacculitis. Prevention Eradication of this infection has been the central objective of official poultry health programmes in most countries. Serology: serum agglutination is the standard screening test. Stunting. Post-mortem lesions     Swollen infraorbital sinuses. Suspect flocks should be re-sampled after 2-3 weeks. Treatment Tilmicosin. HI may also be used. Diagnosis Lesions. Signs        Coughing. demonstration of specific DNA (commercial kit available).

Signs  Swollen sinuses.Mycoplasma immitans infection Introduction Infection with Mycoplasma immitans is seen in geese. Mycoplasma iowae infection. Treatment As for M. Leg lesions can be shown in inoculated birds but do not seem to occur naturally. Prevention As for M. Introduction Infection with Mycoplasma iowae is seen in turkeys.g. Reduced hatchability.i. Signs   Embryonic mortality. perhaps because all affected embryos fail to hatch.g. and partridges (UK). and can occur in other poultry and wild bird species. Post-mortem lesions  Stunted embryos with hepatitis and enlarged spleens. Diagnosis Shows cross reaction in IFA to M. some with down abnormality. ducks (France). Post-mortem lesions  Sinusitis. although DNA homology is only 40%. venereal or horizontal. M.g. Infection occurs via the conjunctiva or upper respiratory tract and transmission among poults may be vertical. 96 .

with transovarian and then lateral spread in meat animals. M. Infected eggs result in widespread distribution of infection and increased risk of further vertical transmission. The infective agent does not survive well outside the bird.-free stock. purchase of M. Stunting. Treatment Pressure differential dipping has been used where breeder flocks are infected.i. Signs        Reduced hatchability.Diagnosis Isolation and identification of the causative organism from dead-in-shell embryos. Mycoplasma meleagridis infection. Infection is via the conjunctiva or upper respiratory tract with an incubation period of 6-10 days. though up to 25% of infected birds show lesions at slaughter. Mild respiratory problems. Slow growth. Prevention Eradication of the infection from breeding stock. The organism has also been isolated from raptors. Mortality is low.m. In adult birds though infection rates are high. Specialised dip tanks are subjected to negative pressure which partially collapses the air cell of the submerged eggs. Antibiotics that have been used are tylosin and enrofloxacin. morbidity may be minimal. it occurs in most turkey-producing countries but is now much rarer in commercial stock. Predisposing factors include stress and viral respiratory infections. Crooked necks. Transmission is venereal in breeders. Pathogenicity is quite variable. Leg problems. When the vacuum is released the eggs draw in antibiotic solution which is subsequently absorbed through the shell membranes. Introduction A disease of turkeys characterised by respiratory and skeletal problems caused by Mycoplasma meleagridis. maintenance of this status by good biosecurity. 97 . For eradication purposes egg injection provides more consistent dosing per egg than does egg dipping. Infected parents may be asymptomatic. This can increase hatchability by 510% in this situation.

spiramycin. or lateral via respiratory aerosols and direct contact. Survival of the infectious agent outwith the bird is poor but fomite transmission between farms is important. all-in/all-out production. Predisposing factors include stress and viral respiratory infections. 11-21 days following contact exposure. and biosecurity. It occurs in most poultry-producing countries. Infected males are particularly prone to transmit infection and may warrant special attention. whilst illness is variable and mortality less than 10%. In some circumstances preventative medication of known infected flocks may be of benefit. Infected birds do develop some immunity. fluoroquinolones. Infectious Synovitis Introduction Infection with Mycoplasma synoviae may be seen in chickens and turkeys in association with synovitis and/or airsacculitis. Differentiate from Mycoplasma gallisepticum. Birds infected from their parents seem to be immuno-tolerant and particularly prone themselves to transmit. especially in commercial layer flocks. Spread is generally rapid within and between houses on a farm. Vaccines are not normally used. other respiratory viruses. Mycoplasma synoviae infection. Diagnosis Lesions. Suspect colonies may be identified by immuno-fluorescence. demonstration of specific DNA (commercial kit available). isolation and identification of organism. Airsacculitis (rarely) seen in adult birds.culture used to confirm. serology. These are based on purchase of uninfected poults.Post-mortem lesions   Airsacculitis in infected pipped embryos and poults. more commonly in Mycoplasma Broth followed by plating out on Mycoplasma Agar. Infection rates may be very high. Culture requires inoculation in mycoplasma-free embryos or. Mycoplasma synoviae. Serology: SAG used routinely . Infection is via the conjunctiva or upper respiratory tract with a long incubation period. 98 . M. Transmission may be transovarian.s. Effort should be made to reduce dust and secondary infections. Prevention Eradication of this infection is also possible using similar techniques as for Mycoplasma gallisepticum. Treatment Tylosin. tetracyclines.

Signs
        There may be no signs. Depression. Inappetance. Ruffled feathers. Lameness. Swelling of hocks, shanks and feet (sometimes severe and bilaterally asymmetrical). Faeces may be green in acute infections. Effects on egg production appear to be minor under good management.

Post-mortem lesions
       Joints and tendon sheaths have viscid grey to yellow exudate. Some strains can lead to amyloidosis. Swollen liver, spleen and kidney have been seen in the past but are not common now. Green liver. Exudate becomes caseous later. Sternal bursitis. Airsacculitis - usually in heavy broilers and associated with condemnations.

Diagnosis
Lesions, serology, isolation (difficult - requires NAD) and identification. Differentiate from viral arthritis, staphylococcal arthritis, Mycoplasma gallisepticum infections,Ornithobacterium rhinotracheale, viral respiratory disease with colibacillosis. Serology: SAG used routinely, Elisa in some countries - PCR and/or culture used to confirm. False positives post inactivated vaccines are, if anything more common than in the case of M.g.

Treatment
Tilmicosin, chlortetracycline, oxytetracycline, tylosin.

Prevention
Eradication of this infection is also possible using similar techniques as described forMycoplasma gallisepticum. These are based on purchase of uninfected chicks, all-in/allout production, and biosecurity. Maintenance of Mycoplasma synoviae free status seems to be more difficult than for Mycoplasma gallisepticum. In some circumstances preventative medication of known infected flocks may be of benefit. Vaccines are not widely used though they are available in some countries. Infected birds do develop some immunity to the effects of repeated inoculation.

99

M.Abubakar.Tahir

Mycotoxicosis
Introduction
Mycotoxicosis refers to all of those diseases caused by the effects of toxins produced by moulds. Disease is often subclinical and may be difficult to diagnose. Problems occur worldwide, but especially climates with high temperature and humidity and where grain is harvested with high water content. Economic impact is considerable in some countries. A number of different types are recognised: aflatoxins are produced by Aspergillus flavus; T2 fusariotoxins by Fusariumspp. (mouth lesions and thin eggshells); ochratoxins byAspergillus ochraceus (interferes with functions of kidney, proventriculus and gizzard); rubratoxin by Penicillium rubrum(interferes with thiamine metabolism and causes symptoms of deficiency). Other mycotoxins certainly occur. Mortality is variable but all are detrimental to bird health and are resistant to heat inactivation. The following species may be affected, in decreasing order of susceptibility: ducks, turkeys, geese, pheasants, chickens. The route of infection is by ingestion of fungal spores, which are readily carried in the air. High grain humidity, and damage due to insects, as well as poor storage conditions are major predisposing causes. Once toxins have been formed it is difficult to avoid their biological effects; they also increase susceptibility to bacterial diseases. Both fungal spores and formed toxins are generally highly resistant. Affected flocks return to normal mortality by 7 to 15 days after removal of the toxins. Some believe that mycotoxicosis is an important factor in fatty liver syndrome. Aflatoxins are known to inibit the synthesis and transport of lipids in the liver. Deficiencies of fat-soluble vitamins (A, D, E, and K) are also sometimes seen in aflatoxicosis. Multiplication of moulds in cereals requires selenium and this element is also important for the production of hepatic lipases. Aflatoxins have been shown to be carcinogenic in rodents so there may be public health issues relating to the effective control of these problems.

Signs
       Signs vary with the species affected, the mycotoxin, the dose ingested and the period of exposure. Diarrhoea. Paralysis or incoordination. Reduced feed efficiency. Reduced weight gain or egg production/hatchability. Increased condemnations. Pale shanks, combs, bone marrows.

Post-mortem lesions
  Lesions also vary in accorance with the same factors as signs. Mycotoxins can cause damage to mucosae with which they come in contact.

100

      

They can also be absorbed and affect blood coagulation, resulting in petechiae and larger haemorrhages in various tissues. Liver and kidney lesions - livers may be enlarged and fatty or show bile retention or tumours. Enteritis of variable degree may be seen. Hydropericardium. Pale bone marrow. Regression of the bursa of Fabricius. Gizzard erosions.

Diagnosis
In severe cases a presumptive diagnosis may be based on the history, signs and lesions. Histology may be beneficial in some cases, as may identification and quantification of toxins in samples of feed or feed residue. Differentiate from poor nutrition, poor management, physical damage to tissues, and infectious bursal disease.

Treatment
The most effective treatment is removal of the source of toxins. Addition of antifungal feed preservatives is also helpful. Increasing protein level in the feed until mortality reduces may also be beneficial. Administration of soluble vitamins and selenium (0.2 ppm), along with finely divided copper sulphate in the feed 1kg/ton for 7 days (where approved) has been used.

Prevention
Mycotoxicoses may be prevented by careful choice of feed raw materials, reduction in water content of the raw materials and hygienic storage. Antimycotic feed additives may also be used but may not deal with toxins already formed. Feeds with high levels of fishmeals are particularly susceptible and should not be stored for more than 3 weeks. Pelletising feed may reduce fungal counts but does not affect toxins. Certain minerals additives have been shown to bind mycotoxins and reduce their effects. Good stock control, management of feeders and bins, and avoidance of feed spillage are all important.

101

Ruffled feathers. Prevention Penicillin in feed is preventive. amoxycillin). Treatment of ducks is not very successful. other debilitating diseases. turkeys and ducks worldwide. Water medication for 3-5 days and in-feed medication for 5-7 days depending on the severity. in drinking water. Reflux of bile-stained liquid in the crop if upper small intestine affected. caused by Clostridium perfringens and characterised by a fibrino-necrotic enteritis. Probiotics may limit multiplication of bacteria and toxin 102 . Closed eyes. usually of the mid. usually in less than 48 hours. Intestinal mucosa with diptheritic membrane.Tahir Necrotic Enteritis Introduction An acute or chronic enterotoxemia seen in chickens. Predisposing factors include coccidiosis/coccidiasis. Inappetance. Mortality may be 5-50%. Signs        Depression. usually around 10%. Infection occurs by faecal-oral transmission. diet (high protein). Spores of the causative organism are highly resistant. Intestinal contents may be dark brown with necrotic material.M. phenoxymethyl penicillin. Treatment Penicillins (e. Post-mortem lesions      Small intestine (usually middle to distal) thickened and distended. 100 ppm). high levels of most growth promotors and normal levels of ionophore anticoccidials also help. neomycin and erythromycin are used in the USA. Diagnosis A presumptive diagnosis may be made based on flock history and gross lesions Confirmation is on the observation of abundant rods in smears from affected tissues and a good response to specific medication.Abubakar. contaminated feed and/or water. Dark coloured diarrhoea. in ducks possibly heavy strains.g. or Bacitracin in feed (e. Immobility.small intestine. Affected birds tend to be dehydrated and to undergo rapid putrefaction.g. Sudden death in good condition (ducks). high viscosity diets (often associated with high rye and wheat inclusions in the diet).

Severe lesions of necrotic enteritis affecting the small intestine of broilers. conjunctivitis in man). sometimes subclinical.production. which is of variable pathogenicity. Signs are typically of disease of the nervous. It is not usually vertical (but chicks may become infected in hatcheries from contaminated shells). It is highly virulent for chickens.Lentogenic .g.Mortality and nervous signs in adult. In many countries local regulations or market conditions prevent the routine use of many of these options. The virus involved is Paramyxovirus PMV-1. Strains can be developed as vaccines. Can affect any age. the upper has formed a thick crust of necrotic material. Newcastle Disease (Paramyxovirus 1) Introduction Paramyxovirus 1 or Newcastle Disease is a highly contagious viral disease affecting poultry of all ages. Affected species include chickens. The sample at the bottom of the picture is still focal.Mild disease.Acute and fatal in chickens of any age causing neurological and some respiratory signs. less for turkeys and relatively apathogenic in psittacines. Four manifestations have been identified:     ND . ND . visitors and imported psittacines (often asymptomatic). pigeons and ducks. Figure 25. Morbidity is usually high and mortality varies 0-100%. respiratory or reproductive systems. ND . Intestinal lesions are absent.Velogenic Viscerotropic (VVND) . Other species can be infected including mammals occasionally (e. fomites. turkeys.Neurotropic Velogenic .Mesogenic . These viruses have sometimes been used as vaccines in previously immunised birds. Transmission is via aerosols. The condition is rarely diagnosed in ducks but is a possible cause of production drops/fertility problems. 103 . ND . Higher mortality is seen in velogenic disease in unvaccinated stock.sometimes called 'asiatic' or exotic. birds.

Necrotic plaques in proventriculus. Pathogenicity evaluated by Mean Death Time in embryos. Paralysis. Inappetance. It is confirmed by isolation in CE.            Sudden Death Depression. Intestinal lesions primarily occur in the viscerotropic form. Nervous signs. Haemorrhage in proventriculus. encephalomyelitis. avian influenza. It is inactivated by temperatures of 56°C for 3 hours or 60°C for 30 min. IFA. antibiotics to control secondary bacteria. and is ether sensitive. formalin and phenol.tracheal or cloacal.The virus survives for long periods at ambient temperature. Differentiate from Infectious bronchitis. Dyspnoea. intestine. Diarrhoea. However it is quite sensitive to disinfectants. post-mortem lesions. encephalomalacia. fumigants and sunlight. Tracheitis. for up to 12 months. the infective dose and the degree of immunity from previous exposure or vaccination. Samples . 104 . HA+. infectious coryza. rising titre in serology. Diagnosis A presumptive diagnosis may be made on signs. Severe drop in egg production. Moult. intracerebral or IV pathogenicity in chicks. pneumovirus infection. Coughing. EDS-76. Signs Signs are highly variable and will depend on the nature of the infecting virus (see above). HI with ND serum or DID (less cross reactions). especially in faeces and can persist in houses (in faeces. acid pH. haemorrhagic disease. intoxications. middle ear infection/skull osteitis. Cross-reactions have mainly been with PMV-3. caecal tonsil. dust etc). laryngotracheitis. Treatment None. Twisted neck. Post-mortem lesions      Airsacculitis.

all-in/all-out production. vaccination. Severe haemorrhagic and necrotic lesions in proventriculus and Peyers patches in the intestines of a broiler chicken suffering from one of the severe forms of Newcastle disease (viscerotropic velogenic). whereas it tends to peak between 6-10 days for chicks that begin eating but then cease. Vaccinal reactions may present as conjunctivitis. Elisa is now also used. especially in breeding birds by the use of routine serological monitoring. 105 . Mortality peaks at 3-5 days for birds that fail to eat at all. Inactivated vaccines have largely replaced the use of live vaccines in lay but they do not prevent local infections. These tests do not directly evaluate mucosal immunity. and occasionally gasping due to a plug of pus in the lower trachea. Use of Mycoplasma gallisepticum free stock under good management reduces the risk of vaccinal reactions. Vaccination programmes should use vaccines of high potency. Morbidity is up to 10% and mortality close to 100%. snicking. The LaSota-type vaccine may even repeated at 35-40 days of age if risk is high. Figure 28. In some countries it has been customary to provide antibiotics prophylactically during periods of anticipated vaccinal reaction. Acute viral infections or heavily contaminated drinking water may have a similar effect to bad management in reducing feed intake. Use of spray application is recommended but it needs to be applied with care to achieve good protection with minimal reaction. HI has been used extensively. It is common to monitor response to vaccination. It is commonest in progeny of young parent flocks (relatively small yolks) or where managers are inexperienced. A typical programme may involve Hitchner B1 vaccine at day old followed by LaSota-type vaccine at 14 days. Non-starter and 'Starve-out's Introduction This is a condition seen worldwide in young chickens and turkeys due to failure to begin normal food consumption. however. which are adequately stored and take into account the local conditions. and is associated with difficulty maintaining brooding temperature and poor management of feeders and drinkers.Prevention Quarantine. To prevent or reduce vaccinal reactions in young chicks it is important that day old have uniform titres of maternal immunity. biosecurity.

Deep Pectoral Myopathy Introduction This condition is so named because it was first identified in adult breeding turkeys in Oregon State. It does not usually cause any mortality or obvious clinical signs and so it is usually identified after slaughter.Signs  Failure to grow. or suffer necrosis. The condition can be reproduced by causing intense exercise of this muscle. Poor development. Gizzard may be impacted with litter. Because it is enclosed in a relatively unyielding membrane. Without adequate blood supply the tissue of the muscle begins to die. Treatment Correction of management problems. Gall bladder distended. Prevention Review brooding management. 106 . any swelling of the muscle tends to cut off the blood supply. Genetics may play a role in that it has been suggested that blood supply to the affected muscles is reduced in some heavy meat type birds. good hygiene and biosecurity in brooding areas to minimise early disease challenges. Oregon Disease . soluble multivitamin supplementation may help. Differentiate from omphalitis/ yolk sac infection. Most organs normal. Post-mortem lesions      Crop empty. good drinking water hygiene. age of collection and weight of hatching eggs. Diagnosis Based on post-mortem lesions. It has since been seen in turkeys. It is caused by a reduction in the blood supply to the deep pectoral muscles. aspergillosis. bile staining of adjacent tissues. nutrition of young parents. in broiler parent chickens and also in large broiler chickens in various places.

The tissue in the centre is dry. with oedema within it and on its surface.Signs  None. It is very difficult to detect affected carcases in standard meat inspection. greenish yellow. artificial insemination in breeding turkeys. If the condition is of over 7 days duration the muscle is dry and often shows greenish tinges. Prevention Avoidance of physical damage of this muscle. A typical case of the chronic stages deep pectoral myopathy in a broiler chicken. weighing birds etc). If inactivated vaccines are administered into the breast muscle it is preferable that they go into the superficial muscle which is better able to cope with swelling. If recent. Treatment Not applicable. Figure 26. in particular excessive exercise. It may also start to be enclosed in a fibrous capsule. Transillumination of the breast may help identify affected carcases and may be worthwhile if the incidence is high. it may become a healed scar. thinning operations in meat birds. the muscle may be swollen and pale. 107 . Diagnosis Lesions. This will normally be due to excessive flapping in association with management activities (e. and flaking. Post-mortem lesions   Acute or chronic necrosis of the deep pectoral muscle on one or both sides. and. If of very long duration.g.

preferably as a flock test comparing results before and after the challenge. Most isolates are oxidase positive and galactosidase positive Serology using Elisa tests has been used. There is some evidence that hatcheries may play a role in the epidemiology. This was first identified as a new disease syndrome of turkeys in Germany in the early 1990s. Infectious Bronchitis). coli infections. sneezing. E. The organism grows slowly producing tiny colonies on blood agar. coli overgrowth may occur. Growth is more rapid and consistent in an anaerobic jar. A range of sero-types have been identified. Post-mortem lesions  Airsacculitis. severe bronchopneumonia. ORT Introduction Ornithobacterium Infection is an infection of chickens and turkeys with the bacterium Ornithobacterium rhinotracheale(ORT). Inoculation of fresh material from a case can reproduce lung lesions similar to those caused by Pasteurella multocida infection in previously uninfected turkeys over 10 weeks of age. Within the poultry house it is likely to be by aerosols. age at infection etc. tracheitis. and E. In broiler chickens its main importance seems to be as a cause of airsacculitis in apparently healthy flocks that is only identified at slaughter. It is a Gram-negative pleomorphic organism. The infection is common in chickens and turkeys. Reduced egg production. The range occurring in turkeys is wider than that seen in chickens. Confirmation is by isolation of the organism. Some uncertainty exists about mechanisms of transmission. Signs    Coughing. Cultures from the trachea of birds showing typical signs are preferred. This can cause significant losses through condemnations. The slow-growing bacterium was named in 1994. ventilation problems. It had been previously isolated in a number of other countries. Diagnosis Clinical signs and lesions. Reduced weight gain.Ornithobacterium Infection. It commonly exacerbates respiratory disease caused by pneumovirus infections in turkeys. direct contact and drinkers. Bordetella aviuminfection. field challenge with respiratory viruses. perhaps through survival of the organism on shell surfaces or shell membranes. 108 . The severity of its effects depends on the pathogenicity of the particular strain and other risk factors such as viral infections. Important cofactors may include respiratory viral vaccines (Newcastle disease.

The lung is solid and covered by pus/ purulent exudate. therapy and vaccination. cost etc. Vaccination of breeder flocks to protect progeny has shown benefits in chickens but. Prevention This is based on good hygiene. Hygiene . Some vaccines seem to have difficulty in producing a longlasting serological response to ORT. Preventative medication with the products listed in the previous section may be beneficial in some circumstances. In France and Belgium most strains were sensitive to enrofloxacin. it requires two doses. also most are sensitive to tiamulin.Treatment The sensitivity of ORT to antibiotic is highly variable. Figure 27. regulation. neomycin and enrofloxacin. Vaccination . Satisfactory disease control depends on good management and biosecurity. Similar lesions may be found in Pasteurellosis. Initially in Germany most strains were sensitive to amoxycillin. An inactivated vaccine is licensed for broiler parents in Europe. Tilmicosin is also effective at 10-20mg/kg and should be used in the early stages of the disease. Severely consolidated lung from an acute ORT infection in 14-week-old turkey growers.there are issues relating to availability. 109 . Routine treatment . ORT is a major problem on multi-age sites.amoxycillin at 250 ppm in water for 3-7 days or chlortetracycline at 500 ppm for 4-5 days. chlortetracycline but not to enrofloxacin.it is very sensitive in vitro to a range of chemicals. Some work has been done on live vaccine in the USA. this is unlikely to work in turkeys. In the USA in 1998 all strains were sensitive to penicillins and many other microbials. though 54% were sensitive to tetracycline. Amoxycillin sensitivity remains good. because of the age of slaughter.

Cage Fatigue Introduction A condition of chickens. 110 . The green discolouration is used to identify carcases that require closer inspection of the other tissues. Predisposing factors include small body size. Enlarged hocks. Turkey Introduction An association has been shown between green discolouration of the livers of turkey growers at slaughter and the occurrence of inflammatory lesions of bones and/or joints. turkeys and ducks seen worldwide and due to Vitamin D or calcium deficiency. Drop in production. Diagnosis Lesions. Prevention Unknown. Birds rest squatting.only identified at slaughter. Birds go off legs. Post-mortem lesions  Green discolouration of the liver at slaughter. Soft-shelled eggs. Treatment Not applicable . Gram-variable pleomorphic bacteria have been isolated from affected livers and bones. high production. Signs  None. Signs        Lameness. Osteoporosis. Soft bones and beak.Osteomyelitis Complex.

place on litter. Epiphyses of long bones enlarged. spondylitis. Diagnosis History. Treatment Over-correct ration vitamin D.M. proper Ca and P levels and ratio. signs. Coughing. Parathyroids enlarged. depending on the species affected and whether infection is complicated by other factors and diseases. Inappetance. calcium carbonate capsules. turkeys and passerine cage birds with Paramyxovirus PMV-2 results in disease with variable mortality.Yucaipa Disease Introduction An infection of chickens. 111 . Paramyxovirus 2 .Tahir Post-mortem lesions      Bones soft and rubbery. whereas turkeys are more severely affected. Beak soft. skeletal size and mineral content at point of lay are critical. Transmission is by wild birds and fomites. antioxidants. In chickens it is usually mild. Drop in egg production. Signs     Depression. Differentiate from Marek's disease. bone ash. Vertical transmission does not usually occur. Wild birds are believed to be especially important. As birds progressively mobilise skeletal calcium for egg production through lay. Post-mortem lesions  Not characteristic. lesions. Beading and fracture of ribs.Abubakar. Prevention Supplementation of vitamin D.

Signs        Depression. Vertical transmission does not usually occur. Diagnosis Isolation in CE. including wild bird contact and fomites. Post-mortem lesions  No specific lesions. The infection is transmitted by birds. haemorrhagic disease. HI with ND serum or DID (less cross reactions). Inappetance. Coughing. Prevention Quarantine. biosecurity. Treatment No specific treatment. Mortality is usually low in poultry. Loss of shell pigment Nervous symptoms (psittacines). laryngotracheitis. occasionally chickens and psittacine cage birds. HA+. antibiotics to control secondary bacteria. 112 . High mortality (cage birds). EDS-76. IFA. Paramyxovirus-3 Introduction Paramyxovirus PMV-3 infects turkeys.Diagnosis Isolation in CE. Drop in egg production (turkeys). Differentiate from Infectious bronchitis. Treatment No specific treatment. antibiotics to control secondary bacteria. HA+. all-in/all-out production. HI with ND serum or DID (less cross reactions). IFA.

A less acute form of the disease appears to produce more of a lingering mortality. Vertical transmission does not usually occur. A range of 113 . antibiotics to control secondary bacteria. Paramyxovirus-6 Introduction Paramyxovirus PMV-6 infection of turkeys. Post-mortem lesions  No specific lesions. Mild respiratory signs. The infection is transmitted by birds. It is an infectious and transmissible cause of sudden increases in mortality in turkeys between 7 and 28 days of age. HA+. Signs   Reduction in egg production. HI with ND serum or DID (less cross reactions). IFA. Treatment No specific treatment. biosecurity. Diagnosis Isolation in CE. Vaccination has been used in turkeys but may not be cost-effective. biosecurity. PEMS and Spiking Mortality of Turkeys Introduction Poult Enteritis and Mortality Syndrome (PEMS) was first identified in high density turkey producing areas of the South Eastern USA in 1991. In both cases mortality can be high and can be associated with a marked depression in growth. all-in/all-out production. Mortality is 0-5%.Prevention Quarantine. Prevention Quarantine. including wild bird contact and fomites. all-in/all-out production. The infection is inapparent in ducks and geese.

This syndrome is clearly distinguished from typical viral enteritis in young turkeys because of the high mortality and severe growth depression. Muscle atrophy. Reduced feed consumption and growth. Good quality diets of a suitable form . Weight loss. Increased water consumption. Droppings watery. Pendulous Crop Introduction A complex condition of turkeys and chickens associated with coarse fibrous feed. Emaciation. huddling. Post-mortem lesions      Dehydration. Diagnosis Signs. All-in/all-out production. Wet litter.5-8% will encourage feed intake and recovery. lesions. Picking at feed. 114 . Treatment A range of antibiotics and arsenicals have been used to control the bacterial component of this condition. eating litter. Prevention Biosecurity to reduce the introduction of new infections into brooding facilities. multivitamins and milk replacer products are helpful for nutritional support in the acute phase. Fluoroquinolone antimicrobials appear to be especially effective.mash and poor quality crumbles increase risk. pale brown.viruses have been isolated from affected flocks. Overdistension of crop in young birds because of an interruption in feed supply may predispose. Liquid intestinal contents. Effective terminal disinfection. Caseous cores in bursae (late in the process). To replicate the condition in full it appears to be necessary to include bacteria in the inoculum. Signs         Initial hyperactivity and increased vocalisation. Increasing weakness. seeking heat. A highly digestible diet with fat at 7.

Lack of muscle tone. Signs    Anaemia. lesions. ulceration.Signs  Enlargement of crop. Tetrameres and Cyrnea are nematodes. They are found in the mucosa of crop and proventriculus causing mainly inapparent infections. Infection is by the oral route on exposure to the intermediate hosts. Emaciation in heavily infected young chicks (Tetrameres). Post-mortem lesions  Inflammation. 115 . if these can be identified. necrosis. have ulcerations and sometimes mycosis. Proventricular Worms Introduction Dispharynx. Diagnosis Macroscopic examination of lesions. spiruroid worm parasites of poultry and game birds. Diagnosis Signs. Post-mortem lesions    Crop distended with feed. haemorrhage. and thickening of mucosa of proventriculus. Diarrhoea. may be impacted. identification of worms. Treatment None. grasshoppers and cockroaches. Prevention Remove predisposing factors. including crustaceans. Crop contents semi-liquid and foul smelling.

other poultry. 116 . duck viral hepatitis. Diarrhoea. tuberculosis. Signs     Weakness. isolation. Sometimes sudden death. colibacillosis. sulphonamides in feed. Prevention Prevention of access to intermediate hosts. Differentiate from Duck viral enteritis. Ruffled feathers. Pseudotuberculosis Introduction An infection of ducks. Diagnosis Lesions.Treatment Not usually required. rodents and man with the bacterium Yersinia pseudotuberculosis. 'hardening off'. The disease has a mortality of 5-75%. Treatment Tetracyclines. wild birds. In peracute disease the only lesion may be enteritis. Prevention Good husbandry and hygiene. coccidiosis. adequate protection. Post-mortem lesions  Miliary lesions in a variety of organs but especially in the liver.

Dark comb and wattles. Watery diarrhoea. Prevention Good management. It is associated with hot weather. Crop distended. Avian Monocytosis Introduction A sudden onset condition of chickens early in lay with high morbidity and a mortality of 050%. Pancreas chalky. Post-mortem lesions         Dehydration. Dehydration.Abubakar. Loss of appetite. coccidiosis. lesions.Tahir Pullet disease. molasses. vibriosis. IBD and typhoid. capillariasis. mucoid casts in intestine. water deprivation.M. Drop in egg production. Affected birds have an increase in circulating monocytes in their blood. Bluecomb. antibiotics. Skeletal muscle necrosis. elimination of other causes. Diagnosis History. Skin cyanosis of head. Signs        Depression. toxin and possibly a virus infection. Treatment Adequate water supply. diet and water supply. Kidneys swollen. Differentiate from fowl cholera. It was commonly reported prior to 1960 but is now rare. Liver swollen with foci. hygiene. Crop distension. Catarrhal enteritis. 117 . multivitamins in water.

For northern fowl mite it is essential to apply approved insecticides to the affected birds. organophosphates. fumigation and insecticide treatment at turnaround. vegetable oil and mineralbased products (both liquid sand dusts) have been used to control red mites in the environment. May cause anaemia and death in young birds. citrus extracts. Pale comb and wattles. Prevention Thorough cleaning. Staff complaints . Spots on eggs.itching. cracks. Treatment Pyrethroids. However keep in mind that the majority of the population of Dermanyssus is in the environment so it is necessary to monitor infection levels on feeder tracks. in nest boxes. Drop in egg production. Ornithonyssus bursae. Filling of cracks and crevices. crevices etc. feeds by sucking blood. Birds restless. Post-mortem lesions  Anaemia. which are external parasites of chickens and turkeys. carbamates.Red Mite and Northern Fowl Mite Introduction Arachnid mites. the Common Red Mite. the Northern Fowl Mite spends its entire life cycle on the bird and can multiply more rapidly as a result. 118 . Diagnosis Number and type of mites identified. Signs        Presence of grey to red mites up to 0. and good design of new equipment to limit harbourages for red mites. Dermanyssus gallinae. Effective monitoring of mite numbers and implementation of control measures before birds are heavily infested improves control.7 mm. mainly at night and may transmit fowl cholera and other diseases. Loss of condition.

E. Lentogenic Newcastle disease virus. may act as 119 .Tahir Respiratory Adenovirus Infection. Infected birds may remain carriers for a few weeks. The virus grows well in tissue culture (CE kidney. Dust. Transmission may be vertical and lateral. intranuclear inclusions in liver. Respiratory Disease Complex Introduction Respiratory infections in chicken and turkeys are seen worldwide but especially in temperate poultry-producing areas in winter months. lesions. Post-mortem lesions  Mild catarrhal tracheitis. Diagnosis History. at least 12 sero-types have been described and these may be isolated from healthy chickens. chloroform. Signs  Mild snick and cough without mortality. ammonia and other gases. Avian pneumovirus. Opinions vary as to whether adenovirus can be characterised as a primary respiratory pathogen. A number of respiratory viruses (Infectious Bronchitis. prevention of immunosuppression. vaccinal and field strains) and bacteria (Ornithobacterium rhinotracheale. Treatment None. The virus is generally resistant to disinfectants (ether. formaldehyde and iodides work better. It may occur as an exacerbating factor in other types of respiratory disease. coli) may be involved. pH).Abubakar. temperature.M. CE liver). and other factors associated with poor ventilation. Prevention Quarantine and good sanitary precautions. and by fomites. 'Mild Respiratory Disease' Introduction An adenovirus infection of chickens with a morbidity of 1-10% and a mortality of 1-10%.

be challenged by some of these pathogens). Diagnosis Lesions. Nasal exudate. Signs       Snick. of course. Figure 29. Severe airsacculitis of thoracic air sacs in a broiler close to slaughter. carefully applied appropriate viral vaccines. There is also percarditis evident (at top right). serology. Rattling noises. Post-mortem lesions    Severe tracheitis with variable exudate . Airsacculitis. Head swelling. response to environmental changes.predisposing factors. Pericarditis. mortality 5. Treatment Antimicrobial treatment of specific bacterial infections. Prevention Effective ventilation. Differentiate from Chronic Respiratory Disease (Mycoplasmosis).catarrhal to purulent. Sneezing. Morbidity is typically 10-20%. and have been cut into to reveal a cheesy (caseous) mass of pus. Conjunctivitis. sanitation of drinking water.10%. If condemned birds are included mortality may be more than 10%. 120 . The air sacs are thickened and congested. Given that many flocks are vaccinated it is necessary to establish normal serological response in vaccinated flocks in the absence of disease (some of which may.

Signs     There may be no obvious signs. Reticuloendotheliosis. Both tracheas were congested and the upper sample had mucopurulent material in the lumen. Leg weakness. Severe tracheitis is broilers with respiratory disease complex. spleen and kidney. ducks. 121 . and the infection can be spread by mosquitoes or in contaminated Marek's disease vaccines. Sometimes nodules in intestine and caecae. usually higher in females than males. turkeys. Post-mortem lesions    Neoplastic lesions in liver.Figure 30. There is an incubation period of 5-15 days. Treatment None. Diarrhoea. Sometimes enteritis and proventriculitis (especially in broilers infected with contaminated Marek's disease vaccine). Diagnosis Pathology. Lympoid Tumour Disease Introduction A retrovirus infection of chickens. geese. chick inoculation. A gradual increase in mortality and poor growth in broilers may be the main signs. Marked stunting when Marek's disease vaccine is contaminated. and quail with morbidity up to 25%. Transmission is lateral and possibly transovarian.

Soft bones and beak. Signs        Lameness. lesions. or Vitamin D or 25-hydroxy vitamin D in drinking water. Avoidance of contamination of live vaccines is the main control measure practised.Prevention Formal control programmes have not been documented as the condition is sporadic and relatively self-limiting. Treatment Over-correct ration with three times vitamin D for 2 weeks. Rickets (hypocalcaemic) Introduction Vitamin D deficiency or phosphorus/calcium imbalance is seen in chickens. Birds go off legs. antioxidants. Post-mortem lesions       Bones soft and rubbery. signs. Hock swelling. Epiphyses of long bones enlarged. Prevention Supplementation of vitamin D. Femoral Head Necrosis. Differentiate from Encephalomalacia. Parathyroids enlarged. Reduction in bodyweight. Beading and fracture of ribs. Diagnosis History. Beak soft. Growth plates widened and disorganised. 122 . proper calcium and phosphorus levels and ratio. turkeys and ducks worldwide. Poor growth. Birds rest squatting.

turkeys and duck is seen worldwide. Growth plates widened and disorganised. Poor growth. Epiphyses of long bones enlarged. antioxidants. proper calcium and phosphorus levels and ratio. Post-mortem lesions       Bones soft and rubbery. signs. Enlarged hocks. Beading and fracture of ribs. Diagnosis History. Signs         Lameness. Intestinal diseases may reduce absorption. Beak soft. This has led feed manufacturers to try various approaches to reduce added phosphorus in diets. Birds rest squatting. Parathyroids enlarged. Soft bones and beak. lesions (analyse Vitamin A or manganese as a guide to premix inclusion). or vitamin D in drinking water. Reduction in bodyweight.Abubakar. Hock swelling.Tahir Rickets (hypophosphataemic) Introduction Phosphorus deficiency in chickens. Prevention Supplementation of Vitamin D.M. 123 . Even subclinical levels of this condition can predispose to Femoral Head Necrosis. Some countries have regulations governing the use of phosphorus in fertiliser with a view to reducing water pollution. Treatment Over-correct ration with 3 times vitamin D for 2 weeks. Birds go off legs.

large . columbae in pigeons. It is not known if vertical transmission occurs though virus has been occasionally isolated from embryonated eggs. Diagnosis Demonstration of virus (PAGE.submit 6 x . Adult birds can tolerate burdens asymptomatically. partridges and pigeons.M. The 124 . Post-mortem lesions  Viruses replicate mainly in the mature villous epithelial cells.Tahir Rotavirus Infection Introduction Rotavirus infection is seen in chickens. The life cycle is similar to that illustrated in the section on the caecal worm Heterakis. guinea fowl. galli in fowl. stout white worms up to 12 cms in length. The route of infection is oral usually by direct ingestion of the embryonated egg and there is a 5-10-week prepatent period. dissimilis in turkeys. Signs  Diarrhoea.Ascaridia Introduction Ascaridia sp. Control of secondary bacterial enteritis may require antimicrobial medication. and A.5 g faeces). pheasants. Roundworm. The route of infection is oral and maximum viral excretion occurs 2-5 days post infection. Virus may be found in asymptomatic birds.Abubakar. turkeys. A. shorter in young birds. Use of a good electrolyte solution is beneficial in the acute stage of infection. Treatment No specific treatment for this infection. are nematode worm parasites. Prevention Good hygiene in brooding areas. seen worldwide. The parasite species vary: A. except that the adults reside in the small intestine and earthworms are not significant paratenic or transport hosts. electron microscopy or Elisa on intestinal contents .

Worms up to 12 cm in length in duodenum and ileum. Poor growth. Listlessness.parasites may be transported by grasshoppers and earthworms and are resistant to environmental effects. pasture rotation and regular treatment. In the bottom left quadrant there are also some immature worms. levamisole. Signs      Loss of condition. A collection of mature roundworms (Ascaridia galli) recovered from the small intestine of a layer chicken in rear. oval smooth-shelled nonembryonated eggs in faeces. piperazine as locally approved. Diagnosis Macroscopic examination with identification of worms. especially for young birds. Figure 31. 125 . Prevention Prevention of contamination of feeders and drinkers with faeces. Post-mortem lesions   Enteritis. Treatment Flubendazole. Diarrhoea. Wasting. mainly in young birds.

Infections still occur worldwide in non-commercial poultry but are rare in most commercial systems now. game birds. Broiler chickens have an avascular area of tendon just above the hock that is the usual site of rupture. canaries and bullfinches.Abubakar.Tahir Ruptured Gastrocnemius Tendon Introduction This is a condition causing severe lameness in roaster type meat chickens and more rarely in turkeys. guinea fowls. Prevention Establishment of a steady growth profile. Affected birds should be culled humanely as soon as they are identified. Histology may be helpful in determining if there is an underlying inflammatory process. Reoviral or staphylococcal arthritis or tenosynovitis may predispose but many cases have no evidence of an inflammatory response. Ruptures of ligaments and joints are also occasionally seen. This can cause mortality in birds of any age. parrots. Chickens are most commonly affected but it also infects turkeys.M. Salmonella Gallinarum. The bird may have the hock dropped to the floor. Treatment None. Post-mortem lesions  The fresh lesion contains a haematoma with the end of the ruptured tendon within or adjacent to it. Avoidance of physical stresses on the musculoskeletal system through careful handling as well as careful design and layout of equipment. Fowl Typhoid Introduction Disease caused by one of the two poultry-adapted strains ofSalmonella bacteria. If there is a greenish tinge to the area of swelling it occurred a few days previously. Signs   Severe lameness. 126 . Diagnosis Signs and lesions are obvious. Salmonella Gallinarum. sparrows. Broiler parents and brown-shell egg layers are especially susceptible.

Enteritis of anterior small intestine.Morbidity is 10-100%. As with other salmonellae. Tube and rapid plate agglutination tests have been the standard serological tests for many years but have only been validated for chickens. The bacterium is fairly resistant to normal climate. egg eating etc. Transmission may be transovarian or horizontal by faecal-oral contamination. both live (usually based on the Houghton 9R strain) and bacterins. Treatment Amoxycillin. pullorum disease and coli-septicaemia. Enrichment procedures usually rely on selenite broth followed by plating on selective media. potentiated sulponamide. Post-mortem lesions     Bronzed enlarged liver with small necrotic foci. Yellow diarrhoea. In clinical cases direct plating on Brilliant Green. Anaemia. recovered birds are resistant to the effects of infection but may remain carriers. even in adults. Prevention Biosecurity. LPS-based Elisa assays have been developed but not widely applied commercially. Signs       Dejection. The route of infection is oral or via the navel/yolk. McConkey and non-selective agar is advisable. Thirst. Vaccines for fowl typhoid have been used in some areas. but is susceptible to normal disinfectants. clean chicks. and/or congestion. 127 . Differentiate from Pasteurellosis. fluoroquinolones. Reluctance to move. Inappetance. Diagnosis Isolation and identification. tetracylines. Ruffled feathers. mortality is increased in stressed or immunocompromised flocks and may be up to 100%. surviving months. Engorgement of kidneys and spleen.

guinea fowls. It still occurs worldwide in noncommercial poultry but is now rare in most commercial systems.Figure 32. Gasping. usually brown-shell egg layers. Depression. this usually only causes mortality in birds up to 3 weeks of age. pale and shows focal necrosis. game birds. surviving months but is susceptible to normal disinfectants. The bacterium is fairly resistant to normal climate. Lameness. Closed eyes. Similar lesions can be seen in Pullorum Disease and with other causes of septicaemia in young chicks. Transmission may be transovarian or horizontal mainly in young birds and may sometimes be associated with cannibalism. White diarrhoea. Loud chirping. but also infects turkeys. Morbidity is 10-80%. in young broiler chickens. ostriches and peafowl. The route of infection is oral or via the navel/yolk. sparrows. Salmonella Pullorum. Bacterial septicaemia caused by Salmonella Gallinarum. the one on the right is slightly enlarged. 'Bacillary White Diarrhoea' Introduction Disease caused by one of the two poultry-adapted strains ofSalmonella bacteria. Ruffled feathers. mortality is increased in stressed or immunocompromised flocks and may be up to 100%. Occasionally it can cause losses in adult birds. parrots. Vent pasting. ring doves. Signs          Inappetance. Salmonella Pullorum. 128 . It affects chickens most commonly. The liver on the left is normal. Pullorum Disease.

S. but S. Derby. Prevention Eradication from breeder flocks. Paratyphoid. Splenomegaly. Pullorum. gizzard wall and heart. As with other salmonellae. Urate crystals in ureters. Many species are intestinal carriers and infection is spread by faeces. In clinical cases direct plating on Brilliant Green. poteniated sulponamide. Vaccines are not normally used as they interfere with serological testing and elimination of carriers. tetracylines. Diagnosis Isolation and identification. McConkey and non-selective agar is advisable. Caecal cores. The route of infection is oral and transmission may be vertical as a result of shell contamination. Certain sero- 129 . Enteritidis andS. Typhimurium (which are considered separately). and also other than S. liver. Intestinal or caecal inflammation.Post-mortem lesions      Grey nodules in lungs. other enterobacteria. Differentiate from Typhoid. S. They infect chickens. recovered birds are resistant to the effects of infection but may remain carriers. S. Even if these infections do not cause clinical disease. Paratyphoid Infections Introduction Salmonellae bacteria other than the species specific sero-typesS. S. Enrichment procedures usually rely on selenite broth followed by plating on selective media. chilling and omphalitis Treatment Amoxycillin. in the environment or in rodent populations. Bredeney are among the more common isolates. Anatum. Montevideo. Salmonellosis. their presence may be significant with respect to carcase contamination as a potential source of human food poisoning. it may become established on certain farms. S. paracolon. Sero-types vary. turkeys and ducks worldwide. fomites and feed (especially protein supplements but also poorly stored grain). Regardless of the initial source of the infection. Morbidity is 0-90% and mortality is usually low. are capable of causing enteritis and septicaemia in young birds. fluoroquinolones. Newport. Gallinarum.

amoxycillin. Ruffled feathers. Pericarditis. Temperatures of around 80°C are effective in eliminating low to moderate infection if applied for 1-2 minutes. Chemotherapy can prolong carrier status in some circumstances. neomycin. Vent pasting. other enterobacteria. but are susceptible to disinfectants that are suitable for the particular contaminated surfaces and conditions. Unabsorbed yolk. other bacterial infections and ornithosis (in ducks). Post-mortem lesions         In acute disease there may be few lesions.types are prone to remain resident in particular installations (e. tetracyclines. chilling. Focal necrotic intestinal lesions. fluoroquinolones. Diagnosis Isolation and identification. Signs        Signs are generally mild compared to host-specific salmonellae.g. Enteritis. Predisposing factors include nutritional deficiencies. Enrichment media such as buffered peptone followed by selective broth or semi-solid media (e. applied at sufficient concentrations. Senftenberg in hatcheries). Loss of appetite and thirst. Differentiate from Pullorum/Typhoid. However this has the potential to reveal the presence of salmonellae that are irrelevant to the clinical problem under investigation. Foci in liver. especially in dry dusty areas. The bacteria are often persistent in the environment. 130 . Good management.g. Rappaport-Vassiliadis) followed by plating on two selective media will greatly increase sensitivity. Closed eyes. Treatment Sulphonamides. S. Diarrhoea. Dejection. Dehydration. This approach is often used in the heat treatment of feed. inadequate water. In clinical cases direct plating on Brilliant Green and McConkey agar may be adequate. or absent. Cheesy cores in caecae.

mills. The route of infection is oral. Routine monitoring of breeding flocks. S. The bacteria are often persistent in the environment. Temperatures of around 80°C are effective in eliminating low to moderate infection if applied for 1-2 minutes. Feed and feed raw material contamination is less common than for other sero-types. breeding and grow-out farms. Many infected birds are culled and others are rejected at slaughter. elimination of resident infections in hatcheries. These are the predominant sero-types associated with human disease in most countries. hatcheries and feed mills is required for effective control. especially phage type 4. especially in dry dusty areas. This approach is often used in the heat treatment of feed. fomites and on eggshells.Typhimurium has remained relatively stable though the spread of the highly antibiotic-resistant strain DT104 in various farmed species gives some reason for concern. secondly. good feed. care in avoiding damage to natural flora. many species are intestinal carriers and infection may be carried by faeces. Salmonella Enteritidis. competitive exclusion. has become much more common in both poultry and humans since the early 80s. all-in/all-out production. Infection results in a strong immune response manifest by progressive reduction in excretion of the organism and reduced disease and excretion on subsequent challenge. Salmonellosis. Vaccines are not generally used for this group of infections. inadequate water and other bacterial infections. applied at sufficient concentrations. 131 . because there are differences in the epidemiology as compared to other salmonellae. Enteritidis and S. fumigate eggs. Infections in chickens.Prevention Uninfected breeders. Vertical transmission may be either by shell contamination or internal transovarian contamination of yolk. these bacteria are often specifically cited in zoonosis control legislation. and.Typhimurium are presented separately from other sero-types of Salmonella because. Typhimurium infections Introduction Salmonella Enteritidis and S. clean nests. but are susceptible to disinfectants that are suitable for the particular contaminated surfaces and conditions. The prevalence of S. Predisposing factors include nutritional deficiencies. on the one hand. chilling. turkeys and ducks cause problems worldwide with morbidity of 0-90% and a low to moderate mortality.

Focal necrotic intestinal lesions. Enteritis. care in avoiding damage to natural flora. Differentiate from Pullorum/Typhoid. other enterobacteria such as E. hatcheries and feed mills is required for effective control.Pullorum serum agglutination tests. neomycin. S. Stunting in older birds. Rappaport-Vassiliadis) followed by plating on two selective media will greatly increase sensitivity. Post-mortem lesions           In acute disease there may be few lesions. all-in/all-out production. Diarrhoea. Ruffled feathers.g. Treatment Sulphonamides. Early depletion of infected breeding stock is required in some countries such as those of the European Union. Routine monitoring of breeding flocks. Pericarditis. Infection 132 .Signs        Dejection. fumigate eggs. Cheesy cores in caecae.Enteritidiscauses cross-reactions which may be detected with S. Chemotherapy can prolong carrier status in some circumstances. However this has the potential to reveal the presence of salmonellae that are irrelevant to the clinical problem under investigation.E. Prevention Uninfected breeders. Misshapen ovules in the ovaries in S. Unabsorbed yolk. coli. Lost of appetite and thirst. breeding and grow-out farms. It is possible to detect reactions with specific antigens in agglutination tests but competitive and direct Elisa tests are more commonly used today. clean nests. elimination of resident infections in hatcheries. Good management. infection Diagnosis Isolation and identification. amoxycillin. tetracyclines. In clinical cases direct plating on Brilliant Green and McConkey agar may be adequate. Closed eyes. Foci in liver. fluoroquinolones in accordance with the sensitivity. competitive exclusion. Dehydration. good feed. Perihepatitis. mills. Enrichment media such as buffered peptone followed by selective broth or semi-solid media (e. Vent pasting.

Anything that damages the epithelium or disturbs normal oviduct motility is likely to increase the likelihood of salpingitis. Distended abdomen. Salpingitis Introduction Salpingitis is an inflammation of the oviduct. are especially prone to increasing salpingitis. Typhimurium infection. Vaccines are increasingly being used for S. which normally has many millions of potentially pathogenic bacteria. The oviduct is a hollow tube joining the normally sterile environment of the body cavity with the cloaca. 133 . It is a complex condition of chickens and ducks associated with various infections including Mycoplasma and bacteria (especially E. Systemic viral infections that cause ovarian regression or damage to the oviduct or cloaca. Enteritidis and S. Post-mortem lesions    Slight to marked distension of oviduct with exudate. Bacteriology of oviduct. coliand occasionally Salmonella spp.results in a strong immune response manifest by progressive reduction in excretion of the organism and reduced disease and excretion on subsequent challenge. Diagnosis Use the signs to select birds for culling and post-mortem investigation. Infection may spread downwards from an infected left abdominal air sac. or may proceed upwards from the cloaca. May form a multi-layered caseous cast in oviduct or be amorphous.). Lesions. The control of infection in this area is probably achieved by ciliated epithelium that mostly wafts a carpet of mucus towards the cloaca. Signs      Sporadic loss of lay. Peritonitis. Death. Some birds may 'lay' a caseous mass of pus (which may be found in a nest or on the egg belt). leaking urates. both inactivated (bacterins) and attenuated live organisms. Damaged vents.

Treatment Multivitamins. 134 . Use of a suitable antimicrobial may be beneficial for birds in the early stages and if associated with efforts to minimise risk factors. immunise effectively against respiratory viral pathogens common in the area.Treatment Birds with well-developed lesions are unlikely to respond to medication. exclusion of other problems. releasing poults into larger areas and in handling heavier birds. Diagnosis Clinical examination. Post-mortem lesions  None. Shaking or quivering of legs after rising. aspirin may be helpful if locally approved. Morbidity is 10-20%. Prevention Control any septicaemia earlier in life. Signs   Stand on toes shaking. Prevention Care in transport of brooded poults. possibly associated with tendon injury. Shaky Leg Syndrome Introduction A condition of turkeys with a course of often 3-4 weeks. use healthy parent flocks.

This appears to be a multifactorial condition. Birds in good condition die after showing neurological signs. Avoidance of physical stress. Excess fluid in lower small intestine and caecae. Death.Spiking Mortality of Chickens Introduction This is a condition characterised by a sudden increase in mortality in young. Post-mortem lesions    Mild enteritis. Treatment Leave affected chicks undisturbed. Provide multivitamins. Mortality drops off as sharply as it started. probably because they are growing faster. Paralysis. Avoidance of interruptions in feed supply. In order to reproduce the typical condition the affected birds are subject to 4 hours without feed and then a mild physical stress such as spraying with cool water. 135 . typically 7-14day-old. Signs      Tremor. Minimise stress. Diagnosis Pattern of mortality. Feed intake. Prevention Good sanitation of the brooding house. Coma. Filtered intestinal contents from affected flocks appear to be capable of reproducing the condition. rapidly growing broiler chickens. Orange mucoid droppings. suggesting a viral component. Signs and lesions. Dehydration. electrolytes and glucose solution to flock. and/or carbohydrate absorption are disturbed resulting in a hypoglycaemia. Males are more susceptible than females.

It is transmitted by arthropods. Cyanosis. Prevention Control vectors. reduced egg production. Often diarrhoea with excessive urates. pheasants. isolate in chicken eggs or chicks or poults. is an intestinal spirochaete that can be associated with inflammation of the large intestine in a broad range of mammals and birds. 136 . vaccines in some countries. Necrotic foci. Thirst. and occasionally by infected faeces. Diagnosis Haematology. Drops in egg production may be seen in both systemic and intestinal forms Post-mortem lesions      Marked splenomegaly. Liver enlarged with small haemorrhages. grouse and canaries with morbidity and mortality up to 100%. Argas persicus. turkey. previously known as Serpulina pilosicoli. Signs       Depression. ducks. Weakness and progressive paralysis.g. and egg soiling in chickens. Treatment Various antibiotics including penicillin.Spirochaetosis Introduction The bacterium Borrelia anserina infects chickens. Mucoid enteritis. geese. It has been associated with typhilitis. The bacterium is poorly resistant outside host but may be carried by Argas persicus for 430 days. Brachyspira pilosicoli. diarrhoea. e. Spleen mottled with ecchymotic haemorrhages.

Post-mortem lesions  Anterior-posterior rotation of the bodies of the last or penultimate thoracic vertebrae resulting in scoliosis just anterior to the kidney. legs extended forward.Tahir Spondylolisthesis. Use of wings to help in walking. Signs    Sitting on hock or rumps. May walk backwards. with rotation of the body of the vertebra and the pinching of the spinal column that causes paralysis. 137 . Treatment None. That on the left shows the typical lesion of spondylolisthesis.Abubakar. Kinky-back Introduction A complex condition of broiler chickens with a morbidity of 1-5% and low mortality associated with rapid growth and possibly having a genetic component. The sample on the right is normal. Diagnosis Symptoms. Prevention Selection for satisfactory conformation in primary breeding. Figure 33. These are cross-sections of the spinal column of 4-5-weekold broilers.M. lesions.

Staphylococcal Arthritis.Abubakar. avoidance of excessive hatching egg storage. The type of chick box liners and the feeding papers used in the brooding house can also influence the occurrence of the condition. Post-mortem lesions  Gross lesions are not usually evident. aureus and seen in chickens and turkeys worldwide. Treatment None. Damaged skin due to nutritional deficiencies (such as of biotin) may also be a point of entry. Prevention All measures that improve chick vitality at hatching are beneficial in reducing this problem. Infection is usually by the respiratory route with an incubation period of 2-3 days seen after artificial infection. mainly S. 138 . These include good breeder nutrition.Tahir Spraddle Legs or Splay Leg Introduction Occurs in all species in the recent hatchling. either accidental or induced by interventions such as beak trimming. Bumble Foot Introduction Caused by Staphylococcus bacteria. Morbidity is usually low and mortality 0-15% though affected birds will often be culled on humane grounds. and careful monitoring of incubation conditions. and toe trimming may be a portal of entry with subsequent spread via the bloodstream to the typical sites of lesions. Wounds. Diagnosis Clinical signs.M. Signs  Legs splay and chick is unable to stand. Staphylococcosis.

especially M. Low mobility. Signs      Ruffled feathers. Infected joints may have clear exudate with fibrin clots.. Mycoplasma spp.. Treatment Antibiotics. low stress and prevention of immunosuppression from any cause will all tend to help. and imunosuppression. Predisposing factors include reovirus infection. in accordance with sensitivity. This condition is a cause of sudden deaths in ducklings of 2-3 weeks of age. Prevention Good hygiene in the nest. synoviae. Salmonella spp. particularly of parent birds. toe clipping). Streptococcus bovis Septicaemia Introduction An infection of ducks with the bacterium Streptococcus bovis. Competitive exclusion with a non-pathogenic Staphylococcushas been shown to be effective (no commercial products yet available based on this technology). Post-mortem lesions   Tenosynovitis. trauma.g.Transmission occurs in the hatchery and in the general farm environment. and by fomites. e. most commonly in the plantar area of the foot or just above the hock joint. Differentiate from septicaemia or tenosynovitis due to Colibacillosis. Diagnosis Lesions. the hatchery and in any intervention or surgery (processing. Lameness. Possibly vaccination against reovirus infection. Recovered birds may have some immunity but vaccination with staphylococci has not been found to be helpful in preventing the disease to date. isolation and identification of pathogen. 139 . This may progress to abscess formation in these areas. Some sudden deaths from acute septicaemia if very heavy challenge. Good management. Swollen above the hock and around the hocks and feet. chronic stress.

Post-mortem lesions     Beak cyanosis. Prevention Good husbandry and hygiene. possibly metabolic.Signs   Sudden deaths. Sudden Death Syndrome. Serum accumulation in lung (may be little if examined shortly after death). It can be induced by lactic acidosis and about 70% of birds affected are males. Treatment Amoxycillin. Affected well-grown birds may appear to have died from smothering. Signs  Sudden death in convulsion. Haemorrhages in muscles and kidneys. Livers heavier than those of pen-mates (as a percentage of bodyweight. 140 .affected birds respond well to saline injection and will actively seek out salt scattered in the litter. Diagnosis History. extra care in the immediate post-brooding period. the ventricles are empty. Lung congestion and oedema. Leg weakness or incoordination in a few birds. Liver congestion.). 'Flipover' Introduction A condition of broiler chickens of unknown cause. lesions. isolation. Post-mortem lesions      Intestine filled with feed. Splenic hyperplasia. most are found lying on their back. The atria of the heart have blood. Sodium deficiency can appear very similar at about the same age .

Diagnosis Identification of the presence of the worms at post-mortem examination. Signs  It is doubtful if any signs are produced under most circumstances. Tapeworms. Treatment None possible. Treatment Flubendazole is effective at a 60 ppm in diet. Prevention Lowering carbohydrate intake (change to mash). or birds' access to them. use of dawn to dusk simulation and avoidance of disturbance. lighting programmes. Most have intermediate invertebrate hosts such as beetles or earthworms. Post-mortem lesions  Occupy space in intestine and create small lesions at point of attachment. feed restriction.Diagnosis Birds found on back with lack of other pathology. 141 . they may not be host specific. Prevention Control the intermediate hosts. Check your local regulations. Cestodes Introduction Cestodes are tapeworms that are seen in many species. low intensity light. however it may not have a zero withdrawal in commercial egg layers.

Swelling and bowing in the region of the knee joints. mild lesions may require histology to distinguish from other problems. Microscopically . Diagnosis Gross pathology. Lameness. in decreasing order of frequency. Signs    There are usually no signs unless the condition is severe. Treatment None. Post-mortem lesions   Plug of cartilage in proximal end of tibia. 142 . distal tibia. chloride levels and acid/base balance. TD Introduction A complex condition seen in chickens. and proximal metatarsus. Mature tapeworms with their heads (scolices) embedded in the intestine. Differentiate from rickets.Figure 34. Tibial Dyschondroplasia. modifications of calcium and phosphorus ratios. It may be associated with rapid growth and have a nutritional factor.a mass of avascular cartilage with transitional chondrocytes. small ovoid lacunae and more matrix than normal. Vitamin D3 supplementation. Lixiscope may identify in vivo as early as 2 weeks of age. Prevention Genetic selection using the Lixiscope to identify bone phenotype. turkeys and ducks.

Diagnosis Identification of the presence of the parasites. Signs       Anaemia. with 143 . and may also transmit spirochaetosis and Pasteurella infection. and is also found on mammals.Abubakar. spends little time on host. These parasites are more likely to be a problem of small scale poultry production in the tropics. Skin blemishes. than in commercial poultry in temperate climates. Post-mortem lesions  Anaemia.Tahir Ticks Introduction Argas persicus is an external parasite of poultry and wild birds. Transmission is lateral with birds and faeces. Prevention As for red mite control. Insecticide sprays in these areas are more likely to be effective than treatment of the birds. Treatment Elimination of cracks and crevices in the poultry housing. Morbidity is close to 100% and mortality is 5-100%.M. The infection is seen in turkeys and sometimes pheasants. Transmissible Enteritis. Bluecomb Introduction Some coronaviruses involved in this condition are considered to be bovine coronaviruses (or closely related thereto). others are avian coronaviruses closely related to infectious bronchitis virus. Emaciation. Weakness. It is more common in warm climates. Reduced productivity. Occasionally paralysis from toxins in the tick saliva.

rapid spread. The course of the disease is about 2 weeks and birds then remain carriers for months. The viruses survive in frozen faeces for months.

Signs
       Anorexia. Depression. Frothy diarrhoea. Subnormal body temperature. Darkening of the head. Loss of weight. Huddling.

Post-mortem lesions
       Dehydration. Emaciation. Enteritis with petechial haemorrhages. Froth ingesta. Sometimes casts. Pancreas chalky. Urates in kidneys/ureters.

Diagnosis
Reproduction with filtered contents, isolation in turkey eggs, electron microscopy, immunofluorescence, Elisa. Commercial M4I IB Elisa will detect some infections.

Treatment
Warmth and good management, antibiotics, milk replacer, potassium chloride. Disinfect and rest houses for 3-4 weeks.

Prevention
All-in/all-out production, good hygiene and biosecurity, good management.

Trichomoniasis, Canker, Frounce
Introduction
Trichomonas gallinae is a protozoan parasite of pigeons and doves (canker), raptors (frounce), turkeys and chickens. It has variable pathogenicity. Morbidity is high and mortality varies but may be high. Transmission is via oral secretions in feed and water, and crop milk.

144

Signs
     Mouth open. Drooling and repeated swallowing movements. Loss of conditon. Watery eyes in some birds. Nervous symptoms (rare).

Post-mortem lesions
  Yellow plaques and raised cheesy masses in mouth, pharynx, oesophagus, crop and proventriculus. Raptors may have liver lesions.

Diagnosis
Lesions, large numbers of protozoa in secretions. Differentiate from Pox and candidiasis.

Treatment
Previously approved products included dimetridazole, nithiazide, and enheptin. Organic arsenical compounds (where approved) and some herbal products may be of some benefit in managing this problem in food animals.

Prevention
Eliminate stagnant water, eliminate known carriers, add no new birds.

Tuberculosis
A bacterial infection, caused by Mycobacterium avium, of poultry, game birds, cage birds etc. Morbidity and mortality are high. Transmission is via faecal excretion, ingestion, inhalation, offal and fomites. The disease has a slow course through a flock. The bacterium resists heat, cold, water, dryness, pH changes and many disinfectants.

Signs
     Severe loss of weight with no loss of appetite. Pale comb. Diarrhoea. Lameness. Sporadic deaths.

Post-mortem lesions
 Emaciation.

145

 

Grey to yellow nodules attached to intestine. Granulomas in liver, spleen and many other tissues, even bone marrow.

Diagnosis
Isolation, acid-fast stain in tissues, TB test. Differentiate from Lymphoid leukosis.

Treatment
None recommended.

Prevention
Market after one season, hygiene, cages, elimination of faeces etc.

Turkey Coryza
Introduction
A condition of turkeys possibly associated with Bordetella avium(previously designated Alkaligenes faecalis) infections. This bacterium usually causes mild respiratory disease in only a proportion of the flocks, and low mortality. It can be synergistic with other respiratory pathogens such as Ornithobacterium,Pasteurella spp, Mycoplasma spp. and pneumoviruses.

Signs
      Decreased appetite, weight gain and feed efficiency. Loss of voice. Ocular and nasal discharge. Conjunctivitis. Snick. Dyspnoea.

Post-mortem lesions
  Excessive mucus in nasal passages and trachea. If there is secondary E. coli infection then pneumonia, airsacculitis and perihepatitis.

Diagnosis
Clinical signs, isolation of agent.

Treatment

146

vertical transmission is uncertain.Antibiotics are not very effective. chlorination of drinking water. possibly involving fomites. Rapid transmission occurs laterally. Prevention All-in/all-out production. Ocular and nasal discharge. Diagnosis Signs. control respiratory stressors. isolation of ciliostatic agent. 147 . Sudden drop in production that lasts 2-3 weeks. Post-mortem lesions  Serous rhinitis and tracheitis. Serology. Loss of voice. Eggs depigmented and thin-shelled. Treatment Antibiotics are not very effective. control respiratory stressors.30%. Prevention All-in/all-out production.live primer followed by inactivated. Morbidity is 10-100% and mortality 1. Signs      Decreased appetite. chlorinate drinking water. Paramyxoviridae. vaccination . maternal antibody may protect. Turkey Rhinotracheitis (Adult) Introduction A disease of turkeys caused by the viruses of the Pneumovirus genus. Good drinking water hygiene.

mortality is 1-25%. Post-mortem lesions   Serous rhinitis and tracheitis. Morbidity is 10-100% and mortality 1. sometimes pus in bronchi. Turkey Viral Hepatitis Introduction An infection of turkeys caused by an unidentified virus.30%. Loss of voice. Morbidity varies. chlorinate drinking water. Transmission may be by direct or indirect contact and possibly vertical. Rapid transmission occurs laterally.Abubakar. Treatment Antibiotics are not very effective. Diagnosis Clinical signs. Conjunctivitis. Ocular and nasal discharge. Vaccination at day-old seems to be most effective. weight gain and feed efficiency. 148 . coli infection then pneumonia. Signs        Decreased appetite. If there is secondary E. Birds remain carriers for up to 16 days. Dyspnoea. Paramyxoviridae. Prevention All-in/all-out production. control respiratory stressors. maternal antibody may protect. Snick. Sinusitis. isolation and identification of the ciliostatic virus.Tahir Turkey Rhinotracheitis (in rear) Introduction A disease of turkeys caused by the viruses of the Pneumovirus genus.M. vertical transmission is uncertain. serology (using an Elisa test to demonstrate rising titre). possibly involving fomites. airsacculitis and perihepatitis.

Post-mortem lesions       Grey foci (c. environment and high growth rate. lesions pathognomonic.Signs   Signs are usually subclinical. Valgus/varus. Focal haemorrhage. Twisted leg Introduction A complex condition seen in chickens and turkeys. 149 . nutrition. Factors involved may include genetics. Diagnosis Isolation in CE. Post-mortem lesions  Linear twisting of growth of long bones.no inclusion bodies. Differentiate from histomonosis. Signs      Lameness. Grey to pink foci in the pancreas. Morbidity is 1-20% and mortality is low. Bile staining. Distortion at hock. Various angulations of leg. 1 mm) coalescing. Prevention Good sanitation and management. Congestion. Depression and sporadic deaths in birds in good condition. Microscopically . with good management many birds recover. Treatment None. bacterial and fungal infections. Gastrocnemius tendon may slip.

IBDV and overcrowding. brunetti). intertarsal angulation up to 10% is physiological. Peritonitis (if ulcers penetrate). Anaemia. Prevention Selection for good conformation in primary breeding. Drooping wings. game birds and pigeons may also be affected. Pale yellow membranes. Blood in intestine. The route of infection is oral and transmission is from faeces of sick or carrier birds or via flies. Quail disease Introduction Ulcerative Enteritis is an acute.. Retracted neck. necatrix. Treatment None. lesions. Partially closed eyes. It can start suddenly and cause high mortality: 100% in quail and 10% in chickens. Post-mortem lesions     Deep ulcers throughout intestine. 150 . Watery white faeces (quail). Signs         Listlessness. E. greater than 20% is abnormal. Ruffled feathers. Ulcerative Enteritis. Differentiate from perosis. Diagnosis Symptoms. tenella. The condition occurs worldwide. Predisposing factors include Coccidiosis (especially E. but mainly ileum and caecae. arthritis and synovitis. Adoption of optimal nutrition and growth patterns for the economic objectives of the production system. The bacterium resists boiling for 3 minutes. which may coalesce and may be round or lenticular. highly contagious disease of chickens and quail caused by the bacterium Clostridium colinumand characterised by ulcers of the intestines and caecae. Diarrhoea. and E. Changed angulation of tibial condyles. Turkeys.

amoxycillin. Loss of condition. Morbidity is low. Transmission is by faecal contamination. Confirmation is on absence of other diseases and isolation of Cl. trichomoniasis. coccidiosis. Response to treatment should occur in 48 to 96 hours. Treatment Streptomycin (44 gm/100 litres water). possibly probiotics. Prevention Infection-free birds. penicillin (50-100 ppm in feed). Diagnosis A presumptive diagnosis may be made on history and lesions. Tetracyclines. The infective agent is rather resistant to environment and disinfectants. salmonellosis. necrotic enteritis. and disease is precipitated by stress. Inappetance. low level antibiotics as per treatment. Bacitracin. 151 . Figure 35. Signs     Dejection. Wall of the caecum of a chicken suffering from ulcerative enteritis Vibrionic Hepatitis. multivitamins. colinum in anaerobic conditions (the agent is often present in pure culture in liver). birds remaining carriers for months. all-in/all-out production. Treat for coccidiosis if this is a factor. Necrotic foci in liver. Diarrhoea. Avian Infectious Hepatitis Introduction An insidious onset disease of chickens caused by Vibrio bacteria. Differentiate from histomonosis ('Blackhead').

   

Pale comb and wattles. Scaly comb. Jaundice. Drop in production/weight gain.

Post-mortem lesions
    Focal hepatic necrosis in 10% of affected. Foci often stellate, or there may be a cauliflower-like 'spotty liver'. Haematocysts under capsule. Swelling of organs. Catarrhal enteritis.

Diagnosis
History, lesions, isolation of infective agent from bile. Differentiate from leukosis, histomonosis, ulcerative enteritis, fowl cholera, and typhoid.

Treatment
Erythromycin, fluoroquinolones.

Prevention
Hygiene, depopulate, obtain birds free of disease, contain stressors.

Viral Arthritis
Introduction
Viral Arthritis is the classic, but by no means the only, manifestation of reovirus infection of chickens; at least 5 sero-types of virus occur. Morbidity is high but mortality is usually low. Transmission is by faecal contamination, and good both laterally and vertically. Birds remain carriers for over 250 days. The virus is resistant to heat, ether, chloroform, pH and environmental factors. Reoviruses vary markedly in pathogenicity and the tissue damaged. Some can cause other disease syndromes such as early chick mortality and malabsorption syndrome. Some strains have shown severe systemic disease including pericarditis in chickens. Others have caused immunosuppression by damaging the cloacal bursa in ducks.

Signs
       Lameness. Low mobility. Poor growth. Inflammation at hock. Swelling of tendon sheaths. Unthriftiness. Rupture of gastrocnemius tendons.

152

Post-mortem lesions
     Swelling and inflammation of digital flexor and metatarsal extensor tendon sheaths. Foot pad swelling. Articular cartilages may be ulcerated. Haemorrhage in tissues. Fibrosis in chronic cases.

Diagnosis
Diagnosis may be based on the history, lesions, IFA and rising antibody titre. Isolation may be readily achieved in CE yolk sac and CAM and also cell cultures (CE kidney or liver cells). Serology may be by DID, FAT or Elisa. 'Silent' infections (not associated with obvious disease) are common. Differentiate from mycoplasmosis, salmonellosis, Marek's, Pasteurella, erysipelas.

Treatment
None.

Prevention
Vaccination is ideally carried out by administering a live vaccine in rear followed by an inactivated vaccine prior to coming into lay. Most vaccines are based on strain 11/33. Rear birds in all-in/all-out production systems.

Visceral Gout, Nephrosis, Baby Chick Nephropathy
Introduction
Visceral gout is the deposition of white urates, which are normally excreted as a white cap on well formed faeces, in various tissues. Urates are also often deposited in joints and in the kidney. This condition can occur as an individual problem at any age. Outbreaks are seen in young chicks in the first week of life (baby chick nephropathy) or in flocks suffering kidney damage, or reduced water intake. All poultry species are susceptible. The kidney damage can arise from infection with certain strains of Infectious Bronchtiis virus, exposure to some mycotoxins or inadequate water intake (often because the birds have not adapated to a new type of drinker). Baby Chick Nephropathy can be due to inappropriate egg storage conditions, excessive water loss during incubation or during chick holding/transport, or inadequate water intake during the first few days of life. Very low humidity in brooding will also increase the likelihood of this problem. The timing of mortality is a reasonable guide as to the source of the problem. In Pekin/mallard ducks the condition is almost always due to inadequate water intake, whereas in muscovy ducks it is seen in breeders allowed to continue laying for over 24 weeks without a rest.

153

Signs
  Depression. Low feed intake and growth.

Post-mortem lesions
  Chalky white deposits on pericardium, liver, air sacs, peritoneum. Similar deposits may be present in joints and are usually present in the kidney.

Diagnosis
Lesions.

Treatment
This is based on correcting any management errors and encouraging water intake. Avoid any intentional or unintentional restriction in water intake. Sodium bicarbonate at 1g/litre water is mildly diuretic, however it could be counter-productive if water intake is in any way restricted.

Prevention
Careful monitoring of the conditions of hatching egg storage and incubation with a view to achieving a standard egg weight loss profile. Humidification of holding rooms and chick transporters may also be beneficial. Humidifiers in chick brooding areas are being used increasingly, especially where whole house hot air brooders are in use. Ample supplies of drinkers should be available and filled with water at house temperature prior to the arrival of the chicks.

Figure 36. Severe visceral gout in a young chick. There are white chalky deposits around the heart (in the pericardium) on all major abdominal organs, including liver, gizzard and intestines, and even in the tissues of the thigh.

154

Abubakar. Differentiate from Infectious coryza. good quality raw materials. classic signs of deficiency are very rare in commercial poultry fed complete diets. infectious sinusitis etc. chronic fowl cholera. lesions. Prevention Supplementation of diet with vitamin A. Microscopically .Tahir Vitamin A Deficiency. Signs       Poor growth. antioxidant.squamous metaplasia of epithelia. Diagnosis Signs. As in the case of other nutritional deficiencies. Excessive urates in kidneys and ureters. feed formulation. Pustules in mouth and pharynx. Pale comb and wattles. Drowsiness. Nasal and ocular discharge. 155 . Post-mortem lesions     Eyelids inflamed and adhered. Nutritional Roup Introduction Vitamin A deficiency is occasionally seen in chickens and turkeys (insufficient vitamin A during 1-7 weeks of age). Eyelids stuck shut with thick exudate. Poor feathering.M. Treatment Vitamin A in drinking water.

Some deficiencies induce characteristic microscopic effects. and egg production in the layer. They act in a broad range of metabolic pathways. The embryo is particularly dependent on having adequate supplies of vitamins deposited in the egg. including growth in the young animal. Diagnosis Signs. exclusion of specific diseases. If it is suspected that the vitamin premix may not have been included in the ration (or included at too low a level) it 156 . Vitamin deficiencies are especially prone to cause problems of hatchability. Simple deficiency is now rare as diets are usually well supplemented.Abubakar. because a continuous supply is required. See the separate discussion under Chondrodystrophy and Fatty Liver and Kidney Syndrome. Most will reduce productivity. response to supplementation.Tahir Vitamin B Deficiencies Introduction The B complex vitamins are water soluble and not stored to any significant extent in the body. However.M. Signs These may be summarised:                     Perosis Curled Toe Paralysis Paralysis/'Stargazing' Dermatitis/Scaly Skin Mouth Lesions Conjunctivitis Anaemia Fatty Liver and Kidney Syndrome Poor Feathering Loose feathers Hatchability problems Embryo with clubbed down Thiamine (B1) Riboflavin (B2) Pantothenic acid Pyridoxine (B6) Niacin Folic Acid Cyanocobalmin (B12) Biotin Post-mortem lesions   Usually the gross lesions are non-specific. damage to the intestine or increased demand for some reason may have an effect.

Uncontrolled movements. Staggering. Green wings. occasionally ducklings and other birds. Encephalomalacia and exudative diathesis tends to be seen in young birds of 1-5 weeks of age. Encephalomalacia. The balance of vitamins present should be similar to the daily nutritional requirement of the stock concerned. Ventral oedema. Good quality multivitamin solutions are beneficial in the supportive care of a range of problems characterised by reduced feed intake. 157 . Post-mortem lesions       Swollen cerebellum with areas of congestion.may be appropriate (faster. less expensive) to analyse feed for a marker substance such as manganese rather than testing for vitamin levels. Treatment If a specific vitamin deficiency is suspected. Vitamin E Deficiency. Falling over. Steatitis. seen worldwide. The problem is associated with feed rancidity typically in diets with high fat. White streaks in muscle. Haemorrhage. Muscular dystrophy is seen more frequently in older and mature birds. Blood-stained or greenish subcutaneous oedema. Necrosis. drinking water supplementation with that vitamin is ideal and usually results in a rapid response in birds that are still drinking. Exudative Diathesis. Signs        Imbalance. characterised by oxidation of various tissues and caused by Vitamin E deficiency. Muscular Dystrophy Introduction A spectrum of diseases of chickens and turkeys. Prevention Adequate supplementation of the feed with all required vitamins in levels which both support normal productivity but also have enough overage to deal with the increased demands that often occur during periods of disease challenge. Paralysis.

'bangers'. Inadequate incubation conditions resulting in excessive water retention and slowly-healing navels and 'tags' of yolk at the navel on hatching also contribute to the problem. and poor hygiene of setters. It is seen where there is poor breeder farm nest hygiene. turkeys and ducks due to bacterial infection of the navel and yolk sac of newly hatched chicks as a result of contamination before healing of the navel. for example poor hygiene of hatching eggs. Omphallitis Introduction A condition seen worldwide in chickens.coli. 158 .Diagnosis Signs. toxicities. feed rancidity. lesions. Staphylococci. use of floor eggs. Closed eyes. histopathology. Treatment Vitamin E and/or selenium in feed and/or water. Loss of appetite. especially E . consistency) that vary according to the bacteria involved.Proteus. Prevention Proper levels of vitamin E. Post-mortem lesions   Enlarged yolk sac with congestion. Diarrhoea. Disease occurs after an incubation period of 1-3 days. necrotic dermatitis. Yolk Sac Infection. selenium. good quality raw materials. Morbidity is 1-10% and mortality is high in affected chicks. Abnormal yolk sac contents (colour. Swollen abdomen. Signs       Dejection. Differentiate from Encephalomyelitis. Broad-spectrum antibiotics where there are extensive skin lesions. inadequate hatchery hygiene or poor incubation conditions. hatchers or chick boxes. Vent pasting. antioxidant. Various bacteria may be involved. response to medication. Pseudomonas.

separate incubation of floor eggs etc.g. 159 . Prevention Prevention is based on a good programme of hygiene and sanitation from the nest through to the chick box (e. There should be routine sanitation monitoring of the hatchery.Diagnosis A presumptive diagnosis is based on the age and typical lesions. frequent collection. sanitation of eggs. Differentiate from incubation problems resulting in weak chicks. Multivitamins in the first few days may generally boost ability to fight off mild infections. however the prognosis for chicks showing obvious signs is poor. exclusion of severely soiled eggs. Confirmation is by isolation and identification of the bacteria involved in the internal lesions. Treatment Antibiotics in accordance with sensitivity may be beneficial in the acute stages. most will die before 7 days of age. clean nests.

You're Reading a Free Preview

Download
scribd
/*********** DO NOT ALTER ANYTHING BELOW THIS LINE ! ************/ var s_code=s.t();if(s_code)document.write(s_code)//-->