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.


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

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

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

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

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

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

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

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

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

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

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


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.


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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Watery diarrhoea that may occasionally be blood stained or contain clumps of mucus or shed mucosa. ruffled feathers. ruptured ligaments. gallopavonis and E. no value to affected bird. correct mineral balance. Coccidiosis of Turkeys Introduction Infection of turkeys with Eimeria spp. The contents may be haemorrhagic or be watery with white material shed from the mucosa. infectious arthritis. Weight loss. 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. Signs      Huddling. E. while E. meleagridis affect the lower small intestine rectum and caecae. infectious synovitis. rickets. Tibia and metatarsus bowed. analysis of feed. meleagrimitis affects the upper small intestine. Treatment For flock proceed as for prevention. Differentiate from twisted leg. Post-mortem lesions  The affected area of intestine shows thickening of the wall and dilation. choline. Depression.Post-mortem lesions     Shortening and thickening of long bones. Diagnosis Lesions. 33 . of which two are associated with significant disease effects. E. dispersa is found in the small intestine. vitamins. adenoides affects the caecae and rectum. Prevention Addition of manganese. Tucked appearance. Five species of Eimeria have been identified that cause lesions in turkeys. Lateral slipping of tendon. while E.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

presumably due to a sudden increase in blood pressure.Dissecting Aneurysm. recovered birds carrying the virus for 8 weeks. was included in feed at 1 ppm for 3-5 days to reduce blood pressure. Aortic Rupture Introduction A complex. Diagnosis History and lesions. Possibly blood in the mouth. Skin pale. 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. pericardial sac. Prevention Limit feed in birds of 16+ weeks. Reserpine. a picornavirus may also 51 . It has been suggested that degenerative changes in the wall of the artery and copper deficiency may be factors. Post-mortem lesions      Carcase anaemic. a tranquilizer. Morbidity is around 100% and mortality 0-95%. Rupture of major blood vessel at base of heart or by the kidneys. A sudden noise or other cause of excitement can lead to an 'outbreak'. birds found on breast or side. A longtitudinal split of the abdominal aorta is the most common lesion. Duck Viral Hepatitis Introduction A viral disease of ducks occurring worldwide and previously a scheduled disease in UK. leg muscles. kidneys. Haemorrhages in lungs. The disease is transmitted by infected ducks and other waterfowl and spreads rapidly. Abdominal cavity full of blood. Aspirin at 250 ppm in feed or water may be of benefit. The infective agent. genetic condition of turkeys linked to male sex and high growth rate.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Formalin-inactivated oil adjuvant vaccines are reported to be highly effective and are used in areas where the condition is endemic.g. Older birds ingest grit to facilitate the grinding activity in the gizzard. histopathology. Lethargy. Congestion of the carcase. Impacted gizzards are then found in 'non-starter' type chicks or poults. This condition usually affects only a small number of birds. and birds of any age can 75 . string etc. Enlarged. treatment of drinking water with 0. Good water sanitation (e. Post-mortem lesions     Excessive straw-coloured fluid distending the pericardium (up to 10 mls).1% of a 2.5% iodophor solution) appears to be beneficial.Signs     Sudden increase in mortality. however sometimes free-range poultry consume large stones. to reduce their particle size to aid digestion. Lungs oedematous. Treatment None. Huddling with ruffled feathers. Grit would not be classed as a foreign body. Impaction and Foreign Bodies of Gizzard Introduction The gizzard or crop may become impacted with litter. pale friable liver and kidney. Control of predisposing immunosuppressive diseases may help limit losses. Yellow mucoid droppings. Most young commercial poultry consume feeds that have a small particle size. Diagnosis Lesions. Gizzard activity also acts as a pacemaker of intestinal activity and controls the speed at which food is passed to the small intestine. Prevention The condition typically occurs in areas of high poultry density where multi-age operation is traditional. however if young chicks to do not begin to eat feed properly they often consume litter instead. The normal function of the gizzard is to aid in the physical grinding of food materials. virology. grass.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

        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.


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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

   

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.


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

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

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

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

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

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