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


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






  • 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.Sc.(Hons) Animal Nutrition

University of Agriculture Faisalabad


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.

   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.

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).

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

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


Anatipestifer Disease, New Duck Syndrome, Duck Sepicaemia
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.

         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.

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.

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.


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

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

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

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

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

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

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

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

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

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

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


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.

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.

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

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.


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

   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.

Clinical signs, exclusion of other causes of similar signs.

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

Check feed particle size by granulometry, grind less finely.

Bedbug Infestation
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.

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


Post-mortem lesions
 Anaemia.

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

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

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

Big Liver and Spleen Disease
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.

    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.


Post-mortem lesions   See signs. 18 . Pale livers and kidneys in fatty liver and kidney syndrome.    Lung congestion Ovarian regression Yolk peritonitis Pale foci and haemorrhages in pancreas. webbing between toes. Sudden deaths in fatty liver and kidney syndrome. Treatment No specific treatment known. 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. Good biosecurity. Signs       Poor growth. Elisa tests have been developed experimentally. 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. Biotin Deficiency. It may be helpful to control other conditions which may be occurring at the same time. Thickened skin under foot pad. A RT-PCR test may be used to detect viral RNA in tissues. Allin/all-out production. Prevention Thorough cleaning and disinfection after depletion of an affected flock. Chondrodystrophy. Diagnosis Typical signs and lesions. Histopathology may also be used but the findings are not specific to this condition. Viral particles may be demonstrated in bile. Drinking water which is well chlorinated should be helpful in reducing challenge by this route. Scabs around eyes and beak. Leg weakness. Must be confirmed by laboratory tests. in embryos. Reduced feed intake and blood sugar can precipitate fatty liver and kidney syndrome.

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

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

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

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

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

It may be that management that favours dry litter reduces the risk of infection and/or transmission within the flock. In poultry they tend to multiply in large numbers in the hindgut. Active ovary with egg in oviduct. The reason for this is unclear. Treatment Provide 5 gm of oyster shell per hen on 3 successive days along with vitamin D in drinking water. 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'. Diagnosis This is made on signs. Congested lungs.Post-mortem lesions    Cyanosis. There are indications that plantar pododermatitis. Campylobacter jejuni is the commonest species found in poultry. and response to treatment. 24 . pets and wild animals. are bacteria that commonly infect a broad range of livestock species. Prevention Keep pullet flocks on low calcium diet until 5% production hen/day. lack of other significant lesions. Infected poultry are a potential reservoir of this zoonosis. Campylobacters are a significant cause of enteritis in man. principally in the caecae. All campylobacters are delicate organisms that survive for relatively short periods outside the host unless protected by organic material. other acute infections and other causes of sudden death. managing birds for maximum uniformity. biofilm or engulfed by protozoa. Differentiate from IB 793b. lesions. There is an annual cycle with increased risk of infection in the summer months in some countries. Campylobacter Infection Introduction Campylobacter spp. carcase quality and litter quality are better on farms which tend to have Campylobacter-negative stock.

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

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

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

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

particularly broiler chickens. Careful flock management with a view to reducing toe wounds has the greatest impact in controlling cellulitis. Signs  Affected flocks tend to have poorer than average productivity and uniformity. The condition is caused by infection of. coli. Treatment Treatment would not be possible if the problem is identified at a final depletion. but the affected birds are not readily detectable prior to slaughter. Prevention Toe scrapes at 15-25 days of age when feather cover is poor are the most likely predisposing factors. Diagnosis Typical lesions.Cellulitis Introduction Cellulitis is literally an inflammation of connective tissues. However its main importance is as a cause of condemnation in meat poultry. which can replicate in the tissues. Routine monitoring of skin damage at about 25 days of age may be helpful in fostering good practices. 29 . often minor. 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. In the USA it is called 'Inflammatory Process'. though most of the birds showing toe scrapes will not go on to develop cellulitis. skin wounds by particular strains of E. It typically occurs between skin and muscles and between muscles and may be an incidental finding in a range of conditions. 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. Many affected birds have no other lesions and are reasonably well grown.

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

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

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

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

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

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

E mitis Introduction This condition of chickens. The infective agent is found in litter. humidity). Treatment Not usually treated but susceptible to the products used for other forms of intestinal coccidiosis.Figure 15. The disease occurring is proportional to the amount of infective agent ingested. Coccidiosis. Predisposing factors include exposure to faeces and litter conditions that favour development of the parasite (temperature. The parasite is moderately resistant in the environment and highly resistant to conventional disinfectants. Signs  Reduced feed conversion efficiency and weight gain. seen worldwide. identification of typical small round oocysts and other stages in fresh scrapings from the small intestine. 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. 36 . is caused by the protozoan parasite Eimeria mitis. which colonises the small intestine. Diagnosis Mild lesions. secondary bacterial enteritis. May predispose to wet litter. Moderate Eimeria tenella infection in the caecae of a chicken (Score 3). 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.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

rickets. Post-mortem studies of birds culled due to lameness and of birds found dead. Careful attention to mineral and Vitamin D nutrition to avoid subclinical. spondylolisthesis. Prevention Exclusion of floor eggs and dirty eggs from the hatchery.75% of all male broilers placed had lesions in the hip bone. Diagnosis Base on post-mortem lesions and isolation of a causative organism. coli. turkeys.Femoral Head Necrosis . staphylococci. Post-mortem lesions  Degeneration of the epiphyses of long bones with thinning of the cortex and tendency to break when force is applied.g. Differentiate from synovitis. Use of a wing for support during walking and hip flexion. E. Signs   Lameness. highly contagious disease caused by the bacterium Pasteurella multocida in a range of avian species including chickens. Pasteurellosis Introduction Fowl Cholera is a serious. Fowl Cholera. especially hypophosphataemic. It is seen worldwide and was one of the first infectious 61 . arthritis. streptococci. Predisposing factors include immunosuppresive viruses such as Infectious Bursal Disease Virus and Chicken Anaemia Virus and non-infectious bone pathologies such as hypophosphaetamic 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. (increasing order of susceptibility). indicated that 0.FHN Introduction A condition of chickens and turkeys that may be associated with several different bacterial infections e. and water fowl. FHN is the commonest infectious cause of lameness in broilers in the UK.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

staples etc. and may penetrate the body wall. caused by an adenovirus. 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 number of different sero-types have been isolated from disease outbreaks but they may also be isolated from healthy chickens. Australia. Signs   Reduced feed intake. Diagnosis Lesions. Obvious non-starters should be culled in this situation. Reduced weight gain. Nails commonly penetrate the lining of the gizzard. It has a course of 9.15 days with a morbidity of 1-10% and a mortality of 1-10%. often with severe anaemia. A foreign body may be found in the interior of the gizzard. The disease was first described in the USA in 1963 and has also been reported in Canada. This usually happens after maintenance activities have been carred out in the housing. Daily monitoring of the crop-fill is a useful procedure. Inclusion Body Hepatitis Introduction A disease of chickens characterised by acute mortality. France and Ireland. the UK. Italy. Sweep floors after maintenance activities to remove nails and other potentially dangerous foreign bodies. and on opening is found to contain a mass of fibrous material. Infected birds remain carriers for a few weeks. Treatment None effective in young birds. 76 . This may extend into the proventriculus and on into the duodeunum. Post-mortem lesions    The gizzard is more firm than normal and.consume nails. Prevention Good brooding management to encourage early adaptation to the diet and adequate consumption of feed and water.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Signs        Reduced hatchability. Specialised dip tanks are subjected to negative pressure which partially collapses the air cell of the submerged eggs. purchase of M. The organism has also been isolated from raptors. Mortality is low.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.m. maintenance of this status by good biosecurity. Introduction A disease of turkeys characterised by respiratory and skeletal problems caused by Mycoplasma meleagridis.i. When the vacuum is released the eggs draw in antibiotic solution which is subsequently absorbed through the shell membranes. Crooked necks. Predisposing factors include stress and viral respiratory infections. Slow growth. For eradication purposes egg injection provides more consistent dosing per egg than does egg dipping. M.-free stock. Infected eggs result in widespread distribution of infection and increased risk of further vertical transmission. Transmission is venereal in breeders. with transovarian and then lateral spread in meat animals. This can increase hatchability by 510% in this situation. Mild respiratory problems. 97 . Treatment Pressure differential dipping has been used where breeder flocks are infected. The infective agent does not survive well outside the bird. though up to 25% of infected birds show lesions at slaughter. Pathogenicity is quite variable. Prevention Eradication of the infection from breeding stock. Antibiotics that have been used are tylosin and enrofloxacin. Infected parents may be asymptomatic. Stunting. In adult birds though infection rates are high. Leg problems. 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. Diagnosis Lesions. other respiratory viruses. or lateral via respiratory aerosols and direct contact. 98 . all-in/all-out production. Infectious Synovitis Introduction Infection with Mycoplasma synoviae may be seen in chickens and turkeys in association with synovitis and/or airsacculitis. Mycoplasma synoviae infection.culture used to confirm. Prevention Eradication of this infection is also possible using similar techniques as for Mycoplasma gallisepticum. Infected males are particularly prone to transmit infection and may warrant special attention. spiramycin. Transmission may be transovarian. In some circumstances preventative medication of known infected flocks may be of benefit. Airsacculitis (rarely) seen in adult birds. 11-21 days following contact exposure. Infection rates may be very high. whilst illness is variable and mortality less than 10%. Culture requires inoculation in mycoplasma-free embryos or. Treatment Tylosin. Spread is generally rapid within and between houses on a farm. fluoroquinolones. Infection is via the conjunctiva or upper respiratory tract with a long incubation period. Infected birds do develop some immunity. isolation and identification of organism. Birds infected from their parents seem to be immuno-tolerant and particularly prone themselves to transmit. Serology: SAG used routinely . M. Survival of the infectious agent outwith the bird is poor but fomite transmission between farms is important. tetracyclines. Effort should be made to reduce dust and secondary infections. Mycoplasma synoviae. demonstration of specific DNA (commercial kit available). Vaccines are not normally used. more commonly in Mycoplasma Broth followed by plating out on Mycoplasma Agar. serology. Suspect colonies may be identified by immuno-fluorescence. It occurs in most poultry-producing countries. and biosecurity.s. Differentiate from Mycoplasma gallisepticum. especially in commercial layer flocks.Post-mortem lesions   Airsacculitis in infected pipped embryos and poults. These are based on purchase of uninfected poults.

        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.

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.

Tilmicosin, chlortetracycline, oxytetracycline, tylosin.

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.



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 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.


      

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.

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.

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.

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.


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

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

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

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

Because it is enclosed in a relatively unyielding membrane. Gall bladder distended. Gizzard may be impacted with litter. It has since been seen in turkeys. nutrition of young parents. bile staining of adjacent tissues. 106 . Treatment Correction of management problems. The condition can be reproduced by causing intense exercise of this muscle. 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. Diagnosis Based on post-mortem lesions. good drinking water hygiene. It is caused by a reduction in the blood supply to the deep pectoral muscles.Signs  Failure to grow. age of collection and weight of hatching eggs.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. Oregon Disease . good hygiene and biosecurity in brooding areas to minimise early disease challenges. Prevention Review brooding management. Without adequate blood supply the tissue of the muscle begins to die. or suffer necrosis. aspergillosis. Differentiate from omphalitis/ yolk sac infection. Post-mortem lesions      Crop empty. in broiler parent chickens and also in large broiler chickens in various places. any swelling of the muscle tends to cut off the blood supply. soluble multivitamin supplementation may help. Poor development. Most organs normal.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

pasture rotation and regular treatment. Post-mortem lesions   Enteritis. Prevention Prevention of contamination of feeders and drinkers with faeces. Listlessness. Worms up to 12 cm in length in duodenum and ileum.parasites may be transported by grasshoppers and earthworms and are resistant to environmental effects. In the bottom left quadrant there are also some immature worms. levamisole. especially for young birds. Wasting. 125 . Signs      Loss of condition. Poor growth. 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. Figure 31. Diagnosis Macroscopic examination with identification of worms. Diarrhoea. mainly in young birds. Treatment Flubendazole. piperazine as locally approved.

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

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

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

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

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

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

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

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

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

Provide multivitamins. 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. Mortality drops off as sharply as it started. and/or carbohydrate absorption are disturbed resulting in a hypoglycaemia. electrolytes and glucose solution to flock. suggesting a viral component. Dehydration. Death. Orange mucoid droppings. Prevention Good sanitation of the brooding house.Spiking Mortality of Chickens Introduction This is a condition characterised by a sudden increase in mortality in young. This appears to be a multifactorial condition. Males are more susceptible than females. Feed intake. Diagnosis Pattern of mortality. typically 7-14day-old. probably because they are growing faster. Avoidance of physical stress. Paralysis. 135 . rapidly growing broiler chickens. Avoidance of interruptions in feed supply. Post-mortem lesions    Mild enteritis. Excess fluid in lower small intestine and caecae. Treatment Leave affected chicks undisturbed. Coma. Minimise stress. Filtered intestinal contents from affected flocks appear to be capable of reproducing the condition. Signs and lesions. Signs      Tremor. Birds in good condition die after showing neurological signs.

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

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

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

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

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

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

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

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

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.

       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.

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

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

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

Trichomoniasis, Canker, Frounce
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.


     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.

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

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.

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

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.

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

Post-mortem lesions
 Emaciation.


 

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

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

None recommended.

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

Turkey Coryza
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.

      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.

Clinical signs, isolation of agent.



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

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

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

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

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

   

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.

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

Erythromycin, fluoroquinolones.

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

Viral Arthritis
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.

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


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 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.


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
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.


  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.


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.

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.


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

Vitamin deficiencies are especially prone to cause problems of hatchability. including growth in the young animal. However. and egg production in the layer. damage to the intestine or increased demand for some reason may have an effect. 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 . They act in a broad range of metabolic pathways. Diagnosis Signs. Simple deficiency is now rare as diets are usually well supplemented. Most will reduce productivity. because a continuous supply is required. 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. The embryo is particularly dependent on having adequate supplies of vitamins deposited in the egg. exclusion of specific diseases. See the separate discussion under Chondrodystrophy and Fatty Liver and Kidney Syndrome. Some deficiencies induce characteristic microscopic effects.Abubakar.M.Tahir Vitamin B Deficiencies Introduction The B complex vitamins are water soluble and not stored to any significant extent in the body. response to supplementation.

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

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

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

You're Reading a Free Preview

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