Poultry Diseases and Their Treatment

By Paul McMullin


M.Sc.(Hons) Animal Nutrition

University of Agriculture Faisalabad


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

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

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

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

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

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


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

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

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

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

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


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

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

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

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

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

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

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

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

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

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

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


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

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

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

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

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


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

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

Post-mortem lesions
 See signs.

Clinical signs, exclusion of other causes of similar signs.

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

Check feed particle size by granulometry, grind less finely.

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

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


Post-mortem lesions
 Anaemia.

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

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

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

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

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

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


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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

History. Use of a multivitamin supplement and facilitating access to water may help. histopathology. Elisa vaccination date prediction < 7 days). weights below 0. Antibiotic medication may be indicated if secondary bacterial infection occurs. 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. Serology: antibodies can be detected as early as 4-7 days after infection and these last for life. Haemorrhages in skeletal muscle (especially on thighs). Half-life of maternally derived antibodies is 3. The normal weight of the bursa in broilers is about 0. Treatment No specific treatment is available.Signs       Depression.4 days. (previously SN and DID). This may be confirmed by demonstrating severe atrophy of the bursa.3% of bodyweight. Post-mortem lesions     Oedematous bursa (may be slightly enlarged. Vent pecking. Haemorrhagic syndrome. Diarrhoea with urates in mucus. rapidly proceeds to atrophy. They are all serotype 1.1% are highly suggestive. especially in the Delmarva Peninsula in the USA. Other possible causes of early immunosuppression are severe mycotoxicosis and managment problems leading to severe stress. Differentiate clinical disease from: Infectious bronchitis (renal).5.A history of chicks with very low levels of maternal antibody (Fewer than 80% positive in the immunodifusion test at day old. normal size or reduced in size depending on the stage). Huddling under equipment. Inappetance. Diagnosis Clinical disease . Subclinical disease . IBD viruses have been isolated and shown to have significant but not complete cross-protection. lesions. especially if present prior to 20 days of age. Tests used are mainly Elisa. Cryptosporidiosis of the bursa (rare). Swollen kidneys with urates. Unsteady gait. Coccidiosis. 84 . subsequent diagnosis of 'immunosuppression diseases' (especially inclusion body hepatitis and gangrenous dermatitis) is highly suggestive. Dehydration. may have haemorrhages. Variants: There have been serious problems with early Gumboro disease in chicks with maternal immunity.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Tilmicosin, chlortetracycline, oxytetracycline, tylosin.

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



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

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

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


      

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

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

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

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


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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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


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

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

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

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

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

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

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

Post-mortem lesions
 Emaciation.


 

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

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

None recommended.

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

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

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

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

Clinical signs, isolation of agent.



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

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

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

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

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

   

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

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

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

Erythromycin, fluoroquinolones.

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

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

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


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

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


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

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


  Depression. Low feed intake and growth.

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


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

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

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


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

Most will reduce productivity. damage to the intestine or increased demand for some reason may have an effect. They act in a broad range of metabolic pathways. including growth in the young animal. See the separate discussion under Chondrodystrophy and Fatty Liver and Kidney Syndrome. because a continuous supply is required. Vitamin deficiencies are especially prone to cause problems of hatchability. response to supplementation. Simple deficiency is now rare as diets are usually well supplemented. exclusion of specific diseases. If it is suspected that the vitamin premix may not have been included in the ration (or included at too low a level) it 156 .M. The embryo is particularly dependent on having adequate supplies of vitamins deposited in the egg. and egg production in the layer.Abubakar. However. Diagnosis Signs. 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. Some deficiencies induce characteristic microscopic effects.Tahir Vitamin B Deficiencies Introduction The B complex vitamins are water soluble and not stored to any significant extent in the body.

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

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

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

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