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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.
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
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.
and is not present in the UK turkey population. Huddling near heat. Unabsorbed yolk sac. Transmission is vertical. feed etc. Autogenous bacterins sometimes used. Arizona infection. Vent-pasting. Figure 40. reptiles. renamed Salmonella Arizonae. cloudiness in eye. rigid depopulation and disinfection. adequate protection. older birds are asymptomatic carriers. Foci in lungs. and also horizontal. sulphonamides in feed. Inactivated and attenuated vaccines available in some countries. from long-term intestinal carriers. It affects turkeys. 4 . transovarian. correct house relative humidity. Arizonosis Introduction Caused by the bacterium Arizona hinshawii. Diarrhoea. Mortality is 10-50% in young birds. Nervous signs. mainly in North America. Congestion of duodenum. 'hardening off'. Inappetance. Paralysis. through faecal contamination of environment. Post-mortem lesions Enlarged mottled liver. rodents. Blindness. Cheesy plugs in intestine or caecum. Signs Dejection.Prevention Good husbandry and hygiene. Erosions of the cartilage of the hock joint in a duck with chronic Riemerella anatipestifer infection.
methods as per Salmonella spp. Diagnosis Isolation and identification. poor ventilation and physiology (oxygen demand. Differentiate from Treatment Injection of streptomycin. Severe muscle congestion. General venous congestion. coli-septicaemia. The disease has a complex aetiology and is predisposed by reduced ventilation. Possibly cyanosis. Dyspnoea. or gentamycin at the hatchery is used in some countries. Signs Sudden deaths in rapidly developing birds. high altitude. Prevention Eradicate from breeder population. Lungs and intestines congested. Dilation of the ventricle. inject eggs or poults with antibiotics. Salpingitis. and respiratory disease. 5 . mortality 1-2% but can be 30% at high altitude. good nest and hatchery hygiene. Pulmonary arterial vasoconstriction appears to be the main mechanism of the condition. Recumbency. Ophthalmitis. Progressive weakness and abdominal distension. Formerly in-feed medication with nitrofurans was also used. Ascites Introduction Associated with inadequate supplies of oxygen. Ascites is a disease of broiler chickens occurring worldwide but especially at high altitude. salmonellosis. Thickening of atrioventricular valve. monitor sensitivity. Post-mortem lesions Thickening of right-side myocardium. Perihepatitis. Morbidity is usually 1-5%. may be related to type of stock and strain). Pericarditis. fumigation of hatching eggs. spectinomycin. Poor development.
A cardiac specific protein (Troponin T) may be measured in the blood. etc. worldwide. Rapid breathing. Weakness. Absidia etc. It affects chickens. in which the typical sign is gasping for breath. Microscopic . The infection has an incubation period of 2-5 days. Diagnosis Gross pathology is characteristic. ducks. especially in young chicks. Treatment Improve ventilation. Ascites. Spleen small. avoid any genetic tendency. penguins. caused by Aspergillus fumigatus. but may be as high as 12%. This may offer the ability to identify genetic predisposition. Nervous signs (rare). Signs Acute form: Inappetance. Spores are highly resistant to disinfectants. Prevention Good ventilation (including in incubation and chick transport). Sometimes the same organism causes eye lesions or chronic lesions in older birds. Occasionally similar lesions are produced by other species ofAspergillus or even other fungi such as Penicillium. control respiratory disease. Vitamin C (500 ppm) has been reported to be of benefit in South America. turkeys. Thirst. Drowsiness. Liver enlargement. Differentiate from broiler Sudden Death Syndrome and bacterial endocarditis. 6 . Pericardial effusion. there is usually little bird-to-bird transmission. Transmission is by inhalation exposure to an environment with a high spore count. Aspergillosis Introduction A fungal infectious disease. Morbidity is usually low. game birds. Mortality among young affected birds is 5-50%. Silent gasping.cartilage nodules increased in lung. The fungus can infect plant material and many species of animals including birds and man. waterfowl.
Thiabendazole or Nystatin has been used in feed. Conjunctivitis/keratitis. trachea. Brain lesions may be seen in some birds with nervous signs. Morbidity 5-60%. The means of transmission is unknown but 7 . Differentiate from excessive exposure to formalin or vaccinal reactions in day olds and from heat stress in older birds. Growth occurs in 24-48 hours and colonies are powdery green/blue in appearance. may have greenish surface. It may be confirmed by isolation of the fungus.M. Post-mortem lesions Yellow to grey nodules or plaques in lungs.Abubakar. good quality litter and feed. See Avian Encephalomyelitis.Tahir 2 Chronic Forms: Ocular discharge (ocular form only). Diagnosis This is usually based on the signs and lesions and microscopic examination for the fungus. plaques in peritoneal cavity. typically by putting small pieces of affected tissue on Sabouraud agar. It affects chickens. mortality none. Amphotericin B and Nystatin have been used in high-value birds. preferably after digestion in 10% potassium hydroxide. turkeys. Epidemic tremors for its effect in young birds. quail. Figure 8. Avian Encephalomyelitis Egg Drop Introduction Avian encephalomyelitis virus infection in laying bird causes inapparent infection or drops in egg production. Wasting. The powdery surface is dark green in colour. 'Furry' airsacculitis in aspergillosis of an adult duck. hygiene. Prevention Dry. Treatment Usually none. pheasants and occurs in most poultry-producing countries. air sacs. Environmental spraying with effective antifungal antiseptic may help reduce challenge.
small (5-10%) and lasting no more than 2 weeks. Predisposed by immunosuppression. Imbalance. turkeys. and there is serious disease in the progeny (see next section). Treatment None. Avian Encephalomyelitis. water etc. It has a worldwide distribution. EDS76. lentogenic Newcastle disease. In breeders there may be a drop in hatchability of about 5%. incubation >10 days. 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. and quail. rising titre to AE virus. Dull expression. Morbidity 5-60% depending on the immune status of the majority of parents. some lateral. Serology . subsequent disease in progeny if breeders. 8 . Diagnosis History. Paralysis. Virus in faeces may survive 4 weeks or more. Virus in faeces may survive 4 weeks or more. with an oral infection route. Post-mortem lesions None. transmission occurs over about 1-2 weeks.probably by faecal contamination of environment. Prevention Vaccination of breeders/layers at 9-15 weeks. mortality high. Differentiate from Infectious Bronchitis. Signs Nervous signs. Vertical transmission is very important. now Elisa is used more commonly. Immunity is usually long lasting. attenuated or not. Ataxia and sitting on hocks. Signs Drop in egg production. lateral transmission is probably by the oral route.The embryo protection test has been used in the past. feed. pheasants.
The virus infects chickens. pigeons. The cause is a virus. signs. especially in turkeys. Marek's disease. quail. Microscopic . The higher the proportion of the chickens dying or showing signs the higher the IVPI. neck and wings. The embryo protection test has been used in the past. and isolates are designated sero-type/ species/location/reference number/year/subtype designation(H/N). Prevention Vaccination of breeders at 9-15 weeks. In addition official control measures disrupt trade in poultry products from affected areas. and ostriches. Brain abscess. and lack of significant lesions. partridges. Treatment None. EE (especially in pheasant in the Americas). Differentiate from Newcastle disease. turkeys.nonpurulent diffuse encephalomyelitis with perivascular cuffing. Fowl One of only two 'Class A' diseases of poultry targeted for emergency disease control measures by OIE. This is a test in which the virus is inoculated into susceptible chickens that are then kept under observation. Avian Influenza-Highly Plague Introduction Pathogenic (HPAI). Enterococcus hirae infection. Immunity is long lasting. Diagnosis A presumptive diagnosis is based on the history. and/or viral isolation may be carried out if required. Effectively all 9 . Post-mortem lesions Gross lesions are mild or absent. riboflavin). Tremor may be inapparent but is accentuated if chicks are held inverted in the hand. the equivalent of the World Health Organisation for animal diseases. A few recovered birds may develop cataracts weeks after infection. vitamin deficiency (E. There may be focal white areas in gizzard muscle (inconstant). its pathogenicity is variable. 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. ducks. Orthomyxovirus type A.2 . now Elisa is used more commonly. Histopathology is usually diagnostic and IFA. Tremor of head. Mycotic Encephalitis. The definitive classification of high pathogenicity is an intravenous pathogenicity test (IVPI) in 6-week-old chickens result of greater than 1. toxicities. pheasants. This viral disease can cause exceptionally high mortality. attenuated or not. A.
It can result in inapparent infection. Nasal and ocular discharge. Broken contaminated eggs may infect chicks in the incubator simulating vertical transmission. More recently outbreaks have occurred in Australia. Transmission is by direct contact with secretions from infected birds. Swollen face. Avian Influenza is a potential zoonosis. Drops in egg production. by oxidising agent and by formalin and iodine compounds. trachea. clothing. even with 'low pathogenicity' strains. Apathogenic and mildly pathogenic influenza A viruses occur worldwide. Highly pathogenic avian influenza A (HPAI) viruses of the H5 and H7 HA subtypes have been isolated occasionally from free-living birds. See current OIE records for up to date information on distribution of HPAI. from December 1999. 550%. drinking water. Mexico and.g. Italy). H5 viruses of low pathogenicity may become highly pathogenic usually after circulating in poultry flocks for a time (Pennsylvania. Marked loss of appetite. A serious outbreak occurred in The Netherlands in 2003 with a few linked cases in Belgium and one in Germany.birds are considered to be at risk of infection. equipment. Signs Sudden death. Depression. It can remain viable for long periods in tissues. Ovarian regression or haemorrhage. waterfowl. The route of infection is probably oral initially. OIE and other bodies are currently examining ways to improve control of LPAI. Morbidity is high but mortality usually relatively low. and the high mortality that 'low-path' AI can cause in turkeys. can survive 4 days in water at 22°C. reduced feed consumption. over 30 days at 0°C. Pakistan. It is inactivated by a temperature of 56°C in 3 hours and 60°Cin 30 min. in northern Italy. Pasteurella) may increase mortality. especially faeces. Outbreaks due to HPAI were recorded in the Pennsylvania area. The small number of human deaths associated with HPAI appear to have resulted from direct exposure to infected birds on farm or in markets. The virus is moderately resistant. in the years 1983-84. Coughing. Infections with other pathogens (e. Cyanosis of comb/wattles. Post-mortem lesions Inflammation of sinuses. Because of this. but possibly by the conjunctival or respiratory route and the incubation period is 3-5 days. air sacs and conjunctiva. Avirulent in one species may be virulent in others. conjunctivitis or severe pneumonia. by acid pH. The virus replicates mainly in respiratory tissues of chickens and turkeys but in the intestinal tract of clinically normal waterfowl. Diarrhoea (often green). 10 . Nervous signs such as paralysis. USA. Cessation of normal flock vocalisation.
To be effective inactivated vaccines must be the right subtype for the particular situation (H5 will not protect against H7 and vice versa). Necrosis of skin of comb and wattles. though there is high mortality of affected birds. Prevention Hygiene. etc. bleeding and vaccination needles. cleaning. HA+. lateral transmission by faecal-oral route (this declines as the bird ages). Congenitally infected birds tend to remain 11 . Myelocytomatosis Introduction Caused by an avian retrovirus. North and South America. The agar gel precipitation test is non-group-specific and is used to confirm any positives. The incubation period is 10-20 weeks. isolation. Minimise contact with wild birds. Survivors can be expected to have a high degree of immunity but may harbour virulent virus. nutrition and antibiotics may reduce losses. Vaccines have been used in recent outbreaks in Mexico and Pakistan. infectious laryngotracheitis. while ducks may be symptomless. Vaccination is not normally recommended because. In outbreaks a regime of slaughter. Muscles congested. other respiratory infections. Diagnosis A presumptive diagnosis may be made on history and postmortem lesions. Transmission is by congenital infection from antibody-negative females. Commercial Elisa test kits are now available. quarantine. fowl cholera. with considerable strain-to-strain variation. as with many such tests occasional false positive reactions can occur. It has occured in Europe. vaccinated birds may remain carriers if exposed to the infection. correct disposal of carcases. Dehydration. Confirmation is by viral isolation in chick embryo. Haemorrhage in proventricular and gizzard mucosae and lymphoid tissue of intestinal tract. Treatment None. Avian Leukosis (Serotype J). DID+. Subcutaneous oedema of head and neck. NDV-. 21-day interval to re-stocking should be followed. This condition has until now been seen only in meat-type chickens. Eradication by slaughter is usual in chickens and turkeys. Turkey lesions tend to be less marked than those of chickens. However. Differentiate from Newcastle disease. disinfection. bacterial sinusitis in ducks. but good husbandry. lesionless carriers of highly pathogenic virus. controlled marketing of recovered birds. all-in/all-out production. although it may reduce losses initially. Morbidity is low.
PCR testing of embryonally infected chicks using DNA testing is uniformly positive for blood and faecal samples. Critical hatchery practices: Separate infected and uninfected lines. Prevent/ reduce cross-infection in hatchery and on farm. 'nonshedders' . often with tumour foci. birds with egg antigen will be antibody negative.only 3% produced infected chicks. Treatment None. Two cell types may be found in the same tumour. Virus survival is poor but sufficient to allow cross contamination in hatcheries and on farm in rear. Diagnosis History.80% produce infected chicks.tumours usually contain well-differentiated myelocytes. Minimise stress. age. Separation in vaccination.most but not all. ribs. Enlargement of abdomen. Loss of weight. There is also evidence that it is slightly more sensitive than conventional testing. Prevention Checking of antigen in the albumen is a basis for eradication .antibody negative. preferably on separate hatch days and in separate machines. particularly of the sternum. shed virus and develop tumours. Splenomegaly and enlarged kidneys also occur. Signs Depression. 'Shedders' . lesions. Persistent low mortality. 12 .an Elisa test is aviailable to identify antibody positive birds. Serology . Lymphoid Leukosis. sacral joint. ultimately identification of virus by isolation and/or PCR. histology. Most characteristically are chalky white tumours in the bone marrow. Microscopic . Post-mortem lesions Liver enlargement. Differentiate from Marek's disease. Emaciation. Handle clean lines before infected lines. Many are asymptomatic. liver.
Many are asymptomatic. fibrosarcomas. There may be increased susceptibility to other infectious diseases due to damage to the immune system. lateral transmission is poor but infection may occur by the faecal-oral route. kidney etc. spleen.egg layers are generally more susceptible to lymphoid leukosis. Liver may be very large. Egg production is somewhat reduced. Mortality tends to be chronically higher than normal for a prolonged period. Leukosis/Sarkoma Group Introduction Lymphoid Leukosis. Delay live vaccine challenges. Avoid migration errors (birds unintentionally moving between pens). Vertical transmission is most important by infection of the egg white in infected breeders (who are long-term carriers). myxosarcomas. Minimise group sizes. 13 . then liver. it may be as short as 6 weeks for some of the other manifestations. erythroblastosis. It affects chickens worldwide with susceptibility varying considerably among different strains and types of stock . especially in young birds. myeloblastosis (see Sero-type J). Signs Depression. age.Farm practices: Brood and rear lines separately and maintain separate for as long as possible. liver or bursa. coligranuloma. osteopetrosis. Enlargement of abdomen. initially in the bursa. The causative viruses are rapidly inactivated at ambient temperature and on exposure to most disinfectants. In lymphoid leukosis the incubation period is about 4-6 months. Microscopic .cells lymphoplastic Diagnosis History. Emaciation. Differentiate from Marek's disease. Morbidity is low but mortality high. Avian Leukosis. A complex of viral diseases with various manifestations such as lymphoid leukosis. cytology. lesions. Persistent low mortality. Post-mortem lesions Focal grey to white tumours. other tumours. Loss of weight.
vertical transmission is uncertain. The incubation period is 5-7 days. eradication . guinea fowl and possibly pheasants seen in Europe. Ocular and nasal discharge. Signs Decreased appetite. all-in/all-out production. Prevention Good hygiene.checking of antigen in the albumen is a basis for eradication (see Sero-type J for details). Diffuse lymphoid tumours in an enlarged liver from a mature broiler parent hen. fomites can be important in moving infection between farms. South America and North America.Treatment None. There is rapid lateral transmission with infection by aerosol through the respiratory route. turkeys (see separate summary). Two subgroups have been identified on the basis of the G-protein sequence: A (original UK isolates) and B (original southern Europe isolates). 14 . weight gain and feed efficiency. Avian Rhinotracheitis 'Swollen Head Syndrome' Introduction A viral disease of chickens. It is caused by a pneumovirus of the Paramyxoviridae family. Figure 9. Africa. Facial and head swelling (though this can occur in other conditions). Conjunctivitis. morbidity is 10-100% and mortality can be 110%. control arthropods. As for many infections. Dyspnoea. Loss of voice. This was a case of Myelocytoma Avian Leukosis (Sero-type J). first isolated from poults in South Africa in 1978. Snick.
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.
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.
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.
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.
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.
Enlarged spleen (over 1gm/kg bodyweight, often with pale foci). Liver usually enlarged, sometimes with subcapsular Affected birds may also have: haemorrhage.
Lung congestion Ovarian regression Yolk peritonitis Pale foci and haemorrhages in pancreas. Serological tests (agar gel immunodiffusion) may be used to detect either the specific antigen (which is likely to be positive first) or the antibody response to it. 18 . Reduced feed intake and blood sugar can precipitate fatty liver and kidney syndrome. in embryos. Allin/all-out production. Thickened skin under foot pad. Sudden deaths in fatty liver and kidney syndrome. Signs Poor growth. Elisa tests have been developed experimentally. Chondrodystrophy. Histopathology may also be used but the findings are not specific to this condition. Viral particles may be demonstrated in bile. Good biosecurity. webbing between toes. Drinking water which is well chlorinated should be helpful in reducing challenge by this route. Must be confirmed by laboratory tests. 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. Treatment No specific treatment known. A RT-PCR test may be used to detect viral RNA in tissues. Prevention Thorough cleaning and disinfection after depletion of an affected flock. Biotin Deficiency. Diagnosis Typical signs and lesions. Scabs around eyes and beak. It may be helpful to control other conditions which may be occurring at the same time. Post-mortem lesions See signs. Leg weakness. Pale livers and kidneys in fatty liver and kidney syndrome.
Loss of vent feathers. Differentiate from pantothenic acid deficiency (skin lesions). Scabs around vent. Irritation. 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. Post-mortem lesions Usually none. Check flocks regulary for rapidly moving insects at the base of the feathers on the abdomen or around the vent. Biting Lice Introduction Various species of lice are common external parasites of poultry worldwide. may be some feather damage and crustiness of skin. lesions. response to treatment/prevention. 19 .Diagnosis Signs. Parasites on birds. Drop in egg production. Loss of condition. has very low bioavailability. Signs Lack of thrift in young birds. especially around vent. They are spread by direct contact between birds and by litter etc.naturally present in many raw materials. Prevention Supplementation of diets with biotin . Lice eggs stuck to feathers. Diagnosis Identification of the parasites. bedbugs. Menocanthus stramineus is the most pathogenic and is said to be capable of causing anaemia in heavy infestations. Differentiate from mites. Away from birds adults survive about 4-5 days. Treatment Addition of biotin in feed or water. Treatment Malathion powders and pyrethroid sprays where approved for bird application.
Post-mortem lesions Anaemia. Blackfly Infestation Introduction Grey-black hump-backed flies. 5 mm long and found in North and South America that are external parasites of birds and mammals. as the larvae within eggs are not killed by most products. 20 . Signs Anaemia in young birds. season. Eggs and larvae survive through the winter to cause new infestations in the following year. Biological control using a strain of Bacillus thuringensis has had some success and is preferable to insecticides. although these insects can travel up to 15 miles. Prevention Similar measures as for mosquito control. Effective removal of all organic material at flock depletion should be practised in all-in/all-out production systems. The condition tends to occur near to rapidly flowing streams. Treatment Treatment is difficult. Examine for lice regularly. local history.Prevention Avoid direct contact with wild and backyard poultry. Swarms of flies. especially in autumn and winter and treat if required. The flies transmit leucocytozoonosis and also a filarial parasite in ducks. It is usually necessary to treat twice at a 7-10 day interval to fully control the condition. Diagnosis Anaemia. Weekly treatments are required.
ducks and other waterfowl occurring worldwide and caused by a bacterial toxin produced byClostridium botulinum mainly types A / C. Maggots or putrid ingesta may be found in the crop. maggots) is consumed by the birds. Feathers may be easily pulled (chicken only). carcases. The toxin and bacterial spores are relatively stable and may survive for some time in the environment. signs. weakness. Diagnosis History. Prevention Preventing access to toxin. A soiled beak. Morbidity is usually low but mortality is high. suspect food and stagnant ponds. Treatment Remove source of toxin. wings then neck. is also quite typical.Botulism Introduction A condition of chickens. Signs Nervous signs. Affected broilers tend to settle with eyes closed when not disturbed. progressive flaccid paralysis of legs. then sudden death. supportive treatment if justifiable. The toxin is produced in decaying animal (usually carcases) and plant waste. Differentiate from acute Marek's disease ('Floppy Broiler Syndrome') by histology of the brain. mouse toxicology on serum or extract of intestinal contents. Mild enteritis if has been affected for some time. selenium. The single most important measure is careful pick-up and removal of all dead birds on a daily basis. especially in hot weather. turkeys. Post-mortem lesions Possibly no significant lesions. Toxin may also be produced by the bacteria in the caecum. because it rests on the litter. and toxin-containing material (pond-mud. 21 . This will reduce the risk of botulism both in the poultry and in any grazing animals on land where poultry litter is spread. antibiotics. 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.
the cause of Blackhead. Morbidity is high but it is not associated with mortality. 22 . and infection withStaphylococcus spp. in chronic cases. leg weakness. and a four-week prepatent period. up to 1.5 cm in length that occur in the caecum. Infection is by the oral route. Morbidity may reach more than 50% but the condition is not fatal. control of leg problems. Treatment Not usually appropriate. Prevention Good litter management and handling. are small whitish worms with a pointed tail. There is an incubation period of 2 weeks for eggs to embryonate. Poor feather cover and caked or wet litter are predisposing factors. Caecal Worm Introduction Heterakis gallinae. Diagnosis Based on lesions. or paratenic hosts with partially developed (L2) larvae. They are found worldwide. bacteria. Earthworms may be transport hosts for eggs. Heterakis gallinaeeggs and larvae are a transport hosts for Histomonas. Post-mortem lesions Inflammation of sternal bursa along the keel bone which may. nematode parasites of poultry and game birds. The meaning of the technical terms relating to parasite life cycle are defined in the glossary. give way to scar tissue.Breast Blister Introduction A complex condition of chickens and turkeys occurring worldwide associated with trauma. Signs Swelling over the keel bone with bruising and discolouration. Signs None.
Diagnosis Adults can be seen in caecal contents at post-mortem examination. Calcium Tetany Introduction A metabolic disease of chickens. Routine anthelmintic treatment. The life cycle ofHeterakis showing the location of adults. an undeveloped egg as found in fresh faeces. and the embryonated egg. possibly with nodule formation. Signs Paralysis. The egg may be ingested directly by a chicken. 23 .Post-mortem lesions Inflammation of caecum. Figure 11. especially broiler parents. Levamisole. Predisposing factors include heat stress with reduced feed intake and panting. or by an earthworm which is in turn ingested by a chicken. are effective. Death from respiratory and cardiac failure. Treatment Flubendazole. Prevention Avoiding access to earth and earthworms.
Campylobacter Infection Introduction Campylobacter spp. Treatment Provide 5 gm of oyster shell per hen on 3 successive days along with vitamin D in drinking water. principally in the caecae. Active ovary with egg in oviduct. are bacteria that commonly infect a broad range of livestock species. managing birds for maximum uniformity. Campylobacter jejuni infection is not currently considered to be pathogenic in poultry though a Campylobacter-like organism is considered to be the cause of 'Vibrionic Hepatitis'. Congested lungs. Campylobacter jejuni is the commonest species found in poultry. lesions. The reason for this is unclear. biofilm or engulfed by protozoa. All campylobacters are delicate organisms that survive for relatively short periods outside the host unless protected by organic material. In poultry they tend to multiply in large numbers in the hindgut. It may be that management that favours dry litter reduces the risk of infection and/or transmission within the flock. Diagnosis This is made on signs.Post-mortem lesions Cyanosis. Differentiate from IB 793b. carcase quality and litter quality are better on farms which tend to have Campylobacter-negative stock. There is an annual cycle with increased risk of infection in the summer months in some countries. other acute infections and other causes of sudden death. and response to treatment. 24 . Campylobacters are a significant cause of enteritis in man. There are indications that plantar pododermatitis. pets and wild animals. Infected poultry are a potential reservoir of this zoonosis. lack of other significant lesions. Prevention Keep pullet flocks on low calcium diet until 5% production hen/day.
For this reason it may be difficult to stop the spread of infection between houses once it becomes established in one house. Treatment Not required on clinical grounds. Prevention In principle. Post-mortem lesions None. as well as processing plant technologies to reduce carcase contamination. sourcing of water from high quality supplies. Many infections are introduced during thinning or other forms of partial depopulation. and changing of overalls and boots on entering bird areas. housed poultry can be maintained free of Campylobacter infection by consistent application of excellent biosecurity. Research is ongoing on the development of vaccines. Key aspects of this include effective sanitation of drinking water. phage treatments and competitive exclusion approaches. The organism is sensitive to air so swabs should be collected into transport medium and other samples placed in airtight containers with minimal airspace. good hand hygiene by stockmen. avoidance of contact with pets and other farmed species. 25 . cloacal swabs or composite faeces. Insects and rodents may act as a means of transfer of the infection from the general environment into the poultry buildings. 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.Signs None. Samples should be tested as quickly as possible after collection.
Ensure good hygiene. Post-mortem lesions White plaques in mouth. Signs Dejection. characterised by thickening and white plaques on the mucosa. intestine and cloaca. copper sulphate (1 kg/tonne feed) for 5 days. microscopic examination of a digested smear (heat in 10% potassium hydroxide) to demonstrate the hyphal forms of the yeast in the tissues. Treatment Nystatin (100 ppm in feed) for 7-10 days. histopathology. smooth and with a yeasty smell. Morbidity and mortality are usually low. Colonies of this fungus appear as white to ivory colour.Candidiasis. Diagnosis Lesions. The cause is a fungal yeast. Control of Candida through drinking water is sometimes practised with chlorination (e. and sometimes other birds and mammals.g. Raised focal lesions may slough into lumen as caseous material. turkeys. Prevention Avoid excessive use of antibiotics and other stressors. Thrush Introduction A disease of the alimentary tract of chickens. 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. sodium or calcium proprionate at 1 kg per tonne continually. possibly confused or masked by signs of the primary disease. Diarrhoea. especially in the crop but sometimes in the proventriculus. 26 . oesophagus. Candida albicans and the condition is seen worldwide. or copper sulphate 1gm/2 litre water for 3 days if approved locally. and associated with gizzard erosion. Poor appetite. Moniliasis. Slow growth. A finely divided powder of copper sulphate (where approved) at 200gm/tonne continually or to 14-16 weeks in replacement pullets. occasionally proventriculus and intestine. proprionic acid. The fungus is resistant to many disinfectants. crop.
It should be repeated periodically. boredom. Prevention Proper density and temperature. Take care to provide fresh clean feed and water. anaemia. low light level. sodium hypochlorite) at 5 ppm. This is economical and effective. through shafts of light in the house). Generalised anaemia. Diagnosis Age. face. Cannibalism. post-mortem cannibalism. uncontaminated by fungi. feed form (mash takes longer to consume than pellets). Differentiate from bacterial dermatitis. Predisposing factors include overcrowding. Signs Pecking at feet (especially young chicks) and vents (adult layers and turkey poults 812 days old). nutritional deficiencies. and strain of bird. excessive light intensity or variation (e. Soluble multivitamins and/ or methionine may be of some benefit in some circumstances. Feather pecking Introduction A complex multifactorial behavioural problem of poultry and game birds seen worldwide. high temperatures. tenosynovitis and other diseases affecting mobility. Post-mortem lesions Skin wounding related to particular signs exhibited. control ectoparasites. Beak trimming may be necessary. Feather-pulling. complying with local regulations and any relevant codes of practice. wings. Morbidity is usually low but mortality is high among affected birds. Treatment Correct any husbandry problems. If so it should be carried out carefully by trained operators. distribution of lesions. head.g. 27 .Chlorox. Provision of a diet that closely matches the nutritional requirements of the stock concerned.
Prevention Separation of birds from possible transport and intermediate hosts. Diagnosis This may be by a combination of macroscopic examination. small intestine or caecum. Some species have earthworms as intermediate hosts.Capillariasis . Morbidity and mortality are usually low. Levamisole. Fenbendazole has been shown to have high efficacy . Worm eggs in the environment are resistant. prepatent period about 21-25 days according to species.Hairworm Infection Introduction Nematode parasitic worms of poultry. Wasting Poor growth. about 0. The worms are 7-18 mm long. game birds and pigeons ofCapillaria species.other approved benzimidazoles can be expected also to have activity. Infection is by the oral route. effective cleaning of houses. 28 . Hairworms in mucosa of crop.05 mm wide and hair-like in appearance. Worm eggs take about 20 days to embryonate with an L1 larvae. seiving intestinal contents. obsignata in the small intestine. C. Signs Diarrhoea. C. Dejection. Treatment Coumphos has been licensed in some markets. Differentiate from other causes of enteritis. contorta in the crop and oesophagus. some are transmitted direct from bird to bird. Post-mortem lesions Enteritis. or characteristic worm eggs in faeces in patent infections.
The condition is caused by infection of. Treatment Treatment would not be possible if the problem is identified at a final depletion.Cellulitis Introduction Cellulitis is literally an inflammation of connective tissues. Prevention Toe scrapes at 15-25 days of age when feather cover is poor are the most likely predisposing factors. skin wounds by particular strains of E. but the affected birds are not readily detectable prior to slaughter. Many meat inspectors become skilled at detecting subtle differences in skin colour in the affected birds. It typically occurs between skin and muscles and between muscles and may be an incidental finding in a range of conditions. In the USA it is called 'Inflammatory Process'. However its main importance is as a cause of condemnation in meat poultry. coli. 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. which can replicate in the tissues. Many affected birds have no other lesions and are reasonably well grown. particularly broiler chickens. often minor. though most of the birds showing toe scrapes will not go on to develop cellulitis. If identified at a thinning there may be time for antibacterial treatment to have some benefit for those birds in the early stages of the problem. Signs Affected flocks tend to have poorer than average productivity and uniformity. Diagnosis Typical lesions. Routine monitoring of skin damage at about 25 days of age may be helpful in fostering good practices. Careful flock management with a view to reducing toe wounds has the greatest impact in controlling cellulitis. 29 .
Prior to confirmation that it is in fact a virus it was known as Chicken Anaemia Agent or CAA. Sudden rise in mortality (usually at 13-16 days of age). PCV of 5-15% (normal 27-36%). Acute mycotic pneumonia. heat (70°C for 1 hour. Treatment Good hygiene and management. and control of other diseases as appropriate.) or poor management (e. Gangrenous dermatitis on feet. lateral transmission may result in poor productivity in broilers. Diagnosis Gross lesions. may be beneficial. Transmission is usually vertical during sero-conversion of a flock in lay. The virus is resistant to pH 2. If gangrenous dermatitis is a problem then periodic medication may be required. Gumboro.g. Hypochlorite appears most effective in vitro. 30 . demonstration of ongoing sero-conversion in parent flock. Mortality is typically 5-10% but may be up to 60% if there are predisposing factors present such as intercurrent disease (Aspergillosis. ether. virus may be isolated in lymphoblastoid cell line (MDCC-MSB1). Atrophy of thymus and bursa. 80°C for 5 minutes) and many disinfectants even for 2 hours at 37°C. legs wings or neck. Pale birds. Discoloured liver and kidney. chloroform.Chicken Anaemia Introduction A viral disease of chickens caused by Chicken Anaemia Virus or CAV. Inclusion body heptatitis etc. No clinical signs or effect on egg production or fertility in parent flock during seroconversion. Signs Poor growth. Post-mortem lesions Pale bone marrow. poor litter quality).
Egg transmission does not occur. Intercurrent salmonellosis and. man. Chlamydiosis. their degree of attenuation is variable. Morbidity is 50-80%. and may be detected by SN. Psittacosis. 15 weeks. Production drops in naive laying flocks Post-mortem lesions Vascular congestion. ducks. Ornithosis Introduction An infection of turkeys. but occurring probably worldwide. Serology: antibodies develop 3-6 weeks after infection. Nasal discharge. Iodophores and formaldehyde are effective disinfecting agents. a bacterium of highly variable pathogenicity. say. It is transmitted by contact. Occasional transient ataxia in pigeons. phenolics are less so. Signs Respiratory signs. Inappetance. 31 . Conjunctivitis. Fibrinous pericarditis. psittacines. or IFA. especially pigeons and robins. Immunity: there is a good response to field challenge (in birds over 4 weeks of age) and to attenuated live vaccines. Weakness. other infections may be predisposing factors. Greenish-yellow diarrhoea. Airsacculitis. perhaps. caused by Chlamydia psittaci. They should be used at least 6 weeks prior to collecting eggs for incubation. pigeons.Prevention Live vaccines are available for parents. Their use may be restricted to those flocks that have not sero-converted by. Elementary bodies are highly resistant and can survive in dried faeces for many months. Wasting. mortality 5-40%. It is a 'Scheduled Disease' rarely diagnosed in UK. faecal dust and wild bird carriers. Weight loss. rarely chickens. Elisa. Depression.
may rupture in pigeons. choline. In embryos parrot beak. Signs Short legs. ducks and turkeys. lesions. Congested lungs and air sacs in the turkey. Perihepatitis. Spleen enlarged and congested. shortened bones. Necrotic foci in liver. Treatment Tetracycline (200-800 ppm in feed for 3-4 weeks) and/or quinolone medication and supervised slaughter. 32 . Fibrinous pneumonia. Distortion of hock. Lameness. Chondrodystrophy. Diagnosis History. exclusion of wild birds. This condition is seen in chickens. zinc. folic acid. Serology: complement fixation. Slipped Tendon or Perosis Introduction Caused by deficiency of manganese. Duck septicaemia. Malposition of leg distal to hock. niacin may also be involved). signs. Live and inactivated vaccines are protective although the former result in carriers and the latter require several applications. Elisa and gel diffusion. In turkeys it may be an inherited deficiency of galactosamine. biotin. Prevention Biosecurity. either singly or in combination (although deficiencies of pyridoxine. Slipping of Achilles tendon (or perosis). Intracytoplasmic inclusions are helpful but confirmation requires demonstration of causal organisms (Giemsa stain. IFA). Differentiate from Duck viral hepatitis.
Prevention Addition of manganese. rickets. Tucked appearance. vitamins. ruptured ligaments. analysis of feed. infectious synovitis. meleagridis affect the lower small intestine rectum and caecae. E. Watery diarrhoea that may occasionally be blood stained or contain clumps of mucus or shed mucosa. gallopavonis and E. Coccidiosis of Turkeys Introduction Infection of turkeys with Eimeria spp. Signs Huddling. ruffled feathers. while E. Diagnosis Lesions. Lateral slipping of tendon. of which two are associated with significant disease effects. Post-mortem lesions The affected area of intestine shows thickening of the wall and dilation. The contents may be haemorrhagic or be watery with white material shed from the mucosa. Depression. while E.Post-mortem lesions Shortening and thickening of long bones. Five species of Eimeria have been identified that cause lesions in turkeys. E. meleagrimitis affects the upper small intestine. Shallow trochlea. adenoides affects the caecae and rectum. This disease is not very common in commercially reared turkeys though most turkey growers receive preventative medication for at least part of their lives. dispersa is found in the small intestine. Treatment For flock proceed as for prevention. 33 . Tibia and metatarsus bowed. infectious arthritis. choline. Weight loss. no value to affected bird. Differentiate from twisted leg. correct mineral balance.
Figure 37. Turkey coccidiosis of the upper small intestine caused by E. 34 . Treatment Toltrazuril. gamonts). typically to 12 weeks of age. Turkey caecal coccidiosis caused by E. meleagrimitis.Diagnosis Signs. Diclazuril is also used for this purpose. Dosage levels of ionophores may be critical to efficacy and safety. lesions. The intestines are dilated. adenoides. Prevention The ionophore coccidiostats lasalocid and monensin are routinely used in turkey growers. Differentiate from necrotic enteritis. Amprolium. microscopic exam of scrapings (oocysts. Sulphaquinoxaline). Exposure of previously unmedicated birds to these compounds can cause toxicity. The exudate can range from semi-liquid to solid white cores. Avoid use of tiamulin in ionophore treated birds. Sulphonamides (e. show some spotty congestion and have abnormal contents due to the sloughed epithelium. Figure 38. Salinomycin is toxic for turkeys even at very low doses.g.
35 . lesions. histomonosis. Signs Depression. Ruffled feathers. Post-mortem lesions Petechiae. mitis (see above). microscopic examination of scrapings. vaccination by controlled exposure. Diagnosis Signs. Production less affected than in some of the other forms of coccidiosis. blood in faeces. Caecal. hygiene. of caecal mucosa. Vitamins A and K in feed or water. Shuttle programmes with chemicals in the starter diet usually improve control. E tenella Introduction This was at one time the commonest type of coccidiosis and is certainly the most easily diagnosed. Morbidity is 10-40% and mortality up to 50%. Differentiate from ulcerative enteritis. Sulphonamides. E. Treatment Toltrazuril. Closed eyes. Amprolium. Diarrhoea.Coccidiosis. ecchymoses. Recovered birds have good immunity to the same parasite. Transmission as for E. Accumulation of varying quantities of blood and caseous necrotic material in the caecum. tenella is more common when 'straight' ionophore programmes are used. In some markets the organic arsenical compound 3-Nitro is used as an aid in the control of caecal coccidiosis. It is caused by Eimeria tenella and results in lesions in the caecum of chickens worldwide. Prevention Coccidiostats in feed. Vaccines are used mainly in breeders but increasingly in broilers. Inappetance. Thickening.
The infective agent is found in litter. humidity). Moderate Eimeria tenella infection in the caecae of a chicken (Score 3). 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. which colonises the small intestine. 36 . The parasite is moderately resistant in the environment and highly resistant to conventional disinfectants. May predispose to wet litter. Diagnosis Mild lesions. Signs Reduced feed conversion efficiency and weight gain. The caecal walls are thickened and haemorrhagic and there is a mass of blood in the caecal lumen. Coccidiosis. is caused by the protozoan parasite Eimeria mitis. seen worldwide. 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. E mitis Introduction This condition of chickens.Figure 15. faeces and on fomites and birds are infected by the oral route with an incubation period of 2-5 days. secondary bacterial enteritis. Predisposing factors include exposure to faeces and litter conditions that favour development of the parasite (temperature.
Poor production. Signs Depression. caecum and rectum. Inappetance. Closed eyes. Coccidiosis. Severe necrotising enteritis. May be included in vaccines. Prevention Coccidiostats in feed. Vitamins A and K in feed or water. microscopic examination of scrapings. it is found in the terminal ileum. caecal coccidiosis. 37 . Morbidity and mortality are variable. extending into caecal tonsils. Diagnosis Signs. Oocysts in caecum and rectum. Treatment Toltrazuril. Ileorectal. Of moderate to high pathogenicity. Ruffled feathers. hygiene.Prevention Normally controlled by anticoccidials in feed. There is good immunity to the same parasite in recovered birds. blood in faeces. Post-mortem lesions Petechiae and thickening of the distal third or more of intestine. Differentiate from ulcerative enteritis. Diarrhoea. E brunetti Introduction A relatively rare form of coccidiosis affecting chickens worldwide caused by Eimeria brunetti. Sulphonamides. Amprolium. lesions. vaccination by controlled exposure. This species is not usually included in vaccines for broilers.
anatipestifer. Signs Sudden death. Amprolium. Tucked appearance. large number of merozoites). Diagnosis Signs. 2 days off. microscopic examination of scrapings (usually few or no oocysts. Moderate Eimeria brunettiinfection in the terminal ileum and rectum of a chicken. Tyzerria has eight sporocysts in each oocyst. lesions. compared to four per oocyst forEimeria. 38 . In the goose E. Blood-stained vent.g. Sulphadimidine 30-600gm/100 birds/day. 3 days on). Post-mortem lesions Massive haemorrhage in upper small intestine. Differentiate from Duck viral hepatitis. Coccidiosis occurs only very rarely in commercially reared ducks in the UK. of Ducks and Geese Introduction Young ducks and geese may suffer from Eimeria spp infection. 3 days on. Intestinal. Duck viral enteritis. Coccidiosis. anseris is the most important. Vitamins A and K in feed or water.Figure 16. Depression. There is thickening of the intestinal mucosa and there are lines of haemorrhagic spots in the mucosa. Treatment Sulphonamides (e. while in ducksTyzzeria perniciosa is most pathogenic.
Signs Depression. Hygiene. Diagnosis Lesions. Kidneys light grey to greyish pink. Reduced feed intake. it can also infect Barbary ducks and swans.Prevention If required coccidiostats could be used in feed. Kidney Introduction A disease of geese caused by Eimeria truncata that can cause high mortality in geese of 312 weeks of age. 39 . presence of coccidial stages in fresh scrapings of kidney lesions. Post-mortem lesions Enlarged kidneys. Coccidiosis. Tiny white foci and petechiae in the kidneys. however this is not routinely practised. Diarrhoea . Treatment Controlled trials of treatments have not been published. Prevention Good Hygiene.faeces tend to be whitish. Weakness.
Depigmentation of skin and plasma is especially evident in this form of cocccidiosis and this is commercially important in some markets. Mild to severe enteritis.Coccidiosis. commercial vaccines commonly contain more than one strain of E. Treatment Sulphonamides. Mid-intestinal. Diagnosis Signs. of moderate to high pathogenicity it is seen worldwide. Closed eyes. non-specific enteritis. contents often orange in colour. This is one of the less immunogenic species. lesions. E maxima Introduction One of the more common forms of coccidiosis in commercial broilers. hygiene. Amprolium. Ruffled feathers. Morbidity and mortality are variable. This infection is often associated with E. Poor absorption of nutrients/pigments. Poor production. microscopic examination of scrapings. Signs Depression. mucosa tends to be pinker than normal. Post-mortem lesions Petechiae and thickening of middle third of intestine. Caused by Eimeria maxima. maxima. Inappetance. Prevention Coccidiostats in feed. Because of the area of intestine affected it tends to have a significant effect on productivity and susceptibility to necrotic enteritis. acervulina coccidiosis and there may be large numbers of characteristic oocysts in smears. vaccination. Differentiate from necrotic enteritis. Vitamins A and K in feed or water. 40 . Blood or pigment in the faeces.
lesions. Coccidiosis. of middle to posterior third or more of small intestine. blood in faeces. microscopic examination of scrapings Differentiate from necrotic enteritis. E necatrix Introduction A highly pathogenic form of coccidiosis. Moderate Eimeria maxima infection in the jejunum of a chicken (Score 2). Deep scrapings necessary to show large schizonts. 'Sausage-like' intestine. Signs Reduced feed consumption. Oocyts in caecal scrapings. The lesions are subtle compared to other forms of coccidiosis. 41 . It occurs in chickens worldwide and has variable morbidity but mortality is high in severely affected birds. Diarrhoea. Post-mortem lesions Petechiae and thickening. Depression. other types of coccidiosis. in which the parasite is present in the small intestine and in the caecum. Schizonts seen as white spots through the serosa interspersed with petechiae. Closed eyes. The intestine is slightly thickened and there are scattered haemorrhages in the mucosa when seen from the inside. caused by Eimeria necatrix. Severe necrotising enteritis. Mid-intestinal. Diagnosis Signs. Ruffled feathers. Poor production.Figure 13. Inappetance.
Eimeria mivatiis currently considered not to be a valid species distinct from E. Diarrhoea. Closed eyes. E acervulina Introduction This is probably the commonest cause of coccidiosis in chickens and occurs worldwide. This is one of the less immunogenic species. Poor production. which is moderately pathogenic. Sulphonamides. maxima. Morbidity is variable and mortality low or absent. Signs Depression. Coccidiosis. commercial vaccines commonly contain more than one strain of E. both alone and in association with other species of coccidia and is caused by Eimeria acervulina. hygiene. vaccination. Depigmentation. Ruffled feathers. Upper Intestinal. Figure 14. Post-mortem lesions 42 . In this case the intestine is thickened and can become ballooned and sausage-like. Prevention Coccidiostats in feed.Treatment Toltrazuril. Haemorrhages and white spots are visible from the outside of the intestine. It is seen in layers and in broilers. Amprolium. Vitamins A and K in feed or water. Inappetance. Moderate Eimeria necatrix infection in the jejunum of a chicken (Score 3). acervulina.
lesions. vaccination by controlled exposure. Moderate Eimeria acervulinainfection (score 2) in chicken duodenum. and other lesions. Treatment Toltrazuril. Differentiate from necrotic and non-specific enteritis. 43 .the duodenum and part of the ileum. Various publications provide a photographic key to severity of lesion. hygiene. In milder infections there may be scattered white spots. Figure 12. Thickening. restricted to upper third of small intestine . Sulphonamides. in severe the entire surface is pale or denuded of epithelium. Petechiae. Immunity is quite short lived (about 30 days) in the absence of continued challenge. microscopic exam of scrapings. Diagnosis Signs. A detailed description is beyond the scope of this book. In severe infections they become confluent and cause sloughing of the mucosa. Prevention Coccidiostats in feed. White spots or bands in the mucosa. Poor absorption of nutrients/pigments. in feed or water. A system of assessing the severity of coccidial challenge by attributing a 'score' is often used. Amprolium. In general terms a score of 0 indicates no lesions and a score of 4 indicates maximal severity of lesion or death.
Reduced appetite. Diagnosis Isolation. Poor navel healing. Synovitis. mucosal damage due to viral infections and immunosuppression are predisposing factors. Infection is by the oral or inhalation routes. Omphalitis. Pericarditis. Colisepticemia Introduction Coli-septicaemia is the commonest infectious disease of farmed poultry. sero-typing. Snick. Omphalitis. etc. water.Colibacillosis. and via shell membranes/yolk/navel. Enteritis. The infectious agent is moderately resistant in the environment. Cellulitis over the abdomen or in the leg. Morbidity varies. Dejection. sneezing. Salpingitis. Arthritis. Poor growth. Aerobic culture yields colonies of 2-5mm on both blood and McConkey agar after 18 hours .most strains are rapidly lactose-fermenting producing 44 . fomites. It is frequently associated with immunosuppressive diseases such as Infectious Bursal Disease Virus (Gumboro Disease) in chickens or Haemorrhagic Enteritis in turkeys. It is most commonly seen following upper respiratory disease (such as Infectious Bronchitis) or Mycoplasmosis. Post-mortem lesions Airsacculitis. Peritonitis. pathology. with an incubation period of 3-5 days. coughing. Swollen liver and spleen. Granulomata in liver and spleen. Signs Respiratory signs. but is susceptible to disinfectants and to temperatures of 80°C. Perihepatitis. or in young birds that are immunologically immature. mortality is 5-20%. turkeys. It is caused by the bacteriumEscherichia coli and is seen worldwide in chickens. Lesions vary from acute to chronic in the various forms of the disease.
flouroquinolones. as well as Pseudomonas. The liver is almost entirely covered by a substantial layer of fibrin and pus. Staphylococcus spp. Treatment Amoxycillin. other enterobacteria such as Proteus. the breast area. Figure 17. when severe. It is seen in growing broiler chickens and turkeys. Severe perihepatitis in colibacillosis in a broiler parent chicken. potentiated sulphonamide. feed and water. Prevention Good hygiene in handling of hatching eggs. whereas others progress to deep ulcers so the size. 45 . Differentiate from acute and chronic infections with Salmonella spp. Immunity is not well documented though both autogenous and commercial vaccines have been used. hatchery hygiene. Control of predisposing factors and infections (usually by vaccination). rear surface of the hock and. Some lesions are superficial. Contact dermatitis is commonly monitored at processing as a means of measuring 'welfare status'. the foot pad. gentamycin or ceftiofur (where hatchery borne). etc. Hock Burn. stage of resolution and severity of lesion is likely to affect the degree of discomfort or pain suffered. tetracyclines. and in broiler parents. Pododermatitis Introduction Contact dermatitis affects skin surfaces which have prolonged contact with litter. Contact Dermatitis.brick-red colonies on McConkey agar. neomycin (intestinal activity only). Well-nourished embryo and optimal incubation to maximise day-old viability. good sanitation of house.
level of soya bean meal in feed (according to some authors. drinker management.Pododermatitis is often related to high droppings pH. Prevention This condition is closely linked to intestinal function as this is the prime determinent of faecal consistency and stickiness. Signs Blackened skin progressing to erosions and fibrosis on the lower surface of the foot pad. See the discussion in the section on Dysbacteriosis. stickiness of droppings). and sometimes in the breast area. It can be reproduced by adding water to the litter. Choice of drinker type (nipple as opposed to bell). Post-mortem lesions As described under signs. and. 46 . litter moisture. most importantly. proper insulation in cold climates. at the back of the hocks. If severe the foot and hock lesions may contribute to lameness or serve as a portal of entry for secondary infections. and adequate ventilation to remove moisture are all important. Figure 18. Diagnosis Signs and lesions. Treatment Not applicable. Moderate pododermatitis on a foot pad.
C. and ducks. although bird strains do not infect mammals very well. White convoluted tracks in the mucosa. Cryptosporidium baileyi can cause respiratory disease in chickens and turkeys. Diagnosis Microscopic examination of mucosal scraping. Avoidance of access to intermediate hosts. A further species causes respiratory disease in quail. The same species causes infections of the hindgut and cloacal bursa in chickens. 47 . acervulinaoocyst). They replicate in the brush border on the surface of epithelial cells. and vice versa. They also differ from coccidia in being poorly host specific. but much smaller (typically oocysts are less than ¼ of the size of an E. Routine worming. Cryptosporidiosis Introduction Cryptosporidia are related to the coccidia. Coumaphos. Some have beetle or earthworms as intermediate hosts. meleagridis also infects both species.Cropworms Introduction The nematode worms Capillaria spp and Gongylonema ingluvicolainfect the mucosa of the crop and oesophagous of poultry and game birds. Treatment Levamisole. Emaciation. The oocysts are excreted ready sporulated in the faeces and infection occurs by inhalation and ingestion. turkeys. Signs Anaemia. Prevention Effective cleaning of housing. Post-mortem lesions Inflammation and thickening of mucosa of crop and oesophagus.
Cough. Torticollis. Signs Incoordination. Low weight gain. Prevention The oocysts of cryptosporidia are extremely resistant to chemical disinfection. coli-septicaemia) there may be benefit in medicating for these. There are no effective preventative medicines or feed additives. 48 . Treatment Unfortunately there is currently no known effective treatment in poultry. Diarrhoea. If other disease processes are complicating the situation (e. Diagnosis Identification of the parasites attached to the epithelium by microscopic examination (smears histopathology acid-fast staining).g. Swollen sinuses.Signs Snick. Tremors. Circling. Pneumonia. recumbency. 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. Post-mortem lesions Sinusitis. It is becoming increasingly common for water companies to screen water supplies for cryptosporidia because of the human health implications of mammalian strains. Airsacculitis.
Reduced breeding performance. Prevention Use fresh dry litter (avoid old sawdust). 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. Diagnosis Lesions. Diagnosis Gross and microscopic lesions. resulting in erosions. Mycotic lesions in lungs. air sacs etc. Treatment 49 . especially of femoral anti-trochanter but also other leg joints. Rapid growth is a possible predisposing factor. The cause remains to be confirmed. Post-mortem lesions Damaged epiphyseal articular cartilage. and cartilage flaps. Microscopically there is necrosis and there may be fissures of articular cartilage and associated osteochondritis. Signs Lameness. or developmental defects. but it may result from physical damage.Post-mortem lesions Necrotic lesions with associated congestion in cerebrum. Treatment None. isolation of the fungus. Degenerative Joint Disease Introduction A condition of chickens and turkeys seen worldwide.
Diagnosis Signs.None available. For small flocks dipping the affected parts in a solution of acaricide may be beneficial. round. pigeons etc.Knemidocoptes spp. microscopic examination for mites in scrapings. Raised thickened scales.5mm in diameter. Mange lesions on legs and unfeathered parts. 50 . The adult females are short legged. There may be a place for growth-control programmes. Post-mortem lesions As described under signs. Exclusion of wild birds from chicken areas is advised as far as possible. up to 0. especially during period of rapid growth. pheasants. Appropriate management of a segregation pen and early marketing of mildly affected birds may limit losses and improve flock welfare. Signs Cause irritation and the bird pulls feathers. Application of mineral or vegetable oil is also beneficial. It may be best to cull affected birds from small flocks. Prevention Careful cleaning of buildings during down-time will help reduce the risk of these infections. Depluming and Scaly Leg Mites Introduction External parasites of adult chickens. Treatment Not usually required in commercial poultry. Prevention Avoidance of physical sources of injury to bones and joints. Unthriftiness.
pericardial sac. a tranquilizer. It has been suggested that degenerative changes in the wall of the artery and copper deficiency may be factors. Aortic Rupture Introduction A complex. The infective agent. Rupture of major blood vessel at base of heart or by the kidneys. genetic condition of turkeys linked to male sex and high growth rate. presumably due to a sudden increase in blood pressure.Dissecting Aneurysm. Skin pale. kidneys. Abdominal cavity full of blood. Morbidity is around 100% and mortality 0-95%. Reserpine in diet of birds of 4+ weeks (no longer licensed in the UK). a picornavirus may also 51 . leg muscles. Possibly blood in the mouth. Diagnosis History and lesions. Duck Viral Hepatitis Introduction A viral disease of ducks occurring worldwide and previously a scheduled disease in UK. Prevention Limit feed in birds of 16+ weeks. Post-mortem lesions Carcase anaemic. Aspirin at 250 ppm in feed or water may be of benefit. A longtitudinal split of the abdominal aorta is the most common lesion. Reserpine. recovered birds carrying the virus for 8 weeks. Haemorrhages in lungs. birds found on breast or side. A sudden noise or other cause of excitement can lead to an 'outbreak'. The disease is transmitted by infected ducks and other waterfowl and spreads rapidly. Signs Sudden death with no warning signs. was included in feed at 1 ppm for 3-5 days to reduce blood pressure. Treatment None currently licensed.
5 ml serum of recovered birds given intramuscularly. arching of back. in USA since 1967. All waterfowl are susceptible and the Barbary duck is more susceptible than the Pekin. Differentiate from Duck plague (viral enteritis). breeder vaccination. A different picornavirus causes a similar condition in North America. Newcastle disease. lesions. bile duct proliferation and inflammation. Diagnosis History. Duck Virus Enteritis. Depression. Treatment Antiserum. Recovered birds may carry the virus for a year. mostly in ornamental collections. Punctate/diffuse haemorrhages. Transmission is by infected birds. rapid deterioration and death. Microscopically . SN serology. Duck septicaemia (anatipestifer). 0. Death in good condition. Duck Plague Introduction A herpesvirus infection of ducks and geese diagnosed in the UK in 1972.survive for ten weeks in brooders and five weeks in faeces. Kidneys and spleen swollen. Signs Sudden death. Fall on side. Post-mortem lesions Liver swollen. Prevention Vaccination and/or antiserum.focal necrosis. 52 . also the Netherlands and other countries. coccidiosis. isolation in CE (causes stunting of 9 day embryo). often in opisthotonus. paddling of legs. The disease follows a very acute course with a morbidity of 5-100% and mortality of 5-100%. Influenza and a 'Type II Variant' hepatitis caused by Astrovirus. fomites and arthropods. only slightly attenuated vaccine is applied at day old by foot web stab and may be repeated in breeding birds to provide maternal immunity. Live.
oesophagitis (birds on restricted feed). Young ducks may show thymic and bursal lesions. The condition is seen mainly in rapidly growing broiler chickens with good food intake. excess caecal volume and fermentation. Paresis. Dysbacteriosis. probably through interference. body cavities. 53 . vent gleet. Prevention Isolation from waterfowl. pasteurellosis. pericardium. spleen. vaccination if approved by authorities (CE adapted live virus). Treatment None. Severe diarrhoea. Dehydration. sometimes dysentery. Crusty plaques from oesophagus to bursa (covered by yellowish plaques in later stages).Signs Sudden deaths. Tremor. HA-. but vaccination in face of outbreak is of value. is common in countries with restrictions on the use of antimicrobial growth promoters and pressure to reduce therapeutic antimicrobial usage. Diagnosis Isolation: Duck CAMs 12 day embryos die in 4 days. Occasionally cyanosis of the bill in the young. Thirst. intranuclear inclusions Differentiate from Duck hepatitis. Occasionally penile prolapse in the penis in drakes. Ataxia. liver. Photophobia. heart. Rapidly spreading disease. coccidiosis. Closed eyes. Haemorrhage in intestine. Post-mortem lesions Severe enteritis. Non-specific Bacterial Enteritis Introduction Inflammation of the small intestine associated with wet litter. Drop egg production.
Argentina. In the autumn of 1976 a distinct egg drop syndrome was first identified in Northern Ireland. Diagnosis Signs. feed interruptions and subclinical coccidiosis may be contributory factors. Prophylactic antimicrobial medication may be necessary in some circumstances. Treatment Amoxycillin and tylosin treatment appear to be beneficial. Peru. first isolated in Northern Ireland in 1976. Mortality is usually negligible. Germany. Apparently a similar disease had been seen over a 4-year period in broiler parents in Holland. Good control of coccidiosis. Signs Diarrhoea. It affects chickens and has occurred in Ireland. microscopic examination of scrapings from the wall of the small intestine (to exclude coccidiosis and perhaps to assess the bacterial flora). Post-mortem lesions Excessive fluid content throughout the small intestine. Circumstantial evidence suggests that the main route of transmission is through the eggs (vertical transmission) 54 . England. Feed acidification may be helpful in some circumstances. Careful choice of any feed enzymes and their matching with local raw materials can have an impact on substrates made available to intestinal bacteria. 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. lesions. Holland. 127. rather we are dealing with a disruption in the normal flora of the gut. Wet faeces in the rectum. Water intake may be increased or irregular. No single bacterium appears to be responsible.Dietary changes. Prevention Competitive exclusion ('normal adult flora') use in day-old chicks reduces the risk of this condition. France. The cause has been identified as Adenovirus BC14. especially where treatment is initiated early. Voluminous caecae. Brazil. often with gas bubbles. Treatment should coincide with good relittering and it is important to provide fresh sanitary drinking water. Uruguay. Spain.
Management problems may be involved: inadequate water supply. Drops may be of 5 to 50% and last for 3-4 weeks. Rough. Marek's disease/Leukosis or any infectious disease causing a significant systemic disturbance (CRD. Serology: HI. Isolation of haemagglutinatin agent in duck eggs or cell culture. Signs Egg drop at peak or failure to peak. 55 . Infectious diseases include Infectious Bronchitis. Poor internal quality. Nutritional deficiency should be considered. Histopathology .followed by latent infection during rear with viral excretion starting shortly before sexual maturity. and D as well as calcium. group antigen distinct from classical adenoviruses (white cells. Avian Encephalomyelitis. Clinical disease occurs during sexual maturity. Diseases in which egg drop occurs. Diphtheritic Fowl Pox). Metabolic diseases include Fatty Liver Syndrome. Loss of shell pigment.only a slight atrophy of ovary and oviduct. as may wildfowl and biting insects. oviduct). sudden changes of feed. intoxication by sulphonamides. may be infectious or metabolic. Infectious Laryngotracheitis. The infection is commonly present in ducks and geese but does not cause disease. signs/lesions (mainly lack of). It is important to rule out other possible reasons for egg drop. inadequate lighting programme. B 12. Elisa. thin or soft-shelled eggs and shell-less eggs. Diagnosis History. insecticides or nicarbazin. selenium. Contamination of egg trays at packing stations may play a part in transmission. Cholera. Lack of signs in the birds themselves. Newcastle disease. DID. Unvaccinated flocks with antibodies before lay do not peak normally. Post-mortem lesions No specific lesion . Coryza.it may be possible to demonstrate degenerative changes in the epithelial cells of the magnum of the oviduct. Spread from house to house may take 5-10 weeks. SN. Parasites. specifically vitamins E. Lateral transmission from bird to bird is slow and may be prevented or slowed for weeks by netting divisions. throat swabs. phosporus. extremes of temperature. which can be caused by a large number of factors acting individually or in combination.
Erysipelothrixetc. Peripheral vessels congested. Signs Fluid-distended abdomen. and /or trauma. growth plate disease. The choice should depend on sensitivity testing of an isolate. Soluble multivitamins may be recommended as a nonspecific measure. Endocarditis Introduction A condition of chickens associated with several bacterial infections such as staphylococci. rickets. 56 . If successive flocks are affected on the same site prophylactic medication ahead of the anticipated problem may be of benefit. streptococci. bacterial infection. Epiphysiolysis Introduction A complex condition of chickens that may be associated with trauma. Culture of lesions to confirm the bacterium involved. Prevention Good hygiene at turn-around. Post-mortem lesions Right ventricular failure and ascites. Treatment Medication is only likely to be of value in reducing deterioration in birds that are starting to develop lesions. osteomyelitis. Prevention Vaccination with inactivated vaccine prior to lay. Diagnosis Differentiate from broiler ascites syndrome by examination of the interior of the heart. Vegetative lesions usually on the right atrioventricular valve.Treatment None.
Treatment Not applicable. Flaccid neck. The natural hosts are wild birds and rodents. Horses are also seriously affected. Diagnosis Gross inspection.Signs Apparent dislocation at extremities of long bones. WEE. Signs Nervous symptoms. chickens. often occurs or is identified in the processed carcase. Post-mortem lesions No gross lesions. wild birds. Paresis. Circling. Ataxia. partridges. It is transmitted between birds by pecking and by mosquitoes. sometimes seen in vivo. 57 . VEE) Introduction A viral disease of pheasants. ducks and pigeons having a high morbidity and high mortality. turkeys. Paralysis. histology may be helpful in identifying underlying problems such as rickets or 'FHN'. These conditions currently only occur from northern South America to North America. Post-mortem lesions Separation of epiphyses at the growth plate. Microscopic lesions not pathognomonic. Prevention Control of predisposing factors. Tremors. May also be asymptomatic. Equine Encephalitis (EEE.
and CE. Chronic scabby skin. The bacterium is fairly resistant to environmental effects or disinfectants and may persist in alkaline soil for years. Sleepiness. kidney. It may be transmitted by faecal carriers for 41 days.Diagnosis Isolation in mice. There is likely to be an increased risk if housing or land has been previously used by pigs or sheep. ID by VN. rarely in geese. COFAL. Joint lesions. Post-mortem lesions Carcase congestion. Endocarditis. ducks. Vaccinate at 5-6 week. spleen swollen. May be diarrhoea and respiratory signs. in soil. Sudden death. pheasants. muscle. especially snood. It is also seen in some mammals. Perineal congestion. control cannibalism. epicardium. fishmeal and semen and by cannibalism. Erysipelas Introduction A sudden onset infection with the bacterium Erysipelothrix insidiosa (E. Swollen snood. 58 . Marked catarrhal enteritis. Treatment None. Liver. water. Depression. TC. Prevention Protection from mosquitoes. Signs Inappetance. rhusiopathiae) seen in turkeys and increasingly in free-range chickens. Haemorrhages in fat.
Death by internal exsanguination after rupture of haematocyst.a combination of the procaine and benzathine salts may be injected. Vaccination or natural infection may cause false positive reactions in the Mycoplasma gallisepticum and M. history. Diagnosis Lesions. vaccine at 16-20 weeks if the condition is enzootic.Diagnosis Isolation on blood agar. synoviae plate tests for a few weeks. Fatty Liver Haemorrhagic Syndrome Introduction A condition occurring worldwide in chickens. the demonstration of the organism in stained impression smears from tissues. Post-mortem lesions Obesity. Sudden death. Headparts pale. and acute Newcastle disease. Sudden drop in egg production. Treatment Penicillin . Differentiate from pasteurellosis. and identification. salmonellosis. especially caged layers and with a complex set of causes including excessive calories. Liver yellow. mycotoxins. Some birds with pale comb and wattles. Signs Overweight typically by 25%. colibacillosis. Tetracyclines in feed may also be helpful. deficiency and stress. often along with bacterin. 59 . Prevention Good biosecurity to prevent spread from other susceptible species. greasy and soft with numerous haemorrhages.
Prevention Feed to avoid obesity.Treatment Reduce energy intake. Favus Introduction A fungal infection. Prevention Good hygiene of facilities. B 12 and inositol. Loss of condition. It is very rare in commercial poultry production. Trichophyton gallinae. of chickens and turkeys. isolation. Feather loss. Diagnosis Lesions. avoid mycotoxins and stress. Post-mortem lesions See signs (above). Treatment Formalin in petroleum jelly. powdery spots and wrinkled crusts and scab on comb and wattles. Thick crusty skin. Signs White. culling affected birds. 'Honeycomb' skin. vitamin E. supplement with choline. 60 .
Predisposing factors include immunosuppresive viruses such as Infectious Bursal Disease Virus and Chicken Anaemia Virus and non-infectious bone pathologies such as hypophosphaetamic rickets. Differentiate from synovitis. 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.Femoral Head Necrosis . and water fowl. spondylolisthesis. It is seen worldwide and was one of the first infectious 61 . Diagnosis Base on post-mortem lesions and isolation of a causative organism. turkeys. Post-mortem studies of birds culled due to lameness and of birds found dead.75% of all male broilers placed had lesions in the hip bone. arthritis. staphylococci. Fowl Cholera.FHN Introduction A condition of chickens and turkeys that may be associated with several different bacterial infections e. E. Careful attention to mineral and Vitamin D nutrition to avoid subclinical. Pasteurellosis Introduction Fowl Cholera is a serious. FHN is the commonest infectious cause of lameness in broilers in the UK. streptococci. highly contagious disease caused by the bacterium Pasteurella multocida in a range of avian species including chickens. rickets. Post-mortem lesions Degeneration of the epiphyses of long bones with thinning of the cortex and tendency to break when force is applied.g. (increasing order of susceptibility). Prevention Exclusion of floor eggs and dirty eggs from the hatchery. coli. especially hypophosphataemic. indicated that 0. Signs Lameness. Use of a wing for support during walking and hip flexion.
erythromycin. tetracyclines. Differentiate from Erysipelas. Diagnosis Impression smears.no growth on McConkey). equipment. Nasal. Sudden death. Reservoirs of infection may be present in other species such as rodents. septicaemic viral and other bacterial diseases. Cellulitis of face and wattles. and possibly pigs. Diarrhoea. Lungs with a consolidated pink 'cooked' appearance in turkeys. cats. confirmed with biochemical tests. Loss of appetite. faeces. Yolk peritonitis. Enteritis. Swollen and cyanotic wattles and face. contaminated soil. isolation (aerobic culture on trypticase soy or blood agar yields colonies up to 3mm in 24 hours . Purulent pneumonia (especially turkeys). Predisposing factors include high density and concurrent infections such as respiratory viruses. The bacterium is easily destroyed by environmental factors and disinfectants. Signs Dejection.diseases to be recognised. Lameness. ocular and oral discharge. Purulent arthritis. necessitating long-term or periodic medication. The incubation period is usually 5-8 days. streptomycin. and people. Swollen joints. Ruffled feathers. Coughing. Treatment Sulphonamides. 62 . The disease often recurs after medication is stopped. The route of infection is oral or nasal with transmission via nasal exudate. penicillin. The disease can range from acute septicaemia to chronic and localised infections and the morbidity and mortality may be up to 100%. or limited to haemorrhages at few sites. Post-mortem lesions Sometimes none. but may persist for prolonged periods in soil. by Louis Pasteur in 1880. Focal hepatitis.
The swelling is made up of oedema and purulent exudates (pus). The virus persists in the environment for months. Infection occurs through skin abrasions and bites. Signs Warty.Prevention Biosecurity. Poor egg production. It is more common in males because of their tendency to fight and cause skin damage. and where there are biting insects. fomites. Poor growth. The duration of the disease is about 14 days on an individual bird basis. 63 . bacterins at 8 and 12 weeks. It is transmitted by birds. Morbidity is 1095% and mortality usually low to moderate. Fowl Pox. Severe localised Pasteurella infection in the swollen wattle of a 30-week-old male broiler parent chicken. live oral vaccine at 6 weeks. hygiene. pigeons and canaries worldwide. 0-50%. Figure 19. turkeys. throat and sometimes trachea. and mosquitoes (infected for 6 weeks). Depression. Caseous deposits in mouth. or by the respiratory route. spreading eruptions and scabs on comb and wattles. Avian Pox Introduction A relatively slow-spreading viral disease characterised by skin lesions and/or plaques in the pharynx and affecting chickens. good rodent control. Pox. Inappetance.
in the diptheritic form.intra-cytoplasmic inclusions (Bollinger bodies) with elementary bodies (Borrel bodies). be caseous plaques in mouth. 64 . Microscopically . Treatment None. DNA probes. There is good cross-immunity among the different viral strains. trachea and/or nasal cavities.Post-mortem lesions Papules progressing to vesicles then pustules and scabs with distribution described above. If there is evidence of secondary bacterial infection broad-spectrum antibiotics may be of some benefit. check take at 7-10 days post vaccination. Differentiate from Trichomoniasis or physical damage to skin. Less commonly there may. Flocks and individuals still unaffected may be vaccinated. Figure 20. signs and post-mortem lesions. Turkeys by thigh-stick at 2-3 months. Fowl pox lesions on the wattle of an adult broiler parent chicken. It is confirmed by IC inclusions in sections/ scrapings. isolation (pocks on CE CAM) with IC inclusions. reproduction in susceptible birds. pharynx. Prevention By vaccination (except canary). usually with chicken strain by wing web puncture. Diagnosis A presumptive diagnosis may be made on history. Chickens well before production.
wattles. Signs Occasionally dejection. wings. especially following congenital Chick Anaemia Virus infection or early Infectious Bursal Disease Virus infection (Gumboro Disease). Morbidity may be up to 50% and mortality is high. Necrotic Dermatitis Introduction A bacterial condition seen in chickens and usually caused byClostridium septicum. Prevention Good hygiene and management. sometimes thighs and other parts. Post-mortem lesions Patches of gangrenous skin with underlying emphysematous and/or sanguinous cellulitis. early Infectious Bursal Disease Virus infection). spleen. It occurs due to invasion of 'normal' wounds by 'normal' bacteria in immunosuppressed birds. usually over wings and breast. Recovery of an abundant growth of causative organism in recently dead birds.Gangrenous Dermatitis. 65 . Gangrenous skin. Foci in liver. Treatment Sulphaquinoxaline. rarely Clostridium noyvi / oedematiens. Loss of appetite. occasionally Staphylococcus aureus. The spores of Clostridial bacteria are highly resistant in the environment. Immunosuppression is therefore a predisposing factor. Diagnosis Clinical signs and/or lesions. Severe cellulitis especially of thighs. Avoid skin trauma and immunosuppression (congenital CAV infection. Swelling and infarction of the liver. penicillin or amoxycillin. Sudden mortality.
pheasants.g. Head shaking. There is an 18-20 day prepatent period. Loss of appetite and condition. and other game and ornamental birds occurring worldwide. Diagnosis Signs and lesions. slugs and snails acting as transfer hosts but the life cycle may also be direct. confirmation of presence of the parasite. The condition is seen more commonly in poultry on free range where ground may be contaminated by wild birds e. a nematode worm parasite of chickens. from rookeries. Signs Gasping. by ingestion of embryonated egg or L3. Prevention Flubendazole. Treatment Flubendazole in feed.Figure 21. Dyspnoea. Infection is by the oral route with earthworms. Gape Introduction Syngamus trachea. levamisole. Post-mortem lesions Tracheitis. 66 . Severe gangrenous dermatitis on the upper surface of the wing of a broiler chicken. turkeys. Presence of worms. paired parasites up to 2 cm long.
Adults are 2-4 cm long and usually bright red. weevils. Grasshoppers. affecting geese and ducks.Gizzard worms . benzimidazoles such as flubendazole. confirmation of presence of the worms. Prevention Prevention of access to intermediate hosts. Diagnosis Lesions. Streptocara. and Histiocephalus are nematode worm parasites of chickens. They are more common in free-range birds because of their increased access to intermediate hosts. Gizzard worms . Loss in condition and weight. Treatment Levamisole. Loss in condition and weight. Cheilospirura and Streptocara are seen worldwide but Histiocephalus is restricted to Europe. beetles etc act as intermediate hosts.Geese Introduction A nematode worm parasite. muscular wall may be sacculated or ruptured. Slow growth. 67 .Chickens Introduction Cheilospirura. necrosis and partial sloughing of gizzard lining. Slow growth. Signs Depression. Worms develop to L3 in eggs and infection is by the oral route direct from environment. Signs Depression. Post-mortem lesions Ulceration. routine worming. Amidostomum anseris.
Loss of down. Losses are negligible in birds over 5 weeks of age. Prevention Rotation of ground on annual basis. Membrane covering tongue. Reduced feed intake. Swelling and congestion of liver. visualisation of worms. benzimidazoles. Profuse white diarrhoea. 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. Derzsy's Disease is caused by a parvovirus distinct from chicken and mammalian parvoviruses.Post-mortem lesions Ulceration. Swollen eyelids and eye and nasal discharge. necrosis and partial sloughing of gizzard lining. Adults are 2-4 cm long and usually bright red. Goose Parvovirus (Derzsy's Disease) Introduction Goose Parvovirus is a highly contagious condition of geese and young Muscovy ducks. spleen and pancreas. 68 . Reddening of skin. Diagnosis Lesions. The younger the bird affected the more acute the condition and the higher the mortality. Treatment Levamisole. Vertical transmission resulting in congenital infection may occur. Post-mortem lesions Pale myocardium. Excessive water intake. Signs Prostration and death in acutely affected goslings. muscular wall may be sacculated or ruptured.
Poor growth. Bone marrow pale with fatty change. heart. Treatment No specific treatment. Administration of immune serum has been shown to be effective but may require two doses (day old and around 3 weeks). Morbidity varies. serosa and mucosae. Ideally flocks that have suffered the disease should not be used for breeding as they may become persistent excreters of the infection. Ascites. Fibrinous perihepatitis. Post-mortem lesions Haemorrhages in one or more sites: skin. Fibrinous pericarditis. Haemorrhagic Disease. Liver yellow. mycotoxins and viral infections and usually following a course of approximately 3 weeks. Aplastic Anaemia. 69 . The preferred approach is to immunise breeding birds with an attenuated live vaccine. Antimicrobials may be of value in reducing the effects of secondary bacterial infections. liver. Signs Dejection. Loss of appetite. Diagnosis Signs and lesions in birds of the appropriate age and species. Carcase anaemia. Pale comb and wattles. Blood in droppings. Haemorrhagic Anaemia Introduction A complex condition of chickens associated with drug toxicities. muscles. Prevention Hatching and brooding geese from different parent flocks together should be avoided. mortality is 5-50%.
Signs Sudden deaths. Blood from vent of moribund birds. Intestine distended with blood. Microscopic . Diarrhoea. double-immuno-diffusion of splenic extract. Serology: DID. The source of virus is unknown but there is easy lateral spread within flocks. reticulo-endothelial hyperplasia and intranuclear inclusions. Diagnosis Typical lesions. similar to pheasant Marble Spleen disease. Post-mortem lesions Petechiae in various tissues. Elisa .Diagnosis History. the virus surviving in frozen faeces for months. add liver solubles to feed.spleen shows lymphoid hyperplasia. reproduction with filtered contents. Drop in feed and water consumption. Spleen mottled and enlarged.sero-conversion frequently occurs in absence of clinical disease. Treatment Vitamin K. signs. Prevention Avoid causative factors. remove sulphonamides. The virulence of the virus varies but morbidity may be 100% and mortality 10-60%. Course 10-21 days. caused by Type II Adenovirus distinct from classical fowl adenovirus and occurring in most turkey-producing areas. 70 . and weeks in litter. May induce immunosupression and precipitate respiratory disease or coccidiosis. Haemorrhagic Enteritis Introduction A viral disease of turkeys. lesions. The route of infection is usually oral.
Immunity to the disease is long lasting. Disinfect and 3-4 weeks house rest. Live vaccines are commonly used in many countries at 4-5 weeks of age. acclimation. Predisposing factors include genetics. Turkeys dying with haemorrhagic enteritis commonly have the small intestine distended with blood. high stocking density. Maternal antibody may interfere with vaccination. oral tetraycline. In this case a loop of intestine has been opened to show the blood.and T-line lymphocytes for up to 5 weeks following exposure. some in turkey B-lymphoblastoid cell lines. Figure 39. 71 . Immunity: there is an early age resistance irrespective of maternal antibody status. drinking water temperature and availability. convalescent serum. feather cover. Pathogenic strains can depress both B. Increased thirst. Heat Stress Introduction A condition seen in chickens. Signs Panting. and turkeys caused by high environmental temperature.Treatment Warmth and good management. Some are produced in live turkeys. Prevention All-in/all-out production. Ducks are relatively resistant to heat stress. nicarbazin in feed. good hygiene and biosecurity. Reduced feed consumption. good management. especially associated with high relative humidity and low air speed.
Prevention Houses of optimal height and insulation. Post-mortem lesions Dehydration. maximise airflow. and some game birds. columbae) is a protozoan parasite of turkeys. Inter-species transmission may occur. Post-mortem lesions Carcases congested. It is transmitted by faeces. Later depression. pigeons. chirping. evaporative coolers. watery diarrhoea. Terminal coma and convulsions. Reduced egg production. fomites. painted white to reflect heat. Intestine flabby with some bulbous dilation. Frothy. 72 . Reductions in stocking density of meat poultry may be quickly achieved by partial depletion ('thinning'). In commercial ducks a related parasiteTetratrichomonas can cause poor growth and drops in egg production. Hexamitiasis Introduction Hexamita meleagridis (pigeons H. carriers. lesions. Inappetance. Diagnosis Temperature records. Prostration. pheasants. if relative humidity is low then wet the roof and fog. Feeding during cooler hours may be beneficial. Treatment Cool water. signs. pattern of losses. contains excessive mucus and gas. Signs Initially birds nervous. Mucoid exudate in nostrils and mouth. Legs and wings outstretched. Loss in weight. exclusion of other conditions. feed with a reduced protein:energy ratio.
The problem is seen in high-biosecurity facilities. Diagnosis Lesions. significant disease has been seen in breeding chickens and free-range layers. Poor growth. Within a turkey shed transmission is rapid in spite of the fact that it is difficult to infect birds orally with unprotected parasites. presumably introduced with worm eggs. Blood in faeces (chickens). Cyanosis of head. 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. Differentiate from transmissible enteritis. Caecal tonsils congested. Treatment Tetracycline. Histomoniasis. gallinae the parasite is easily destroyed. Histamonosis. Blackhead Introduction Histomonas melagridis is a protozoan parasite of turkeys. histomonosis. if possible. Signs Depression. Furazolidone. scrapings from fresh material. all-in/all-out production. increase ambient temperature. trichomoniasis. The effect of antibiotic may be related to the control of secondary bacterial enteritis. First half of intestine inflamed. Prevention Depopulation. It has recently been demonstrated that infection occurs readily via the cloaca when birds are on contaminated litter. dimetridazole. This condition has high morbidity and mortality in turkeys. and also. paratyphoid. pheasants and game birds that acts together with facultative bacteria to produce the condition of Blackhead. hygiene. avoid interspecies mixing. and occasionally chickens. Sulphur-yellow diarrhoea. and mixing groups of different ages. Although chickens are relatively resistant to the condition. Outwith earth worms orH. dimetridazole and ipronidazole have been used in the past. Inappetance. 73 . Progressive depression and emaciation.
nitrofurans (e. however they may not be present in the early stages. The disease is readily reproduced by inoculating birds with a bacteria-free filtrate of a liver extract from an affected bird. At the time of writing no products of these groups are approved for use in the European Union. Diagnosis Lesions. Having both chickens and turkeys on the same property is likely to increase the risk of this disease in turkeys. nifursol) and arsenicals (e.Tahir Post-mortem lesions Enlargement of caeca. possibly in combination with an RNA virus and immunosuppression caused by Chick Anaemia Virus or Infectious Bursal Disease. 'Herban)' have been used with some apparent success though controlled trials and formal approval for this purpose are not recorded. Use of an anti-histomonas product in feed where such products are approved but due care with respect to residue avoidance would be required. Prevention Good sanitation. furazolidone.g. especially in chickens. Hydropericardium-Hepatitis Syndrome. 74 . Regular worming to help control the intermediate hosts. Ulcers. Some herbal products based on the essential oils (e.g.M. concrete floors. Mortality may reach 60% but more typically 10-30%. caseous cores with yellow. Angara Disease Introduction This condition was first identified in broilers in Pakistan in 1987.Abubakar. dimetridazole). It is a condition caused by an adenovirus. Liver may have irregular-round depressed lesions. given recent new knowledge on the mechanism of transmission.g. usually grey in colour. scrapings from fresh material. and only nitarsone is approved in the USA.nitarsone) have been used to treat this important disease of poultry. grey or green areas. avoid mixing species. 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. Treatment Historically nitro-imidazoles (e. Arsenicals are less effective in treatment than they are in prevention.g. It affects mainly broilers and broiler parents in rear and has also been seen in pigeons. Intensive relittering may help reduce the level of infection.
Most young commercial poultry consume feeds that have a small particle size. string etc. Good water sanitation (e. Treatment None. Prevention The condition typically occurs in areas of high poultry density where multi-age operation is traditional. 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. Enlarged. Older birds ingest grit to facilitate the grinding activity in the gizzard. Post-mortem lesions Excessive straw-coloured fluid distending the pericardium (up to 10 mls).1% of a 2.g. treatment of drinking water with 0. Control of predisposing immunosuppressive diseases may help limit losses. grass. The normal function of the gizzard is to aid in the physical grinding of food materials. however if young chicks to do not begin to eat feed properly they often consume litter instead. Formalin-inactivated oil adjuvant vaccines are reported to be highly effective and are used in areas where the condition is endemic. This condition usually affects only a small number of birds. pale friable liver and kidney. Gizzard activity also acts as a pacemaker of intestinal activity and controls the speed at which food is passed to the small intestine. Yellow mucoid droppings. virology. Lungs oedematous. Congestion of the carcase. Impacted gizzards are then found in 'non-starter' type chicks or poults. however sometimes free-range poultry consume large stones. Huddling with ruffled feathers. to reduce their particle size to aid digestion. Diagnosis Lesions.5% iodophor solution) appears to be beneficial. and birds of any age can 75 . histopathology. Lethargy.Signs Sudden increase in mortality.
A foreign body may be found in the interior of the gizzard. It has a course of 9. Nails commonly penetrate the lining of the gizzard. Infected birds remain carriers for a few weeks.consume nails. 76 . Obvious non-starters should be culled in this situation. Daily monitoring of the crop-fill is a useful procedure. Italy.15 days with a morbidity of 1-10% and a mortality of 1-10%. Reduced weight gain. Prevention Good brooding management to encourage early adaptation to the diet and adequate consumption of feed and water. Treatment None effective in young birds. This usually happens after maintenance activities have been carred out in the housing. and on opening is found to contain a mass of fibrous material. A number of different sero-types have been isolated from disease outbreaks but they may also be isolated from healthy chickens. The disease was first described in the USA in 1963 and has also been reported in Canada. caused by an adenovirus. and may penetrate the body wall. This may extend into the proventriculus and on into the duodeunum. Diagnosis Lesions. staples etc. France and Ireland. Australia. Sweep floors after maintenance activities to remove nails and other potentially dangerous foreign bodies. 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. Inclusion Body Hepatitis Introduction A disease of chickens characterised by acute mortality. the UK. Post-mortem lesions The gizzard is more firm than normal and. Signs Reduced feed intake. often with severe anaemia.
Ruffled feathers. Microscopically . may be important. isolation alone does not confirm that they are the cause of a particular problem. Post-mortem lesions Liver swollen. Signs Depression. many different sero-types have been isolated from different cases. perhaps because they have lower levels of maternal antibody. and deficiency of vitamin B12. A form of the disease affecting birds under 3 weeks of age in Australia has been reproduced with serotype 8 adenovirus. chloroform. Serology: DID for group antigen. Differentiate from Chick anaemia syndrome.Transmission may be vertical or lateral and may involve fomites. Confirmation is made on finding inclusions in the liver. Bursa and spleen small. The virus is generally resistant to disinfectants (ether. 77 . Since adenoviruses are commonly found in healthy poultry. Treatment None.basophilic intranuclear inclusions. Pallor of comb and wattles. Progeny of high health status breeding flocks appear to be at greater risk. Infectious Bursal Disease. Soluble multivitamins may help with the recovery process. CEL). Inappetance. but on the other hand many field cases show eosinophilic inclusions that do not appear to have adenovirus particles. Kidneys and bone marrow pale. Immunosuppression. and high temperatures. sulphonamide intoxication. Formaldehyde and iodides work better. The virus grows well in tissue culture (CEK. Blood thin. yellow. for instance due to early IBD challenge or congenital CAV infection. SN for individual sero-types. Curiously. fatty liver syndrome. vibrionic hepatitis. pH). mottled with petechiae and ecchymoses. Diagnosis A presumptive diagnosis may be made on history and lesions.
fomites or aerosol. Huddling. heat (56°C for 15 mins). gasping. is sensitive to solvents. Infectious Bronchitis. Post-mortem lesions Mild to moderate respiratory tract inflammation. prior vaccination. was first described in the USA (N. maternal immunity (young birds). dyspnoea. Infection is via the conjunctiva or upper respiratory tract with an incubation period of 18-36 hours. Its affects vary with: the virulence of the virus. Wet litter. Airsacculitis. Tracheal oedema. Kidneys and bronchi may be swollen and they and the ureters may have urates. The cause is a Coronavirus that is antigenically highly variable. which may survive 4 weeks in premises. Signs Depression. coli. IB Introduction This infection. 78 . Dakota. Diarrhoea. Coughing. Loss of appetite. probably the commonest respiratory disease of chickens. prevention of immunosuppression. E. Newcastle disease). These differences are due to structural differences in the spike proteins (S1 fraction). depending on secondary infections. alkalis. About eight sero-groups are recognised by sero-neutralization. and complicating infections (Mycoplasma. The virus. Diuresis. disinfectants (Formal 1% for 3 mins). Caseous plugs in bronchi. 1931). The infection is highly contagious and spreads rapidly by contact.Prevention Quarantine and good sanitary precautions. Tracheitis. Typing by haemagglutination-inhibition is also used. Some birds/viral strains can be carriers to 1 year. Morbidity may vary 50-100% and mortality 0-25%. new sero-types continue to emerge. Poor ventilation and high density are predisposing factors. the age of the bird.
alkalis. Maternal immunity provides protection for 2-3 weeks. Muscular shivering. depending on secondary infections. Infectious Bronchitis. HA negative. Treatment Sodium salicylate 1gm/litre (acute phase) where permitted . Local immunity is first line of defence. disinfectants (Formal 1% for 3 mins). The infection spreads rapidly by contact. Definitive diagnosis is based on viral isolation after 3-5 passages in chick embryo. Prevention Live vaccines of appropriate sero-type and attenuation. Signs Sudden death. Avian Influenza and Laryngotracheitis. Serology: HI. The virus. lesions and serology. mycoplasmosis. Poor ventilation and high density are predisposing factors. is sensitive to solvents.v. heat (56°C for 15 mins). which may survive 4 weeks in premises. possible reactions depending on virulence and particle size. with typical lesions. vaccinal reactions.antibiotics to control secondary colibacillosis (q. Cellmediated immunity may also be important.). DID (poor sensitivity. Elisa (both group specific). SN (type specific). group specific).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. Some birds/viral strains can be carriers for up to 1 year. Humoral immunity appears 10-14 days post vaccination. Infection is via the conjunctiva or upper respiratory tract with an incubation period of 18-36 hours. Differentiate from Newcastle disease (lentogenic and mesogenic forms).Diagnosis Tentative diagnosis is based on clinical sgns. 79 . flourescent antibody positive and ciliostasis in tracheal organ culture. IB . short duration. fomites or aerosol.
The virus is moderately resistant and may survive 4 weeks in premises. In layers the ovules may be intensely congested. lesions progress to necrosis and scarring of deep pectorals in convalescence. Rough shells. IB Egg-layers Introduction A Coronavirus infection of chickens. CK) only after adaptation Serology: HI. A few birds are carriers up to 49 days post infection. Prevention Live vaccines of appropriate sero-type and attenuation.). sneezing. typical lesions. ciliostatic in tracheal organ culture. Infection is via the conjunctiva or upper respiratory tract. SN (type specific). DID (poor sensitivity. Diagnosis 3-5 passages in CE allantoic cavity. short duration. The condition has a morbidity of 10-100% and mortality of 0-1%. Signs Drop in egg production (20-50%). cell culture (Vero. FA.v. HA-. Poor ventilation and high density are predisposing factors. Elisa (both group specific). fomites or aerosol. group specific).antibiotics to control secondary colibacillosis (q. Infectious Bronchitis. Treatment Sodium salicylate 1gm/litre (acute phase) where permitted . Soft-shelled eggs. possible reactions depending on virulence and particle size. Rales may or may not be present. Coughing. with much antigenic variation. Loss of internal egg quality.Post-mortem lesions Oedema of pectoral muscles and subcutaneously on abdomen. Other lesions of 'classical' IB may be encountered. 80 . There is rapid spread by contact.
HA-. virulence. Cell-mediated immunity may also be important. typical lesions.antibiotics to control secondary colibacillosis (q.v. Diagnosis 3-5 passages in CE. Yolk in peritoneal cavity (non-specific).Post-mortem lesions Follicles flaccid. SN. Humoral immunity appears 10-14 days post vaccination. Elisa. Treatment Sodium salicylate 1gm/litre (acute phase) where permitted . Figure 22. EDS76.). Differentiate from Egg Drop Syndrome. Prevention Live vaccines of appropriate sero-type and attenuation. Maternal immunity provides protection for 2-3 weeks. although reactions can occur depending on prior immunity. Local immunity is the first line of defence. Serology: HI. 81 . Flaccid ovarian follicles in a broiler parent chicken undergoing challenge with Infectious Bronchitis virus. FA. particle size (if sprayed) and general health status. DID.
Coughing. Yolk in peritoneal cavity (non-specific). The virus is moderately resistant and may survive 4 weeks in premises. Elisa. Local immunity is the first line of defence. typical lesions.). Poor ventilation and high density are predisposing factors. A few birds are carriers up to 49 days post infection.Infectious Bronchitis. Cell-mediated immunity may also be important. Rales may or may not be present. virulence. The condition has a morbidity of 10-100% and mortality of 0-1%. Treatment Sodium salicylate 1gm/litre (acute phase) where permitted . IB Egg-layers Introduction A Coronavirus infection of chickens. There is rapid spread by contact. with much antigenic variation. 82 . FA.v. Loss of internal egg quality. EDS76. particle size (if sprayed) and general health status. Maternal immunity provides protection for 2-3 weeks. Infection is via the conjunctiva or upper respiratory tract. Humoral immunity appears 10-14 days post vaccination.antibiotics to control secondary colibacillosis (q. Rough shells. Post-mortem lesions Follicles flaccid. fomites or aerosol. Diagnosis 3-5 passages in CE. HA-. DID. SN. Prevention Live vaccines of appropriate sero-type and attenuation. Serology: HI. Differentiate from Egg Drop Syndrome. sneezing. although reactions can occur depending on prior immunity. Soft-shelled eggs. Signs Drop in egg production (20-50%).
The virus is very resistant. especially with sero-type 2). The age up to which infection can cause serious immunosuppression varies between 14 and 28 days according to the antigen in question. IBD. Sero-type 1 only. 83 . There is no vertical transmission. the damage caused to the immune system interacts with other pathogens to cause significant effects. with an incubation period of 2-3 days. Signs are most pronounced in birds of 4-6 weeks and White Leghorns are more susceptible than broilers and brown-egg layers. and affected birds excrete large amounts of virus for about 2 weeks post infection.Figure 22. Generally speaking the earlier the damage occurs the more severe the effects. The route of infection is usually oral. Morbidity is high with a mortality usually 0. Infectious Bursal Disease. The infective agent is a Birnavirus (Birnaviridae). Subclinical infection in young chicks results in: deficient immunological response to Newcastle disease. Gumboro Introduction A viral disease. first identified in the USA in 1962. Mealworms and litter mites may harbour the virus for 8 weeks. susceptibility to Inclusion Body Hepatitis and gangrenous dermatitis and increased susceptibility to CRD.20% but sometimes up to 60%. Marek's disease and Infectious Bronchitis. persisting for months in houses. but may be via the conjunctiva or respiratory tract. The disease is highly contagious. seen worldwide. In addition to the direct economic effects of the clinical disease. faeces etc. (Turkeys and ducks show infection only. Flaccid ovarian follicles in a broiler parent chicken undergoing challenge with Infectious Bronchitis virus. which targets the bursal component of the immune system of chickens.
Inappetance. 84 . Antibiotic medication may be indicated if secondary bacterial infection occurs. lesions.5. Variants: There have been serious problems with early Gumboro disease in chicks with maternal immunity. Coccidiosis. Use of a multivitamin supplement and facilitating access to water may help. normal size or reduced in size depending on the stage). Elisa vaccination date prediction < 7 days). Haemorrhagic syndrome. Serology: antibodies can be detected as early as 4-7 days after infection and these last for life. Diagnosis Clinical disease . rapidly proceeds to atrophy. This may be confirmed by demonstrating severe atrophy of the bursa. Unsteady gait. Post-mortem lesions Oedematous bursa (may be slightly enlarged. The normal weight of the bursa in broilers is about 0. weights below 0. Vent pecking. histopathology. Treatment No specific treatment is available. IBD viruses have been isolated and shown to have significant but not complete cross-protection. Dehydration. Swollen kidneys with urates. 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. Haemorrhages in skeletal muscle (especially on thighs).Signs Depression.History. Diarrhoea with urates in mucus. may have haemorrhages.1% are highly suggestive.3% of bodyweight. Tests used are mainly Elisa. Other possible causes of early immunosuppression are severe mycotoxicosis and managment problems leading to severe stress. Cryptosporidiosis of the bursa (rare). (previously SN and DID). Subclinical disease . especially in the Delmarva Peninsula in the USA. Huddling under equipment. especially if present prior to 20 days of age.A history of chicks with very low levels of maternal antibody (Fewer than 80% positive in the immunodifusion test at day old. Differentiate clinical disease from: Infectious bronchitis (renal).4 days. Half-life of maternally derived antibodies is 3. They are all serotype 1. subsequent diagnosis of 'immunosuppression diseases' (especially inclusion body hepatitis and gangrenous dermatitis) is highly suggestive.
85 . This bursa is from an acutely affected broiler. sometimes chronic. 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. the rectum and the vent. characterised by catarrhal inflammation of the upper respiratory tract. occasionally pheasants and guinea-fowl. Morbidity is high but mortality low if uncomplicated although it may be up to 20%.Prevention Vaccination. highly infectious disease of chickens. Figure 23. including passive protection via breeders. 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. It is enlarged. biosecurity measures may be helpful in limiting the spread between sites. When outbreaks do occur. It is not egg transmitted. Infectious Coryza Introduction A usually acute. Carriers are important with transmission via exudates and by direct contact. Infectious Coryza is caused by the bacterium Haemophilus paragallinarum and is seen in many countries especially in multi-age farms that are never depopulated. and tracing of contacts may indicate sites on which a more rebust vaccination programme is indicated. especially nasal and sinus mucosae. resulting in increased culling. A strong immunity follows field challenge. Immunity after a live vaccine can be poor if maternal antibody was still high at the time of vaccination. vaccination of progeny depending on virulence and age of challenge. This shows the anatomical relationship between the bursa. turgid and oedematous.
Drop in egg production of 10-40%. agglutination and IF have all been used but are not routine. Post-mortem lesions Catarrhal inflammation of nasal passages and sinuses. Dihydrostreptomycin. Caseous material in conjunctiva/sinus. Sneezing. tylosin. Swollen wattles. Signs Facial swelling. Eye-lid adherence. 86 . chronic or localised pasteurellosis and vitamin A deficiency. Flouroquinolones are bactericidal and might prevent carriers. Live attenutated strains have been used but are more risky. DID. Vaccines are used in areas of high incidence. sulphonamides. Diagnosis A presumptive diagnosis may be made on signs. Intercurrent respiratory viral and bacterial infections are predisposing factors. respiratory viruses. drying and disinfectants. lesions. Tracheitis. Treatment Streptomycin. Dyspnoea. Confirmation is by isolation and identification .requires X (Haematin) and V (NAD) factors. Inappetance. Commercial bacterins may not fully protect against all field strains but reduce the severity of reactions. Purulent ocular and nasal discharge. Bacterin at intervals if history justifies or if multi-age. preferably in raised CO 2 such as a candle jar. while bacterins only protect against homologous strains. erythromycin. identification of the bacteria in a Gram-stained smear from sinus. Birds recovered from challenge of one serotype are resistant to others. Differentiate from Mycoplasmosis. Prevention Stock coryza-free birds on an all-in/all-out production policy. Conjunctivitis. at least two doses are required. Loss in condition. Serology: HI.The bacterium survives 2-3 days outside the bird but is easily killed by heat. Controlled exposure has also been practised.
Differentiate from Newcastle disease. lesions. vaccination. 87 . if enzootic or epizootic in an area. ILT Introduction A herpesvirus (pathogenicity can vary) infection of chickens. Diagnosis Signs.intranuclear inclusions in tracheal epithelium. Isolation in CE CAMs. IFA. Ocular discharge. All-in/allout operation. Nasal discharge (low pathogenicity strains). Gasping. The route of infection is via upper respiratory tract and conjunctiva or possibly oral and the course of the disease is up to 6 weeks. Prevention Quarantine. Coughing of mucus and blood. Treatment None. Sinusitis. Transmission between farms can occur by airborne particles or fomites. severe bronchitis. Keep susceptible stock separate from vaccinated or recovered birds. Post-mortem lesions Severe laryngotracheitis. Movement and mixing of stock and reaching point of lay are predisposing factors. histology. Apply strict biosecurity in moving equipment or materials between these these categories of stock. peafowl and turkeys with a morbidity of 50-100% and a mortality usually 10-20% but sometimes up to 70%. after 4 weeks of age. Sera may be examined by VN or Elisa. Microscopically . caseous plugs may be present. Fairly slow lateral spread occurs in houses. Signs Dyspnoea.Infectious Laryngotracheitis. Drop in egg production. in severe form may be enough. antibiotics to control secondary bacterial infection if this is marked. pheasants. PCR. The virus is highly resistant outside host but is susceptible to disinfectants. often with blood in lumen. Recovered and vaccinated birds are long-term carriers.
Thirst. protozoan parasites of turkeys. Leukocytozoonosis Introduction Caused by Leucocytozoon species. Survivors may carry infection. Asia and Africa. Post-mortem lesions Telescoping of the bowel. Different species of this parasite have been reported from North America. Signs Sudden onset of depression. Rapid breathing. rarely chickens. it may actually protrude at the vent and be cannibalised. Careful attention to feeding practices to avoid anticipation of feed arrival if on restricted feeding. Prevention Control of coccidiosis and other causes of intestinal inflammation. Loss of equilibrium. Anorexia. ducks. Diagnosis Typical post-mortem lesions Treatment As appropriate for the underlying disease condition. worms and other forms of enteritis are predisposing factors. guinea fowl. Signs Mainly sudden deaths.Intussusception Introduction A condition of chickens associated with increased intestinal motility. Simulid flies or culicoid midges are intermediate hosts. Coccidiosis. 88 . usually in the lower small intestine. The disease has a short course and morbidity and mortality are high.
schizonts in liver. Treatment 89 . Persistent low mortality. Diagnosis History. Signs Depression. Diagnosis Lesions. gametes in erythrocytes. May be asymptomatic. Enlargement of abdomen. Lymphoproliferative Disease (LPD) Introduction A Type C retrovirus infection of turkeys with low morbidity and high mortality. especially in enlarged spleen. lesions. Anaemia. Prevention Separation from intermediate hosts. Microscopically . Differentiate from Reticuloendotheliosis. age. Anaemia.megaschizonts in brains of birds with nervous signs. Treatment None known. Emaciation. cytology. Hepatomegaly. Post-mortem lesions Splenomegaly. disposal of recovered birds. histology and blood smears. Loss of weight. liver or bursa. Post-mortem lesions Focal tumours.
Pancreatic atrophy/fibrosis and pancreatic atrophy (rather variable). reoviruses. rotavirus etc. Signs Uneven growth. Abnormal feathers ('helicopter wings' 'yellow-heads'). Poor feathering.Tahir None. It is suspected that these viruses can be vertically transmitted and the most severe signs in young birds are associated with this. Diarrhoea. all-in/all-out production. direct electron microscope examination of intestinal contents. Poor early management (feed and water supply. North and South America and Australia. Sometimes osteomyelitis and/or rickets. Treatment Daily cull of affected birds between 14 and 28 days.(maize-) fed birds (often associated with orange intestinal contents and/or faeces). Runting (permanent). The condition has been seen in Europe.M. for example enteroviruses. control arthropods. in future eradication. Prevention Good hygiene. temperature control) may lead to a similar picture in the absence of specific infection. Poor management may contribute to the problem. Pot-bellied appearance. Diarrhoea in older birds may be an effect of on-farm infection.Abubakar. Runting/Stunting Introduction A condition of chickens and turkeys that may be associated with several different viruses. Malabsorption Syndrome. 90 . enterovirus-like particles. Diagnosis Pathology. Pale shanks in corn. Post-mortem lesions Enteritis. Stunting (temporary). Eating faeces.
avoidance of intercurrent disease and management problems (such as chilling). Intestines of a young broiler chick suffering from malabsorption syndrome. lungs. Figure 24.Tumours in heart. fomites. both parasitic and bacterial. Morbidity is 10-50% and mortality up to 100%. c) Cutaneous . as well as more longstanding paralysis of legs or wings and eye lesions. seen worldwide. The virus survives at ambient temperature for a long time (65 weeks) when cell associated 91 . b) Visceral .poorly digested food enclosed in mucus. Infected birds remain viraemic for life. Vertical transmission is not considered to be important.Acute infiltration of the CNS and nerves resulting in 'floppy broiler syndrome' and transient paralysis.Prevention Good broiler farm hygiene. A sample of the faeces produced is shown at the bottom of the picture . Mortality in an affected flock typically continues at a moderate or high rate for quite a few weeks. good parent nutrition and egg selection and santitation. In 'late' Marek's the mortality can extend to 40 weeks of age. From the 1980s and 1990s highly virulent strains have become a problem in North America and Europe. tests. ovary. muscles. The route of infection is usually respiratory and the disease is highly contagious being spread by infective feather-follicle dander. Marek's disease Introduction Marek's disease is a Herpes virus infection of chickens. They are distended with poorly digested feed. and rarely turkeys in close association with chickens. etc. Affected birds are more susceptible to other diseases.Tumours of feather follicles. The disease has various manifestations: a) Neurological .
chronic respiratory disease in chickens. deficiency of thiamine. Signs Paralysis of legs. distribution of lesions. Diagnosis History. association with other strains (SB1 Sero-type 2) and Rispen's. Loss of weight. spleen. vaccination generally with 1500 PFU of HVT at day old (but increasingly by in-ovo application at transfer).and is resistant to some disinfectants (quaternary ammonium and phenol). especially at the start of lay.g. Skin around feather follicles raised and roughened. game birds.lymphoid infiltration is polymorphic. histopathology. Genetics can help by increasing the frequency of the B21 gene that confers increased resistance to Marek's disease challenge. kidney.. Post-mortem lesions Grey-white foci of neoplastic tissue in liver.Chicken Introduction Infection with Mycoplasma gallisepticum is associated with slow onset. Thickening of nerve trunks and loss of striation. lung. botulism. gonads. Mycoplasma gallisepticum infection. It is inactivated rapidly when frozen and thawed. Prevention Hygiene. turkeys. Grey iris or irregular pupil. all-in/all-out production. clinical signs. pigeons and other wild birds. wings and neck. Treatment None. Chronic Respiratory Disease . and skeletal muscle. age affected. Differentiate from Lymphoid leukosis. heart. It is common practice to use combinations of the different vaccine types in an effort to broaden the protection achieved. M. Vision impairment. Microscopically . deficiency of Ca/Phosphorus/Vitamin D. resistant strains. Ducks and geese can 92 .
tenosynovitis and salpingitis in chickens. The condition occurs worldwide. morbidity may be minimal and mortality varies. Intercurrent infection with respiratory viruses (IB. Slow growth. and to a lesser extent fomites. more commonly in Mycoplasma Broth followed by plating out on Mycoplasma Agar. 93 . subsequent stress may cause recurrence of disease. Nasal and ocular discharge. ART). Suspect colonies may be identified by immuno-flourescence. Transmission may be transovarian. Occasionally arthritis. and in lyophilised material. though infection rates are high. Leg problems. though in some countries this infection is now rare in commercial poultry. coli. In turkeys it is most associated with severe sinusitis (see separate description in the turkey section). and inadequate environmental conditions are predisposing factors for clinical disease. ND. Post-mortem lesions Airsacculitis. demonstration of specific DNA (commercial PCR kit available). coli infection). Haemophilus. or by direct contact with birds. Survival seems to be improved on hair and feathers. Fomites appear to a significant factor in transmission between farms. Occasional encephalopathy and abnormal feathers. sinuses. Reduced hatchability and chick viability. Diagnosis Lesions. Catarrhal inflammation of nasal passages. Pericarditis. The route of infection is via the conjunctiva or upper respiratory tract with an incubation period of 6-10 days. Perihepatitis (especially with secondary E. serology. Spread is slow between houses and pens suggesting that aerosols are not normally a major route of transmission. airborne dust and feathers. Recovered birds remain infected for life. virulent E.become infected when held with infected chickens. Culture requires inoculation in mycoplasma-free embryos or. The infectious agent survives for only a matter of days outwith birds although prolonged survival has been reported in egg yolk and allantoic fluid. Stunting. exudates. Signs Coughing. trachea and bronchi. aerosols. Poor productivity. In others it is actually increasing because of more birds in extensive production systems that expose them more to wild birds. Pasteurella spp. In adult birds. isolation and identification of organism. Inappetance.
and fomites.Turkeys Introduction A slow onset chronic respiratory disease of turkeys often with severe sinusitis and associated with Mycoplasma gallisepticuminfection. therefore M. Morbidity is low to moderate and mortality low. Differentiate from Infectious Coryza. suspect reactions are examined further by heat inactivation and/or dilution. M.g. These programmes are based on purchase of uninfected chicks. Mycoplasma gallisepticum infection. Treatment Tilmicosin. Productivity in challenged and vaccinated birds is not as good as in M. or by direct contact with birds. Effort should be made to reduce dust and secondary infections. fluoroquinolones. HI may be used.-free stock.. tetracyclines.g. viral respiratory diseases. PCR is possible if it is urgent to determine the flock status. It is seen worldwide. Live attenuated or naturally mild strains are used in some countries and may be helpful in gradually displacing field strains on multi-age sites. aerosols. Suspect flocks should be re-sampled after 2-3 weeks. Prevention Eradication of this infection has been the central objective of official poultry health programmes in most countries. Elisa is accepted as the primary screening test in some countries. Infectious Sinusitis . vitamin A deficiency. Transmission may be transovarian. subsequent stress may cause recurrence of disease. all-in/all-out production. synoviae and M. tylosin. Aspergillosis. The route of infection is via the conjunctiva or upper respiratory tract with an incubation period of 6-10 days. generally as a confirmatory test. spiramycin. Some inactivated vaccines for other diseases induce 'false positives' in serological testing for 3-8 weeks. Recovered birds remain infected for life.g. In some circumstances preventative medication of known infected flocks may be of benefit. 94 . other Mycoplasma infections such as M. hatchingeggs and chicks.Serology: serum agglutination is the standard screening test. though in many countries this infection is now rare in commercial poultry. biosecurity. exudates. meleagridis(turkeys). and routine serological monitoring. infection status is important for trade in birds.
although prolonged survival has been reported in egg yolk and allantoic fluid. Suspect colonies may be identified by immunofluorescence. Effort should be made to reduce dust and secondary infections. Culture. Some inactivated vaccines induce 'false positives' in serological testing. serology. Leg problems. Prevention Eradication of this infection has been the central objective of official poultry health programmes in most countries. Slow growth. requires inoculation in mycoplasma-free embryos or. Nasal and ocular discharge. 95 . all-in/allout production. especially Turkey Rhinotracheitis. Differentiate from viral respiratory disease. intercurrent viral disease such as Newcastle disease (even lentogenic) and Turkey Rhinotracheitis are predisposing factors. Survival seems to be improved on hair and feathers. spiramycin. Signs Coughing. often with inspissated pus. Swollen sinuses. PCR is possible if it is urgent to determine the flock status. more commonly in Mycoplasma Broth followed by plating out on Mycoplasma Agar. suspect reactions are examined further by heat inactivation and/or dilution. Inappetance. of swabs taken from the trachea or lesions. Perihepatitis. Post-mortem lesions Swollen infraorbital sinuses. Suspect flocks should be re-sampled after 2-3 weeks. tylosin. Serology: serum agglutination is the standard screening test. Airsacculitis. Stunting. In some circumstances preventative medication of known infected flocks may be of benefit. tetracyclines. fluoroquinolones. isolation and identification of organism. Pericarditis. Diagnosis Lesions. These are based on purchase of uninfected poults. demonstration of specific DNA (commercial kit available). and in lyophilised material. Stress.The infectious agent survives for only a matter of days outwith birds. HI may also be used. Treatment Tilmicosin. malnutrition. and biosecurity.
perhaps because all affected embryos fail to hatch. Leg lesions can be shown in inoculated birds but do not seem to occur naturally. although DNA homology is only 40%. ducks (France).g.Mycoplasma immitans infection Introduction Infection with Mycoplasma immitans is seen in geese. Infection occurs via the conjunctiva or upper respiratory tract and transmission among poults may be vertical. Diagnosis Shows cross reaction in IFA to M.g. Signs Embryonic mortality.g. Mycoplasma iowae infection. Post-mortem lesions Sinusitis. Reduced hatchability. and can occur in other poultry and wild bird species.i. some with down abnormality. venereal or horizontal. M. 96 . Treatment As for M. Introduction Infection with Mycoplasma iowae is seen in turkeys. and partridges (UK). Signs Swollen sinuses. Prevention As for M. Post-mortem lesions Stunted embryos with hepatitis and enlarged spleens.
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. Signs Reduced hatchability.i. with transovarian and then lateral spread in meat animals. Crooked necks. M.-free stock. When the vacuum is released the eggs draw in antibiotic solution which is subsequently absorbed through the shell membranes. Introduction A disease of turkeys characterised by respiratory and skeletal problems caused by Mycoplasma meleagridis. Mycoplasma meleagridis infection. In adult birds though infection rates are high. Infected parents may be asymptomatic. purchase of M. Pathogenicity is quite variable. Stunting. Infection is via the conjunctiva or upper respiratory tract with an incubation period of 6-10 days. Slow growth. Leg problems. The organism has also been isolated from raptors.m. Treatment Pressure differential dipping has been used where breeder flocks are infected. Antibiotics that have been used are tylosin and enrofloxacin. Mild respiratory problems. Infected eggs result in widespread distribution of infection and increased risk of further vertical transmission. it occurs in most turkey-producing countries but is now much rarer in commercial stock. 97 . though up to 25% of infected birds show lesions at slaughter. maintenance of this status by good biosecurity. This can increase hatchability by 510% in this situation. Specialised dip tanks are subjected to negative pressure which partially collapses the air cell of the submerged eggs. The infective agent does not survive well outside the bird. Transmission is venereal in breeders. Prevention Eradication of the infection from breeding stock. morbidity may be minimal. Predisposing factors include stress and viral respiratory infections. Mortality is low.
Effort should be made to reduce dust and secondary infections. and biosecurity. Differentiate from Mycoplasma gallisepticum. spiramycin. Mycoplasma synoviae. isolation and identification of organism. M. fluoroquinolones. Infection rates may be very high. Infected birds do develop some immunity. Mycoplasma synoviae infection. Birds infected from their parents seem to be immuno-tolerant and particularly prone themselves to transmit. 98 . serology. Spread is generally rapid within and between houses on a farm. Survival of the infectious agent outwith the bird is poor but fomite transmission between farms is important. 11-21 days following contact exposure. Diagnosis Lesions. Prevention Eradication of this infection is also possible using similar techniques as for Mycoplasma gallisepticum.culture used to confirm.Post-mortem lesions Airsacculitis in infected pipped embryos and poults. whilst illness is variable and mortality less than 10%. demonstration of specific DNA (commercial kit available). more commonly in Mycoplasma Broth followed by plating out on Mycoplasma Agar.s. Infected males are particularly prone to transmit infection and may warrant special attention. In some circumstances preventative medication of known infected flocks may be of benefit. especially in commercial layer flocks. Infection is via the conjunctiva or upper respiratory tract with a long incubation period. Serology: SAG used routinely . Airsacculitis (rarely) seen in adult birds. other respiratory viruses. These are based on purchase of uninfected poults. Predisposing factors include stress and viral respiratory infections. Suspect colonies may be identified by immuno-fluorescence. It occurs in most poultry-producing countries. all-in/all-out production. Culture requires inoculation in mycoplasma-free embryos or. Treatment Tylosin. tetracyclines. Vaccines are not normally used. Infectious Synovitis Introduction Infection with Mycoplasma synoviae may be seen in chickens and turkeys in association with synovitis and/or airsacculitis. Transmission may be transovarian. or lateral via respiratory aerosols and direct contact.
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.
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.
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.
100 ppm). Treatment of ducks is not very successful.Tahir Necrotic Enteritis Introduction An acute or chronic enterotoxemia seen in chickens. Inappetance. Immobility. usually of the mid. high levels of most growth promotors and normal levels of ionophore anticoccidials also help. turkeys and ducks worldwide. Prevention Penicillin in feed is preventive.Abubakar. Mortality may be 5-50%. or Bacitracin in feed (e. other debilitating diseases. diet (high protein). Signs Depression. Intestinal contents may be dark brown with necrotic material. usually in less than 48 hours. in drinking water. Closed eyes. neomycin and erythromycin are used in the USA. Ruffled feathers. phenoxymethyl penicillin. Probiotics may limit multiplication of bacteria and toxin 102 . Water medication for 3-5 days and in-feed medication for 5-7 days depending on the severity. amoxycillin). high viscosity diets (often associated with high rye and wheat inclusions in the diet). Intestinal mucosa with diptheritic membrane. Affected birds tend to be dehydrated and to undergo rapid putrefaction. Reflux of bile-stained liquid in the crop if upper small intestine affected. in ducks possibly heavy strains. 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. Post-mortem lesions Small intestine (usually middle to distal) thickened and distended. Predisposing factors include coccidiosis/coccidiasis. Sudden death in good condition (ducks).g. Dark coloured diarrhoea.small intestine. Infection occurs by faecal-oral transmission. usually around 10%. contaminated feed and/or water. Spores of the causative organism are highly resistant. caused by Clostridium perfringens and characterised by a fibrino-necrotic enteritis.g. Treatment Penicillins (e.M.
Acute and fatal in chickens of any age causing neurological and some respiratory signs.g. Strains can be developed as vaccines. Intestinal lesions are absent. Morbidity is usually high and mortality varies 0-100%. respiratory or reproductive systems. ND . In many countries local regulations or market conditions prevent the routine use of many of these options.Mesogenic .Mild disease.Lentogenic .sometimes called 'asiatic' or exotic.Neurotropic Velogenic . The virus involved is Paramyxovirus PMV-1. Four manifestations have been identified: ND .production.Mortality and nervous signs in adult. These viruses have sometimes been used as vaccines in previously immunised birds. Newcastle Disease (Paramyxovirus 1) Introduction Paramyxovirus 1 or Newcastle Disease is a highly contagious viral disease affecting poultry of all ages. Severe lesions of necrotic enteritis affecting the small intestine of broilers. Affected species include chickens. It is highly virulent for chickens. Figure 25. less for turkeys and relatively apathogenic in psittacines. ND . It is not usually vertical (but chicks may become infected in hatcheries from contaminated shells). fomites. pigeons and ducks. The condition is rarely diagnosed in ducks but is a possible cause of production drops/fertility problems. Signs are typically of disease of the nervous. sometimes subclinical. which is of variable pathogenicity. visitors and imported psittacines (often asymptomatic). The sample at the bottom of the picture is still focal. Transmission is via aerosols. Can affect any age. the upper has formed a thick crust of necrotic material. Other species can be infected including mammals occasionally (e. 103 . turkeys. birds.Velogenic Viscerotropic (VVND) . ND . conjunctivitis in man). Higher mortality is seen in velogenic disease in unvaccinated stock.
Cross-reactions have mainly been with PMV-3. encephalomyelitis. caecal tonsil. dust etc). especially in faeces and can persist in houses (in faeces. Twisted neck. Moult. intracerebral or IV pathogenicity in chicks. Severe drop in egg production. Signs Signs are highly variable and will depend on the nature of the infecting virus (see above). laryngotracheitis. post-mortem lesions. Paralysis. IFA. Necrotic plaques in proventriculus. Coughing. It is inactivated by temperatures of 56°C for 3 hours or 60°C for 30 min. It is confirmed by isolation in CE. rising titre in serology.The virus survives for long periods at ambient temperature. haemorrhagic disease. Sudden Death Depression. Differentiate from Infectious bronchitis.tracheal or cloacal. and is ether sensitive. Diarrhoea. Intestinal lesions primarily occur in the viscerotropic form. the infective dose and the degree of immunity from previous exposure or vaccination. Nervous signs. Diagnosis A presumptive diagnosis may be made on signs. Pathogenicity evaluated by Mean Death Time in embryos. However it is quite sensitive to disinfectants. HA+. for up to 12 months. intoxications. intestine. Dyspnoea. Haemorrhage in proventriculus. EDS-76. infectious coryza. 104 . Inappetance. Tracheitis. formalin and phenol. Samples . avian influenza. fumigants and sunlight. HI with ND serum or DID (less cross reactions). acid pH. pneumovirus infection. encephalomalacia. middle ear infection/skull osteitis. antibiotics to control secondary bacteria. Post-mortem lesions Airsacculitis. Treatment None.
Non-starter and 'Starve-out's Introduction This is a condition seen worldwide in young chickens and turkeys due to failure to begin normal food consumption. Use of Mycoplasma gallisepticum free stock under good management reduces the risk of vaccinal reactions. and occasionally gasping due to a plug of pus in the lower trachea. biosecurity. Severe haemorrhagic and necrotic lesions in proventriculus and Peyers patches in the intestines of a broiler chicken suffering from one of the severe forms of Newcastle disease (viscerotropic velogenic). whereas it tends to peak between 6-10 days for chicks that begin eating but then cease. To prevent or reduce vaccinal reactions in young chicks it is important that day old have uniform titres of maternal immunity. It is commonest in progeny of young parent flocks (relatively small yolks) or where managers are inexperienced. Figure 28. Inactivated vaccines have largely replaced the use of live vaccines in lay but they do not prevent local infections. It is common to monitor response to vaccination. Mortality peaks at 3-5 days for birds that fail to eat at all. snicking. Morbidity is up to 10% and mortality close to 100%. 105 . especially in breeding birds by the use of routine serological monitoring. which are adequately stored and take into account the local conditions. Vaccination programmes should use vaccines of high potency. and is associated with difficulty maintaining brooding temperature and poor management of feeders and drinkers. Acute viral infections or heavily contaminated drinking water may have a similar effect to bad management in reducing feed intake. In some countries it has been customary to provide antibiotics prophylactically during periods of anticipated vaccinal reaction. Use of spray application is recommended but it needs to be applied with care to achieve good protection with minimal reaction. The LaSota-type vaccine may even repeated at 35-40 days of age if risk is high. HI has been used extensively. These tests do not directly evaluate mucosal immunity. Elisa is now also used. however. Vaccinal reactions may present as conjunctivitis. A typical programme may involve Hitchner B1 vaccine at day old followed by LaSota-type vaccine at 14 days. vaccination. all-in/all-out production.Prevention Quarantine.
soluble multivitamin supplementation may help. 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. Because it is enclosed in a relatively unyielding membrane. Most organs normal. Treatment Correction of management problems. It has since been seen in turkeys. The condition can be reproduced by causing intense exercise of this muscle. bile staining of adjacent tissues. Diagnosis Based on post-mortem lesions. any swelling of the muscle tends to cut off the blood supply. in broiler parent chickens and also in large broiler chickens in various places. Gall bladder distended. good drinking water hygiene. Differentiate from omphalitis/ yolk sac infection. Prevention Review brooding management. Gizzard may be impacted with litter.Deep Pectoral Myopathy Introduction This condition is so named because it was first identified in adult breeding turkeys in Oregon State. It does not usually cause any mortality or obvious clinical signs and so it is usually identified after slaughter. It is caused by a reduction in the blood supply to the deep pectoral muscles. Oregon Disease . Poor development. aspergillosis. 106 . good hygiene and biosecurity in brooding areas to minimise early disease challenges.Signs Failure to grow. or suffer necrosis. nutrition of young parents. Without adequate blood supply the tissue of the muscle begins to die. Post-mortem lesions Crop empty. age of collection and weight of hatching eggs.
If of very long duration. and flaking. greenish yellow. Treatment Not applicable. It is very difficult to detect affected carcases in standard meat inspection. weighing birds etc). 107 . Transillumination of the breast may help identify affected carcases and may be worthwhile if the incidence is high. Prevention Avoidance of physical damage of this muscle. It may also start to be enclosed in a fibrous capsule. Post-mortem lesions Acute or chronic necrosis of the deep pectoral muscle on one or both sides. the muscle may be swollen and pale. Figure 26. The tissue in the centre is dry. in particular excessive exercise.g. it may become a healed scar. Diagnosis Lesions.Signs None. If recent. thinning operations in meat birds. with oedema within it and on its surface. artificial insemination in breeding turkeys. 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. and. This will normally be due to excessive flapping in association with management activities (e. A typical case of the chronic stages deep pectoral myopathy in a broiler chicken. If the condition is of over 7 days duration the muscle is dry and often shows greenish tinges.
There is some evidence that hatcheries may play a role in the epidemiology. Growth is more rapid and consistent in an anaerobic jar. Signs Coughing. Reduced weight gain. preferably as a flock test comparing results before and after the challenge. The range occurring in turkeys is wider than that seen in chickens. It is a Gram-negative pleomorphic organism. Bordetella aviuminfection. Important cofactors may include respiratory viral vaccines (Newcastle disease. coli overgrowth may occur. ORT Introduction Ornithobacterium Infection is an infection of chickens and turkeys with the bacterium Ornithobacterium rhinotracheale(ORT). Reduced egg production. E. sneezing. 108 . perhaps through survival of the organism on shell surfaces or shell membranes. Most isolates are oxidase positive and galactosidase positive Serology using Elisa tests has been used. Some uncertainty exists about mechanisms of transmission. Within the poultry house it is likely to be by aerosols. coli infections. It had been previously isolated in a number of other countries. The organism grows slowly producing tiny colonies on blood agar. ventilation problems. This was first identified as a new disease syndrome of turkeys in Germany in the early 1990s.Ornithobacterium Infection. Cultures from the trachea of birds showing typical signs are preferred. This can cause significant losses through condemnations. Post-mortem lesions Airsacculitis. In broiler chickens its main importance seems to be as a cause of airsacculitis in apparently healthy flocks that is only identified at slaughter. A range of sero-types have been identified. severe bronchopneumonia. direct contact and drinkers. field challenge with respiratory viruses. age at infection etc. Confirmation is by isolation of the organism. The infection is common in chickens and turkeys. Infectious Bronchitis). 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. tracheitis. Diagnosis Clinical signs and lesions. The slow-growing bacterium was named in 1994. It commonly exacerbates respiratory disease caused by pneumovirus infections in turkeys. The severity of its effects depends on the pathogenicity of the particular strain and other risk factors such as viral infections. and E.
Figure 27. 109 .amoxycillin at 250 ppm in water for 3-7 days or chlortetracycline at 500 ppm for 4-5 days. Satisfactory disease control depends on good management and biosecurity. Initially in Germany most strains were sensitive to amoxycillin. In France and Belgium most strains were sensitive to enrofloxacin. Some work has been done on live vaccine in the USA. it requires two doses. Prevention This is based on good hygiene. Some vaccines seem to have difficulty in producing a longlasting serological response to ORT. Amoxycillin sensitivity remains good. cost etc. Vaccination of breeder flocks to protect progeny has shown benefits in chickens but. therapy and vaccination. though 54% were sensitive to tetracycline. neomycin and enrofloxacin. Preventative medication with the products listed in the previous section may be beneficial in some circumstances. chlortetracycline but not to enrofloxacin. Routine treatment . this is unlikely to work in turkeys.there are issues relating to availability. In the USA in 1998 all strains were sensitive to penicillins and many other microbials. Hygiene . An inactivated vaccine is licensed for broiler parents in Europe. Tilmicosin is also effective at 10-20mg/kg and should be used in the early stages of the disease. Similar lesions may be found in Pasteurellosis. Severely consolidated lung from an acute ORT infection in 14-week-old turkey growers. ORT is a major problem on multi-age sites. regulation.Treatment The sensitivity of ORT to antibiotic is highly variable. The lung is solid and covered by pus/ purulent exudate.it is very sensitive in vitro to a range of chemicals. also most are sensitive to tiamulin. because of the age of slaughter. Vaccination .
Post-mortem lesions Green discolouration of the liver at slaughter. Soft-shelled eggs.only identified at slaughter. Prevention Unknown. Gram-variable pleomorphic bacteria have been isolated from affected livers and bones. Drop in production.Osteomyelitis Complex. Enlarged hocks. Osteoporosis. high production. Signs None. turkeys and ducks seen worldwide and due to Vitamin D or calcium deficiency. Diagnosis Lesions. Soft bones and beak. Birds rest squatting. 110 . Treatment Not applicable . The green discolouration is used to identify carcases that require closer inspection of the other tissues. Predisposing factors include small body size. Turkey Introduction An association has been shown between green discolouration of the livers of turkey growers at slaughter and the occurrence of inflammatory lesions of bones and/or joints. Signs Lameness. Cage Fatigue Introduction A condition of chickens. Birds go off legs.
turkeys and passerine cage birds with Paramyxovirus PMV-2 results in disease with variable mortality. Epiphyses of long bones enlarged. In chickens it is usually mild. lesions.Tahir Post-mortem lesions Bones soft and rubbery. Diagnosis History. bone ash. Parathyroids enlarged. Vertical transmission does not usually occur. Beak soft.M. depending on the species affected and whether infection is complicated by other factors and diseases. spondylitis. Paramyxovirus 2 . Prevention Supplementation of vitamin D. Treatment Over-correct ration vitamin D. place on litter. Drop in egg production.Yucaipa Disease Introduction An infection of chickens. Beading and fracture of ribs. signs. calcium carbonate capsules. As birds progressively mobilise skeletal calcium for egg production through lay. skeletal size and mineral content at point of lay are critical. Transmission is by wild birds and fomites. Wild birds are believed to be especially important. Post-mortem lesions Not characteristic. whereas turkeys are more severely affected. Differentiate from Marek's disease. Inappetance. antioxidants. Coughing.Abubakar. proper Ca and P levels and ratio. Signs Depression. 111 .
antibiotics to control secondary bacteria. IFA. Drop in egg production (turkeys). Differentiate from Infectious bronchitis. Vertical transmission does not usually occur. Coughing. Treatment No specific treatment. High mortality (cage birds). Post-mortem lesions No specific lesions. antibiotics to control secondary bacteria. HA+. Signs Depression. all-in/all-out production. laryngotracheitis. 112 . The infection is transmitted by birds. Loss of shell pigment Nervous symptoms (psittacines). occasionally chickens and psittacine cage birds. IFA. including wild bird contact and fomites. Treatment No specific treatment. Inappetance.Diagnosis Isolation in CE. HI with ND serum or DID (less cross reactions). Diagnosis Isolation in CE. HI with ND serum or DID (less cross reactions). haemorrhagic disease. EDS-76. Paramyxovirus-3 Introduction Paramyxovirus PMV-3 infects turkeys. HA+. biosecurity. Prevention Quarantine. Mortality is usually low in poultry.
Diagnosis Isolation in CE. Signs Reduction in egg production. biosecurity. Vertical transmission does not usually occur. The infection is transmitted by birds. Mortality is 0-5%. A range of 113 . antibiotics to control secondary bacteria. biosecurity. Treatment No specific treatment. A less acute form of the disease appears to produce more of a lingering mortality.Prevention Quarantine. Mild respiratory signs. In both cases mortality can be high and can be associated with a marked depression in growth. Paramyxovirus-6 Introduction Paramyxovirus PMV-6 infection of turkeys. 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. including wild bird contact and fomites. It is an infectious and transmissible cause of sudden increases in mortality in turkeys between 7 and 28 days of age. Post-mortem lesions No specific lesions. HI with ND serum or DID (less cross reactions). all-in/all-out production. all-in/all-out production. The infection is inapparent in ducks and geese. Prevention Quarantine. Vaccination has been used in turkeys but may not be cost-effective. IFA.
huddling. Caseous cores in bursae (late in the process). Droppings watery. A highly digestible diet with fat at 7. pale brown. Weight loss. Diagnosis Signs. multivitamins and milk replacer products are helpful for nutritional support in the acute phase. This syndrome is clearly distinguished from typical viral enteritis in young turkeys because of the high mortality and severe growth depression. Effective terminal disinfection.5-8% will encourage feed intake and recovery. Emaciation. Wet litter. Treatment A range of antibiotics and arsenicals have been used to control the bacterial component of this condition. Overdistension of crop in young birds because of an interruption in feed supply may predispose. Prevention Biosecurity to reduce the introduction of new infections into brooding facilities. Good quality diets of a suitable form . eating litter. Reduced feed consumption and growth. Increasing weakness. Liquid intestinal contents. Post-mortem lesions Dehydration. All-in/all-out production. Picking at feed. lesions.mash and poor quality crumbles increase risk. Pendulous Crop Introduction A complex condition of turkeys and chickens associated with coarse fibrous feed. To replicate the condition in full it appears to be necessary to include bacteria in the inoculum. Increased water consumption. 114 . seeking heat. Fluoroquinolone antimicrobials appear to be especially effective. Signs Initial hyperactivity and increased vocalisation. Muscle atrophy.viruses have been isolated from affected flocks.
lesions. Crop contents semi-liquid and foul smelling. Lack of muscle tone. They are found in the mucosa of crop and proventriculus causing mainly inapparent infections. Post-mortem lesions Inflammation. including crustaceans.Signs Enlargement of crop. Treatment None. have ulcerations and sometimes mycosis. Proventricular Worms Introduction Dispharynx. Diagnosis Signs. and thickening of mucosa of proventriculus. haemorrhage. necrosis. Emaciation in heavily infected young chicks (Tetrameres). 115 . ulceration. Prevention Remove predisposing factors. spiruroid worm parasites of poultry and game birds. Signs Anaemia. may be impacted. Tetrameres and Cyrnea are nematodes. identification of worms. Diarrhoea. if these can be identified. Diagnosis Macroscopic examination of lesions. Infection is by the oral route on exposure to the intermediate hosts. grasshoppers and cockroaches. Post-mortem lesions Crop distended with feed.
other poultry. Signs Weakness. Sometimes sudden death. 'hardening off'. coccidiosis. Treatment Tetracyclines. wild birds. In peracute disease the only lesion may be enteritis. tuberculosis. Ruffled feathers. isolation. duck viral hepatitis.Treatment Not usually required. The disease has a mortality of 5-75%. rodents and man with the bacterium Yersinia pseudotuberculosis. colibacillosis. sulphonamides in feed. adequate protection. Diarrhoea. Pseudotuberculosis Introduction An infection of ducks. Diagnosis Lesions. Prevention Good husbandry and hygiene. Post-mortem lesions Miliary lesions in a variety of organs but especially in the liver. Differentiate from Duck viral enteritis. Prevention Prevention of access to intermediate hosts. 116 .
Dehydration. Diagnosis History. toxin and possibly a virus infection. Pancreas chalky. Treatment Adequate water supply. 117 . Prevention Good management. coccidiosis. Loss of appetite. antibiotics. diet and water supply. Differentiate from fowl cholera. Affected birds have an increase in circulating monocytes in their blood. Watery diarrhoea. Liver swollen with foci. Crop distended. elimination of other causes. Drop in egg production. Kidneys swollen. It is associated with hot weather. water deprivation. Catarrhal enteritis. It was commonly reported prior to 1960 but is now rare. Dark comb and wattles.M. IBD and typhoid. mucoid casts in intestine.Tahir Pullet disease. multivitamins in water. Crop distension.Abubakar. hygiene. vibriosis. Bluecomb. capillariasis. molasses. Skin cyanosis of head. Skeletal muscle necrosis. Signs Depression. Post-mortem lesions Dehydration. lesions. Avian Monocytosis Introduction A sudden onset condition of chickens early in lay with high morbidity and a mortality of 050%.
Red Mite and Northern Fowl Mite Introduction Arachnid mites. Treatment Pyrethroids. crevices etc. Loss of condition. Ornithonyssus bursae. 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. Effective monitoring of mite numbers and implementation of control measures before birds are heavily infested improves control. Birds restless.itching. carbamates. organophosphates. 118 . the Common Red Mite. For northern fowl mite it is essential to apply approved insecticides to the affected birds. and good design of new equipment to limit harbourages for red mites. Filling of cracks and crevices. Dermanyssus gallinae. in nest boxes. Spots on eggs. Pale comb and wattles. mainly at night and may transmit fowl cholera and other diseases. the Northern Fowl Mite spends its entire life cycle on the bird and can multiply more rapidly as a result. citrus extracts.7 mm. fumigation and insecticide treatment at turnaround. Signs Presence of grey to red mites up to 0. Staff complaints . Drop in egg production. Diagnosis Number and type of mites identified. vegetable oil and mineralbased products (both liquid sand dusts) have been used to control red mites in the environment. Prevention Thorough cleaning. Post-mortem lesions Anaemia. feeds by sucking blood. May cause anaemia and death in young birds. which are external parasites of chickens and turkeys. cracks.
Treatment None. may act as 119 . vaccinal and field strains) and bacteria (Ornithobacterium rhinotracheale. and by fomites. It may occur as an exacerbating factor in other types of respiratory disease. A number of respiratory viruses (Infectious Bronchitis. Lentogenic Newcastle disease virus.Abubakar.Tahir Respiratory Adenovirus Infection. Infected birds may remain carriers for a few weeks. Post-mortem lesions Mild catarrhal tracheitis. intranuclear inclusions in liver.M. formaldehyde and iodides work better. coli) may be involved. at least 12 sero-types have been described and these may be isolated from healthy chickens. 'Mild Respiratory Disease' Introduction An adenovirus infection of chickens with a morbidity of 1-10% and a mortality of 1-10%. pH). The virus grows well in tissue culture (CE kidney. Dust. Diagnosis History. CE liver). E. and other factors associated with poor ventilation. The virus is generally resistant to disinfectants (ether. temperature. Respiratory Disease Complex Introduction Respiratory infections in chicken and turkeys are seen worldwide but especially in temperate poultry-producing areas in winter months. lesions. chloroform. Prevention Quarantine and good sanitary precautions. Avian pneumovirus. Signs Mild snick and cough without mortality. Transmission may be vertical and lateral. prevention of immunosuppression. ammonia and other gases. Opinions vary as to whether adenovirus can be characterised as a primary respiratory pathogen.
Rattling noises. Signs Snick. be challenged by some of these pathogens). Severe airsacculitis of thoracic air sacs in a broiler close to slaughter. Airsacculitis.catarrhal to purulent. sanitation of drinking water. serology. Head swelling. If condemned birds are included mortality may be more than 10%. and have been cut into to reveal a cheesy (caseous) mass of pus. Treatment Antimicrobial treatment of specific bacterial infections. Post-mortem lesions Severe tracheitis with variable exudate . Given that many flocks are vaccinated it is necessary to establish normal serological response in vaccinated flocks in the absence of disease (some of which may. Conjunctivitis. Sneezing. mortality 5. 120 . carefully applied appropriate viral vaccines. There is also percarditis evident (at top right). Figure 29.10%. Pericarditis. of course. Prevention Effective ventilation.predisposing factors. Nasal exudate. The air sacs are thickened and congested. response to environmental changes. Differentiate from Chronic Respiratory Disease (Mycoplasmosis). Morbidity is typically 10-20%. Diagnosis Lesions.
Both tracheas were congested and the upper sample had mucopurulent material in the lumen. and the infection can be spread by mosquitoes or in contaminated Marek's disease vaccines. Diarrhoea. Diagnosis Pathology. turkeys. chick inoculation. Treatment None. usually higher in females than males. Post-mortem lesions Neoplastic lesions in liver. Sometimes enteritis and proventriculitis (especially in broilers infected with contaminated Marek's disease vaccine). There is an incubation period of 5-15 days. Transmission is lateral and possibly transovarian. ducks. and quail with morbidity up to 25%. 121 . A gradual increase in mortality and poor growth in broilers may be the main signs. Sometimes nodules in intestine and caecae. Leg weakness. spleen and kidney. Signs There may be no obvious signs. geese. Severe tracheitis is broilers with respiratory disease complex. Reticuloendotheliosis. Marked stunting when Marek's disease vaccine is contaminated.Figure 30. Lympoid Tumour Disease Introduction A retrovirus infection of chickens.
turkeys and ducks worldwide. Reduction in bodyweight. Parathyroids enlarged. Birds rest squatting. Rickets (hypocalcaemic) Introduction Vitamin D deficiency or phosphorus/calcium imbalance is seen in chickens. antioxidants. Poor growth. Soft bones and beak. Beak soft. Beading and fracture of ribs. Prevention Supplementation of vitamin D. Birds go off legs. Growth plates widened and disorganised. Treatment Over-correct ration with three times vitamin D for 2 weeks. Avoidance of contamination of live vaccines is the main control measure practised. Hock swelling. lesions.Prevention Formal control programmes have not been documented as the condition is sporadic and relatively self-limiting. Signs Lameness. signs. or Vitamin D or 25-hydroxy vitamin D in drinking water. Post-mortem lesions Bones soft and rubbery. Epiphyses of long bones enlarged. 122 . proper calcium and phosphorus levels and ratio. Diagnosis History. Femoral Head Necrosis. Differentiate from Encephalomalacia.
Soft bones and beak. Beak soft. Parathyroids enlarged. Some countries have regulations governing the use of phosphorus in fertiliser with a view to reducing water pollution. Birds rest squatting. signs. Diagnosis History. Birds go off legs. Even subclinical levels of this condition can predispose to Femoral Head Necrosis. Treatment Over-correct ration with 3 times vitamin D for 2 weeks. proper calcium and phosphorus levels and ratio. lesions (analyse Vitamin A or manganese as a guide to premix inclusion). This has led feed manufacturers to try various approaches to reduce added phosphorus in diets. Enlarged hocks. Post-mortem lesions Bones soft and rubbery. Intestinal diseases may reduce absorption. Hock swelling. antioxidants. Reduction in bodyweight.M. Growth plates widened and disorganised. 123 .Abubakar. Beading and fracture of ribs. Signs Lameness. turkeys and duck is seen worldwide. Epiphyses of long bones enlarged. Poor growth. or vitamin D in drinking water.Tahir Rickets (hypophosphataemic) Introduction Phosphorus deficiency in chickens. Prevention Supplementation of Vitamin D.
Treatment No specific treatment for this infection. The parasite species vary: A. dissimilis in turkeys. partridges and pigeons. are nematode worm parasites. electron microscopy or Elisa on intestinal contents . turkeys.Ascaridia Introduction Ascaridia sp. galli in fowl. and A. Use of a good electrolyte solution is beneficial in the acute stage of infection. The route of infection is oral and maximum viral excretion occurs 2-5 days post infection. Control of secondary bacterial enteritis may require antimicrobial medication. The life cycle is similar to that illustrated in the section on the caecal worm Heterakis.5 g faeces). stout white worms up to 12 cms in length. Diagnosis Demonstration of virus (PAGE. shorter in young birds. columbae in pigeons. Virus may be found in asymptomatic birds. The 124 . Roundworm. It is not known if vertical transmission occurs though virus has been occasionally isolated from embryonated eggs. except that the adults reside in the small intestine and earthworms are not significant paratenic or transport hosts. The route of infection is oral usually by direct ingestion of the embryonated egg and there is a 5-10-week prepatent period. guinea fowl.submit 6 x .Abubakar.M. Post-mortem lesions Viruses replicate mainly in the mature villous epithelial cells. Prevention Good hygiene in brooding areas. large . pheasants. Signs Diarrhoea. seen worldwide.Tahir Rotavirus Infection Introduction Rotavirus infection is seen in chickens. Adult birds can tolerate burdens asymptomatically. A.
A collection of mature roundworms (Ascaridia galli) recovered from the small intestine of a layer chicken in rear. pasture rotation and regular treatment. 125 . especially for young birds. Post-mortem lesions Enteritis. Worms up to 12 cm in length in duodenum and ileum. levamisole. Diarrhoea. piperazine as locally approved. oval smooth-shelled nonembryonated eggs in faeces. Wasting. Poor growth. mainly in young birds. Figure 31. In the bottom left quadrant there are also some immature worms. Diagnosis Macroscopic examination with identification of worms.parasites may be transported by grasshoppers and earthworms and are resistant to environmental effects. Listlessness. Prevention Prevention of contamination of feeders and drinkers with faeces. Signs Loss of condition. Treatment Flubendazole.
This can cause mortality in birds of any age.Abubakar. 126 . Salmonella Gallinarum. parrots. canaries and bullfinches. Infections still occur worldwide in non-commercial poultry but are rare in most commercial systems now. Broiler parents and brown-shell egg layers are especially susceptible.Tahir Ruptured Gastrocnemius Tendon Introduction This is a condition causing severe lameness in roaster type meat chickens and more rarely in turkeys. Avoidance of physical stresses on the musculoskeletal system through careful handling as well as careful design and layout of equipment. Fowl Typhoid Introduction Disease caused by one of the two poultry-adapted strains ofSalmonella bacteria. guinea fowls. Affected birds should be culled humanely as soon as they are identified. Diagnosis Signs and lesions are obvious. game birds. Treatment None.M. Ruptures of ligaments and joints are also occasionally seen. The bird may have the hock dropped to the floor. If there is a greenish tinge to the area of swelling it occurred a few days previously. Signs Severe lameness. Reoviral or staphylococcal arthritis or tenosynovitis may predispose but many cases have no evidence of an inflammatory response. sparrows. Prevention Establishment of a steady growth profile. Histology may be helpful in determining if there is an underlying inflammatory process. Salmonella Gallinarum. Post-mortem lesions The fresh lesion contains a haematoma with the end of the ruptured tendon within or adjacent to it. Chickens are most commonly affected but it also infects turkeys. Broiler chickens have an avascular area of tendon just above the hock that is the usual site of rupture.
both live (usually based on the Houghton 9R strain) and bacterins. fluoroquinolones. Tube and rapid plate agglutination tests have been the standard serological tests for many years but have only been validated for chickens. Treatment Amoxycillin. potentiated sulponamide. Transmission may be transovarian or horizontal by faecal-oral contamination. Post-mortem lesions Bronzed enlarged liver with small necrotic foci. In clinical cases direct plating on Brilliant Green. Inappetance. Anaemia. Enrichment procedures usually rely on selenite broth followed by plating on selective media. McConkey and non-selective agar is advisable. 127 . Ruffled feathers. pullorum disease and coli-septicaemia. Prevention Biosecurity. LPS-based Elisa assays have been developed but not widely applied commercially. but is susceptible to normal disinfectants. even in adults. surviving months. Differentiate from Pasteurellosis. Thirst. Reluctance to move. The route of infection is oral or via the navel/yolk. recovered birds are resistant to the effects of infection but may remain carriers. Signs Dejection. Diagnosis Isolation and identification. Vaccines for fowl typhoid have been used in some areas. clean chicks. Enteritis of anterior small intestine. Engorgement of kidneys and spleen. mortality is increased in stressed or immunocompromised flocks and may be up to 100%. egg eating etc. As with other salmonellae. tetracylines. The bacterium is fairly resistant to normal climate. Yellow diarrhoea.Morbidity is 10-100%. and/or congestion.
Gasping. White diarrhoea. Salmonella Pullorum. Salmonella Pullorum. game birds. Signs Inappetance. 'Bacillary White Diarrhoea' Introduction Disease caused by one of the two poultry-adapted strains ofSalmonella bacteria. ostriches and peafowl. in young broiler chickens. but also infects turkeys. Bacterial septicaemia caused by Salmonella Gallinarum. pale and shows focal necrosis. The liver on the left is normal.Figure 32. usually brown-shell egg layers. surviving months but is susceptible to normal disinfectants. Depression. The route of infection is oral or via the navel/yolk. Transmission may be transovarian or horizontal mainly in young birds and may sometimes be associated with cannibalism. the one on the right is slightly enlarged. Pullorum Disease. Morbidity is 10-80%. guinea fowls. Occasionally it can cause losses in adult birds. Similar lesions can be seen in Pullorum Disease and with other causes of septicaemia in young chicks. Loud chirping. ring doves. Lameness. It affects chickens most commonly. Ruffled feathers. sparrows. Vent pasting. 128 . It still occurs worldwide in noncommercial poultry but is now rare in most commercial systems. mortality is increased in stressed or immunocompromised flocks and may be up to 100%. The bacterium is fairly resistant to normal climate. Closed eyes. parrots. this usually only causes mortality in birds up to 3 weeks of age.
Urate crystals in ureters. Derby. fluoroquinolones. Paratyphoid Infections Introduction Salmonellae bacteria other than the species specific sero-typesS. Vaccines are not normally used as they interfere with serological testing and elimination of carriers. Typhimurium (which are considered separately). Regardless of the initial source of the infection. In clinical cases direct plating on Brilliant Green. Many species are intestinal carriers and infection is spread by faeces. S. and also other than S. Montevideo. Enrichment procedures usually rely on selenite broth followed by plating on selective media. recovered birds are resistant to the effects of infection but may remain carriers. other enterobacteria. Intestinal or caecal inflammation. their presence may be significant with respect to carcase contamination as a potential source of human food poisoning. chilling and omphalitis Treatment Amoxycillin. Anatum. They infect chickens. paracolon. are capable of causing enteritis and septicaemia in young birds. gizzard wall and heart. S. Gallinarum. McConkey and non-selective agar is advisable. poteniated sulponamide. Enteritidis andS. Caecal cores. S. As with other salmonellae. turkeys and ducks worldwide. Pullorum. Morbidity is 0-90% and mortality is usually low. Diagnosis Isolation and identification. tetracylines. but S. Prevention Eradication from breeder flocks. The route of infection is oral and transmission may be vertical as a result of shell contamination. fomites and feed (especially protein supplements but also poorly stored grain). S. Certain sero- 129 . Salmonellosis. in the environment or in rodent populations. Sero-types vary. it may become established on certain farms. liver. S. Differentiate from Typhoid. Bredeney are among the more common isolates. Splenomegaly. Newport. Paratyphoid. Even if these infections do not cause clinical disease.Post-mortem lesions Grey nodules in lungs.
Good management. Enrichment media such as buffered peptone followed by selective broth or semi-solid media (e. Predisposing factors include nutritional deficiencies. neomycin. chilling.types are prone to remain resident in particular installations (e. The bacteria are often persistent in the environment. but are susceptible to disinfectants that are suitable for the particular contaminated surfaces and conditions.g. Pericarditis. other enterobacteria. Differentiate from Pullorum/Typhoid. Diarrhoea. Loss of appetite and thirst. 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. especially in dry dusty areas. Vent pasting. This approach is often used in the heat treatment of feed. tetracyclines. amoxycillin. Senftenberg in hatcheries). Cheesy cores in caecae. or absent. Foci in liver. Enteritis. Diagnosis Isolation and identification. Temperatures of around 80°C are effective in eliminating low to moderate infection if applied for 1-2 minutes. other bacterial infections and ornithosis (in ducks). Focal necrotic intestinal lesions. Ruffled feathers. Treatment Sulphonamides. 130 . fluoroquinolones. Dejection. Dehydration. applied at sufficient concentrations. Closed eyes. However this has the potential to reveal the presence of salmonellae that are irrelevant to the clinical problem under investigation. Chemotherapy can prolong carrier status in some circumstances. Unabsorbed yolk. inadequate water. Post-mortem lesions In acute disease there may be few lesions. S.g. Signs Signs are generally mild compared to host-specific salmonellae.
Typhimurium has remained relatively stable though the spread of the highly antibiotic-resistant strain DT104 in various farmed species gives some reason for concern. Predisposing factors include nutritional deficiencies. because there are differences in the epidemiology as compared to other salmonellae. elimination of resident infections in hatcheries. The prevalence of S. breeding and grow-out farms. turkeys and ducks cause problems worldwide with morbidity of 0-90% and a low to moderate mortality. many species are intestinal carriers and infection may be carried by faeces. Typhimurium infections Introduction Salmonella Enteritidis and S. applied at sufficient concentrations. The route of infection is oral. Enteritidis and S. Many infected birds are culled and others are rejected at slaughter. Routine monitoring of breeding flocks. clean nests. especially phage type 4. all-in/all-out production. S. The bacteria are often persistent in the environment. fomites and on eggshells. Infection results in a strong immune response manifest by progressive reduction in excretion of the organism and reduced disease and excretion on subsequent challenge. good feed. Salmonellosis. Temperatures of around 80°C are effective in eliminating low to moderate infection if applied for 1-2 minutes. has become much more common in both poultry and humans since the early 80s. inadequate water and other bacterial infections. Vaccines are not generally used for this group of infections. secondly. This approach is often used in the heat treatment of feed. Salmonella Enteritidis.Typhimurium are presented separately from other sero-types of Salmonella because. These are the predominant sero-types associated with human disease in most countries. Infections in chickens. Feed and feed raw material contamination is less common than for other sero-types. competitive exclusion. 131 .Prevention Uninfected breeders. especially in dry dusty areas. these bacteria are often specifically cited in zoonosis control legislation. on the one hand. mills. and. Vertical transmission may be either by shell contamination or internal transovarian contamination of yolk. fumigate eggs. hatcheries and feed mills is required for effective control. chilling. care in avoiding damage to natural flora. but are susceptible to disinfectants that are suitable for the particular contaminated surfaces and conditions.
Rappaport-Vassiliadis) followed by plating on two selective media will greatly increase sensitivity. It is possible to detect reactions with specific antigens in agglutination tests but competitive and direct Elisa tests are more commonly used today. However this has the potential to reveal the presence of salmonellae that are irrelevant to the clinical problem under investigation. Cheesy cores in caecae. Pericarditis. Good management. Lost of appetite and thirst. Differentiate from Pullorum/Typhoid. Ruffled feathers. mills. Prevention Uninfected breeders. Focal necrotic intestinal lesions. breeding and grow-out farms. neomycin. other enterobacteria such as E. Diarrhoea. amoxycillin. Post-mortem lesions In acute disease there may be few lesions. Dehydration. Infection 132 . Chemotherapy can prolong carrier status in some circumstances. coli.Pullorum serum agglutination tests. In clinical cases direct plating on Brilliant Green and McConkey agar may be adequate. S. Stunting in older birds. Treatment Sulphonamides. care in avoiding damage to natural flora. Enrichment media such as buffered peptone followed by selective broth or semi-solid media (e. Early depletion of infected breeding stock is required in some countries such as those of the European Union. infection Diagnosis Isolation and identification. Vent pasting. competitive exclusion. hatcheries and feed mills is required for effective control. Enteritis. Misshapen ovules in the ovaries in S. tetracyclines. good feed. all-in/all-out production. elimination of resident infections in hatcheries. Unabsorbed yolk.Signs Dejection.E. Routine monitoring of breeding flocks. fumigate eggs.g. Closed eyes. clean nests. fluoroquinolones in accordance with the sensitivity. Perihepatitis.Enteritidiscauses cross-reactions which may be detected with S. Foci in liver.
Systemic viral infections that cause ovarian regression or damage to the oviduct or cloaca. Peritonitis. Diagnosis Use the signs to select birds for culling and post-mortem investigation. leaking urates. or may proceed upwards from the cloaca. The control of infection in this area is probably achieved by ciliated epithelium that mostly wafts a carpet of mucus towards the cloaca. Some birds may 'lay' a caseous mass of pus (which may be found in a nest or on the egg belt). The oviduct is a hollow tube joining the normally sterile environment of the body cavity with the cloaca. Damaged vents. coliand occasionally Salmonella spp. Salpingitis Introduction Salpingitis is an inflammation of the oviduct. Distended abdomen. May form a multi-layered caseous cast in oviduct or be amorphous. Vaccines are increasingly being used for S. both inactivated (bacterins) and attenuated live organisms. Infection may spread downwards from an infected left abdominal air sac.). Typhimurium infection. Bacteriology of oviduct. Anything that damages the epithelium or disturbs normal oviduct motility is likely to increase the likelihood of salpingitis. It is a complex condition of chickens and ducks associated with various infections including Mycoplasma and bacteria (especially E. are especially prone to increasing salpingitis. which normally has many millions of potentially pathogenic bacteria. Enteritidis and S. Death. Signs Sporadic loss of lay. 133 . Post-mortem lesions Slight to marked distension of oviduct with exudate.results in a strong immune response manifest by progressive reduction in excretion of the organism and reduced disease and excretion on subsequent challenge. Lesions.
immunise effectively against respiratory viral pathogens common in the area. Shaking or quivering of legs after rising. Post-mortem lesions None.Treatment Birds with well-developed lesions are unlikely to respond to medication. Signs Stand on toes shaking. aspirin may be helpful if locally approved. Diagnosis Clinical examination. releasing poults into larger areas and in handling heavier birds. Use of a suitable antimicrobial may be beneficial for birds in the early stages and if associated with efforts to minimise risk factors. Prevention Control any septicaemia earlier in life. use healthy parent flocks. 134 . Treatment Multivitamins. exclusion of other problems. possibly associated with tendon injury. Prevention Care in transport of brooded poults. Morbidity is 10-20%. Shaky Leg Syndrome Introduction A condition of turkeys with a course of often 3-4 weeks.
This appears to be a multifactorial condition. Orange mucoid droppings. Mortality drops off as sharply as it started. Post-mortem lesions Mild enteritis. Minimise stress. 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. suggesting a viral component. 135 . Provide multivitamins. typically 7-14day-old. Feed intake. electrolytes and glucose solution to flock.Spiking Mortality of Chickens Introduction This is a condition characterised by a sudden increase in mortality in young. Filtered intestinal contents from affected flocks appear to be capable of reproducing the condition. Prevention Good sanitation of the brooding house. Dehydration. Signs Tremor. Excess fluid in lower small intestine and caecae. Diagnosis Pattern of mortality. Avoidance of interruptions in feed supply. rapidly growing broiler chickens. Birds in good condition die after showing neurological signs. Males are more susceptible than females. and/or carbohydrate absorption are disturbed resulting in a hypoglycaemia. Coma. Avoidance of physical stress. probably because they are growing faster. Signs and lesions. Death. Treatment Leave affected chicks undisturbed. Paralysis.
ducks. and egg soiling in chickens. Weakness and progressive paralysis. Signs Depression. pheasants. e. Necrotic foci.g. 136 . isolate in chicken eggs or chicks or poults. Mucoid enteritis. geese. diarrhoea. grouse and canaries with morbidity and mortality up to 100%. It has been associated with typhilitis.Spirochaetosis Introduction The bacterium Borrelia anserina infects chickens. previously known as Serpulina pilosicoli. Cyanosis. Often diarrhoea with excessive urates. reduced egg production. is an intestinal spirochaete that can be associated with inflammation of the large intestine in a broad range of mammals and birds. and occasionally by infected faeces. Liver enlarged with small haemorrhages. Diagnosis Haematology. It is transmitted by arthropods. The bacterium is poorly resistant outside host but may be carried by Argas persicus for 430 days. Drops in egg production may be seen in both systemic and intestinal forms Post-mortem lesions Marked splenomegaly. vaccines in some countries. Brachyspira pilosicoli. Argas persicus. Prevention Control vectors. Spleen mottled with ecchymotic haemorrhages. turkey. Thirst. Treatment Various antibiotics including penicillin.
That on the left shows the typical lesion of spondylolisthesis.Abubakar.M. Post-mortem lesions Anterior-posterior rotation of the bodies of the last or penultimate thoracic vertebrae resulting in scoliosis just anterior to the kidney. Signs Sitting on hock or rumps. 137 . lesions. Diagnosis Symptoms. May walk backwards. These are cross-sections of the spinal column of 4-5-weekold broilers. Treatment None. Use of wings to help in walking. The sample on the right is normal. Kinky-back Introduction A complex condition of broiler chickens with a morbidity of 1-5% and low mortality associated with rapid growth and possibly having a genetic component. Prevention Selection for satisfactory conformation in primary breeding. legs extended forward. with rotation of the body of the vertebra and the pinching of the spinal column that causes paralysis.Tahir Spondylolisthesis. Figure 33.
Infection is usually by the respiratory route with an incubation period of 2-3 days seen after artificial infection. Wounds. Treatment None. Damaged skin due to nutritional deficiencies (such as of biotin) may also be a point of entry. Diagnosis Clinical signs. aureus and seen in chickens and turkeys worldwide. mainly S. Post-mortem lesions Gross lesions are not usually evident.Abubakar. Morbidity is usually low and mortality 0-15% though affected birds will often be culled on humane grounds. Staphylococcal Arthritis.M. and toe trimming may be a portal of entry with subsequent spread via the bloodstream to the typical sites of lesions. 138 . Signs Legs splay and chick is unable to stand. Staphylococcosis. The type of chick box liners and the feeding papers used in the brooding house can also influence the occurrence of the condition. avoidance of excessive hatching egg storage. These include good breeder nutrition. either accidental or induced by interventions such as beak trimming. Prevention All measures that improve chick vitality at hatching are beneficial in reducing this problem. Bumble Foot Introduction Caused by Staphylococcus bacteria.Tahir Spraddle Legs or Splay Leg Introduction Occurs in all species in the recent hatchling. and careful monitoring of incubation conditions.
Recovered birds may have some immunity but vaccination with staphylococci has not been found to be helpful in preventing the disease to date. 139 .. Prevention Good hygiene in the nest. and by fomites. This may progress to abscess formation in these areas. Possibly vaccination against reovirus infection. toe clipping). Good management. synoviae. low stress and prevention of immunosuppression from any cause will all tend to help. Signs Ruffled feathers. the hatchery and in any intervention or surgery (processing. in accordance with sensitivity. isolation and identification of pathogen. Low mobility. Lameness. e.. particularly of parent birds. Treatment Antibiotics. trauma. and imunosuppression. especially M. Mycoplasma spp.g. Post-mortem lesions Tenosynovitis. Differentiate from septicaemia or tenosynovitis due to Colibacillosis. chronic stress. This condition is a cause of sudden deaths in ducklings of 2-3 weeks of age. Some sudden deaths from acute septicaemia if very heavy challenge. Infected joints may have clear exudate with fibrin clots. Swollen above the hock and around the hocks and feet. most commonly in the plantar area of the foot or just above the hock joint. Diagnosis Lesions.Transmission occurs in the hatchery and in the general farm environment. Salmonella spp. Competitive exclusion with a non-pathogenic Staphylococcushas been shown to be effective (no commercial products yet available based on this technology). Predisposing factors include reovirus infection. Streptococcus bovis Septicaemia Introduction An infection of ducks with the bacterium Streptococcus bovis.
most are found lying on their back. Post-mortem lesions Intestine filled with feed. Sudden Death Syndrome. Leg weakness or incoordination in a few birds. Liver congestion. lesions.).affected birds respond well to saline injection and will actively seek out salt scattered in the litter. Lung congestion and oedema. The atria of the heart have blood. 140 . the ventricles are empty. Treatment Amoxycillin. possibly metabolic. Post-mortem lesions Beak cyanosis. Signs Sudden death in convulsion. Prevention Good husbandry and hygiene. 'Flipover' Introduction A condition of broiler chickens of unknown cause. Sodium deficiency can appear very similar at about the same age . It can be induced by lactic acidosis and about 70% of birds affected are males. isolation.Signs Sudden deaths. Livers heavier than those of pen-mates (as a percentage of bodyweight. Serum accumulation in lung (may be little if examined shortly after death). Haemorrhages in muscles and kidneys. Splenic hyperplasia. Diagnosis History. Affected well-grown birds may appear to have died from smothering. extra care in the immediate post-brooding period.
or birds' access to them. they may not be host specific. low intensity light. Prevention Lowering carbohydrate intake (change to mash). Cestodes Introduction Cestodes are tapeworms that are seen in many species. lighting programmes.Diagnosis Birds found on back with lack of other pathology. 141 . Check your local regulations. however it may not have a zero withdrawal in commercial egg layers. Post-mortem lesions Occupy space in intestine and create small lesions at point of attachment. Diagnosis Identification of the presence of the worms at post-mortem examination. Most have intermediate invertebrate hosts such as beetles or earthworms. Tapeworms. Treatment None possible. use of dawn to dusk simulation and avoidance of disturbance. Prevention Control the intermediate hosts. Treatment Flubendazole is effective at a 60 ppm in diet. feed restriction. Signs It is doubtful if any signs are produced under most circumstances.
Tibial Dyschondroplasia. distal tibia. Diagnosis Gross pathology. Differentiate from rickets.a mass of avascular cartilage with transitional chondrocytes. Signs There are usually no signs unless the condition is severe. Mature tapeworms with their heads (scolices) embedded in the intestine. TD Introduction A complex condition seen in chickens.Figure 34. Post-mortem lesions Plug of cartilage in proximal end of tibia. Lixiscope may identify in vivo as early as 2 weeks of age. Microscopically . It may be associated with rapid growth and have a nutritional factor. chloride levels and acid/base balance. mild lesions may require histology to distinguish from other problems. small ovoid lacunae and more matrix than normal. 142 . Treatment None. Vitamin D3 supplementation. turkeys and ducks. Swelling and bowing in the region of the knee joints. Lameness. modifications of calcium and phosphorus ratios. and proximal metatarsus. Prevention Genetic selection using the Lixiscope to identify bone phenotype. in decreasing order of frequency.
than in commercial poultry in temperate climates. and is also found on mammals. Weakness. These parasites are more likely to be a problem of small scale poultry production in the tropics. Reduced productivity. Transmission is lateral with birds and faeces.M. The infection is seen in turkeys and sometimes pheasants. Post-mortem lesions Anaemia. Occasionally paralysis from toxins in the tick saliva. It is more common in warm climates. Morbidity is close to 100% and mortality is 5-100%. with 143 .Abubakar. Insecticide sprays in these areas are more likely to be effective than treatment of the birds. spends little time on host. Emaciation. Prevention As for red mite control. Transmissible Enteritis. and may also transmit spirochaetosis and Pasteurella infection. Bluecomb Introduction Some coronaviruses involved in this condition are considered to be bovine coronaviruses (or closely related thereto). Signs Anaemia. others are avian coronaviruses closely related to infectious bronchitis virus. Skin blemishes.Tahir Ticks Introduction Argas persicus is an external parasite of poultry and wild birds. Treatment Elimination of cracks and crevices in the poultry housing. Diagnosis Identification of the presence of the parasites.
rapid spread. The course of the disease is about 2 weeks and birds then remain carriers for months. The viruses survive in frozen faeces for months.
Anorexia. Depression. Frothy diarrhoea. Subnormal body temperature. Darkening of the head. Loss of weight. Huddling.
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).
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.
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.
Market after one season, hygiene, cages, elimination of faeces etc.
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.
Excessive mucus in nasal passages and trachea. If there is secondary E. coli infection then pneumonia, airsacculitis and perihepatitis.
Clinical signs, isolation of agent.
maternal antibody may protect. chlorination of drinking water.Antibiotics are not very effective. Diagnosis Signs. Good drinking water hygiene. chlorinate drinking water. 147 . Ocular and nasal discharge. control respiratory stressors. Serology. Morbidity is 10-100% and mortality 1. Sudden drop in production that lasts 2-3 weeks. Prevention All-in/all-out production. Loss of voice. control respiratory stressors. vaccination . Eggs depigmented and thin-shelled.live primer followed by inactivated.30%. Turkey Rhinotracheitis (Adult) Introduction A disease of turkeys caused by the viruses of the Pneumovirus genus. vertical transmission is uncertain. Treatment Antibiotics are not very effective. isolation of ciliostatic agent. Prevention All-in/all-out production. Signs Decreased appetite. possibly involving fomites. Post-mortem lesions Serous rhinitis and tracheitis. Paramyxoviridae. Rapid transmission occurs laterally.
30%. Treatment Antibiotics are not very effective.M. Rapid transmission occurs laterally. Dyspnoea. Vaccination at day-old seems to be most effective. possibly involving fomites. Snick. sometimes pus in bronchi. maternal antibody may protect. airsacculitis and perihepatitis. mortality is 1-25%. weight gain and feed efficiency. Birds remain carriers for up to 16 days. Conjunctivitis. 148 . control respiratory stressors. Paramyxoviridae. isolation and identification of the ciliostatic virus. vertical transmission is uncertain. Sinusitis. If there is secondary E.Abubakar. Ocular and nasal discharge.Tahir Turkey Rhinotracheitis (in rear) Introduction A disease of turkeys caused by the viruses of the Pneumovirus genus. Signs Decreased appetite. Transmission may be by direct or indirect contact and possibly vertical. Prevention All-in/all-out production. serology (using an Elisa test to demonstrate rising titre). Morbidity is 10-100% and mortality 1. Post-mortem lesions Serous rhinitis and tracheitis. Loss of voice. Turkey Viral Hepatitis Introduction An infection of turkeys caused by an unidentified virus. Morbidity varies. chlorinate drinking water. Diagnosis Clinical signs. coli infection then pneumonia.
Microscopically . Twisted leg Introduction A complex condition seen in chickens and turkeys. Distortion at hock. Grey to pink foci in the pancreas. Signs Lameness. Factors involved may include genetics. Congestion. Differentiate from histomonosis. Treatment None. environment and high growth rate. Focal haemorrhage. 1 mm) coalescing. Valgus/varus.Signs Signs are usually subclinical. Post-mortem lesions Linear twisting of growth of long bones. lesions pathognomonic. Various angulations of leg. Diagnosis Isolation in CE. 149 . Bile staining. Prevention Good sanitation and management. Depression and sporadic deaths in birds in good condition. Post-mortem lesions Grey foci (c.no inclusion bodies. with good management many birds recover. Gastrocnemius tendon may slip. nutrition. Morbidity is 1-20% and mortality is low. bacterial and fungal infections.
Ruffled feathers. Prevention Selection for good conformation in primary breeding. The bacterium resists boiling for 3 minutes. Differentiate from perosis. Diarrhoea. Watery white faeces (quail). Changed angulation of tibial condyles. The route of infection is oral and transmission is from faeces of sick or carrier birds or via flies. Anaemia. Post-mortem lesions Deep ulcers throughout intestine. Retracted neck. Adoption of optimal nutrition and growth patterns for the economic objectives of the production system. 150 . Treatment None. Turkeys. brunetti).. Signs Listlessness. but mainly ileum and caecae. It can start suddenly and cause high mortality: 100% in quail and 10% in chickens. and E. Predisposing factors include Coccidiosis (especially E. The condition occurs worldwide. Pale yellow membranes. Ulcerative Enteritis. highly contagious disease of chickens and quail caused by the bacterium Clostridium colinumand characterised by ulcers of the intestines and caecae. greater than 20% is abnormal. Quail disease Introduction Ulcerative Enteritis is an acute. necatrix. lesions. arthritis and synovitis. Blood in intestine. Partially closed eyes. E. intertarsal angulation up to 10% is physiological. tenella. Drooping wings. game birds and pigeons may also be affected. Diagnosis Symptoms. IBDV and overcrowding. which may coalesce and may be round or lenticular. Peritonitis (if ulcers penetrate).
Treat for coccidiosis if this is a factor. Avian Infectious Hepatitis Introduction An insidious onset disease of chickens caused by Vibrio bacteria. Response to treatment should occur in 48 to 96 hours. Prevention Infection-free birds. Inappetance. birds remaining carriers for months. Loss of condition. colinum in anaerobic conditions (the agent is often present in pure culture in liver). and disease is precipitated by stress. Transmission is by faecal contamination. salmonellosis. low level antibiotics as per treatment. Tetracyclines. Signs Dejection. Diarrhoea. The infective agent is rather resistant to environment and disinfectants. Confirmation is on absence of other diseases and isolation of Cl. possibly probiotics. all-in/all-out production. Treatment Streptomycin (44 gm/100 litres water). multivitamins. Morbidity is low. coccidiosis. penicillin (50-100 ppm in feed). Figure 35. Diagnosis A presumptive diagnosis may be made on history and lesions. 151 . Necrotic foci in liver. Wall of the caecum of a chicken suffering from ulcerative enteritis Vibrionic Hepatitis. Differentiate from histomonosis ('Blackhead'). amoxycillin. trichomoniasis. necrotic enteritis. Bacitracin.
Pale comb and wattles. Scaly comb. Jaundice. Drop in production/weight gain.
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.
Hygiene, depopulate, obtain birds free of disease, contain stressors.
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.
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.
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.
antioxidant. Nutritional Roup Introduction Vitamin A deficiency is occasionally seen in chickens and turkeys (insufficient vitamin A during 1-7 weeks of age). Microscopically . Poor feathering. Pustules in mouth and pharynx. chronic fowl cholera.Abubakar. Drowsiness. As in the case of other nutritional deficiencies.squamous metaplasia of epithelia. lesions. Treatment Vitamin A in drinking water. infectious sinusitis etc. 155 .M. Differentiate from Infectious coryza. Nasal and ocular discharge. Post-mortem lesions Eyelids inflamed and adhered. Prevention Supplementation of diet with vitamin A. Diagnosis Signs. good quality raw materials. Eyelids stuck shut with thick exudate. feed formulation. Excessive urates in kidneys and ureters.Tahir Vitamin A Deficiency. classic signs of deficiency are very rare in commercial poultry fed complete diets. Signs Poor growth. Pale comb and wattles.
Most will reduce productivity. Some deficiencies induce characteristic microscopic effects. They act in a broad range of metabolic pathways. and egg production in the layer.Tahir Vitamin B Deficiencies Introduction The B complex vitamins are water soluble and not stored to any significant extent in the body.M. including growth in the young animal. The embryo is particularly dependent on having adequate supplies of vitamins deposited in the egg. Simple deficiency is now rare as diets are usually well supplemented. response to supplementation. exclusion of specific diseases. See the separate discussion under Chondrodystrophy and Fatty Liver and Kidney Syndrome.Abubakar. Vitamin deficiencies are especially prone to cause problems of hatchability. Diagnosis Signs. 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 . damage to the intestine or increased demand for some reason may have an effect. However. Signs These may be summarised: Perosis Curled Toe Paralysis Paralysis/'Stargazing' Dermatitis/Scaly Skin Mouth Lesions Conjunctivitis Anaemia Fatty Liver and Kidney Syndrome Poor Feathering Loose feathers Hatchability problems Embryo with clubbed down Thiamine (B1) Riboflavin (B2) Pantothenic acid Pyridoxine (B6) Niacin Folic Acid Cyanocobalmin (B12) Biotin Post-mortem lesions Usually the gross lesions are non-specific.
Vitamin E Deficiency. Green wings. Muscular dystrophy is seen more frequently in older and mature birds. Post-mortem lesions Swollen cerebellum with areas of congestion. The balance of vitamins present should be similar to the daily nutritional requirement of the stock concerned. Uncontrolled movements. Haemorrhage. Paralysis. 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. Steatitis. characterised by oxidation of various tissues and caused by Vitamin E deficiency. Encephalomalacia. Staggering. Encephalomalacia and exudative diathesis tends to be seen in young birds of 1-5 weeks of age. Falling over. occasionally ducklings and other birds. The problem is associated with feed rancidity typically in diets with high fat. seen worldwide. Exudative Diathesis. Necrosis. Treatment If a specific vitamin deficiency is suspected. Ventral oedema. less expensive) to analyse feed for a marker substance such as manganese rather than testing for vitamin levels. Muscular Dystrophy Introduction A spectrum of diseases of chickens and turkeys. drinking water supplementation with that vitamin is ideal and usually results in a rapid response in birds that are still drinking. Good quality multivitamin solutions are beneficial in the supportive care of a range of problems characterised by reduced feed intake. White streaks in muscle.may be appropriate (faster. 157 . Signs Imbalance. Blood-stained or greenish subcutaneous oedema.
Loss of appetite. It is seen where there is poor breeder farm nest hygiene. necrotic dermatitis.Proteus. good quality raw materials. Disease occurs after an incubation period of 1-3 days. Post-mortem lesions Enlarged yolk sac with congestion. and poor hygiene of setters. histopathology. 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. especially E . 158 . use of floor eggs. Pseudomonas. response to medication. lesions.coli. hatchers or chick boxes. feed rancidity. 'bangers'. Differentiate from Encephalomyelitis. Morbidity is 1-10% and mortality is high in affected chicks. Diarrhoea. Signs Dejection. Swollen abdomen. selenium. Staphylococci.Diagnosis Signs. consistency) that vary according to the bacteria involved. inadequate hatchery hygiene or poor incubation conditions. Yolk Sac Infection. Abnormal yolk sac contents (colour. Broad-spectrum antibiotics where there are extensive skin lesions. antioxidant. Various bacteria may be involved. Omphallitis Introduction A condition seen worldwide in chickens. for example poor hygiene of hatching eggs. 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. Prevention Proper levels of vitamin E. Vent pasting. Treatment Vitamin E and/or selenium in feed and/or water. Closed eyes. toxicities.
g. sanitation of eggs. 159 . There should be routine sanitation monitoring of the hatchery. Treatment Antibiotics in accordance with sensitivity may be beneficial in the acute stages. most will die before 7 days of age.Diagnosis A presumptive diagnosis is based on the age and typical lesions. Confirmation is by isolation and identification of the bacteria involved in the internal lesions. separate incubation of floor eggs etc. however the prognosis for chicks showing obvious signs is poor. frequent collection. Differentiate from incubation problems resulting in weak chicks. Prevention Prevention is based on a good programme of hygiene and sanitation from the nest through to the chick box (e. exclusion of severely soiled eggs. clean nests. Multivitamins in the first few days may generally boost ability to fight off mild infections.