Poultry Diseases and Their Treatment

By Paul McMullin

M.Abubakar.Tahir

M.Sc.(Hons) Animal Nutrition

University of Agriculture Faisalabad
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M.Abubakar.Tahir

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Sinusitis.

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

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

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

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

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

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

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

Post-mortem lesions
 See signs.

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

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

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

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

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

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Post-mortem lesions
 Anaemia.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Treatment
Tilmicosin, chlortetracycline, oxytetracycline, tylosin.

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

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M.Abubakar.Tahir

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

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

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

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      

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Post-mortem lesions
 Emaciation.

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 

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

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

Treatment
None recommended.

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

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

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

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

Diagnosis
Clinical signs, isolation of agent.

Treatment

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

Diagnosis Clinical signs. Ocular and nasal discharge. Sinusitis. Morbidity varies.M.Tahir Turkey Rhinotracheitis (in rear) Introduction A disease of turkeys caused by the viruses of the Pneumovirus genus. Vaccination at day-old seems to be most effective. Paramyxoviridae. vertical transmission is uncertain. Prevention All-in/all-out production. Transmission may be by direct or indirect contact and possibly vertical. Loss of voice. Signs        Decreased appetite. If there is secondary E. isolation and identification of the ciliostatic virus. chlorinate drinking water. weight gain and feed efficiency. 148 . mortality is 1-25%. Turkey Viral Hepatitis Introduction An infection of turkeys caused by an unidentified virus. serology (using an Elisa test to demonstrate rising titre). control respiratory stressors. possibly involving fomites. maternal antibody may protect. Morbidity is 10-100% and mortality 1.30%.Abubakar. Treatment Antibiotics are not very effective. airsacculitis and perihepatitis. coli infection then pneumonia. sometimes pus in bronchi. Birds remain carriers for up to 16 days. Conjunctivitis. Dyspnoea. Rapid transmission occurs laterally. Snick. Post-mortem lesions   Serous rhinitis and tracheitis.

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

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

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

   

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

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

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

Treatment
Erythromycin, fluoroquinolones.

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

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

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

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

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

Treatment
None.

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

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

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Signs
  Depression. Low feed intake and growth.

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

Diagnosis
Lesions.

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

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

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

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

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

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

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

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

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