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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.
Diarrhoea. Arizonosis Introduction Caused by the bacterium Arizona hinshawii. Cheesy plugs in intestine or caecum. Signs Dejection. from long-term intestinal carriers. Paralysis. Figure 40. Erosions of the cartilage of the hock joint in a duck with chronic Riemerella anatipestifer infection. transovarian. Congestion of duodenum. mainly in North America. sulphonamides in feed. through faecal contamination of environment. Unabsorbed yolk sac. and is not present in the UK turkey population. Inappetance. Vent-pasting. 4 . reptiles. Inactivated and attenuated vaccines available in some countries. rodents.Prevention Good husbandry and hygiene. Transmission is vertical. 'hardening off'. feed etc. Nervous signs. correct house relative humidity. Foci in lungs. Post-mortem lesions Enlarged mottled liver. older birds are asymptomatic carriers. cloudiness in eye. Mortality is 10-50% in young birds. Blindness. renamed Salmonella Arizonae. rigid depopulation and disinfection. and also horizontal. adequate protection. It affects turkeys. Autogenous bacterins sometimes used. Arizona infection. Huddling near heat.
and respiratory disease. Post-mortem lesions Thickening of right-side myocardium. fumigation of hatching eggs. Formerly in-feed medication with nitrofurans was also used. Pulmonary arterial vasoconstriction appears to be the main mechanism of the condition. spectinomycin. Ascites is a disease of broiler chickens occurring worldwide but especially at high altitude. The disease has a complex aetiology and is predisposed by reduced ventilation. Thickening of atrioventricular valve. Pericarditis. Signs Sudden deaths in rapidly developing birds. good nest and hatchery hygiene. Recumbency. Progressive weakness and abdominal distension. Dilation of the ventricle. or gentamycin at the hatchery is used in some countries. Prevention Eradicate from breeder population. high altitude. inject eggs or poults with antibiotics. monitor sensitivity. Ophthalmitis. poor ventilation and physiology (oxygen demand. Diagnosis Isolation and identification. methods as per Salmonella spp. 5 . Poor development. mortality 1-2% but can be 30% at high altitude. Severe muscle congestion. Perihepatitis. Differentiate from Treatment Injection of streptomycin. Salpingitis. Dyspnoea. General venous congestion. Possibly cyanosis. salmonellosis. Ascites Introduction Associated with inadequate supplies of oxygen. coli-septicaemia. may be related to type of stock and strain). Morbidity is usually 1-5%. Lungs and intestines congested.
Differentiate from broiler Sudden Death Syndrome and bacterial endocarditis. Diagnosis Gross pathology is characteristic. The fungus can infect plant material and many species of animals including birds and man. in which the typical sign is gasping for breath. Silent gasping. Weakness. 6 . especially in young chicks. worldwide. Liver enlargement. Thirst. turkeys. Spleen small. Aspergillosis Introduction A fungal infectious disease. Treatment Improve ventilation. This may offer the ability to identify genetic predisposition. but may be as high as 12%. ducks. Microscopic . Occasionally similar lesions are produced by other species ofAspergillus or even other fungi such as Penicillium. Absidia etc. Transmission is by inhalation exposure to an environment with a high spore count. avoid any genetic tendency. etc. Ascites. penguins. caused by Aspergillus fumigatus. Signs Acute form: Inappetance. Nervous signs (rare). control respiratory disease. It affects chickens. A cardiac specific protein (Troponin T) may be measured in the blood. 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. there is usually little bird-to-bird transmission.cartilage nodules increased in lung. game birds. Morbidity is usually low. Drowsiness. Pericardial effusion. The infection has an incubation period of 2-5 days. waterfowl. Vitamin C (500 ppm) has been reported to be of benefit in South America. Mortality among young affected birds is 5-50%. Rapid breathing.
hygiene. Growth occurs in 24-48 hours and colonies are powdery green/blue in appearance. mortality none. Amphotericin B and Nystatin have been used in high-value birds. trachea.Abubakar. Conjunctivitis/keratitis. The powdery surface is dark green in colour. Epidemic tremors for its effect in young birds. air sacs. Diagnosis This is usually based on the signs and lesions and microscopic examination for the fungus. The means of transmission is unknown but 7 . pheasants and occurs in most poultry-producing countries. Figure 8. quail. Treatment Usually none. good quality litter and feed. Wasting. See Avian Encephalomyelitis.M. Thiabendazole or Nystatin has been used in feed. Morbidity 5-60%. Brain lesions may be seen in some birds with nervous signs. plaques in peritoneal cavity. It affects chickens.Tahir 2 Chronic Forms: Ocular discharge (ocular form only). typically by putting small pieces of affected tissue on Sabouraud agar. Environmental spraying with effective antifungal antiseptic may help reduce challenge. may have greenish surface. turkeys. Prevention Dry. Post-mortem lesions Yellow to grey nodules or plaques in lungs. Avian Encephalomyelitis Egg Drop Introduction Avian encephalomyelitis virus infection in laying bird causes inapparent infection or drops in egg production. It may be confirmed by isolation of the fungus. preferably after digestion in 10% potassium hydroxide. Differentiate from excessive exposure to formalin or vaccinal reactions in day olds and from heat stress in older birds. 'Furry' airsacculitis in aspergillosis of an adult duck.
Virus in faeces may survive 4 weeks or more. pheasants. and quail.probably by faecal contamination of environment. Prevention Vaccination of breeders/layers at 9-15 weeks. water etc. mortality high. turkeys. now Elisa is used more commonly. lateral transmission is probably by the oral route. Signs Nervous signs. Imbalance. It has a worldwide distribution. Signs Drop in egg production. and there is serious disease in the progeny (see next section). feed. Paralysis. Differentiate from Infectious Bronchitis. some lateral. Morbidity 5-60% depending on the immune status of the majority of parents. Dull expression. The route of infection is transovarian with an incubation period of 1-7 days. small (5-10%) and lasting no more than 2 weeks. Vertical transmission is very important. attenuated or not. incubation >10 days. 8 . Serology . Virus in faeces may survive 4 weeks or more. Avian Encephalomyelitis. with an oral infection route. EDS76. transmission occurs over about 1-2 weeks. rising titre to AE virus. subsequent disease in progeny if breeders.The embryo protection test has been used in the past. Epidemic Tremors Introduction Avian encephalomyelitis is a viral disease of the central nervous system of chickens. lentogenic Newcastle disease. In breeders there may be a drop in hatchability of about 5%. Treatment None. Immunity is usually long lasting. Post-mortem lesions None. Diagnosis History. Predisposed by immunosuppression. Ataxia and sitting on hocks.
Fowl One of only two 'Class A' diseases of poultry targeted for emergency disease control measures by OIE. Effectively all 9 . and isolates are designated sero-type/ species/location/reference number/year/subtype designation(H/N).2 . The embryo protection test has been used in the past. The cause is a virus. The higher the proportion of the chickens dying or showing signs the higher the IVPI. Microscopic . the equivalent of the World Health Organisation for animal diseases. Tremor of head. 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. There may be focal white areas in gizzard muscle (inconstant). signs. The definitive classification of high pathogenicity is an intravenous pathogenicity test (IVPI) in 6-week-old chickens result of greater than 1. toxicities. The virus infects chickens. quail. Avian Influenza-Highly Plague Introduction Pathogenic (HPAI). Orthomyxovirus type A. Post-mortem lesions Gross lesions are mild or absent. and ostriches. ducks. Immunity is long lasting. Mycotic Encephalitis. A. Marek's disease. attenuated or not. pheasants. neck and wings. Enterococcus hirae infection. EE (especially in pheasant in the Americas). Diagnosis A presumptive diagnosis is based on the history. Tremor may be inapparent but is accentuated if chicks are held inverted in the hand. Brain abscess.nonpurulent diffuse encephalomyelitis with perivascular cuffing. its pathogenicity is variable. A few recovered birds may develop cataracts weeks after infection. partridges. now Elisa is used more commonly. Prevention Vaccination of breeders at 9-15 weeks. In addition official control measures disrupt trade in poultry products from affected areas. pigeons. and/or viral isolation may be carried out if required. This viral disease can cause exceptionally high mortality. especially in turkeys. This is a test in which the virus is inoculated into susceptible chickens that are then kept under observation. vitamin deficiency (E. turkeys. Differentiate from Newcastle disease. Histopathology is usually diagnostic and IFA. and lack of significant lesions. Treatment None. riboflavin).
The small number of human deaths associated with HPAI appear to have resulted from direct exposure to infected birds on farm or in markets. It is inactivated by a temperature of 56°C in 3 hours and 60°Cin 30 min. Transmission is by direct contact with secretions from infected birds. Outbreaks due to HPAI were recorded in the Pennsylvania area. in northern Italy. can survive 4 days in water at 22°C. but possibly by the conjunctival or respiratory route and the incubation period is 3-5 days. Pasteurella) may increase mortality. USA. even with 'low pathogenicity' strains. over 30 days at 0°C. clothing. reduced feed consumption. conjunctivitis or severe pneumonia. Apathogenic and mildly pathogenic influenza A viruses occur worldwide. drinking water. See current OIE records for up to date information on distribution of HPAI. OIE and other bodies are currently examining ways to improve control of LPAI.birds are considered to be at risk of infection. Morbidity is high but mortality usually relatively low. 550%. Avirulent in one species may be virulent in others. Diarrhoea (often green). in the years 1983-84. Pakistan. Cyanosis of comb/wattles. A serious outbreak occurred in The Netherlands in 2003 with a few linked cases in Belgium and one in Germany. Avian Influenza is a potential zoonosis. Ovarian regression or haemorrhage. Swollen face. Broken contaminated eggs may infect chicks in the incubator simulating vertical transmission. trachea. More recently outbreaks have occurred in Australia. Drops in egg production. air sacs and conjunctiva. Mexico and. Cessation of normal flock vocalisation. Signs Sudden death. Marked loss of appetite. Nervous signs such as paralysis. Because of this.g. waterfowl. equipment. The virus replicates mainly in respiratory tissues of chickens and turkeys but in the intestinal tract of clinically normal waterfowl. The route of infection is probably oral initially. Highly pathogenic avian influenza A (HPAI) viruses of the H5 and H7 HA subtypes have been isolated occasionally from free-living birds. especially faeces. by acid pH. Nasal and ocular discharge. Coughing. H5 viruses of low pathogenicity may become highly pathogenic usually after circulating in poultry flocks for a time (Pennsylvania. Italy). It can result in inapparent infection. and the high mortality that 'low-path' AI can cause in turkeys. Infections with other pathogens (e. It can remain viable for long periods in tissues. 10 . Depression. from December 1999. The virus is moderately resistant. by oxidising agent and by formalin and iodine compounds. Post-mortem lesions Inflammation of sinuses.
Morbidity is low. To be effective inactivated vaccines must be the right subtype for the particular situation (H5 will not protect against H7 and vice versa). other respiratory infections. Eradication by slaughter is usual in chickens and turkeys. North and South America. though there is high mortality of affected birds. Differentiate from Newcastle disease. fowl cholera. cleaning. infectious laryngotracheitis. with considerable strain-to-strain variation. while ducks may be symptomless. Subcutaneous oedema of head and neck. Transmission is by congenital infection from antibody-negative females. Diagnosis A presumptive diagnosis may be made on history and postmortem lesions. nutrition and antibiotics may reduce losses. Muscles congested. It has occured in Europe. disinfection. lateral transmission by faecal-oral route (this declines as the bird ages). vaccinated birds may remain carriers if exposed to the infection. etc. Necrosis of skin of comb and wattles. Prevention Hygiene. The agar gel precipitation test is non-group-specific and is used to confirm any positives. Congenitally infected birds tend to remain 11 . DID+. NDV-. Confirmation is by viral isolation in chick embryo. Vaccines have been used in recent outbreaks in Mexico and Pakistan. bleeding and vaccination needles. correct disposal of carcases. In outbreaks a regime of slaughter. This condition has until now been seen only in meat-type chickens. Survivors can be expected to have a high degree of immunity but may harbour virulent virus. Turkey lesions tend to be less marked than those of chickens. although it may reduce losses initially. Treatment None. Minimise contact with wild birds. Myelocytomatosis Introduction Caused by an avian retrovirus. lesionless carriers of highly pathogenic virus. Haemorrhage in proventricular and gizzard mucosae and lymphoid tissue of intestinal tract. Avian Leukosis (Serotype J). all-in/all-out production. 21-day interval to re-stocking should be followed. The incubation period is 10-20 weeks. isolation. Commercial Elisa test kits are now available. controlled marketing of recovered birds. Dehydration. HA+. as with many such tests occasional false positive reactions can occur. but good husbandry. However. quarantine. Vaccination is not normally recommended because. bacterial sinusitis in ducks.
sacral joint.tumours usually contain well-differentiated myelocytes. Enlargement of abdomen. Two cell types may be found in the same tumour. particularly of the sternum. shed virus and develop tumours. 'Shedders' . Separation in vaccination. Post-mortem lesions Liver enlargement. ribs. lesions. Microscopic .80% produce infected chicks. ultimately identification of virus by isolation and/or PCR. Emaciation.antibody negative. Lymphoid Leukosis. 12 . Minimise stress. birds with egg antigen will be antibody negative. Most characteristically are chalky white tumours in the bone marrow.most but not all. Many are asymptomatic. Diagnosis History. Splenomegaly and enlarged kidneys also occur. Loss of weight. PCR testing of embryonally infected chicks using DNA testing is uniformly positive for blood and faecal samples. histology. Prevention Checking of antigen in the albumen is a basis for eradication . often with tumour foci. Differentiate from Marek's disease.only 3% produced infected chicks. Virus survival is poor but sufficient to allow cross contamination in hatcheries and on farm in rear. Persistent low mortality. age.an Elisa test is aviailable to identify antibody positive birds. preferably on separate hatch days and in separate machines. liver. Treatment None. Prevent/ reduce cross-infection in hatchery and on farm. Serology . Critical hatchery practices: Separate infected and uninfected lines. 'nonshedders' . Signs Depression. Handle clean lines before infected lines. There is also evidence that it is slightly more sensitive than conventional testing.
initially in the bursa. cytology. fibrosarcomas. Microscopic . kidney etc. Differentiate from Marek's disease. myxosarcomas. age. spleen. A complex of viral diseases with various manifestations such as lymphoid leukosis. There may be increased susceptibility to other infectious diseases due to damage to the immune system. Morbidity is low but mortality high. lesions. It affects chickens worldwide with susceptibility varying considerably among different strains and types of stock . Vertical transmission is most important by infection of the egg white in infected breeders (who are long-term carriers). Many are asymptomatic. Avoid migration errors (birds unintentionally moving between pens). it may be as short as 6 weeks for some of the other manifestations. Leukosis/Sarkoma Group Introduction Lymphoid Leukosis. Signs Depression. The causative viruses are rapidly inactivated at ambient temperature and on exposure to most disinfectants. Emaciation. coligranuloma. Post-mortem lesions Focal grey to white tumours.Farm practices: Brood and rear lines separately and maintain separate for as long as possible. myeloblastosis (see Sero-type J). erythroblastosis. especially in young birds. Liver may be very large. Minimise group sizes. osteopetrosis. Persistent low mortality. liver or bursa. Delay live vaccine challenges.egg layers are generally more susceptible to lymphoid leukosis. 13 . Avian Leukosis. Enlargement of abdomen. In lymphoid leukosis the incubation period is about 4-6 months. lateral transmission is poor but infection may occur by the faecal-oral route. Mortality tends to be chronically higher than normal for a prolonged period. other tumours. Loss of weight. then liver. Egg production is somewhat reduced.cells lymphoplastic Diagnosis History.
checking of antigen in the albumen is a basis for eradication (see Sero-type J for details). Two subgroups have been identified on the basis of the G-protein sequence: A (original UK isolates) and B (original southern Europe isolates).Treatment None. Facial and head swelling (though this can occur in other conditions). first isolated from poults in South Africa in 1978. fomites can be important in moving infection between farms. Conjunctivitis. There is rapid lateral transmission with infection by aerosol through the respiratory route. Diffuse lymphoid tumours in an enlarged liver from a mature broiler parent hen. Figure 9. Snick. Ocular and nasal discharge. This was a case of Myelocytoma Avian Leukosis (Sero-type J). control arthropods. It is caused by a pneumovirus of the Paramyxoviridae family. turkeys (see separate summary). Signs Decreased appetite. guinea fowl and possibly pheasants seen in Europe. Prevention Good hygiene. 14 . As for many infections. Dyspnoea. morbidity is 10-100% and mortality can be 110%. South America and North America. Africa. all-in/all-out production. Avian Rhinotracheitis 'Swollen Head Syndrome' Introduction A viral disease of chickens. vertical transmission is uncertain. weight gain and feed efficiency. eradication . The incubation period is 5-7 days. Loss of voice.
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.
Scabs around eyes and beak. 18 . Pale livers and kidneys in fatty liver and kidney syndrome. Good biosecurity. Lung congestion Ovarian regression Yolk peritonitis Pale foci and haemorrhages in pancreas. Treatment No specific treatment known. in embryos. A RT-PCR test may be used to detect viral RNA in tissues. Biotin Deficiency. Allin/all-out production. Post-mortem lesions See signs. Thickened skin under foot pad. Prevention Thorough cleaning and disinfection after depletion of an affected flock. Leg weakness. Diagnosis Typical signs and lesions. Reduced feed intake and blood sugar can precipitate fatty liver and kidney syndrome. 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. Sudden deaths in fatty liver and kidney syndrome. Signs Poor growth. Histopathology may also be used but the findings are not specific to this condition. Drinking water which is well chlorinated should be helpful in reducing challenge by this route. Viral particles may be demonstrated in bile. 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. webbing between toes. Elisa tests have been developed experimentally. It may be helpful to control other conditions which may be occurring at the same time. Chondrodystrophy.
bedbugs. Differentiate from pantothenic acid deficiency (skin lesions). Signs Lack of thrift in young birds. Prevention Supplementation of diets with biotin . Treatment Addition of biotin in feed or water. Check flocks regulary for rapidly moving insects at the base of the feathers on the abdomen or around the vent. Parasites on birds. response to treatment/prevention. Menocanthus stramineus is the most pathogenic and is said to be capable of causing anaemia in heavy infestations. may be some feather damage and crustiness of skin. They are spread by direct contact between birds and by litter etc. Away from birds adults survive about 4-5 days. Diagnosis Identification of the parasites. Differentiate from mites. Loss of condition. Drop in egg production.naturally present in many raw materials. Lice eggs stuck to feathers.Diagnosis Signs. The parasites are 1-6 mm in size and their life cycle takes about 3 weeks. lesions. Loss of vent feathers. has very low bioavailability. Treatment Malathion powders and pyrethroid sprays where approved for bird application. Biting Lice Introduction Various species of lice are common external parasites of poultry worldwide. Irritation. Scabs around vent. Crusty clumps of eggs ('nits') may be visible at the base of feathers. Post-mortem lesions Usually none. 19 . especially around vent.
Treatment Treatment is difficult. Examine for lice regularly. although these insects can travel up to 15 miles. It is usually necessary to treat twice at a 7-10 day interval to fully control the condition. Weekly treatments are required. Diagnosis Anaemia. The condition tends to occur near to rapidly flowing streams. Eggs and larvae survive through the winter to cause new infestations in the following year. Effective removal of all organic material at flock depletion should be practised in all-in/all-out production systems.Prevention Avoid direct contact with wild and backyard poultry. 5 mm long and found in North and South America that are external parasites of birds and mammals. Post-mortem lesions Anaemia. as the larvae within eggs are not killed by most products. 20 . Signs Anaemia in young birds. Swarms of flies. The flies transmit leucocytozoonosis and also a filarial parasite in ducks. especially in autumn and winter and treat if required. Biological control using a strain of Bacillus thuringensis has had some success and is preferable to insecticides. local history. season. Blackfly Infestation Introduction Grey-black hump-backed flies. Prevention Similar measures as for mosquito control.
mouse toxicology on serum or extract of intestinal contents. turkeys.Botulism Introduction A condition of chickens. The single most important measure is careful pick-up and removal of all dead birds on a daily basis. Maggots or putrid ingesta may be found in the crop. Differentiate from acute Marek's disease ('Floppy Broiler Syndrome') by histology of the brain. supportive treatment if justifiable. maggots) is consumed by the birds. The toxin and bacterial spores are relatively stable and may survive for some time in the environment. Morbidity is usually low but mortality is high. especially in hot weather. progressive flaccid paralysis of legs. because it rests on the litter. Feathers may be easily pulled (chicken only). selenium. ducks and other waterfowl occurring worldwide and caused by a bacterial toxin produced byClostridium botulinum mainly types A / C. antibiotics. The toxin is produced in decaying animal (usually carcases) and plant waste. 21 . Prevention Preventing access to toxin. signs. Post-mortem lesions Possibly no significant lesions. Signs Nervous signs. 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. suspect food and stagnant ponds. Affected broilers tend to settle with eyes closed when not disturbed. carcases. is also quite typical. A soiled beak. then sudden death. This will reduce the risk of botulism both in the poultry and in any grazing animals on land where poultry litter is spread. Treatment Remove source of toxin. weakness. Diagnosis History. and toxin-containing material (pond-mud. Toxin may also be produced by the bacteria in the caecum. wings then neck. Mild enteritis if has been affected for some time.
Morbidity is high but it is not associated with mortality. There is an incubation period of 2 weeks for eggs to embryonate. are small whitish worms with a pointed tail. Post-mortem lesions Inflammation of sternal bursa along the keel bone which may. the cause of Blackhead.5 cm in length that occur in the caecum. Caecal Worm Introduction Heterakis gallinae. 22 . leg weakness. Heterakis gallinaeeggs and larvae are a transport hosts for Histomonas. and infection withStaphylococcus spp. Treatment Not usually appropriate. and a four-week prepatent period. nematode parasites of poultry and game birds. Earthworms may be transport hosts for eggs. Morbidity may reach more than 50% but the condition is not fatal.Breast Blister Introduction A complex condition of chickens and turkeys occurring worldwide associated with trauma. up to 1. Poor feather cover and caked or wet litter are predisposing factors. The meaning of the technical terms relating to parasite life cycle are defined in the glossary. Infection is by the oral route. control of leg problems. bacteria. in chronic cases. Signs None. Diagnosis Based on lesions. They are found worldwide. or paratenic hosts with partially developed (L2) larvae. Prevention Good litter management and handling. Signs Swelling over the keel bone with bruising and discolouration. give way to scar tissue.
Predisposing factors include heat stress with reduced feed intake and panting. possibly with nodule formation. Calcium Tetany Introduction A metabolic disease of chickens. Prevention Avoiding access to earth and earthworms. and the embryonated egg. 23 . are effective. an undeveloped egg as found in fresh faeces. Levamisole. Treatment Flubendazole. Routine anthelmintic treatment. Death from respiratory and cardiac failure. The egg may be ingested directly by a chicken. Figure 11. The life cycle ofHeterakis showing the location of adults. or by an earthworm which is in turn ingested by a chicken. Signs Paralysis.Post-mortem lesions Inflammation of caecum. Diagnosis Adults can be seen in caecal contents at post-mortem examination. especially broiler parents.
Infected poultry are a potential reservoir of this zoonosis. lesions. It may be that management that favours dry litter reduces the risk of infection and/or transmission within the flock. lack of other significant lesions. are bacteria that commonly infect a broad range of livestock species. Campylobacter jejuni is the commonest species found in poultry. principally in the caecae. The reason for this is unclear. There is an annual cycle with increased risk of infection in the summer months in some countries. There are indications that plantar pododermatitis. 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. Prevention Keep pullet flocks on low calcium diet until 5% production hen/day. carcase quality and litter quality are better on farms which tend to have Campylobacter-negative stock. managing birds for maximum uniformity. All campylobacters are delicate organisms that survive for relatively short periods outside the host unless protected by organic material. Active ovary with egg in oviduct. Treatment Provide 5 gm of oyster shell per hen on 3 successive days along with vitamin D in drinking water. pets and wild animals. and response to treatment.Post-mortem lesions Cyanosis. In poultry they tend to multiply in large numbers in the hindgut. biofilm or engulfed by protozoa. 24 . Differentiate from IB 793b. Campylobacter Infection Introduction Campylobacter spp. other acute infections and other causes of sudden death. Campylobacters are a significant cause of enteritis in man. Diagnosis This is made on signs.
Diagnosis Isolation of the organism from caecal contents. Post-mortem lesions None. sourcing of water from high quality supplies. Key aspects of this include effective sanitation of drinking water. phage treatments and competitive exclusion approaches. Many infections are introduced during thinning or other forms of partial depopulation. cloacal swabs or composite faeces. and changing of overalls and boots on entering bird areas. as well as processing plant technologies to reduce carcase contamination.Signs None. In practice the success of this will also depend upon the degree of environmental contamination by the organism. avoidance of contact with pets and other farmed species. Treatment Not required on clinical grounds. Samples should be tested as quickly as possible after collection. good hand hygiene by stockmen. housed poultry can be maintained free of Campylobacter infection by consistent application of excellent biosecurity. 25 . Prevention In principle. The organism is sensitive to air so swabs should be collected into transport medium and other samples placed in airtight containers with minimal airspace. Insects and rodents may act as a means of transfer of the infection from the general environment into the poultry buildings. Research is ongoing on the development of vaccines. For this reason it may be difficult to stop the spread of infection between houses once it becomes established in one house.
Candidiasis. characterised by thickening and white plaques on the mucosa. microscopic examination of a digested smear (heat in 10% potassium hydroxide) to demonstrate the hyphal forms of the yeast in the tissues. and sometimes other birds and mammals. The cause is a fungal yeast. Diagnosis Lesions. Slow growth. Colonies of this fungus appear as white to ivory colour. histopathology. The route of infection is normally oral and the organism is often present in healthy animals with disease occurring secondary to stress and poor hygiene.g. Poor appetite. Signs Dejection. sodium or calcium proprionate at 1 kg per tonne continually. occasionally proventriculus and intestine. Candida albicans and the condition is seen worldwide. or copper sulphate 1gm/2 litre water for 3 days if approved locally. Raised focal lesions may slough into lumen as caseous material. Thrush Introduction A disease of the alimentary tract of chickens. Post-mortem lesions White plaques in mouth. possibly confused or masked by signs of the primary disease. A finely divided powder of copper sulphate (where approved) at 200gm/tonne continually or to 14-16 weeks in replacement pullets. turkeys. copper sulphate (1 kg/tonne feed) for 5 days. Morbidity and mortality are usually low. 26 . smooth and with a yeasty smell. oesophagus. Prevention Avoid excessive use of antibiotics and other stressors. crop. The fungus is resistant to many disinfectants. Treatment Nystatin (100 ppm in feed) for 7-10 days. Ensure good hygiene. Moniliasis. proprionic acid. Diarrhoea. intestine and cloaca. Control of Candida through drinking water is sometimes practised with chlorination (e. especially in the crop but sometimes in the proventriculus. and associated with gizzard erosion.
excessive light intensity or variation (e. Generalised anaemia. Morbidity is usually low but mortality is high among affected birds. Diagnosis Age. Cannibalism. distribution of lesions. 27 . control ectoparasites. and strain of bird.g.Chlorox. Post-mortem lesions Skin wounding related to particular signs exhibited. Treatment Correct any husbandry problems. Signs Pecking at feet (especially young chicks) and vents (adult layers and turkey poults 812 days old). tenosynovitis and other diseases affecting mobility. Differentiate from bacterial dermatitis. feed form (mash takes longer to consume than pellets). If so it should be carried out carefully by trained operators. Take care to provide fresh clean feed and water. sodium hypochlorite) at 5 ppm. wings. nutritional deficiencies. complying with local regulations and any relevant codes of practice. Beak trimming may be necessary. uncontaminated by fungi. boredom. through shafts of light in the house). anaemia. Prevention Proper density and temperature. head. Feather pecking Introduction A complex multifactorial behavioural problem of poultry and game birds seen worldwide. high temperatures. post-mortem cannibalism. Predisposing factors include overcrowding. Soluble multivitamins and/ or methionine may be of some benefit in some circumstances. It should be repeated periodically. low light level. Provision of a diet that closely matches the nutritional requirements of the stock concerned. face. This is economical and effective. Feather-pulling.
Fenbendazole has been shown to have high efficacy . small intestine or caecum. or characteristic worm eggs in faeces in patent infections. Post-mortem lesions Enteritis. prepatent period about 21-25 days according to species.05 mm wide and hair-like in appearance. Some species have earthworms as intermediate hosts. Hairworms in mucosa of crop. Worm eggs in the environment are resistant. some are transmitted direct from bird to bird. The worms are 7-18 mm long.Hairworm Infection Introduction Nematode parasitic worms of poultry. C. Prevention Separation of birds from possible transport and intermediate hosts.other approved benzimidazoles can be expected also to have activity. Wasting Poor growth. C. Treatment Coumphos has been licensed in some markets. seiving intestinal contents. Infection is by the oral route. obsignata in the small intestine. Differentiate from other causes of enteritis. Morbidity and mortality are usually low. effective cleaning of houses. Signs Diarrhoea. game birds and pigeons ofCapillaria species. 28 . Dejection.Capillariasis . Worm eggs take about 20 days to embryonate with an L1 larvae. about 0. contorta in the crop and oesophagus. Levamisole. Diagnosis This may be by a combination of macroscopic examination.
Careful flock management with a view to reducing toe wounds has the greatest impact in controlling cellulitis. Diagnosis Typical lesions. but the affected birds are not readily detectable prior to slaughter. It typically occurs between skin and muscles and between muscles and may be an incidental finding in a range of conditions. which can replicate in the tissues. Routine monitoring of skin damage at about 25 days of age may be helpful in fostering good practices. 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. Many meat inspectors become skilled at detecting subtle differences in skin colour in the affected birds. The condition is caused by infection of. Signs Affected flocks tend to have poorer than average productivity and uniformity. 29 . However its main importance is as a cause of condemnation in meat poultry. 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. 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. Treatment Treatment would not be possible if the problem is identified at a final depletion. though most of the birds showing toe scrapes will not go on to develop cellulitis. particularly broiler chickens. Many affected birds have no other lesions and are reasonably well grown. often minor. coli. In the USA it is called 'Inflammatory Process'.Cellulitis Introduction Cellulitis is literally an inflammation of connective tissues.
virus may be isolated in lymphoblastoid cell line (MDCC-MSB1). 30 . PCV of 5-15% (normal 27-36%). Post-mortem lesions Pale bone marrow. and control of other diseases as appropriate. Prior to confirmation that it is in fact a virus it was known as Chicken Anaemia Agent or CAA. chloroform. Pale birds. may be beneficial. The virus is resistant to pH 2. Sudden rise in mortality (usually at 13-16 days of age).Chicken Anaemia Introduction A viral disease of chickens caused by Chicken Anaemia Virus or CAV. Transmission is usually vertical during sero-conversion of a flock in lay. Gangrenous dermatitis on feet. Discoloured liver and kidney. poor litter quality). ether. Mortality is typically 5-10% but may be up to 60% if there are predisposing factors present such as intercurrent disease (Aspergillosis. Diagnosis Gross lesions. Signs Poor growth. demonstration of ongoing sero-conversion in parent flock. Inclusion body heptatitis etc. 80°C for 5 minutes) and many disinfectants even for 2 hours at 37°C. Gumboro. heat (70°C for 1 hour. If gangrenous dermatitis is a problem then periodic medication may be required. Treatment Good hygiene and management. Hypochlorite appears most effective in vitro. Atrophy of thymus and bursa.) or poor management (e.g. legs wings or neck. No clinical signs or effect on egg production or fertility in parent flock during seroconversion. Acute mycotic pneumonia. lateral transmission may result in poor productivity in broilers.
Their use may be restricted to those flocks that have not sero-converted by. rarely chickens. Egg transmission does not occur. Airsacculitis. caused by Chlamydia psittaci. Elisa.Prevention Live vaccines are available for parents. Inappetance. Wasting. Weakness. Ornithosis Introduction An infection of turkeys. Serology: antibodies develop 3-6 weeks after infection. but occurring probably worldwide. 31 . ducks. Iodophores and formaldehyde are effective disinfecting agents. Nasal discharge. their degree of attenuation is variable. Greenish-yellow diarrhoea. phenolics are less so. Chlamydiosis. say. Elementary bodies are highly resistant and can survive in dried faeces for many months. It is transmitted by contact. man. 15 weeks. or IFA. Signs Respiratory signs. Morbidity is 50-80%. It is a 'Scheduled Disease' rarely diagnosed in UK. Immunity: there is a good response to field challenge (in birds over 4 weeks of age) and to attenuated live vaccines. Production drops in naive laying flocks Post-mortem lesions Vascular congestion. a bacterium of highly variable pathogenicity. other infections may be predisposing factors. Weight loss. Psittacosis. mortality 5-40%. Depression. and may be detected by SN. Conjunctivitis. faecal dust and wild bird carriers. especially pigeons and robins. Occasional transient ataxia in pigeons. Fibrinous pericarditis. pigeons. They should be used at least 6 weeks prior to collecting eggs for incubation. Intercurrent salmonellosis and. perhaps. psittacines.
signs. Necrotic foci in liver. Differentiate from Duck viral hepatitis. ducks and turkeys. Spleen enlarged and congested. In embryos parrot beak. Diagnosis History. Prevention Biosecurity. Malposition of leg distal to hock. Intracytoplasmic inclusions are helpful but confirmation requires demonstration of causal organisms (Giemsa stain. biotin. lesions. Elisa and gel diffusion. shortened bones. This condition is seen in chickens. folic acid. Signs Short legs. Perihepatitis. niacin may also be involved). exclusion of wild birds. Congested lungs and air sacs in the turkey. Fibrinous pneumonia. In turkeys it may be an inherited deficiency of galactosamine. Lameness. Live and inactivated vaccines are protective although the former result in carriers and the latter require several applications. Treatment Tetracycline (200-800 ppm in feed for 3-4 weeks) and/or quinolone medication and supervised slaughter. IFA). Duck septicaemia. 32 . Slipping of Achilles tendon (or perosis). Chondrodystrophy. choline. zinc. may rupture in pigeons. Slipped Tendon or Perosis Introduction Caused by deficiency of manganese. Serology: complement fixation. either singly or in combination (although deficiencies of pyridoxine. Distortion of hock.
Weight loss. Watery diarrhoea that may occasionally be blood stained or contain clumps of mucus or shed mucosa. vitamins. while E. adenoides affects the caecae and rectum. Differentiate from twisted leg. rickets. Five species of Eimeria have been identified that cause lesions in turkeys. The contents may be haemorrhagic or be watery with white material shed from the mucosa. 33 . while E. Shallow trochlea. Depression. of which two are associated with significant disease effects. infectious synovitis. Prevention Addition of manganese. Diagnosis Lesions. ruptured ligaments. choline. Coccidiosis of Turkeys Introduction Infection of turkeys with Eimeria spp. E. gallopavonis and E. dispersa is found in the small intestine. E. Lateral slipping of tendon. meleagridis affect the lower small intestine rectum and caecae. Tibia and metatarsus bowed. Treatment For flock proceed as for prevention. meleagrimitis affects the upper small intestine. ruffled feathers. no value to affected bird. Tucked appearance. This disease is not very common in commercially reared turkeys though most turkey growers receive preventative medication for at least part of their lives. infectious arthritis. Signs Huddling. correct mineral balance. analysis of feed.Post-mortem lesions Shortening and thickening of long bones. Post-mortem lesions The affected area of intestine shows thickening of the wall and dilation.
Figure 38. Figure 37. lesions. meleagrimitis.g. 34 . Turkey coccidiosis of the upper small intestine caused by E. Sulphonamides (e. adenoides. Salinomycin is toxic for turkeys even at very low doses. Exposure of previously unmedicated birds to these compounds can cause toxicity. Treatment Toltrazuril. gamonts). show some spotty congestion and have abnormal contents due to the sloughed epithelium. The exudate can range from semi-liquid to solid white cores. Diclazuril is also used for this purpose. Prevention The ionophore coccidiostats lasalocid and monensin are routinely used in turkey growers. Sulphaquinoxaline). Amprolium. Turkey caecal coccidiosis caused by E. The intestines are dilated. Avoid use of tiamulin in ionophore treated birds. microscopic exam of scrapings (oocysts.Diagnosis Signs. Differentiate from necrotic enteritis. typically to 12 weeks of age. Dosage levels of ionophores may be critical to efficacy and safety.
Accumulation of varying quantities of blood and caseous necrotic material in the caecum. blood in faeces. E. Treatment Toltrazuril. Shuttle programmes with chemicals in the starter diet usually improve control.Coccidiosis. In some markets the organic arsenical compound 3-Nitro is used as an aid in the control of caecal coccidiosis. Post-mortem lesions Petechiae. Diarrhoea. Differentiate from ulcerative enteritis. Vaccines are used mainly in breeders but increasingly in broilers. lesions. Closed eyes. of caecal mucosa. Ruffled feathers. Transmission as for E. Inappetance. histomonosis. mitis (see above). Caecal. Amprolium. Sulphonamides. Thickening. Production less affected than in some of the other forms of coccidiosis. tenella is more common when 'straight' ionophore programmes are used. vaccination by controlled exposure. microscopic examination of scrapings. Signs Depression. Recovered birds have good immunity to the same parasite. Prevention Coccidiostats in feed. 35 . Morbidity is 10-40% and mortality up to 50%. It is caused by Eimeria tenella and results in lesions in the caecum of chickens worldwide. ecchymoses. E tenella Introduction This was at one time the commonest type of coccidiosis and is certainly the most easily diagnosed. Vitamins A and K in feed or water. hygiene. Diagnosis Signs.
The caecal walls are thickened and haemorrhagic and there is a mass of blood in the caecal lumen. Post-mortem lesions The lesions are minimal and located in the lower small intestine (ileum) which tends to be pale and flaccid with scattered petechiae. The disease occurring is proportional to the amount of infective agent ingested. Signs Reduced feed conversion efficiency and weight gain. The parasite is moderately resistant in the environment and highly resistant to conventional disinfectants. Moderate Eimeria tenella infection in the caecae of a chicken (Score 3). is caused by the protozoan parasite Eimeria mitis. seen worldwide.Figure 15. humidity). faeces and on fomites and birds are infected by the oral route with an incubation period of 2-5 days. The infective agent is found in litter. identification of typical small round oocysts and other stages in fresh scrapings from the small intestine. May predispose to wet litter. Predisposing factors include exposure to faeces and litter conditions that favour development of the parasite (temperature. Treatment Not usually treated but susceptible to the products used for other forms of intestinal coccidiosis. E mitis Introduction This condition of chickens. 36 . Coccidiosis. secondary bacterial enteritis. which colonises the small intestine. Diagnosis Mild lesions.
May be included in vaccines. Post-mortem lesions Petechiae and thickening of the distal third or more of intestine. caecum and rectum. Closed eyes. Signs Depression. Sulphonamides. Ruffled feathers. Diagnosis Signs. Amprolium. This species is not usually included in vaccines for broilers. Ileorectal. lesions. microscopic examination of scrapings. Prevention Coccidiostats in feed. Differentiate from ulcerative enteritis. caecal coccidiosis. Severe necrotising enteritis. 37 . Inappetance. Diarrhoea. Oocysts in caecum and rectum. blood in faeces. it is found in the terminal ileum. Of moderate to high pathogenicity. extending into caecal tonsils. Coccidiosis. Poor production. hygiene. E brunetti Introduction A relatively rare form of coccidiosis affecting chickens worldwide caused by Eimeria brunetti. vaccination by controlled exposure. There is good immunity to the same parasite in recovered birds. Treatment Toltrazuril. Vitamins A and K in feed or water. Morbidity and mortality are variable.Prevention Normally controlled by anticoccidials in feed.
Diagnosis Signs. Coccidiosis occurs only very rarely in commercially reared ducks in the UK. compared to four per oocyst forEimeria. There is thickening of the intestinal mucosa and there are lines of haemorrhagic spots in the mucosa. while in ducksTyzzeria perniciosa is most pathogenic. 38 . Tyzerria has eight sporocysts in each oocyst. Blood-stained vent. Coccidiosis. Duck viral enteritis. Depression. anatipestifer. Differentiate from Duck viral hepatitis. lesions.Figure 16. Intestinal. 3 days on). anseris is the most important. Vitamins A and K in feed or water. large number of merozoites). Amprolium. In the goose E. Tucked appearance. 3 days on. of Ducks and Geese Introduction Young ducks and geese may suffer from Eimeria spp infection. Signs Sudden death. Sulphadimidine 30-600gm/100 birds/day.g. 2 days off. microscopic examination of scrapings (usually few or no oocysts. Post-mortem lesions Massive haemorrhage in upper small intestine. Treatment Sulphonamides (e. Moderate Eimeria brunettiinfection in the terminal ileum and rectum of a chicken.
however this is not routinely practised. Kidney Introduction A disease of geese caused by Eimeria truncata that can cause high mortality in geese of 312 weeks of age. Diarrhoea . Hygiene. presence of coccidial stages in fresh scrapings of kidney lesions. Diagnosis Lesions. it can also infect Barbary ducks and swans. 39 . Prevention Good Hygiene.Prevention If required coccidiostats could be used in feed. Kidneys light grey to greyish pink.faeces tend to be whitish. Weakness. Coccidiosis. Post-mortem lesions Enlarged kidneys. Treatment Controlled trials of treatments have not been published. Tiny white foci and petechiae in the kidneys. Reduced feed intake. Signs Depression.
Ruffled feathers. Morbidity and mortality are variable. Diagnosis Signs. Inappetance. Prevention Coccidiostats in feed. Depigmentation of skin and plasma is especially evident in this form of cocccidiosis and this is commercially important in some markets. Post-mortem lesions Petechiae and thickening of middle third of intestine. 40 .Coccidiosis. Closed eyes. Blood or pigment in the faeces. Poor production. contents often orange in colour. acervulina coccidiosis and there may be large numbers of characteristic oocysts in smears. vaccination. Treatment Sulphonamides. mucosa tends to be pinker than normal. E maxima Introduction One of the more common forms of coccidiosis in commercial broilers. Vitamins A and K in feed or water. Poor absorption of nutrients/pigments. This infection is often associated with E. microscopic examination of scrapings. Caused by Eimeria maxima. commercial vaccines commonly contain more than one strain of E. Mild to severe enteritis. Mid-intestinal. Differentiate from necrotic enteritis. of moderate to high pathogenicity it is seen worldwide. Signs Depression. hygiene. Because of the area of intestine affected it tends to have a significant effect on productivity and susceptibility to necrotic enteritis. Amprolium. lesions. maxima. non-specific enteritis. This is one of the less immunogenic species.
Poor production. Post-mortem lesions Petechiae and thickening. Closed eyes. Schizonts seen as white spots through the serosa interspersed with petechiae. The intestine is slightly thickened and there are scattered haemorrhages in the mucosa when seen from the inside. microscopic examination of scrapings Differentiate from necrotic enteritis. It occurs in chickens worldwide and has variable morbidity but mortality is high in severely affected birds. Deep scrapings necessary to show large schizonts. Mid-intestinal. lesions. other types of coccidiosis. Inappetance. E necatrix Introduction A highly pathogenic form of coccidiosis. caused by Eimeria necatrix. of middle to posterior third or more of small intestine. Diarrhoea. blood in faeces.Figure 13. in which the parasite is present in the small intestine and in the caecum. Coccidiosis. Severe necrotising enteritis. Diagnosis Signs. Depression. 'Sausage-like' intestine. Oocyts in caecal scrapings. The lesions are subtle compared to other forms of coccidiosis. Moderate Eimeria maxima infection in the jejunum of a chicken (Score 2). Ruffled feathers. 41 . Signs Reduced feed consumption.
Treatment Toltrazuril. Post-mortem lesions 42 . Depigmentation. This is one of the less immunogenic species. Haemorrhages and white spots are visible from the outside of the intestine. both alone and in association with other species of coccidia and is caused by Eimeria acervulina. Inappetance. Sulphonamides. Ruffled feathers. In this case the intestine is thickened and can become ballooned and sausage-like. Vitamins A and K in feed or water. Coccidiosis. Amprolium. hygiene. Upper Intestinal. Eimeria mivatiis currently considered not to be a valid species distinct from E. commercial vaccines commonly contain more than one strain of E. maxima. E acervulina Introduction This is probably the commonest cause of coccidiosis in chickens and occurs worldwide. Closed eyes. Morbidity is variable and mortality low or absent. Figure 14. Diarrhoea. Prevention Coccidiostats in feed. Signs Depression. It is seen in layers and in broilers. which is moderately pathogenic. acervulina. Poor production. vaccination. Moderate Eimeria necatrix infection in the jejunum of a chicken (Score 3).
Treatment Toltrazuril. A system of assessing the severity of coccidial challenge by attributing a 'score' is often used. and other lesions. restricted to upper third of small intestine . Figure 12. Prevention Coccidiostats in feed. Sulphonamides. 43 . In severe infections they become confluent and cause sloughing of the mucosa.the duodenum and part of the ileum. Thickening. In milder infections there may be scattered white spots. Moderate Eimeria acervulinainfection (score 2) in chicken duodenum. in severe the entire surface is pale or denuded of epithelium. in feed or water. Petechiae. Poor absorption of nutrients/pigments. A detailed description is beyond the scope of this book. Diagnosis Signs. White spots or bands in the mucosa. hygiene. Various publications provide a photographic key to severity of lesion. vaccination by controlled exposure. Amprolium. microscopic exam of scrapings. Differentiate from necrotic and non-specific enteritis. Immunity is quite short lived (about 30 days) in the absence of continued challenge. lesions. In general terms a score of 0 indicates no lesions and a score of 4 indicates maximal severity of lesion or death.
coughing. Enteritis. Lesions vary from acute to chronic in the various forms of the disease. Morbidity varies. Omphalitis. It is caused by the bacteriumEscherichia coli and is seen worldwide in chickens. but is susceptible to disinfectants and to temperatures of 80°C. Signs Respiratory signs. Poor growth. Reduced appetite. sneezing. Synovitis. with an incubation period of 3-5 days. The infectious agent is moderately resistant in the environment. fomites. Cellulitis over the abdomen or in the leg. sero-typing. Infection is by the oral or inhalation routes. pathology. Post-mortem lesions Airsacculitis. Poor navel healing. Pericarditis. and via shell membranes/yolk/navel. Colisepticemia Introduction Coli-septicaemia is the commonest infectious disease of farmed poultry. Swollen liver and spleen. Omphalitis. water. Snick. or in young birds that are immunologically immature. It is frequently associated with immunosuppressive diseases such as Infectious Bursal Disease Virus (Gumboro Disease) in chickens or Haemorrhagic Enteritis in turkeys. Peritonitis. Dejection. mortality is 5-20%. It is most commonly seen following upper respiratory disease (such as Infectious Bronchitis) or Mycoplasmosis. Diagnosis Isolation.Colibacillosis. etc. Salpingitis. mucosal damage due to viral infections and immunosuppression are predisposing factors. Arthritis. Perihepatitis. turkeys. Granulomata in liver and spleen. Aerobic culture yields colonies of 2-5mm on both blood and McConkey agar after 18 hours .most strains are rapidly lactose-fermenting producing 44 .
potentiated sulphonamide. tetracyclines. the breast area. Severe perihepatitis in colibacillosis in a broiler parent chicken. whereas others progress to deep ulcers so the size. Pododermatitis Introduction Contact dermatitis affects skin surfaces which have prolonged contact with litter. feed and water. other enterobacteria such as Proteus. good sanitation of house. flouroquinolones. Staphylococcus spp. stage of resolution and severity of lesion is likely to affect the degree of discomfort or pain suffered. Immunity is not well documented though both autogenous and commercial vaccines have been used. as well as Pseudomonas. hatchery hygiene. Figure 17. when severe. the foot pad. 45 . It is seen in growing broiler chickens and turkeys. Well-nourished embryo and optimal incubation to maximise day-old viability. Control of predisposing factors and infections (usually by vaccination). etc.brick-red colonies on McConkey agar. Contact dermatitis is commonly monitored at processing as a means of measuring 'welfare status'. Some lesions are superficial. Differentiate from acute and chronic infections with Salmonella spp. Hock Burn. Prevention Good hygiene in handling of hatching eggs. The liver is almost entirely covered by a substantial layer of fibrin and pus. Contact Dermatitis. and in broiler parents. gentamycin or ceftiofur (where hatchery borne). neomycin (intestinal activity only). rear surface of the hock and. Treatment Amoxycillin.
Prevention This condition is closely linked to intestinal function as this is the prime determinent of faecal consistency and stickiness. See the discussion in the section on Dysbacteriosis. level of soya bean meal in feed (according to some authors. and adequate ventilation to remove moisture are all important. Choice of drinker type (nipple as opposed to bell). proper insulation in cold climates. most importantly. Post-mortem lesions As described under signs. It can be reproduced by adding water to the litter. and sometimes in the breast area. at the back of the hocks. stickiness of droppings). Signs Blackened skin progressing to erosions and fibrosis on the lower surface of the foot pad. litter moisture. drinker management. Moderate pododermatitis on a foot pad. Treatment Not applicable.Pododermatitis is often related to high droppings pH. 46 . Diagnosis Signs and lesions. If severe the foot and hock lesions may contribute to lameness or serve as a portal of entry for secondary infections. Figure 18. and.
meleagridis also infects both species. White convoluted tracks in the mucosa. Some have beetle or earthworms as intermediate hosts. The same species causes infections of the hindgut and cloacal bursa in chickens. Signs Anaemia. but much smaller (typically oocysts are less than ¼ of the size of an E. Coumaphos. They replicate in the brush border on the surface of epithelial cells. 47 . Cryptosporidiosis Introduction Cryptosporidia are related to the coccidia. Post-mortem lesions Inflammation and thickening of mucosa of crop and oesophagus. and ducks. Routine worming. acervulinaoocyst).Cropworms Introduction The nematode worms Capillaria spp and Gongylonema ingluvicolainfect the mucosa of the crop and oesophagous of poultry and game birds. A further species causes respiratory disease in quail.C. although bird strains do not infect mammals very well. They also differ from coccidia in being poorly host specific. and vice versa. The oocysts are excreted ready sporulated in the faeces and infection occurs by inhalation and ingestion. turkeys. Avoidance of access to intermediate hosts. Diagnosis Microscopic examination of mucosal scraping. Emaciation. Treatment Levamisole. Cryptosporidium baileyi can cause respiratory disease in chickens and turkeys. Prevention Effective cleaning of housing.
Circling. Swollen sinuses. Pneumonia. 48 . Diagnosis Identification of the parasites attached to the epithelium by microscopic examination (smears histopathology acid-fast staining). There are no effective preventative medicines or feed additives. Treatment Unfortunately there is currently no known effective treatment in poultry.g. It is becoming increasingly common for water companies to screen water supplies for cryptosporidia because of the human health implications of mammalian strains. Airsacculitis. Tremors. coli-septicaemia) there may be benefit in medicating for these. Cough. recumbency. Signs Incoordination. Diarrhoea. Post-mortem lesions Sinusitis. Torticollis. Low weight gain. If other disease processes are complicating the situation (e.Signs Snick. Prevention The oocysts of cryptosporidia are extremely resistant to chemical disinfection. 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.
isolation of the fungus. 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.Post-mortem lesions Necrotic lesions with associated congestion in cerebrum. resulting in erosions. and cartilage flaps. or developmental defects. Treatment 49 . air sacs etc. Diagnosis Lesions. Signs Lameness. especially of femoral anti-trochanter but also other leg joints. Post-mortem lesions Damaged epiphyseal articular cartilage. Diagnosis Gross and microscopic lesions. Rapid growth is a possible predisposing factor. The cause remains to be confirmed. Degenerative Joint Disease Introduction A condition of chickens and turkeys seen worldwide. Mycotic lesions in lungs. Microscopically there is necrosis and there may be fissures of articular cartilage and associated osteochondritis. Reduced breeding performance. but it may result from physical damage. Treatment None.
Prevention Avoidance of physical sources of injury to bones and joints. The adult females are short legged. especially during period of rapid growth. Appropriate management of a segregation pen and early marketing of mildly affected birds may limit losses and improve flock welfare. Depluming and Scaly Leg Mites Introduction External parasites of adult chickens. Unthriftiness. There may be a place for growth-control programmes.5mm in diameter. 50 . Prevention Careful cleaning of buildings during down-time will help reduce the risk of these infections. up to 0. pheasants. Diagnosis Signs. Application of mineral or vegetable oil is also beneficial. Signs Cause irritation and the bird pulls feathers. Post-mortem lesions As described under signs. Mange lesions on legs and unfeathered parts.Knemidocoptes spp. Exclusion of wild birds from chicken areas is advised as far as possible. For small flocks dipping the affected parts in a solution of acaricide may be beneficial. It may be best to cull affected birds from small flocks. Treatment Not usually required in commercial poultry. Raised thickened scales. round. microscopic examination for mites in scrapings.None available. pigeons etc.
kidneys. presumably due to a sudden increase in blood pressure. Aortic Rupture Introduction A complex. Reserpine in diet of birds of 4+ weeks (no longer licensed in the UK). Rupture of major blood vessel at base of heart or by the kidneys. Haemorrhages in lungs.Dissecting Aneurysm. Treatment None currently licensed. Signs Sudden death with no warning signs. Possibly blood in the mouth. genetic condition of turkeys linked to male sex and high growth rate. Prevention Limit feed in birds of 16+ weeks. A sudden noise or other cause of excitement can lead to an 'outbreak'. Duck Viral Hepatitis Introduction A viral disease of ducks occurring worldwide and previously a scheduled disease in UK. A longtitudinal split of the abdominal aorta is the most common lesion. leg muscles. Reserpine. The infective agent. was included in feed at 1 ppm for 3-5 days to reduce blood pressure. Abdominal cavity full of blood. Diagnosis History and lesions. a tranquilizer. Aspirin at 250 ppm in feed or water may be of benefit. a picornavirus may also 51 . Skin pale. recovered birds carrying the virus for 8 weeks. The disease is transmitted by infected ducks and other waterfowl and spreads rapidly. Post-mortem lesions Carcase anaemic. It has been suggested that degenerative changes in the wall of the artery and copper deficiency may be factors. pericardial sac. birds found on breast or side. Morbidity is around 100% and mortality 0-95%.
in USA since 1967. 52 . fomites and arthropods. Newcastle disease. coccidiosis. Kidneys and spleen swollen. also the Netherlands and other countries. Death in good condition. Depression. Transmission is by infected birds. All waterfowl are susceptible and the Barbary duck is more susceptible than the Pekin. Differentiate from Duck plague (viral enteritis). Influenza and a 'Type II Variant' hepatitis caused by Astrovirus. Microscopically . Fall on side. Duck Virus Enteritis. Treatment Antiserum. Recovered birds may carry the virus for a year. rapid deterioration and death. isolation in CE (causes stunting of 9 day embryo). Live.survive for ten weeks in brooders and five weeks in faeces. often in opisthotonus. paddling of legs. SN serology. arching of back. Prevention Vaccination and/or antiserum. bile duct proliferation and inflammation.focal necrosis. only slightly attenuated vaccine is applied at day old by foot web stab and may be repeated in breeding birds to provide maternal immunity. 0. Diagnosis History. A different picornavirus causes a similar condition in North America. Post-mortem lesions Liver swollen. Signs Sudden death. Duck Plague Introduction A herpesvirus infection of ducks and geese diagnosed in the UK in 1972.5 ml serum of recovered birds given intramuscularly. Duck septicaemia (anatipestifer). The disease follows a very acute course with a morbidity of 5-100% and mortality of 5-100%. Punctate/diffuse haemorrhages. mostly in ornamental collections. breeder vaccination. lesions.
Photophobia. but vaccination in face of outbreak is of value. Dysbacteriosis. Occasionally penile prolapse in the penis in drakes. sometimes dysentery. pericardium. Thirst. spleen. oesophagitis (birds on restricted feed). pasteurellosis. excess caecal volume and fermentation. vent gleet. body cavities. is common in countries with restrictions on the use of antimicrobial growth promoters and pressure to reduce therapeutic antimicrobial usage. Tremor. Diagnosis Isolation: Duck CAMs 12 day embryos die in 4 days. Post-mortem lesions Severe enteritis. coccidiosis. Crusty plaques from oesophagus to bursa (covered by yellowish plaques in later stages). HA-. intranuclear inclusions Differentiate from Duck hepatitis. Haemorrhage in intestine. Non-specific Bacterial Enteritis Introduction Inflammation of the small intestine associated with wet litter. Prevention Isolation from waterfowl. Treatment None. probably through interference. 53 . Closed eyes. Dehydration. vaccination if approved by authorities (CE adapted live virus). liver. Young ducks may show thymic and bursal lesions.Signs Sudden deaths. Ataxia. heart. Drop egg production. Rapidly spreading disease. Occasionally cyanosis of the bill in the young. Severe diarrhoea. Paresis. The condition is seen mainly in rapidly growing broiler chickens with good food intake.
Diagnosis Signs. No single bacterium appears to be responsible. Uruguay. England. Treatment should coincide with good relittering and it is important to provide fresh sanitary drinking water. Peru. The cause has been identified as Adenovirus BC14. It affects chickens and has occurred in Ireland. lesions. 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. Circumstantial evidence suggests that the main route of transmission is through the eggs (vertical transmission) 54 . often with gas bubbles. Spain. Brazil. first isolated in Northern Ireland in 1976. Water intake may be increased or irregular. Argentina. Prevention Competitive exclusion ('normal adult flora') use in day-old chicks reduces the risk of this condition. Holland. microscopic examination of scrapings from the wall of the small intestine (to exclude coccidiosis and perhaps to assess the bacterial flora). France. In the autumn of 1976 a distinct egg drop syndrome was first identified in Northern Ireland.Dietary changes. Treatment Amoxycillin and tylosin treatment appear to be beneficial. 127. Post-mortem lesions Excessive fluid content throughout the small intestine. Voluminous caecae. Signs Diarrhoea. feed interruptions and subclinical coccidiosis may be contributory factors. rather we are dealing with a disruption in the normal flora of the gut. Apparently a similar disease had been seen over a 4-year period in broiler parents in Holland. Prophylactic antimicrobial medication may be necessary in some circumstances. Feed acidification may be helpful in some circumstances. especially where treatment is initiated early. Careful choice of any feed enzymes and their matching with local raw materials can have an impact on substrates made available to intestinal bacteria. Wet faeces in the rectum. Mortality is usually negligible. Germany. Good control of coccidiosis.
Drops may be of 5 to 50% and last for 3-4 weeks. insecticides or nicarbazin. SN. Diagnosis History. Parasites. DID. which can be caused by a large number of factors acting individually or in combination. oviduct). Metabolic diseases include Fatty Liver Syndrome. Cholera. Coryza. thin or soft-shelled eggs and shell-less eggs. Post-mortem lesions No specific lesion . Loss of shell pigment. Infectious Laryngotracheitis. group antigen distinct from classical adenoviruses (white cells. Marek's disease/Leukosis or any infectious disease causing a significant systemic disturbance (CRD. B 12. specifically vitamins E. Diseases in which egg drop occurs. Management problems may be involved: inadequate water supply. 55 . Newcastle disease. Lack of signs in the birds themselves.followed by latent infection during rear with viral excretion starting shortly before sexual maturity. intoxication by sulphonamides. and D as well as calcium. Signs Egg drop at peak or failure to peak. Contamination of egg trays at packing stations may play a part in transmission. Serology: HI. Histopathology . Isolation of haemagglutinatin agent in duck eggs or cell culture. Poor internal quality.it may be possible to demonstrate degenerative changes in the epithelial cells of the magnum of the oviduct. phosporus. Clinical disease occurs during sexual maturity. Elisa. The infection is commonly present in ducks and geese but does not cause disease. sudden changes of feed. It is important to rule out other possible reasons for egg drop. Lateral transmission from bird to bird is slow and may be prevented or slowed for weeks by netting divisions. Nutritional deficiency should be considered. Diphtheritic Fowl Pox). selenium. may be infectious or metabolic. signs/lesions (mainly lack of). extremes of temperature. Rough. Spread from house to house may take 5-10 weeks. throat swabs. Avian Encephalomyelitis.only a slight atrophy of ovary and oviduct. as may wildfowl and biting insects. inadequate lighting programme. Infectious diseases include Infectious Bronchitis. Unvaccinated flocks with antibodies before lay do not peak normally.
osteomyelitis. growth plate disease. 56 . Vegetative lesions usually on the right atrioventricular valve. Culture of lesions to confirm the bacterium involved. streptococci. Diagnosis Differentiate from broiler ascites syndrome by examination of the interior of the heart.Treatment None. Post-mortem lesions Right ventricular failure and ascites. Erysipelothrixetc. Signs Fluid-distended abdomen. If successive flocks are affected on the same site prophylactic medication ahead of the anticipated problem may be of benefit. Epiphysiolysis Introduction A complex condition of chickens that may be associated with trauma. Prevention Vaccination with inactivated vaccine prior to lay. bacterial infection. Treatment Medication is only likely to be of value in reducing deterioration in birds that are starting to develop lesions. and /or trauma. The choice should depend on sensitivity testing of an isolate. Prevention Good hygiene at turn-around. rickets. Soluble multivitamins may be recommended as a nonspecific measure. Peripheral vessels congested. Endocarditis Introduction A condition of chickens associated with several bacterial infections such as staphylococci.
It is transmitted between birds by pecking and by mosquitoes. VEE) Introduction A viral disease of pheasants. Paralysis. Horses are also seriously affected. Ataxia. Treatment Not applicable. often occurs or is identified in the processed carcase.Signs Apparent dislocation at extremities of long bones. Signs Nervous symptoms. partridges. chickens. The natural hosts are wild birds and rodents. Microscopic lesions not pathognomonic. sometimes seen in vivo. Post-mortem lesions Separation of epiphyses at the growth plate. May also be asymptomatic. WEE. Tremors. Flaccid neck. turkeys. 57 . Equine Encephalitis (EEE. histology may be helpful in identifying underlying problems such as rickets or 'FHN'. Paresis. Prevention Control of predisposing factors. Circling. wild birds. Post-mortem lesions No gross lesions. ducks and pigeons having a high morbidity and high mortality. Diagnosis Gross inspection. These conditions currently only occur from northern South America to North America.
control cannibalism. Post-mortem lesions Carcase congestion.Diagnosis Isolation in mice. It is also seen in some mammals. Vaccinate at 5-6 week. It may be transmitted by faecal carriers for 41 days. Endocarditis. Swollen snood. TC. 58 . rhusiopathiae) seen in turkeys and increasingly in free-range chickens. ID by VN. Prevention Protection from mosquitoes. epicardium. Joint lesions. pheasants. kidney. Erysipelas Introduction A sudden onset infection with the bacterium Erysipelothrix insidiosa (E. Liver. spleen swollen. in soil. water. COFAL. muscle. The bacterium is fairly resistant to environmental effects or disinfectants and may persist in alkaline soil for years. Perineal congestion. and CE. Signs Inappetance. Sleepiness. Treatment None. especially snood. There is likely to be an increased risk if housing or land has been previously used by pigs or sheep. ducks. fishmeal and semen and by cannibalism. Chronic scabby skin. Marked catarrhal enteritis. rarely in geese. May be diarrhoea and respiratory signs. Depression. Sudden death. Haemorrhages in fat.
and acute Newcastle disease. Liver yellow.a combination of the procaine and benzathine salts may be injected. history. synoviae plate tests for a few weeks. Sudden drop in egg production. Tetracyclines in feed may also be helpful. Diagnosis Lesions. Death by internal exsanguination after rupture of haematocyst. Treatment Penicillin . Fatty Liver Haemorrhagic Syndrome Introduction A condition occurring worldwide in chickens. Differentiate from pasteurellosis. Prevention Good biosecurity to prevent spread from other susceptible species. especially caged layers and with a complex set of causes including excessive calories.Diagnosis Isolation on blood agar. often along with bacterin. Some birds with pale comb and wattles. the demonstration of the organism in stained impression smears from tissues. salmonellosis. colibacillosis. Signs Overweight typically by 25%. mycotoxins. Headparts pale. vaccine at 16-20 weeks if the condition is enzootic. and identification. Vaccination or natural infection may cause false positive reactions in the Mycoplasma gallisepticum and M. Sudden death. 59 . Post-mortem lesions Obesity. greasy and soft with numerous haemorrhages. deficiency and stress.
Favus Introduction A fungal infection. isolation. Treatment Formalin in petroleum jelly. Signs White. 60 . Loss of condition.Treatment Reduce energy intake. Prevention Feed to avoid obesity. Trichophyton gallinae. Prevention Good hygiene of facilities. Post-mortem lesions See signs (above). vitamin E. B 12 and inositol. culling affected birds. of chickens and turkeys. avoid mycotoxins and stress. Feather loss. powdery spots and wrinkled crusts and scab on comb and wattles. supplement with choline. Thick crusty skin. Diagnosis Lesions. It is very rare in commercial poultry production. 'Honeycomb' skin.
It is seen worldwide and was one of the first infectious 61 . (increasing order of susceptibility). turkeys.g. 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. indicated that 0. E. Careful attention to mineral and Vitamin D nutrition to avoid subclinical.Femoral Head Necrosis . Signs Lameness. Post-mortem lesions Degeneration of the epiphyses of long bones with thinning of the cortex and tendency to break when force is applied.75% of all male broilers placed had lesions in the hip bone. arthritis. Use of a wing for support during walking and hip flexion. FHN is the commonest infectious cause of lameness in broilers in the UK. and water fowl. highly contagious disease caused by the bacterium Pasteurella multocida in a range of avian species including chickens. Fowl Cholera. streptococci. coli. Diagnosis Base on post-mortem lesions and isolation of a causative organism.FHN Introduction A condition of chickens and turkeys that may be associated with several different bacterial infections e. Differentiate from synovitis. Post-mortem studies of birds culled due to lameness and of birds found dead. staphylococci. especially hypophosphataemic. rickets. spondylolisthesis. Pasteurellosis Introduction Fowl Cholera is a serious. Prevention Exclusion of floor eggs and dirty eggs from the hatchery. Predisposing factors include immunosuppresive viruses such as Infectious Bursal Disease Virus and Chicken Anaemia Virus and non-infectious bone pathologies such as hypophosphaetamic rickets.
The disease often recurs after medication is stopped. Treatment Sulphonamides. cats. necessitating long-term or periodic medication. Ruffled feathers. equipment. isolation (aerobic culture on trypticase soy or blood agar yields colonies up to 3mm in 24 hours . The route of infection is oral or nasal with transmission via nasal exudate. but may persist for prolonged periods in soil. The incubation period is usually 5-8 days. Diagnosis Impression smears. Reservoirs of infection may be present in other species such as rodents. and people. Loss of appetite. Focal hepatitis. Sudden death. Swollen joints. The bacterium is easily destroyed by environmental factors and disinfectants. and possibly pigs. penicillin. Post-mortem lesions Sometimes none. contaminated soil. confirmed with biochemical tests. or limited to haemorrhages at few sites. Yolk peritonitis. Cellulitis of face and wattles. Purulent pneumonia (especially turkeys). Diarrhoea. Predisposing factors include high density and concurrent infections such as respiratory viruses. The disease can range from acute septicaemia to chronic and localised infections and the morbidity and mortality may be up to 100%. Coughing. Lungs with a consolidated pink 'cooked' appearance in turkeys. 62 . faeces. Differentiate from Erysipelas. Signs Dejection. erythromycin.no growth on McConkey).diseases to be recognised. ocular and oral discharge. Purulent arthritis. tetracyclines. septicaemic viral and other bacterial diseases. Swollen and cyanotic wattles and face. Enteritis. by Louis Pasteur in 1880. streptomycin. Nasal. Lameness.
turkeys. It is more common in males because of their tendency to fight and cause skin damage. Depression. throat and sometimes trachea. spreading eruptions and scabs on comb and wattles. hygiene. The virus persists in the environment for months. Figure 19. Poor egg production. Morbidity is 1095% and mortality usually low to moderate. and where there are biting insects. Signs Warty. The duration of the disease is about 14 days on an individual bird basis. Fowl Pox. It is transmitted by birds. pigeons and canaries worldwide. bacterins at 8 and 12 weeks. or by the respiratory route. Severe localised Pasteurella infection in the swollen wattle of a 30-week-old male broiler parent chicken. good rodent control. live oral vaccine at 6 weeks.Prevention Biosecurity. 0-50%. Inappetance. fomites. Poor growth. Avian Pox Introduction A relatively slow-spreading viral disease characterised by skin lesions and/or plaques in the pharynx and affecting chickens. The swelling is made up of oedema and purulent exudates (pus). 63 . and mosquitoes (infected for 6 weeks). Infection occurs through skin abrasions and bites. Pox. Caseous deposits in mouth.
intra-cytoplasmic inclusions (Bollinger bodies) with elementary bodies (Borrel bodies). Flocks and individuals still unaffected may be vaccinated. usually with chicken strain by wing web puncture. pharynx. isolation (pocks on CE CAM) with IC inclusions. signs and post-mortem lesions. Fowl pox lesions on the wattle of an adult broiler parent chicken. Figure 20. in the diptheritic form. DNA probes. check take at 7-10 days post vaccination. Less commonly there may. It is confirmed by IC inclusions in sections/ scrapings. trachea and/or nasal cavities. Chickens well before production. Differentiate from Trichomoniasis or physical damage to skin.Post-mortem lesions Papules progressing to vesicles then pustules and scabs with distribution described above. Diagnosis A presumptive diagnosis may be made on history. 64 . reproduction in susceptible birds. Prevention By vaccination (except canary). Microscopically . If there is evidence of secondary bacterial infection broad-spectrum antibiotics may be of some benefit. There is good cross-immunity among the different viral strains. be caseous plaques in mouth. Treatment None. Turkeys by thigh-stick at 2-3 months.
Signs Occasionally dejection. 65 . sometimes thighs and other parts. occasionally Staphylococcus aureus. Loss of appetite. Treatment Sulphaquinoxaline. Severe cellulitis especially of thighs. Recovery of an abundant growth of causative organism in recently dead birds. early Infectious Bursal Disease Virus infection). spleen. Foci in liver.Gangrenous Dermatitis. Sudden mortality. Post-mortem lesions Patches of gangrenous skin with underlying emphysematous and/or sanguinous cellulitis. especially following congenital Chick Anaemia Virus infection or early Infectious Bursal Disease Virus infection (Gumboro Disease). Diagnosis Clinical signs and/or lesions. wattles. usually over wings and breast. wings. rarely Clostridium noyvi / oedematiens. Immunosuppression is therefore a predisposing factor. penicillin or amoxycillin. Morbidity may be up to 50% and mortality is high. Avoid skin trauma and immunosuppression (congenital CAV infection. Swelling and infarction of the liver. It occurs due to invasion of 'normal' wounds by 'normal' bacteria in immunosuppressed birds. Necrotic Dermatitis Introduction A bacterial condition seen in chickens and usually caused byClostridium septicum. Prevention Good hygiene and management. Gangrenous skin. The spores of Clostridial bacteria are highly resistant in the environment.
Dyspnoea. Loss of appetite and condition. slugs and snails acting as transfer hosts but the life cycle may also be direct. Gape Introduction Syngamus trachea. Diagnosis Signs and lesions. There is an 18-20 day prepatent period. a nematode worm parasite of chickens. from rookeries. levamisole. confirmation of presence of the parasite. paired parasites up to 2 cm long. The condition is seen more commonly in poultry on free range where ground may be contaminated by wild birds e. Severe gangrenous dermatitis on the upper surface of the wing of a broiler chicken. Treatment Flubendazole in feed. Signs Gasping.Figure 21. Head shaking. Prevention Flubendazole. turkeys. Presence of worms. Infection is by the oral route with earthworms. 66 .g. Post-mortem lesions Tracheitis. pheasants. by ingestion of embryonated egg or L3. and other game and ornamental birds occurring worldwide.
Gizzard worms . weevils. Signs Depression. Amidostomum anseris. 67 . Diagnosis Lesions. Grasshoppers. muscular wall may be sacculated or ruptured. and Histiocephalus are nematode worm parasites of chickens. Slow growth. Treatment Levamisole. Slow growth. Post-mortem lesions Ulceration. Adults are 2-4 cm long and usually bright red. confirmation of presence of the worms. Loss in condition and weight. Streptocara. Signs Depression.Geese Introduction A nematode worm parasite.Chickens Introduction Cheilospirura. routine worming. Gizzard worms . Prevention Prevention of access to intermediate hosts. Worms develop to L3 in eggs and infection is by the oral route direct from environment. Cheilospirura and Streptocara are seen worldwide but Histiocephalus is restricted to Europe. beetles etc act as intermediate hosts. Loss in condition and weight. benzimidazoles such as flubendazole. affecting geese and ducks. They are more common in free-range birds because of their increased access to intermediate hosts. necrosis and partial sloughing of gizzard lining.
Vertical transmission resulting in congenital infection may occur. Prevention Rotation of ground on annual basis. Reduced feed intake. muscular wall may be sacculated or ruptured. 68 . Diagnosis Lesions. visualisation of worms. The amount of maternal antibody passed from the breeding birds will affect the severity and timing and severity of the condition in the young birds. Derzsy's Disease is caused by a parvovirus distinct from chicken and mammalian parvoviruses. Adults are 2-4 cm long and usually bright red. Membrane covering tongue. The younger the bird affected the more acute the condition and the higher the mortality. Loss of down. necrosis and partial sloughing of gizzard lining. Profuse white diarrhoea.Post-mortem lesions Ulceration. Swollen eyelids and eye and nasal discharge. Signs Prostration and death in acutely affected goslings. Goose Parvovirus (Derzsy's Disease) Introduction Goose Parvovirus is a highly contagious condition of geese and young Muscovy ducks. spleen and pancreas. Losses are negligible in birds over 5 weeks of age. Excessive water intake. benzimidazoles. Reddening of skin. Treatment Levamisole. Swelling and congestion of liver. Post-mortem lesions Pale myocardium.
Loss of appetite. Carcase anaemia. mycotoxins and viral infections and usually following a course of approximately 3 weeks. Aplastic Anaemia. Ascites. 69 . Ideally flocks that have suffered the disease should not be used for breeding as they may become persistent excreters of the infection. Prevention Hatching and brooding geese from different parent flocks together should be avoided. Antimicrobials may be of value in reducing the effects of secondary bacterial infections. Treatment No specific treatment. heart. Pale comb and wattles. Morbidity varies. Signs Dejection. Fibrinous pericarditis. Bone marrow pale with fatty change. Poor growth. Liver yellow. Diagnosis Signs and lesions in birds of the appropriate age and species. Post-mortem lesions Haemorrhages in one or more sites: skin. Haemorrhagic Disease. liver. Haemorrhagic Anaemia Introduction A complex condition of chickens associated with drug toxicities. mortality is 5-50%. muscles. Fibrinous perihepatitis. The preferred approach is to immunise breeding birds with an attenuated live vaccine. Administration of immune serum has been shown to be effective but may require two doses (day old and around 3 weeks). Blood in droppings. serosa and mucosae.
Diagnosis History.spleen shows lymphoid hyperplasia. Elisa . Signs Sudden deaths. Spleen mottled and enlarged. lesions. reproduction with filtered contents. Serology: DID. Microscopic . The source of virus is unknown but there is easy lateral spread within flocks. May induce immunosupression and precipitate respiratory disease or coccidiosis. Treatment Vitamin K. reticulo-endothelial hyperplasia and intranuclear inclusions. the virus surviving in frozen faeces for months. add liver solubles to feed. Prevention Avoid causative factors. Post-mortem lesions Petechiae in various tissues. remove sulphonamides. Diagnosis Typical lesions. The route of infection is usually oral.sero-conversion frequently occurs in absence of clinical disease. similar to pheasant Marble Spleen disease. Course 10-21 days. signs. Drop in feed and water consumption. Intestine distended with blood. Haemorrhagic Enteritis Introduction A viral disease of turkeys. Blood from vent of moribund birds. Diarrhoea. and weeks in litter. 70 . The virulence of the virus varies but morbidity may be 100% and mortality 10-60%. double-immuno-diffusion of splenic extract. caused by Type II Adenovirus distinct from classical fowl adenovirus and occurring in most turkey-producing areas.
oral tetraycline. good hygiene and biosecurity. feather cover. 71 . Pathogenic strains can depress both B. Live vaccines are commonly used in many countries at 4-5 weeks of age. In this case a loop of intestine has been opened to show the blood.Treatment Warmth and good management. Turkeys dying with haemorrhagic enteritis commonly have the small intestine distended with blood. Immunity to the disease is long lasting. Reduced feed consumption. drinking water temperature and availability. acclimation. Ducks are relatively resistant to heat stress. especially associated with high relative humidity and low air speed. some in turkey B-lymphoblastoid cell lines. Disinfect and 3-4 weeks house rest. Immunity: there is an early age resistance irrespective of maternal antibody status. Increased thirst. Signs Panting. high stocking density. Some are produced in live turkeys. Prevention All-in/all-out production. nicarbazin in feed. good management. and turkeys caused by high environmental temperature. Figure 39. convalescent serum. Heat Stress Introduction A condition seen in chickens. Predisposing factors include genetics.and T-line lymphocytes for up to 5 weeks following exposure. Maternal antibody may interfere with vaccination.
Post-mortem lesions Carcases congested. Mucoid exudate in nostrils and mouth. columbae) is a protozoan parasite of turkeys. Hexamitiasis Introduction Hexamita meleagridis (pigeons H. In commercial ducks a related parasiteTetratrichomonas can cause poor growth and drops in egg production. contains excessive mucus and gas. Frothy. Intestine flabby with some bulbous dilation. Legs and wings outstretched. carriers. and some game birds. Later depression. Loss in weight. Reductions in stocking density of meat poultry may be quickly achieved by partial depletion ('thinning'). pigeons. Terminal coma and convulsions. painted white to reflect heat. 72 . Post-mortem lesions Dehydration. Feeding during cooler hours may be beneficial. Treatment Cool water. Inter-species transmission may occur. chirping. Signs Initially birds nervous. Prostration. if relative humidity is low then wet the roof and fog. evaporative coolers. signs. exclusion of other conditions. Prevention Houses of optimal height and insulation. feed with a reduced protein:energy ratio. maximise airflow. Reduced egg production. It is transmitted by faeces. fomites. Inappetance. watery diarrhoea. pheasants. lesions. pattern of losses. Diagnosis Temperature records.
Caecal tonsils congested. Outwith earth worms orH. increase ambient temperature. First half of intestine inflamed. significant disease has been seen in breeding chickens and free-range layers. Progressive depression and emaciation. The problem is seen in high-biosecurity facilities. Blackhead Introduction Histomonas melagridis is a protozoan parasite of turkeys. This condition has high morbidity and mortality in turkeys. Poor growth. Sulphur-yellow diarrhoea. Histomoniasis. 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. Diagnosis Lesions. The effect of antibiotic may be related to the control of secondary bacterial enteritis. all-in/all-out production. trichomoniasis. Histamonosis. Prevention Depopulation. and occasionally chickens. 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. avoid interspecies mixing. Treatment Tetracycline. and also. 73 . hygiene. dimetridazole. gallinae the parasite is easily destroyed. paratyphoid. Inappetance. Signs Depression. and mixing groups of different ages. Furazolidone. It has recently been demonstrated that infection occurs readily via the cloaca when birds are on contaminated litter. histomonosis. Cyanosis of head. Although chickens are relatively resistant to the condition. scrapings from fresh material. dimetridazole and ipronidazole have been used in the past. Blood in faeces (chickens). if possible. Differentiate from transmissible enteritis. pheasants and game birds that acts together with facultative bacteria to produce the condition of Blackhead.
furazolidone. Angara Disease Introduction This condition was first identified in broilers in Pakistan in 1987. 74 .Tahir Post-mortem lesions Enlargement of caeca. Having both chickens and turkeys on the same property is likely to increase the risk of this disease in turkeys. dimetridazole). Arsenicals are less effective in treatment than they are in prevention. Ulcers.g. especially in chickens. Treatment Historically nitro-imidazoles (e.nitarsone) have been used to treat this important disease of poultry.g. usually grey in colour. Some herbal products based on the essential oils (e. scrapings from fresh material. nitrofurans (e. Regular worming to help control the intermediate hosts. At the time of writing no products of these groups are approved for use in the European Union. grey or green areas. Hydropericardium-Hepatitis Syndrome. Use of an anti-histomonas product in feed where such products are approved but due care with respect to residue avoidance would be required. possibly in combination with an RNA virus and immunosuppression caused by Chick Anaemia Virus or Infectious Bursal Disease. caseous cores with yellow. given recent new knowledge on the mechanism of transmission. Liver may have irregular-round depressed lesions. It is a condition caused by an adenovirus. Intensive relittering may help reduce the level of infection. Diagnosis Lesions. concrete floors. Mortality may reach 60% but more typically 10-30%. 'Herban)' have been used with some apparent success though controlled trials and formal approval for this purpose are not recorded.g. however they may not be present in the early stages. and only nitarsone is approved in the USA. Prevention Good sanitation. 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. nifursol) and arsenicals (e.M. The disease is readily reproduced by inoculating birds with a bacteria-free filtrate of a liver extract from an affected bird.g.Abubakar. avoid mixing species. It affects mainly broilers and broiler parents in rear and has also been seen in pigeons.
Prevention The condition typically occurs in areas of high poultry density where multi-age operation is traditional. Impacted gizzards are then found in 'non-starter' type chicks or poults. Grit would not be classed as a foreign body. Formalin-inactivated oil adjuvant vaccines are reported to be highly effective and are used in areas where the condition is endemic. Congestion of the carcase. virology. Huddling with ruffled feathers. pale friable liver and kidney. treatment of drinking water with 0. Post-mortem lesions Excessive straw-coloured fluid distending the pericardium (up to 10 mls). Most young commercial poultry consume feeds that have a small particle size. Yellow mucoid droppings. Lungs oedematous.5% iodophor solution) appears to be beneficial. Enlarged. Diagnosis Lesions. and birds of any age can 75 . Gizzard activity also acts as a pacemaker of intestinal activity and controls the speed at which food is passed to the small intestine. Impaction and Foreign Bodies of Gizzard Introduction The gizzard or crop may become impacted with litter. to reduce their particle size to aid digestion. Older birds ingest grit to facilitate the grinding activity in the gizzard. Lethargy.1% of a 2.Signs Sudden increase in mortality. grass. Control of predisposing immunosuppressive diseases may help limit losses. histopathology.g. however sometimes free-range poultry consume large stones. Good water sanitation (e. This condition usually affects only a small number of birds. The normal function of the gizzard is to aid in the physical grinding of food materials. string etc. Treatment None. however if young chicks to do not begin to eat feed properly they often consume litter instead.
Treatment None effective in young birds. Sweep floors after maintenance activities to remove nails and other potentially dangerous foreign bodies. Diagnosis Lesions. Daily monitoring of the crop-fill is a useful procedure. Italy. and may penetrate the body wall. Prevention Good brooding management to encourage early adaptation to the diet and adequate consumption of feed and water. Inclusion Body Hepatitis Introduction A disease of chickens characterised by acute mortality. Signs Reduced feed intake. the UK. The disease was first described in the USA in 1963 and has also been reported in Canada. France and Ireland. often with severe anaemia. 76 . 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. This usually happens after maintenance activities have been carred out in the housing. 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. staples etc.15 days with a morbidity of 1-10% and a mortality of 1-10%. A number of different sero-types have been isolated from disease outbreaks but they may also be isolated from healthy chickens. Post-mortem lesions The gizzard is more firm than normal and.consume nails. caused by an adenovirus. Reduced weight gain. Australia. This may extend into the proventriculus and on into the duodeunum. Obvious non-starters should be culled in this situation. and on opening is found to contain a mass of fibrous material. Infected birds remain carriers for a few weeks.
The virus is generally resistant to disinfectants (ether.Transmission may be vertical or lateral and may involve fomites. The virus grows well in tissue culture (CEK. Ruffled feathers. many different sero-types have been isolated from different cases.basophilic intranuclear inclusions. Serology: DID for group antigen. and high temperatures. Treatment None. Post-mortem lesions Liver swollen. Diagnosis A presumptive diagnosis may be made on history and lesions. 77 . CEL). Kidneys and bone marrow pale. Formaldehyde and iodides work better. and deficiency of vitamin B12. Infectious Bursal Disease. may be important. vibrionic hepatitis. A form of the disease affecting birds under 3 weeks of age in Australia has been reproduced with serotype 8 adenovirus. pH). for instance due to early IBD challenge or congenital CAV infection. Blood thin. Since adenoviruses are commonly found in healthy poultry. Inappetance. fatty liver syndrome. Signs Depression. Progeny of high health status breeding flocks appear to be at greater risk. Differentiate from Chick anaemia syndrome. Microscopically . sulphonamide intoxication. Confirmation is made on finding inclusions in the liver. Bursa and spleen small. chloroform. but on the other hand many field cases show eosinophilic inclusions that do not appear to have adenovirus particles. isolation alone does not confirm that they are the cause of a particular problem. perhaps because they have lower levels of maternal antibody. Immunosuppression. mottled with petechiae and ecchymoses. Soluble multivitamins may help with the recovery process. SN for individual sero-types. Pallor of comb and wattles. Curiously. yellow.
Diuresis. Tracheal oedema. E. fomites or aerosol. Signs Depression. new sero-types continue to emerge. Its affects vary with: the virulence of the virus. Diarrhoea. and complicating infections (Mycoplasma. Poor ventilation and high density are predisposing factors. These differences are due to structural differences in the spike proteins (S1 fraction). was first described in the USA (N. probably the commonest respiratory disease of chickens. disinfectants (Formal 1% for 3 mins). Post-mortem lesions Mild to moderate respiratory tract inflammation. Airsacculitis.Prevention Quarantine and good sanitary precautions. Coughing. coli. Newcastle disease). Tracheitis. Huddling. Caseous plugs in bronchi. depending on secondary infections. Infection is via the conjunctiva or upper respiratory tract with an incubation period of 18-36 hours. heat (56°C for 15 mins). Loss of appetite. Dakota. prevention of immunosuppression. Infectious Bronchitis. Morbidity may vary 50-100% and mortality 0-25%. is sensitive to solvents. the age of the bird. The virus. Kidneys and bronchi may be swollen and they and the ureters may have urates. The cause is a Coronavirus that is antigenically highly variable. gasping. alkalis. Wet litter. Some birds/viral strains can be carriers to 1 year. 1931). prior vaccination. maternal immunity (young birds). IB Introduction This infection. dyspnoea. The infection is highly contagious and spreads rapidly by contact. Typing by haemagglutination-inhibition is also used. 78 . which may survive 4 weeks in premises. About eight sero-groups are recognised by sero-neutralization.
Local immunity is first line of defence. heat (56°C for 15 mins). Some birds/viral strains can be carriers for up to 1 year. mycoplasmosis. Avian Influenza and Laryngotracheitis. group specific). 79 . short duration. IB . Serology: HI. Muscular shivering. Poor ventilation and high density are predisposing factors. DID (poor sensitivity. Definitive diagnosis is based on viral isolation after 3-5 passages in chick embryo. The infection spreads rapidly by contact. Infection is via the conjunctiva or upper respiratory tract with an incubation period of 18-36 hours. SN (type specific). disinfectants (Formal 1% for 3 mins). Differentiate from Newcastle disease (lentogenic and mesogenic forms). which may survive 4 weeks in premises.v.antibiotics to control secondary colibacillosis (q. Cellmediated immunity may also be important. Infectious Bronchitis. vaccinal reactions. with typical lesions. Prevention Live vaccines of appropriate sero-type and attenuation. Treatment Sodium salicylate 1gm/litre (acute phase) where permitted .Diagnosis Tentative diagnosis is based on clinical sgns. flourescent antibody positive and ciliostasis in tracheal organ culture. Otherwise as for standard IB.).793b Variant Sudden Death Syndrome in Broiler Parents Introduction A Coronavirus infection of chickens with a morbidity of 50-100% and a mortality 0-25%. depending on secondary infections. fomites or aerosol. is sensitive to solvents. alkalis. possible reactions depending on virulence and particle size. The virus. lesions and serology. Humoral immunity appears 10-14 days post vaccination. HA negative. Signs Sudden death. Maternal immunity provides protection for 2-3 weeks. Elisa (both group specific).
Loss of internal egg quality. The condition has a morbidity of 10-100% and mortality of 0-1%.antibiotics to control secondary colibacillosis (q. ciliostatic in tracheal organ culture. lesions progress to necrosis and scarring of deep pectorals in convalescence. Prevention Live vaccines of appropriate sero-type and attenuation. group specific). Diagnosis 3-5 passages in CE allantoic cavity. The virus is moderately resistant and may survive 4 weeks in premises. There is rapid spread by contact. Treatment Sodium salicylate 1gm/litre (acute phase) where permitted . FA. CK) only after adaptation Serology: HI. HA-. IB Egg-layers Introduction A Coronavirus infection of chickens. short duration. Rales may or may not be present. Coughing. sneezing. possible reactions depending on virulence and particle size. fomites or aerosol. Poor ventilation and high density are predisposing factors. A few birds are carriers up to 49 days post infection. DID (poor sensitivity. Elisa (both group specific).Post-mortem lesions Oedema of pectoral muscles and subcutaneously on abdomen. Soft-shelled eggs.). Infection is via the conjunctiva or upper respiratory tract.v. cell culture (Vero. 80 . typical lesions. Rough shells. In layers the ovules may be intensely congested. Other lesions of 'classical' IB may be encountered. Infectious Bronchitis. Signs Drop in egg production (20-50%). with much antigenic variation. SN (type specific).
Local immunity is the first line of defence. Diagnosis 3-5 passages in CE. although reactions can occur depending on prior immunity. virulence.v. particle size (if sprayed) and general health status. Treatment Sodium salicylate 1gm/litre (acute phase) where permitted . SN. Humoral immunity appears 10-14 days post vaccination. HA-. 81 .Post-mortem lesions Follicles flaccid. Elisa. Yolk in peritoneal cavity (non-specific). FA. Figure 22. typical lesions. DID. Prevention Live vaccines of appropriate sero-type and attenuation. Maternal immunity provides protection for 2-3 weeks. Differentiate from Egg Drop Syndrome.antibiotics to control secondary colibacillosis (q. Flaccid ovarian follicles in a broiler parent chicken undergoing challenge with Infectious Bronchitis virus.). Serology: HI. Cell-mediated immunity may also be important. EDS76.
). Treatment Sodium salicylate 1gm/litre (acute phase) where permitted . HA-. Prevention Live vaccines of appropriate sero-type and attenuation. Elisa. DID. A few birds are carriers up to 49 days post infection. typical lesions.antibiotics to control secondary colibacillosis (q. SN. Post-mortem lesions Follicles flaccid. Cell-mediated immunity may also be important. Poor ventilation and high density are predisposing factors. sneezing. Humoral immunity appears 10-14 days post vaccination. The virus is moderately resistant and may survive 4 weeks in premises. Local immunity is the first line of defence. Rough shells. The condition has a morbidity of 10-100% and mortality of 0-1%. 82 . fomites or aerosol. Soft-shelled eggs. Differentiate from Egg Drop Syndrome.v. with much antigenic variation.Infectious Bronchitis. IB Egg-layers Introduction A Coronavirus infection of chickens. Infection is via the conjunctiva or upper respiratory tract. Coughing. Rales may or may not be present. Serology: HI. EDS76. Diagnosis 3-5 passages in CE. Signs Drop in egg production (20-50%). FA. Yolk in peritoneal cavity (non-specific). particle size (if sprayed) and general health status. There is rapid spread by contact. although reactions can occur depending on prior immunity. Loss of internal egg quality. Maternal immunity provides protection for 2-3 weeks. virulence.
Generally speaking the earlier the damage occurs the more severe the effects. Sero-type 1 only. The age up to which infection can cause serious immunosuppression varies between 14 and 28 days according to the antigen in question. (Turkeys and ducks show infection only. susceptibility to Inclusion Body Hepatitis and gangrenous dermatitis and increased susceptibility to CRD. Morbidity is high with a mortality usually 0. especially with sero-type 2). with an incubation period of 2-3 days. Subclinical infection in young chicks results in: deficient immunological response to Newcastle disease. The infective agent is a Birnavirus (Birnaviridae). 83 . Gumboro Introduction A viral disease. In addition to the direct economic effects of the clinical disease. The route of infection is usually oral. which targets the bursal component of the immune system of chickens. and affected birds excrete large amounts of virus for about 2 weeks post infection. Mealworms and litter mites may harbour the virus for 8 weeks. the damage caused to the immune system interacts with other pathogens to cause significant effects.Figure 22. faeces etc. persisting for months in houses. Infectious Bursal Disease. The virus is very resistant. Marek's disease and Infectious Bronchitis. seen worldwide.20% but sometimes up to 60%. There is no vertical transmission. The disease is highly contagious. Signs are most pronounced in birds of 4-6 weeks and White Leghorns are more susceptible than broilers and brown-egg layers. IBD. Flaccid ovarian follicles in a broiler parent chicken undergoing challenge with Infectious Bronchitis virus. first identified in the USA in 1962. but may be via the conjunctiva or respiratory tract.
rapidly proceeds to atrophy. lesions. Vent pecking. This may be confirmed by demonstrating severe atrophy of the bursa. Diagnosis Clinical disease . Elisa vaccination date prediction < 7 days). Haemorrhages in skeletal muscle (especially on thighs). Huddling under equipment. Use of a multivitamin supplement and facilitating access to water may help. Diarrhoea with urates in mucus. Inappetance. Cryptosporidiosis of the bursa (rare). Unsteady gait. Half-life of maternally derived antibodies is 3. Swollen kidneys with urates. may have haemorrhages.A history of chicks with very low levels of maternal antibody (Fewer than 80% positive in the immunodifusion test at day old. Serology: antibodies can be detected as early as 4-7 days after infection and these last for life. Variants: There have been serious problems with early Gumboro disease in chicks with maternal immunity. IBD viruses have been isolated and shown to have significant but not complete cross-protection.5. weights below 0. Other possible causes of early immunosuppression are severe mycotoxicosis and managment problems leading to severe stress. 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. Haemorrhagic syndrome. Dehydration. Post-mortem lesions Oedematous bursa (may be slightly enlarged. Coccidiosis.3% of bodyweight. Subclinical disease .1% are highly suggestive. The normal weight of the bursa in broilers is about 0. especially if present prior to 20 days of age. Antibiotic medication may be indicated if secondary bacterial infection occurs. normal size or reduced in size depending on the stage). They are all serotype 1. Tests used are mainly Elisa.History.4 days. especially in the Delmarva Peninsula in the USA. (previously SN and DID).Signs Depression. subsequent diagnosis of 'immunosuppression diseases' (especially inclusion body hepatitis and gangrenous dermatitis) is highly suggestive. 84 . Differentiate clinical disease from: Infectious bronchitis (renal). Treatment No specific treatment is available. histopathology.
Morbidity is high but mortality low if uncomplicated although it may be up to 20%. especially nasal and sinus mucosae. occasionally pheasants and guinea-fowl. This bursa is from an acutely affected broiler. The route of infection is conjunctival or nasal with an incubation period of 1-3 days followed by rapid onset of disease over a 2-3 day period with the whole flock affected within 10 days. Infectious Coryza Introduction A usually acute. the rectum and the vent. It is not egg transmitted. including passive protection via breeders. Immunity after a live vaccine can be poor if maternal antibody was still high at the time of vaccination. It is enlarged. and tracing of contacts may indicate sites on which a more rebust vaccination programme is indicated. 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. When outbreaks do occur. vaccination of progeny depending on virulence and age of challenge. Figure 23.Prevention Vaccination. highly infectious disease of chickens. Infectious Coryza is caused by the bacterium Haemophilus paragallinarum and is seen in many countries especially in multi-age farms that are never depopulated. 85 . turgid and oedematous. A strong immunity follows field challenge. resulting in increased culling. biosecurity measures may be helpful in limiting the spread between sites. characterised by catarrhal inflammation of the upper respiratory tract. This shows the anatomical relationship between the bursa. Carriers are important with transmission via exudates and by direct contact.
Intercurrent respiratory viral and bacterial infections are predisposing factors. Conjunctivitis. identification of the bacteria in a Gram-stained smear from sinus. Swollen wattles. Differentiate from Mycoplasmosis. Dyspnoea. erythromycin. Live attenutated strains have been used but are more risky. Inappetance. Birds recovered from challenge of one serotype are resistant to others. Bacterin at intervals if history justifies or if multi-age. Dihydrostreptomycin. Prevention Stock coryza-free birds on an all-in/all-out production policy. Commercial bacterins may not fully protect against all field strains but reduce the severity of reactions. Confirmation is by isolation and identification . preferably in raised CO 2 such as a candle jar. agglutination and IF have all been used but are not routine. at least two doses are required. Diagnosis A presumptive diagnosis may be made on signs. Vaccines are used in areas of high incidence. Controlled exposure has also been practised. lesions. 86 .requires X (Haematin) and V (NAD) factors. chronic or localised pasteurellosis and vitamin A deficiency. Tracheitis. drying and disinfectants. Purulent ocular and nasal discharge. Drop in egg production of 10-40%. Sneezing. Caseous material in conjunctiva/sinus. Signs Facial swelling. Loss in condition. Serology: HI. Post-mortem lesions Catarrhal inflammation of nasal passages and sinuses. respiratory viruses. Treatment Streptomycin. DID. Flouroquinolones are bactericidal and might prevent carriers.The bacterium survives 2-3 days outside the bird but is easily killed by heat. while bacterins only protect against homologous strains. sulphonamides. Eye-lid adherence. tylosin.
antibiotics to control secondary bacterial infection if this is marked. Microscopically . Keep susceptible stock separate from vaccinated or recovered birds. Treatment None. peafowl and turkeys with a morbidity of 50-100% and a mortality usually 10-20% but sometimes up to 70%. Fairly slow lateral spread occurs in houses.Infectious Laryngotracheitis. histology.intranuclear inclusions in tracheal epithelium. The route of infection is via upper respiratory tract and conjunctiva or possibly oral and the course of the disease is up to 6 weeks. Prevention Quarantine. All-in/allout operation. Gasping. Sera may be examined by VN or Elisa. often with blood in lumen. The virus is highly resistant outside host but is susceptible to disinfectants. Diagnosis Signs. PCR. 87 . Drop in egg production. pheasants. Transmission between farms can occur by airborne particles or fomites. in severe form may be enough. Post-mortem lesions Severe laryngotracheitis. caseous plugs may be present. lesions. Apply strict biosecurity in moving equipment or materials between these these categories of stock. severe bronchitis. Movement and mixing of stock and reaching point of lay are predisposing factors. Differentiate from Newcastle disease. Signs Dyspnoea. Nasal discharge (low pathogenicity strains). Isolation in CE CAMs. vaccination. Sinusitis. Coughing of mucus and blood. after 4 weeks of age. ILT Introduction A herpesvirus (pathogenicity can vary) infection of chickens. Recovered and vaccinated birds are long-term carriers. Ocular discharge. if enzootic or epizootic in an area. IFA.
protozoan parasites of turkeys. Survivors may carry infection. Asia and Africa. Different species of this parasite have been reported from North America. usually in the lower small intestine. ducks. it may actually protrude at the vent and be cannibalised. Anorexia. Signs Mainly sudden deaths. Signs Sudden onset of depression. 88 . Careful attention to feeding practices to avoid anticipation of feed arrival if on restricted feeding. worms and other forms of enteritis are predisposing factors. Loss of equilibrium. Post-mortem lesions Telescoping of the bowel. Leukocytozoonosis Introduction Caused by Leucocytozoon species. Thirst.Intussusception Introduction A condition of chickens associated with increased intestinal motility. Simulid flies or culicoid midges are intermediate hosts. Diagnosis Typical post-mortem lesions Treatment As appropriate for the underlying disease condition. Rapid breathing. rarely chickens. Coccidiosis. guinea fowl. The disease has a short course and morbidity and mortality are high. Prevention Control of coccidiosis and other causes of intestinal inflammation.
Prevention Separation from intermediate hosts. schizonts in liver. Lymphoproliferative Disease (LPD) Introduction A Type C retrovirus infection of turkeys with low morbidity and high mortality. histology and blood smears. Treatment 89 . age. Loss of weight. Diagnosis Lesions. Treatment None known. lesions. liver or bursa. Persistent low mortality. Anaemia. Post-mortem lesions Splenomegaly.megaschizonts in brains of birds with nervous signs. Post-mortem lesions Focal tumours. Signs Depression. disposal of recovered birds. Enlargement of abdomen. Anaemia. Differentiate from Reticuloendotheliosis. Diagnosis History. Microscopically . May be asymptomatic. Emaciation. especially in enlarged spleen. gametes in erythrocytes. cytology. Hepatomegaly.
Eating faeces. The condition has been seen in Europe.(maize-) fed birds (often associated with orange intestinal contents and/or faeces). Diarrhoea in older birds may be an effect of on-farm infection. direct electron microscope examination of intestinal contents. Runting (permanent). in future eradication. reoviruses. Sometimes osteomyelitis and/or rickets. It is suspected that these viruses can be vertically transmitted and the most severe signs in young birds are associated with this. temperature control) may lead to a similar picture in the absence of specific infection. Poor feathering. Diarrhoea. 90 . for example enteroviruses. Pot-bellied appearance. Poor management may contribute to the problem.M. all-in/all-out production. enterovirus-like particles. Prevention Good hygiene. Pancreatic atrophy/fibrosis and pancreatic atrophy (rather variable). Treatment Daily cull of affected birds between 14 and 28 days. control arthropods. Poor early management (feed and water supply. Pale shanks in corn. North and South America and Australia.Abubakar. Malabsorption Syndrome. Stunting (temporary). Abnormal feathers ('helicopter wings' 'yellow-heads'). Post-mortem lesions Enteritis. rotavirus etc. Signs Uneven growth. Runting/Stunting Introduction A condition of chickens and turkeys that may be associated with several different viruses. Diagnosis Pathology.Tahir None.
Prevention Good broiler farm hygiene. Vertical transmission is not considered to be important. good parent nutrition and egg selection and santitation. ovary. A sample of the faeces produced is shown at the bottom of the picture .poorly digested food enclosed in mucus. Figure 24. The disease has various manifestations: a) Neurological .Acute infiltration of the CNS and nerves resulting in 'floppy broiler syndrome' and transient paralysis. Intestines of a young broiler chick suffering from malabsorption syndrome. In 'late' Marek's the mortality can extend to 40 weeks of age. They are distended with poorly digested feed. avoidance of intercurrent disease and management problems (such as chilling). Morbidity is 10-50% and mortality up to 100%. Affected birds are more susceptible to other diseases.Tumours in heart. The route of infection is usually respiratory and the disease is highly contagious being spread by infective feather-follicle dander. c) Cutaneous . Mortality in an affected flock typically continues at a moderate or high rate for quite a few weeks. tests. both parasitic and bacterial. muscles.Tumours of feather follicles. lungs. b) Visceral . etc. From the 1980s and 1990s highly virulent strains have become a problem in North America and Europe. and rarely turkeys in close association with chickens. as well as more longstanding paralysis of legs or wings and eye lesions. seen worldwide. Infected birds remain viraemic for life. fomites. The virus survives at ambient temperature for a long time (65 weeks) when cell associated 91 . Marek's disease Introduction Marek's disease is a Herpes virus infection of chickens.
all-in/all-out production. clinical signs. deficiency of thiamine. Grey iris or irregular pupil. Post-mortem lesions Grey-white foci of neoplastic tissue in liver. It is inactivated rapidly when frozen and thawed. histopathology.lymphoid infiltration is polymorphic. association with other strains (SB1 Sero-type 2) and Rispen's. distribution of lesions. resistant strains. botulism. Mycoplasma gallisepticum infection. Differentiate from Lymphoid leukosis..g. deficiency of Ca/Phosphorus/Vitamin D. chronic respiratory disease in chickens. wings and neck. vaccination generally with 1500 PFU of HVT at day old (but increasingly by in-ovo application at transfer). kidney. Thickening of nerve trunks and loss of striation. Microscopically .and is resistant to some disinfectants (quaternary ammonium and phenol). age affected. Treatment None. Prevention Hygiene. and skeletal muscle. spleen. lung. Chronic Respiratory Disease . gonads. Ducks and geese can 92 . game birds. Vision impairment.Chicken Introduction Infection with Mycoplasma gallisepticum is associated with slow onset. turkeys. heart. Genetics can help by increasing the frequency of the B21 gene that confers increased resistance to Marek's disease challenge. M. It is common practice to use combinations of the different vaccine types in an effort to broaden the protection achieved. especially at the start of lay. Loss of weight. Diagnosis History. pigeons and other wild birds. Skin around feather follicles raised and roughened. Signs Paralysis of legs.
ART). Occasional encephalopathy and abnormal feathers. Perihepatitis (especially with secondary E. Recovered birds remain infected for life. Occasionally arthritis. In turkeys it is most associated with severe sinusitis (see separate description in the turkey section). Pasteurella spp. Survival seems to be improved on hair and feathers. isolation and identification of organism. Fomites appear to a significant factor in transmission between farms.become infected when held with infected chickens. Signs Coughing. ND. and inadequate environmental conditions are predisposing factors for clinical disease. Post-mortem lesions Airsacculitis. The route of infection is via the conjunctiva or upper respiratory tract with an incubation period of 6-10 days. aerosols. Haemophilus. though in some countries this infection is now rare in commercial poultry. In others it is actually increasing because of more birds in extensive production systems that expose them more to wild birds. In adult birds. The infectious agent survives for only a matter of days outwith birds although prolonged survival has been reported in egg yolk and allantoic fluid. and in lyophilised material. morbidity may be minimal and mortality varies. The condition occurs worldwide. subsequent stress may cause recurrence of disease. exudates. though infection rates are high. more commonly in Mycoplasma Broth followed by plating out on Mycoplasma Agar. Inappetance. Diagnosis Lesions. Pericarditis. virulent E. Suspect colonies may be identified by immuno-flourescence. demonstration of specific DNA (commercial PCR kit available). Intercurrent infection with respiratory viruses (IB. airborne dust and feathers. and to a lesser extent fomites. Reduced hatchability and chick viability. Slow growth. trachea and bronchi. Leg problems. Poor productivity. Culture requires inoculation in mycoplasma-free embryos or. or by direct contact with birds. serology. Stunting. Transmission may be transovarian. Nasal and ocular discharge. tenosynovitis and salpingitis in chickens. Spread is slow between houses and pens suggesting that aerosols are not normally a major route of transmission. 93 . coli infection). coli. Catarrhal inflammation of nasal passages. sinuses.
all-in/all-out production. Effort should be made to reduce dust and secondary infections. Aspergillosis..-free stock. Elisa is accepted as the primary screening test in some countries. and fomites. other Mycoplasma infections such as M. Productivity in challenged and vaccinated birds is not as good as in M. fluoroquinolones. tetracyclines. Infectious Sinusitis . Differentiate from Infectious Coryza.Serology: serum agglutination is the standard screening test. viral respiratory diseases. It is seen worldwide. Recovered birds remain infected for life. exudates.g. meleagridis(turkeys).Turkeys Introduction A slow onset chronic respiratory disease of turkeys often with severe sinusitis and associated with Mycoplasma gallisepticuminfection.g.g. 94 . and routine serological monitoring. PCR is possible if it is urgent to determine the flock status. generally as a confirmatory test. vitamin A deficiency. The route of infection is via the conjunctiva or upper respiratory tract with an incubation period of 6-10 days. Treatment Tilmicosin. M. Mycoplasma gallisepticum infection. spiramycin. tylosin. synoviae and M. aerosols. therefore M. hatchingeggs and chicks. suspect reactions are examined further by heat inactivation and/or dilution. Suspect flocks should be re-sampled after 2-3 weeks. though in many countries this infection is now rare in commercial poultry. Transmission may be transovarian. HI may be used. In some circumstances preventative medication of known infected flocks may be of benefit. infection status is important for trade in birds. or by direct contact with birds. Live attenuated or naturally mild strains are used in some countries and may be helpful in gradually displacing field strains on multi-age sites. Some inactivated vaccines for other diseases induce 'false positives' in serological testing for 3-8 weeks. Morbidity is low to moderate and mortality low. Prevention Eradication of this infection has been the central objective of official poultry health programmes in most countries. subsequent stress may cause recurrence of disease. These programmes are based on purchase of uninfected chicks. biosecurity.
Suspect flocks should be re-sampled after 2-3 weeks. intercurrent viral disease such as Newcastle disease (even lentogenic) and Turkey Rhinotracheitis are predisposing factors. HI may also be used. Some inactivated vaccines induce 'false positives' in serological testing. especially Turkey Rhinotracheitis. Signs Coughing. These are based on purchase of uninfected poults. Perihepatitis. and biosecurity. often with inspissated pus. Suspect colonies may be identified by immunofluorescence. PCR is possible if it is urgent to determine the flock status. Differentiate from viral respiratory disease. and in lyophilised material. tetracyclines. although prolonged survival has been reported in egg yolk and allantoic fluid. demonstration of specific DNA (commercial kit available). Slow growth. Pericarditis. malnutrition.The infectious agent survives for only a matter of days outwith birds. requires inoculation in mycoplasma-free embryos or. In some circumstances preventative medication of known infected flocks may be of benefit. more commonly in Mycoplasma Broth followed by plating out on Mycoplasma Agar. tylosin. Prevention Eradication of this infection has been the central objective of official poultry health programmes in most countries. Nasal and ocular discharge. fluoroquinolones. Treatment Tilmicosin. Swollen sinuses. Stress. Culture. Inappetance. Survival seems to be improved on hair and feathers. isolation and identification of organism. Leg problems. Stunting. suspect reactions are examined further by heat inactivation and/or dilution. Airsacculitis. Post-mortem lesions Swollen infraorbital sinuses. of swabs taken from the trachea or lesions. Serology: serum agglutination is the standard screening test. Effort should be made to reduce dust and secondary infections. serology. all-in/allout production. Diagnosis Lesions. spiramycin. 95 .
Post-mortem lesions Stunted embryos with hepatitis and enlarged spleens. Signs Embryonic mortality. perhaps because all affected embryos fail to hatch. some with down abnormality. although DNA homology is only 40%. 96 . Reduced hatchability. and partridges (UK).i. Introduction Infection with Mycoplasma iowae is seen in turkeys. Leg lesions can be shown in inoculated birds but do not seem to occur naturally. Diagnosis Shows cross reaction in IFA to M.Mycoplasma immitans infection Introduction Infection with Mycoplasma immitans is seen in geese. Post-mortem lesions Sinusitis. Prevention As for M. venereal or horizontal. ducks (France). M.g.g.g. Mycoplasma iowae infection. Infection occurs via the conjunctiva or upper respiratory tract and transmission among poults may be vertical. Signs Swollen sinuses. and can occur in other poultry and wild bird species. Treatment As for M.
-free stock. Infection is via the conjunctiva or upper respiratory tract with an incubation period of 6-10 days. Transmission is venereal in breeders. Pathogenicity is quite variable. maintenance of this status by good biosecurity. Leg problems. though up to 25% of infected birds show lesions at slaughter. The infective agent does not survive well outside the bird. Predisposing factors include stress and viral respiratory infections. 97 . Mortality is low. Infected parents may be asymptomatic. Antibiotics that have been used are tylosin and enrofloxacin. Signs Reduced hatchability. Treatment Pressure differential dipping has been used where breeder flocks are infected. Specialised dip tanks are subjected to negative pressure which partially collapses the air cell of the submerged eggs. Crooked necks. This can increase hatchability by 510% in this situation. with transovarian and then lateral spread in meat animals. Introduction A disease of turkeys characterised by respiratory and skeletal problems caused by Mycoplasma meleagridis. Stunting.Diagnosis Isolation and identification of the causative organism from dead-in-shell embryos. In adult birds though infection rates are high. Infected eggs result in widespread distribution of infection and increased risk of further vertical transmission. Mycoplasma meleagridis infection. M.m. The organism has also been isolated from raptors. morbidity may be minimal. purchase of M. Prevention Eradication of the infection from breeding stock. When the vacuum is released the eggs draw in antibiotic solution which is subsequently absorbed through the shell membranes. Slow growth. For eradication purposes egg injection provides more consistent dosing per egg than does egg dipping.i. it occurs in most turkey-producing countries but is now much rarer in commercial stock. Mild respiratory problems.
Vaccines are not normally used. Survival of the infectious agent outwith the bird is poor but fomite transmission between farms is important. It occurs in most poultry-producing countries. Infected males are particularly prone to transmit infection and may warrant special attention.s. Predisposing factors include stress and viral respiratory infections. Serology: SAG used routinely . 98 . Airsacculitis (rarely) seen in adult birds.culture used to confirm. Infection rates may be very high. isolation and identification of organism. tetracyclines. especially in commercial layer flocks. Prevention Eradication of this infection is also possible using similar techniques as for Mycoplasma gallisepticum. Infected birds do develop some immunity. spiramycin. or lateral via respiratory aerosols and direct contact. Effort should be made to reduce dust and secondary infections. Birds infected from their parents seem to be immuno-tolerant and particularly prone themselves to transmit. demonstration of specific DNA (commercial kit available). 11-21 days following contact exposure. Spread is generally rapid within and between houses on a farm. These are based on purchase of uninfected poults. Culture requires inoculation in mycoplasma-free embryos or. Treatment Tylosin. more commonly in Mycoplasma Broth followed by plating out on Mycoplasma Agar. 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. serology. In some circumstances preventative medication of known infected flocks may be of benefit. all-in/all-out production. Mycoplasma synoviae infection. M. Differentiate from Mycoplasma gallisepticum. Suspect colonies may be identified by immuno-fluorescence. fluoroquinolones. Infection is via the conjunctiva or upper respiratory tract with a long incubation period. and biosecurity. other respiratory viruses. whilst illness is variable and mortality less than 10%. Diagnosis Lesions. Mycoplasma synoviae.Post-mortem lesions Airsacculitis in infected pipped embryos and poults.
There may be no signs. Depression. Inappetance. Ruffled feathers. Lameness. Swelling of hocks, shanks and feet (sometimes severe and bilaterally asymmetrical). Faeces may be green in acute infections. Effects on egg production appear to be minor under good management.
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.
Post-mortem lesions Small intestine (usually middle to distal) thickened and distended. Affected birds tend to be dehydrated and to undergo rapid putrefaction.g. Ruffled feathers. amoxycillin).small intestine. other debilitating diseases.g. Intestinal contents may be dark brown with necrotic material. Reflux of bile-stained liquid in the crop if upper small intestine affected. Spores of the causative organism are highly resistant. 100 ppm). diet (high protein). high viscosity diets (often associated with high rye and wheat inclusions in the diet). usually of the mid. Sudden death in good condition (ducks). Treatment Penicillins (e. Diagnosis A presumptive diagnosis may be made based on flock history and gross lesions Confirmation is on the observation of abundant rods in smears from affected tissues and a good response to specific medication. Infection occurs by faecal-oral transmission. Prevention Penicillin in feed is preventive. Inappetance. neomycin and erythromycin are used in the USA. Closed eyes. in ducks possibly heavy strains. turkeys and ducks worldwide. usually around 10%.M. in drinking water. or Bacitracin in feed (e.Tahir Necrotic Enteritis Introduction An acute or chronic enterotoxemia seen in chickens. contaminated feed and/or water. Signs Depression. caused by Clostridium perfringens and characterised by a fibrino-necrotic enteritis. Water medication for 3-5 days and in-feed medication for 5-7 days depending on the severity. Predisposing factors include coccidiosis/coccidiasis. Immobility. usually in less than 48 hours. Mortality may be 5-50%. high levels of most growth promotors and normal levels of ionophore anticoccidials also help. Treatment of ducks is not very successful. Probiotics may limit multiplication of bacteria and toxin 102 .Abubakar. phenoxymethyl penicillin. Intestinal mucosa with diptheritic membrane. Dark coloured diarrhoea.
which is of variable pathogenicity. In many countries local regulations or market conditions prevent the routine use of many of these options. ND . Other species can be infected including mammals occasionally (e. the upper has formed a thick crust of necrotic material.Velogenic Viscerotropic (VVND) . The sample at the bottom of the picture is still focal. Newcastle Disease (Paramyxovirus 1) Introduction Paramyxovirus 1 or Newcastle Disease is a highly contagious viral disease affecting poultry of all ages. ND . Transmission is via aerosols.sometimes called 'asiatic' or exotic.Mesogenic .Lentogenic . These viruses have sometimes been used as vaccines in previously immunised birds. The condition is rarely diagnosed in ducks but is a possible cause of production drops/fertility problems. The virus involved is Paramyxovirus PMV-1. ND .Mortality and nervous signs in adult.production. Affected species include chickens. sometimes subclinical. Higher mortality is seen in velogenic disease in unvaccinated stock. respiratory or reproductive systems. birds. Severe lesions of necrotic enteritis affecting the small intestine of broilers. Strains can be developed as vaccines. It is highly virulent for chickens.Mild disease. conjunctivitis in man).g. 103 . It is not usually vertical (but chicks may become infected in hatcheries from contaminated shells). Signs are typically of disease of the nervous. Morbidity is usually high and mortality varies 0-100%. fomites. pigeons and ducks. Four manifestations have been identified: ND . turkeys. Figure 25. Can affect any age. Intestinal lesions are absent. visitors and imported psittacines (often asymptomatic). less for turkeys and relatively apathogenic in psittacines.Neurotropic Velogenic .Acute and fatal in chickens of any age causing neurological and some respiratory signs.
Paralysis. fumigants and sunlight. especially in faeces and can persist in houses (in faeces. Haemorrhage in proventriculus. Dyspnoea. Treatment None. acid pH. Tracheitis. Post-mortem lesions Airsacculitis. HI with ND serum or DID (less cross reactions). encephalomyelitis. Nervous signs. pneumovirus infection. caecal tonsil. antibiotics to control secondary bacteria. avian influenza. Severe drop in egg production.The virus survives for long periods at ambient temperature. intoxications. HA+. Sudden Death Depression. However it is quite sensitive to disinfectants. haemorrhagic disease. Intestinal lesions primarily occur in the viscerotropic form. IFA. Inappetance. Differentiate from Infectious bronchitis. post-mortem lesions. middle ear infection/skull osteitis. for up to 12 months. Diarrhoea. Necrotic plaques in proventriculus. Samples . the infective dose and the degree of immunity from previous exposure or vaccination. encephalomalacia. Twisted neck. Signs Signs are highly variable and will depend on the nature of the infecting virus (see above). dust etc). laryngotracheitis. infectious coryza. It is inactivated by temperatures of 56°C for 3 hours or 60°C for 30 min. It is confirmed by isolation in CE. Diagnosis A presumptive diagnosis may be made on signs. Cross-reactions have mainly been with PMV-3. rising titre in serology. intracerebral or IV pathogenicity in chicks.tracheal or cloacal. and is ether sensitive. Pathogenicity evaluated by Mean Death Time in embryos. 104 . EDS-76. intestine. Coughing. Moult. formalin and phenol.
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). The LaSota-type vaccine may even repeated at 35-40 days of age if risk is high. 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. These tests do not directly evaluate mucosal immunity. Inactivated vaccines have largely replaced the use of live vaccines in lay but they do not prevent local infections. Figure 28.Prevention Quarantine. vaccination. Elisa is now also used. snicking. Vaccinal reactions may present as conjunctivitis. 105 . HI has been used extensively. A typical programme may involve Hitchner B1 vaccine at day old followed by LaSota-type vaccine at 14 days. especially in breeding birds by the use of routine serological monitoring. all-in/all-out production. It is commonest in progeny of young parent flocks (relatively small yolks) or where managers are inexperienced. Use of spray application is recommended but it needs to be applied with care to achieve good protection with minimal reaction. Use of Mycoplasma gallisepticum free stock under good management reduces the risk of vaccinal reactions. Mortality peaks at 3-5 days for birds that fail to eat at all. Vaccination programmes should use vaccines of high potency. biosecurity. and is associated with difficulty maintaining brooding temperature and poor management of feeders and drinkers. which are adequately stored and take into account the local conditions. It is common to monitor response to vaccination. To prevent or reduce vaccinal reactions in young chicks it is important that day old have uniform titres of maternal immunity. and occasionally gasping due to a plug of pus in the lower trachea. whereas it tends to peak between 6-10 days for chicks that begin eating but then cease. however. In some countries it has been customary to provide antibiotics prophylactically during periods of anticipated vaccinal reaction. Acute viral infections or heavily contaminated drinking water may have a similar effect to bad management in reducing feed intake. Morbidity is up to 10% and mortality close to 100%.
age of collection and weight of hatching eggs. nutrition of young parents. It has since been seen in turkeys. Without adequate blood supply the tissue of the muscle begins to die. Because it is enclosed in a relatively unyielding membrane. good drinking water hygiene. in broiler parent chickens and also in large broiler chickens in various places. soluble multivitamin supplementation may help. or suffer necrosis. Poor development. Most organs normal.Signs Failure to grow. Gall bladder distended. Treatment Correction of management problems. good hygiene and biosecurity in brooding areas to minimise early disease challenges. It does not usually cause any mortality or obvious clinical signs and so it is usually identified after slaughter. any swelling of the muscle tends to cut off the blood supply. Prevention Review brooding management. 106 . Genetics may play a role in that it has been suggested that blood supply to the affected muscles is reduced in some heavy meat type birds. The condition can be reproduced by causing intense exercise of this muscle.Deep Pectoral Myopathy Introduction This condition is so named because it was first identified in adult breeding turkeys in Oregon State. bile staining of adjacent tissues. Differentiate from omphalitis/ yolk sac infection. Post-mortem lesions Crop empty. It is caused by a reduction in the blood supply to the deep pectoral muscles. Gizzard may be impacted with litter. aspergillosis. Diagnosis Based on post-mortem lesions. Oregon Disease .
This will normally be due to excessive flapping in association with management activities (e. If recent.Signs None. Diagnosis Lesions. Prevention Avoidance of physical damage of this muscle. If of very long duration. If inactivated vaccines are administered into the breast muscle it is preferable that they go into the superficial muscle which is better able to cope with swelling. Post-mortem lesions Acute or chronic necrosis of the deep pectoral muscle on one or both sides. It is very difficult to detect affected carcases in standard meat inspection. weighing birds etc). and. it may become a healed scar. greenish yellow. Treatment Not applicable. thinning operations in meat birds. artificial insemination in breeding turkeys. Transillumination of the breast may help identify affected carcases and may be worthwhile if the incidence is high. with oedema within it and on its surface. It may also start to be enclosed in a fibrous capsule. The tissue in the centre is dry. Figure 26. in particular excessive exercise. 107 . the muscle may be swollen and pale. and flaking.g. If the condition is of over 7 days duration the muscle is dry and often shows greenish tinges. A typical case of the chronic stages deep pectoral myopathy in a broiler chicken.
The infection is common in chickens and turkeys. Bordetella aviuminfection. sneezing. age at infection etc. field challenge with respiratory viruses. It is a Gram-negative pleomorphic organism. and E. Important cofactors may include respiratory viral vaccines (Newcastle disease. There is some evidence that hatcheries may play a role in the epidemiology. tracheitis. This can cause significant losses through condemnations. direct contact and drinkers. 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. Post-mortem lesions Airsacculitis. ventilation problems. The range occurring in turkeys is wider than that seen in chickens. Cultures from the trachea of birds showing typical signs are preferred. coli infections. Diagnosis Clinical signs and lesions. coli overgrowth may occur. This was first identified as a new disease syndrome of turkeys in Germany in the early 1990s. ORT Introduction Ornithobacterium Infection is an infection of chickens and turkeys with the bacterium Ornithobacterium rhinotracheale(ORT). preferably as a flock test comparing results before and after the challenge. Reduced egg production. E. Most isolates are oxidase positive and galactosidase positive Serology using Elisa tests has been used.Ornithobacterium Infection. The severity of its effects depends on the pathogenicity of the particular strain and other risk factors such as viral infections. Signs Coughing. It commonly exacerbates respiratory disease caused by pneumovirus infections in turkeys. perhaps through survival of the organism on shell surfaces or shell membranes. Confirmation is by isolation of the organism. The organism grows slowly producing tiny colonies on blood agar. Some uncertainty exists about mechanisms of transmission. Infectious Bronchitis). The slow-growing bacterium was named in 1994. Within the poultry house it is likely to be by aerosols. It had been previously isolated in a number of other countries. Growth is more rapid and consistent in an anaerobic jar. Reduced weight gain. 108 . 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. severe bronchopneumonia.
it requires two doses. Vaccination . In the USA in 1998 all strains were sensitive to penicillins and many other microbials. regulation. In France and Belgium most strains were sensitive to enrofloxacin. also most are sensitive to tiamulin. Prevention This is based on good hygiene.amoxycillin at 250 ppm in water for 3-7 days or chlortetracycline at 500 ppm for 4-5 days. though 54% were sensitive to tetracycline. Some work has been done on live vaccine in the USA. cost etc. chlortetracycline but not to enrofloxacin. Initially in Germany most strains were sensitive to amoxycillin. this is unlikely to work in turkeys. because of the age of slaughter. Amoxycillin sensitivity remains good. 109 . Preventative medication with the products listed in the previous section may be beneficial in some circumstances. Severely consolidated lung from an acute ORT infection in 14-week-old turkey growers. An inactivated vaccine is licensed for broiler parents in Europe. Some vaccines seem to have difficulty in producing a longlasting serological response to ORT. Routine treatment .Treatment The sensitivity of ORT to antibiotic is highly variable. ORT is a major problem on multi-age sites. Satisfactory disease control depends on good management and biosecurity. The lung is solid and covered by pus/ purulent exudate. Vaccination of breeder flocks to protect progeny has shown benefits in chickens but. neomycin and enrofloxacin.there are issues relating to availability.it is very sensitive in vitro to a range of chemicals. Figure 27. therapy and vaccination. Tilmicosin is also effective at 10-20mg/kg and should be used in the early stages of the disease. Hygiene . Similar lesions may be found in Pasteurellosis.
Birds go off legs. Post-mortem lesions Green discolouration of the liver at slaughter. turkeys and ducks seen worldwide and due to Vitamin D or calcium deficiency. Predisposing factors include small body size. The green discolouration is used to identify carcases that require closer inspection of the other tissues. Osteoporosis. Prevention Unknown. Soft-shelled eggs. Drop in production. Enlarged hocks. Cage Fatigue Introduction A condition of chickens. Turkey Introduction An association has been shown between green discolouration of the livers of turkey growers at slaughter and the occurrence of inflammatory lesions of bones and/or joints. Gram-variable pleomorphic bacteria have been isolated from affected livers and bones.Osteomyelitis Complex. high production. Signs Lameness. Birds rest squatting. Treatment Not applicable . Diagnosis Lesions. Signs None.only identified at slaughter. 110 . Soft bones and beak.
Yucaipa Disease Introduction An infection of chickens. Diagnosis History. As birds progressively mobilise skeletal calcium for egg production through lay. whereas turkeys are more severely affected. spondylitis. turkeys and passerine cage birds with Paramyxovirus PMV-2 results in disease with variable mortality. Wild birds are believed to be especially important. lesions. 111 . signs. Beading and fracture of ribs. Parathyroids enlarged. proper Ca and P levels and ratio. Post-mortem lesions Not characteristic. bone ash.Tahir Post-mortem lesions Bones soft and rubbery. Differentiate from Marek's disease. Transmission is by wild birds and fomites. Treatment Over-correct ration vitamin D. skeletal size and mineral content at point of lay are critical. calcium carbonate capsules. antioxidants. depending on the species affected and whether infection is complicated by other factors and diseases. Prevention Supplementation of vitamin D. Signs Depression. Inappetance. Drop in egg production.M. Paramyxovirus 2 . Epiphyses of long bones enlarged. Coughing. Vertical transmission does not usually occur. place on litter.Abubakar. Beak soft. In chickens it is usually mild.
The infection is transmitted by birds. HA+. Mortality is usually low in poultry. Inappetance. biosecurity. occasionally chickens and psittacine cage birds. Differentiate from Infectious bronchitis. Prevention Quarantine. Loss of shell pigment Nervous symptoms (psittacines). Post-mortem lesions No specific lesions. Diagnosis Isolation in CE. HI with ND serum or DID (less cross reactions). 112 . Paramyxovirus-3 Introduction Paramyxovirus PMV-3 infects turkeys. HI with ND serum or DID (less cross reactions). HA+. IFA. Drop in egg production (turkeys). Treatment No specific treatment. all-in/all-out production. Signs Depression. antibiotics to control secondary bacteria. including wild bird contact and fomites. Vertical transmission does not usually occur. EDS-76.Diagnosis Isolation in CE. haemorrhagic disease. Treatment No specific treatment. laryngotracheitis. High mortality (cage birds). Coughing. IFA. antibiotics to control secondary bacteria.
Paramyxovirus-6 Introduction Paramyxovirus PMV-6 infection of turkeys. all-in/all-out production. all-in/all-out production. A less acute form of the disease appears to produce more of a lingering mortality. antibiotics to control secondary bacteria. Vaccination has been used in turkeys but may not be cost-effective. Mortality is 0-5%. In both cases mortality can be high and can be associated with a marked depression in growth. HA+. biosecurity. including wild bird contact and fomites. Mild respiratory signs. IFA. 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. The infection is transmitted by birds. Treatment No specific treatment. Signs Reduction in egg production. Post-mortem lesions No specific lesions. Vertical transmission does not usually occur. Diagnosis Isolation in CE. It is an infectious and transmissible cause of sudden increases in mortality in turkeys between 7 and 28 days of age. biosecurity. Prevention Quarantine. The infection is inapparent in ducks and geese.Prevention Quarantine. A range of 113 . HI with ND serum or DID (less cross reactions).
Muscle atrophy. Prevention Biosecurity to reduce the introduction of new infections into brooding facilities. Post-mortem lesions Dehydration. Weight loss.mash and poor quality crumbles increase risk. 114 . A highly digestible diet with fat at 7. multivitamins and milk replacer products are helpful for nutritional support in the acute phase. Diagnosis Signs. pale brown. Increased water consumption. Reduced feed consumption and growth. Treatment A range of antibiotics and arsenicals have been used to control the bacterial component of this condition. Liquid intestinal contents.viruses have been isolated from affected flocks. lesions. Pendulous Crop Introduction A complex condition of turkeys and chickens associated with coarse fibrous feed. huddling. Wet litter. Picking at feed. All-in/all-out production. Effective terminal disinfection. Overdistension of crop in young birds because of an interruption in feed supply may predispose. seeking heat. Emaciation. Signs Initial hyperactivity and increased vocalisation. Increasing weakness. eating litter. Good quality diets of a suitable form . Fluoroquinolone antimicrobials appear to be especially effective.5-8% will encourage feed intake and recovery. To replicate the condition in full it appears to be necessary to include bacteria in the inoculum. Caseous cores in bursae (late in the process). Droppings watery. This syndrome is clearly distinguished from typical viral enteritis in young turkeys because of the high mortality and severe growth depression.
including crustaceans. Lack of muscle tone. They are found in the mucosa of crop and proventriculus causing mainly inapparent infections. Prevention Remove predisposing factors. Diagnosis Signs. Crop contents semi-liquid and foul smelling. necrosis. lesions. may be impacted. grasshoppers and cockroaches. Emaciation in heavily infected young chicks (Tetrameres). Post-mortem lesions Inflammation. spiruroid worm parasites of poultry and game birds. haemorrhage. Treatment None. have ulcerations and sometimes mycosis. 115 . Diagnosis Macroscopic examination of lesions. ulceration. if these can be identified.Signs Enlargement of crop. Proventricular Worms Introduction Dispharynx. and thickening of mucosa of proventriculus. Tetrameres and Cyrnea are nematodes. Post-mortem lesions Crop distended with feed. Diarrhoea. Infection is by the oral route on exposure to the intermediate hosts. identification of worms. Signs Anaemia.
Differentiate from Duck viral enteritis. isolation. In peracute disease the only lesion may be enteritis.Treatment Not usually required. Diagnosis Lesions. 116 . duck viral hepatitis. Sometimes sudden death. Prevention Prevention of access to intermediate hosts. Diarrhoea. Treatment Tetracyclines. adequate protection. rodents and man with the bacterium Yersinia pseudotuberculosis. Signs Weakness. Ruffled feathers. 'hardening off'. colibacillosis. The disease has a mortality of 5-75%. Pseudotuberculosis Introduction An infection of ducks. tuberculosis. sulphonamides in feed. wild birds. coccidiosis. Prevention Good husbandry and hygiene. Post-mortem lesions Miliary lesions in a variety of organs but especially in the liver. other poultry.
Tahir Pullet disease. lesions. molasses. Loss of appetite. Differentiate from fowl cholera. toxin and possibly a virus infection. elimination of other causes. Avian Monocytosis Introduction A sudden onset condition of chickens early in lay with high morbidity and a mortality of 050%. 117 . vibriosis. Crop distended. Signs Depression. Skeletal muscle necrosis. Pancreas chalky. coccidiosis. Prevention Good management. Kidneys swollen. Post-mortem lesions Dehydration. hygiene. Dark comb and wattles. capillariasis.Abubakar. IBD and typhoid. It was commonly reported prior to 1960 but is now rare. water deprivation.M. Dehydration. Bluecomb. It is associated with hot weather. Watery diarrhoea. Catarrhal enteritis. diet and water supply. Crop distension. Treatment Adequate water supply. Affected birds have an increase in circulating monocytes in their blood. Liver swollen with foci. Diagnosis History. Drop in egg production. mucoid casts in intestine. multivitamins in water. Skin cyanosis of head. antibiotics.
For northern fowl mite it is essential to apply approved insecticides to the affected birds. cracks. the Northern Fowl Mite spends its entire life cycle on the bird and can multiply more rapidly as a result. Diagnosis Number and type of mites identified. Treatment Pyrethroids. Spots on eggs. Effective monitoring of mite numbers and implementation of control measures before birds are heavily infested improves control. Staff complaints . and good design of new equipment to limit harbourages for red mites.itching. Loss of condition. Dermanyssus gallinae. organophosphates. 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. Signs Presence of grey to red mites up to 0. Ornithonyssus bursae. Prevention Thorough cleaning. fumigation and insecticide treatment at turnaround. Post-mortem lesions Anaemia. 118 . mainly at night and may transmit fowl cholera and other diseases.7 mm. crevices etc.Red Mite and Northern Fowl Mite Introduction Arachnid mites. May cause anaemia and death in young birds. vegetable oil and mineralbased products (both liquid sand dusts) have been used to control red mites in the environment. Drop in egg production. the Common Red Mite. Filling of cracks and crevices. citrus extracts. in nest boxes. Pale comb and wattles. Birds restless. feeds by sucking blood. which are external parasites of chickens and turkeys. carbamates.
Avian pneumovirus. Opinions vary as to whether adenovirus can be characterised as a primary respiratory pathogen.Abubakar. chloroform. Post-mortem lesions Mild catarrhal tracheitis. lesions. Infected birds may remain carriers for a few weeks. ammonia and other gases. Signs Mild snick and cough without mortality. Respiratory Disease Complex Introduction Respiratory infections in chicken and turkeys are seen worldwide but especially in temperate poultry-producing areas in winter months. It may occur as an exacerbating factor in other types of respiratory disease. Prevention Quarantine and good sanitary precautions. Dust. may act as 119 . Diagnosis History. intranuclear inclusions in liver.Tahir Respiratory Adenovirus Infection. and other factors associated with poor ventilation. prevention of immunosuppression. vaccinal and field strains) and bacteria (Ornithobacterium rhinotracheale. at least 12 sero-types have been described and these may be isolated from healthy chickens. coli) may be involved. Treatment None. E.M. The virus is generally resistant to disinfectants (ether. 'Mild Respiratory Disease' Introduction An adenovirus infection of chickens with a morbidity of 1-10% and a mortality of 1-10%. A number of respiratory viruses (Infectious Bronchitis. The virus grows well in tissue culture (CE kidney. formaldehyde and iodides work better. Lentogenic Newcastle disease virus. Transmission may be vertical and lateral. and by fomites. temperature. pH). CE liver).
Head swelling.predisposing factors. Figure 29. Differentiate from Chronic Respiratory Disease (Mycoplasmosis).catarrhal to purulent. Severe airsacculitis of thoracic air sacs in a broiler close to slaughter. Nasal exudate. be challenged by some of these pathogens). Rattling noises. sanitation of drinking water. Conjunctivitis. Airsacculitis. serology. Sneezing. mortality 5. carefully applied appropriate viral vaccines. Morbidity is typically 10-20%. If condemned birds are included mortality may be more than 10%. Given that many flocks are vaccinated it is necessary to establish normal serological response in vaccinated flocks in the absence of disease (some of which may. Signs Snick. There is also percarditis evident (at top right). Prevention Effective ventilation. Post-mortem lesions Severe tracheitis with variable exudate . The air sacs are thickened and congested. and have been cut into to reveal a cheesy (caseous) mass of pus. Diagnosis Lesions. of course. Pericarditis.10%. response to environmental changes. 120 . Treatment Antimicrobial treatment of specific bacterial infections.
There is an incubation period of 5-15 days. Lympoid Tumour Disease Introduction A retrovirus infection of chickens. Leg weakness. spleen and kidney. Treatment None. A gradual increase in mortality and poor growth in broilers may be the main signs. chick inoculation. Sometimes nodules in intestine and caecae. Post-mortem lesions Neoplastic lesions in liver. Sometimes enteritis and proventriculitis (especially in broilers infected with contaminated Marek's disease vaccine). Severe tracheitis is broilers with respiratory disease complex. Both tracheas were congested and the upper sample had mucopurulent material in the lumen. turkeys. Transmission is lateral and possibly transovarian. Signs There may be no obvious signs.Figure 30. Marked stunting when Marek's disease vaccine is contaminated. Diarrhoea. and the infection can be spread by mosquitoes or in contaminated Marek's disease vaccines. 121 . usually higher in females than males. Diagnosis Pathology. geese. and quail with morbidity up to 25%. Reticuloendotheliosis. ducks.
or Vitamin D or 25-hydroxy vitamin D in drinking water. Prevention Supplementation of vitamin D. Hock swelling. Post-mortem lesions Bones soft and rubbery. Birds go off legs.Prevention Formal control programmes have not been documented as the condition is sporadic and relatively self-limiting. Beak soft. Poor growth. Rickets (hypocalcaemic) Introduction Vitamin D deficiency or phosphorus/calcium imbalance is seen in chickens. Treatment Over-correct ration with three times vitamin D for 2 weeks. signs. Avoidance of contamination of live vaccines is the main control measure practised. 122 . Soft bones and beak. Femoral Head Necrosis. Epiphyses of long bones enlarged. lesions. Birds rest squatting. Reduction in bodyweight. Beading and fracture of ribs. proper calcium and phosphorus levels and ratio. Parathyroids enlarged. antioxidants. turkeys and ducks worldwide. Signs Lameness. Diagnosis History. Growth plates widened and disorganised. Differentiate from Encephalomalacia.
Abubakar. 123 . Soft bones and beak.Tahir Rickets (hypophosphataemic) Introduction Phosphorus deficiency in chickens. Intestinal diseases may reduce absorption. or vitamin D in drinking water. Epiphyses of long bones enlarged. Poor growth. Enlarged hocks. Some countries have regulations governing the use of phosphorus in fertiliser with a view to reducing water pollution. Parathyroids enlarged. 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. antioxidants. Growth plates widened and disorganised. Hock swelling. turkeys and duck is seen worldwide. Reduction in bodyweight.M. Signs Lameness. Birds rest squatting. Diagnosis History. Beading and fracture of ribs. Beak soft. Prevention Supplementation of Vitamin D. signs. Post-mortem lesions Bones soft and rubbery. Treatment Over-correct ration with 3 times vitamin D for 2 weeks. Birds go off legs. Even subclinical levels of this condition can predispose to Femoral Head Necrosis.
The parasite species vary: A.5 g faeces). guinea fowl. Virus may be found in asymptomatic birds. A. The route of infection is oral usually by direct ingestion of the embryonated egg and there is a 5-10-week prepatent period. Use of a good electrolyte solution is beneficial in the acute stage of infection. Post-mortem lesions Viruses replicate mainly in the mature villous epithelial cells. The life cycle is similar to that illustrated in the section on the caecal worm Heterakis. Prevention Good hygiene in brooding areas. and A. large . Signs Diarrhoea.submit 6 x . are nematode worm parasites. pheasants. Treatment No specific treatment for this infection. partridges and pigeons. galli in fowl. Roundworm. seen worldwide. except that the adults reside in the small intestine and earthworms are not significant paratenic or transport hosts.Ascaridia Introduction Ascaridia sp. The 124 . columbae in pigeons.M.Tahir Rotavirus Infection Introduction Rotavirus infection is seen in chickens. Diagnosis Demonstration of virus (PAGE. electron microscopy or Elisa on intestinal contents . Control of secondary bacterial enteritis may require antimicrobial medication.Abubakar. turkeys. The route of infection is oral and maximum viral excretion occurs 2-5 days post infection. shorter in young birds. stout white worms up to 12 cms in length. dissimilis in turkeys. It is not known if vertical transmission occurs though virus has been occasionally isolated from embryonated eggs. Adult birds can tolerate burdens asymptomatically.
pasture rotation and regular treatment. levamisole. A collection of mature roundworms (Ascaridia galli) recovered from the small intestine of a layer chicken in rear. Wasting. Treatment Flubendazole. 125 . Poor growth. Prevention Prevention of contamination of feeders and drinkers with faeces. especially for young birds. Signs Loss of condition. Worms up to 12 cm in length in duodenum and ileum. Diarrhoea. Figure 31. Listlessness. Post-mortem lesions Enteritis. oval smooth-shelled nonembryonated eggs in faeces.parasites may be transported by grasshoppers and earthworms and are resistant to environmental effects. Diagnosis Macroscopic examination with identification of worms. mainly in young birds. piperazine as locally approved. In the bottom left quadrant there are also some immature worms.
Ruptures of ligaments and joints are also occasionally seen.M. This can cause mortality in birds of any age. Chickens are most commonly affected but it also infects turkeys.Tahir Ruptured Gastrocnemius Tendon Introduction This is a condition causing severe lameness in roaster type meat chickens and more rarely in turkeys. Histology may be helpful in determining if there is an underlying inflammatory process. Prevention Establishment of a steady growth profile. Broiler parents and brown-shell egg layers are especially susceptible. Infections still occur worldwide in non-commercial poultry but are rare in most commercial systems now. Salmonella Gallinarum. Post-mortem lesions The fresh lesion contains a haematoma with the end of the ruptured tendon within or adjacent to it. Avoidance of physical stresses on the musculoskeletal system through careful handling as well as careful design and layout of equipment. canaries and bullfinches. Broiler chickens have an avascular area of tendon just above the hock that is the usual site of rupture. Affected birds should be culled humanely as soon as they are identified. The bird may have the hock dropped to the floor. 126 . guinea fowls. Diagnosis Signs and lesions are obvious. If there is a greenish tinge to the area of swelling it occurred a few days previously.Abubakar. Signs Severe lameness. Fowl Typhoid Introduction Disease caused by one of the two poultry-adapted strains ofSalmonella bacteria. game birds. sparrows. Reoviral or staphylococcal arthritis or tenosynovitis may predispose but many cases have no evidence of an inflammatory response. Salmonella Gallinarum. Treatment None. parrots.
Prevention Biosecurity. Ruffled feathers. clean chicks. surviving months. Engorgement of kidneys and spleen. Diagnosis Isolation and identification. even in adults. Signs Dejection. Enteritis of anterior small intestine. Tube and rapid plate agglutination tests have been the standard serological tests for many years but have only been validated for chickens. The route of infection is oral or via the navel/yolk. Yellow diarrhoea. pullorum disease and coli-septicaemia. tetracylines. McConkey and non-selective agar is advisable. Differentiate from Pasteurellosis. Enrichment procedures usually rely on selenite broth followed by plating on selective media. both live (usually based on the Houghton 9R strain) and bacterins. Vaccines for fowl typhoid have been used in some areas. but is susceptible to normal disinfectants. Thirst. recovered birds are resistant to the effects of infection but may remain carriers. Transmission may be transovarian or horizontal by faecal-oral contamination. 127 . Post-mortem lesions Bronzed enlarged liver with small necrotic foci. Reluctance to move. fluoroquinolones. mortality is increased in stressed or immunocompromised flocks and may be up to 100%. Anaemia. and/or congestion. potentiated sulponamide. egg eating etc. In clinical cases direct plating on Brilliant Green.Morbidity is 10-100%. Inappetance. The bacterium is fairly resistant to normal climate. LPS-based Elisa assays have been developed but not widely applied commercially. Treatment Amoxycillin. As with other salmonellae.
The liver on the left is normal. Closed eyes. Transmission may be transovarian or horizontal mainly in young birds and may sometimes be associated with cannibalism. Salmonella Pullorum. guinea fowls. Bacterial septicaemia caused by Salmonella Gallinarum. Morbidity is 10-80%. Lameness. sparrows. the one on the right is slightly enlarged. Occasionally it can cause losses in adult birds. It affects chickens most commonly. Gasping. but also infects turkeys. usually brown-shell egg layers. White diarrhoea.Figure 32. ring doves. this usually only causes mortality in birds up to 3 weeks of age. Pullorum Disease. surviving months but is susceptible to normal disinfectants. The route of infection is oral or via the navel/yolk. 'Bacillary White Diarrhoea' Introduction Disease caused by one of the two poultry-adapted strains ofSalmonella bacteria. Vent pasting. Depression. It still occurs worldwide in noncommercial poultry but is now rare in most commercial systems. Salmonella Pullorum. game birds. parrots. ostriches and peafowl. Signs Inappetance. Similar lesions can be seen in Pullorum Disease and with other causes of septicaemia in young chicks. Ruffled feathers. in young broiler chickens. mortality is increased in stressed or immunocompromised flocks and may be up to 100%. 128 . Loud chirping. The bacterium is fairly resistant to normal climate. pale and shows focal necrosis.
The route of infection is oral and transmission may be vertical as a result of shell contamination. fluoroquinolones. other enterobacteria. Sero-types vary. Regardless of the initial source of the infection. S. Vaccines are not normally used as they interfere with serological testing and elimination of carriers. Even if these infections do not cause clinical disease. Paratyphoid Infections Introduction Salmonellae bacteria other than the species specific sero-typesS. Newport. Differentiate from Typhoid. In clinical cases direct plating on Brilliant Green. are capable of causing enteritis and septicaemia in young birds. They infect chickens. Prevention Eradication from breeder flocks. in the environment or in rodent populations. chilling and omphalitis Treatment Amoxycillin. Gallinarum. Splenomegaly. As with other salmonellae. recovered birds are resistant to the effects of infection but may remain carriers. fomites and feed (especially protein supplements but also poorly stored grain). turkeys and ducks worldwide. and also other than S. McConkey and non-selective agar is advisable. but S. Diagnosis Isolation and identification. Paratyphoid.Post-mortem lesions Grey nodules in lungs. poteniated sulponamide. liver. it may become established on certain farms. Urate crystals in ureters. Intestinal or caecal inflammation. Montevideo. paracolon. Bredeney are among the more common isolates. Derby. Anatum. Certain sero- 129 . Pullorum. Enteritidis andS. S. S. S. Many species are intestinal carriers and infection is spread by faeces. S. Caecal cores. tetracylines. Salmonellosis. gizzard wall and heart. Morbidity is 0-90% and mortality is usually low. their presence may be significant with respect to carcase contamination as a potential source of human food poisoning. Enrichment procedures usually rely on selenite broth followed by plating on selective media. Typhimurium (which are considered separately).
Treatment Sulphonamides. other bacterial infections and ornithosis (in ducks). Post-mortem lesions In acute disease there may be few lesions. Rappaport-Vassiliadis) followed by plating on two selective media will greatly increase sensitivity. Dehydration. Diarrhoea. amoxycillin. Dejection. Unabsorbed yolk. Vent pasting. Differentiate from Pullorum/Typhoid. Ruffled feathers. This approach is often used in the heat treatment of feed. The bacteria are often persistent in the environment. Predisposing factors include nutritional deficiencies. Diagnosis Isolation and identification. Signs Signs are generally mild compared to host-specific salmonellae. Enteritis. Chemotherapy can prolong carrier status in some circumstances. fluoroquinolones. chilling. Loss of appetite and thirst.g. Senftenberg in hatcheries). neomycin. especially in dry dusty areas.types are prone to remain resident in particular installations (e. Good management. Enrichment media such as buffered peptone followed by selective broth or semi-solid media (e. In clinical cases direct plating on Brilliant Green and McConkey agar may be adequate. other enterobacteria. S. Pericarditis. inadequate water. tetracyclines. Cheesy cores in caecae. or absent. Focal necrotic intestinal lesions. Closed eyes. However this has the potential to reveal the presence of salmonellae that are irrelevant to the clinical problem under investigation. Foci in liver. but are susceptible to disinfectants that are suitable for the particular contaminated surfaces and conditions. Temperatures of around 80°C are effective in eliminating low to moderate infection if applied for 1-2 minutes. applied at sufficient concentrations.g. 130 .
especially phage type 4. Routine monitoring of breeding flocks. but are susceptible to disinfectants that are suitable for the particular contaminated surfaces and conditions. mills. The route of infection is oral. these bacteria are often specifically cited in zoonosis control legislation. fomites and on eggshells. Enteritidis and S. secondly. clean nests. good feed. turkeys and ducks cause problems worldwide with morbidity of 0-90% and a low to moderate mortality. especially in dry dusty areas. Infections in chickens. fumigate eggs. Infection results in a strong immune response manifest by progressive reduction in excretion of the organism and reduced disease and excretion on subsequent challenge. and. chilling. many species are intestinal carriers and infection may be carried by faeces. This approach is often used in the heat treatment of feed. Temperatures of around 80°C are effective in eliminating low to moderate infection if applied for 1-2 minutes. Feed and feed raw material contamination is less common than for other sero-types.Typhimurium are presented separately from other sero-types of Salmonella because. competitive exclusion. on the one hand. Salmonella Enteritidis. 131 . S. Many infected birds are culled and others are rejected at slaughter. Vertical transmission may be either by shell contamination or internal transovarian contamination of yolk. Predisposing factors include nutritional deficiencies.Prevention Uninfected breeders. care in avoiding damage to natural flora. hatcheries and feed mills is required for effective control. Typhimurium infections Introduction Salmonella Enteritidis and S. elimination of resident infections in hatcheries. The prevalence of S. has become much more common in both poultry and humans since the early 80s. because there are differences in the epidemiology as compared to other salmonellae. Salmonellosis. Vaccines are not generally used for this group of infections. all-in/all-out production. The bacteria are often persistent in the environment. applied at sufficient concentrations. These are the predominant sero-types associated with human disease in most countries. inadequate water and other bacterial infections.Typhimurium has remained relatively stable though the spread of the highly antibiotic-resistant strain DT104 in various farmed species gives some reason for concern. breeding and grow-out farms.
It is possible to detect reactions with specific antigens in agglutination tests but competitive and direct Elisa tests are more commonly used today.Pullorum serum agglutination tests. Dehydration. fluoroquinolones in accordance with the sensitivity. In clinical cases direct plating on Brilliant Green and McConkey agar may be adequate. all-in/all-out production. Chemotherapy can prolong carrier status in some circumstances. Diarrhoea. Vent pasting. coli. clean nests. Stunting in older birds. elimination of resident infections in hatcheries. Lost of appetite and thirst.E. neomycin. hatcheries and feed mills is required for effective control. Unabsorbed yolk. good feed. Prevention Uninfected breeders. Early depletion of infected breeding stock is required in some countries such as those of the European Union. Foci in liver. Perihepatitis. breeding and grow-out farms. care in avoiding damage to natural flora. amoxycillin. tetracyclines.g. mills. Pericarditis. Cheesy cores in caecae. However this has the potential to reveal the presence of salmonellae that are irrelevant to the clinical problem under investigation. S. Focal necrotic intestinal lesions. Enrichment media such as buffered peptone followed by selective broth or semi-solid media (e. Infection 132 . Misshapen ovules in the ovaries in S. Enteritis. Rappaport-Vassiliadis) followed by plating on two selective media will greatly increase sensitivity. Routine monitoring of breeding flocks.Enteritidiscauses cross-reactions which may be detected with S. Differentiate from Pullorum/Typhoid. other enterobacteria such as E. Ruffled feathers.Signs Dejection. Post-mortem lesions In acute disease there may be few lesions. infection Diagnosis Isolation and identification. Treatment Sulphonamides. fumigate eggs. competitive exclusion. Good management. Closed eyes.
Anything that damages the epithelium or disturbs normal oviduct motility is likely to increase the likelihood of salpingitis. coliand occasionally Salmonella spp. Systemic viral infections that cause ovarian regression or damage to the oviduct or cloaca. 133 . It is a complex condition of chickens and ducks associated with various infections including Mycoplasma and bacteria (especially E. or may proceed upwards from the cloaca. Diagnosis Use the signs to select birds for culling and post-mortem investigation. The control of infection in this area is probably achieved by ciliated epithelium that mostly wafts a carpet of mucus towards the cloaca. May form a multi-layered caseous cast in oviduct or be amorphous. Vaccines are increasingly being used for S. Bacteriology of oviduct. which normally has many millions of potentially pathogenic bacteria. Death. both inactivated (bacterins) and attenuated live organisms. are especially prone to increasing salpingitis. The oviduct is a hollow tube joining the normally sterile environment of the body cavity with the cloaca. Typhimurium infection. leaking urates. Post-mortem lesions Slight to marked distension of oviduct with exudate. Infection may spread downwards from an infected left abdominal air sac. Signs Sporadic loss of lay. Damaged vents.). Enteritidis and S.results in a strong immune response manifest by progressive reduction in excretion of the organism and reduced disease and excretion on subsequent challenge. Some birds may 'lay' a caseous mass of pus (which may be found in a nest or on the egg belt). Salpingitis Introduction Salpingitis is an inflammation of the oviduct. Lesions. Distended abdomen. Peritonitis.
Treatment Birds with well-developed lesions are unlikely to respond to medication. Shaking or quivering of legs after rising. use healthy parent flocks. 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. Signs Stand on toes shaking. Diagnosis Clinical examination. possibly associated with tendon injury. aspirin may be helpful if locally approved. Morbidity is 10-20%. 134 . Shaky Leg Syndrome Introduction A condition of turkeys with a course of often 3-4 weeks. releasing poults into larger areas and in handling heavier birds. immunise effectively against respiratory viral pathogens common in the area. exclusion of other problems. Post-mortem lesions None. Treatment Multivitamins. Prevention Care in transport of brooded poults.
135 . This appears to be a multifactorial condition. Dehydration. Prevention Good sanitation of the brooding house. and/or carbohydrate absorption are disturbed resulting in a hypoglycaemia. Mortality drops off as sharply as it started. Provide multivitamins. Treatment Leave affected chicks undisturbed. Minimise stress. suggesting a viral component. Signs and lesions. Males are more susceptible than females. Signs Tremor. Feed intake. Avoidance of physical stress. Filtered intestinal contents from affected flocks appear to be capable of reproducing the condition. Death. electrolytes and glucose solution to flock. Excess fluid in lower small intestine and caecae. Orange mucoid droppings. Birds in good condition die after showing neurological signs. Diagnosis Pattern of mortality. typically 7-14day-old. rapidly growing broiler chickens. Paralysis. 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. probably because they are growing faster.Spiking Mortality of Chickens Introduction This is a condition characterised by a sudden increase in mortality in young. Avoidance of interruptions in feed supply. Post-mortem lesions Mild enteritis. Coma.
Mucoid enteritis.g. isolate in chicken eggs or chicks or poults. The bacterium is poorly resistant outside host but may be carried by Argas persicus for 430 days. reduced egg production. grouse and canaries with morbidity and mortality up to 100%. is an intestinal spirochaete that can be associated with inflammation of the large intestine in a broad range of mammals and birds. Drops in egg production may be seen in both systemic and intestinal forms Post-mortem lesions Marked splenomegaly. and egg soiling in chickens. pheasants. Argas persicus. 136 . Treatment Various antibiotics including penicillin. Signs Depression. Thirst. Necrotic foci. Diagnosis Haematology. Prevention Control vectors. turkey. geese. ducks. Spleen mottled with ecchymotic haemorrhages. It is transmitted by arthropods. It has been associated with typhilitis. Liver enlarged with small haemorrhages. and occasionally by infected faeces. diarrhoea. vaccines in some countries. e. Often diarrhoea with excessive urates. Brachyspira pilosicoli. previously known as Serpulina pilosicoli.Spirochaetosis Introduction The bacterium Borrelia anserina infects chickens. Weakness and progressive paralysis. Cyanosis.
137 . Figure 33. Treatment None. with rotation of the body of the vertebra and the pinching of the spinal column that causes paralysis. That on the left shows the typical lesion of spondylolisthesis.Tahir Spondylolisthesis.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. legs extended forward. Diagnosis Symptoms. These are cross-sections of the spinal column of 4-5-weekold broilers. Prevention Selection for satisfactory conformation in primary breeding. lesions. 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. May walk backwards. Use of wings to help in walking.Abubakar.
aureus and seen in chickens and turkeys worldwide. Treatment None. and careful monitoring of incubation conditions.Abubakar. These include good breeder nutrition. Wounds. Morbidity is usually low and mortality 0-15% though affected birds will often be culled on humane grounds. and toe trimming may be a portal of entry with subsequent spread via the bloodstream to the typical sites of lesions. Staphylococcosis. The type of chick box liners and the feeding papers used in the brooding house can also influence the occurrence of the condition. Infection is usually by the respiratory route with an incubation period of 2-3 days seen after artificial infection. Damaged skin due to nutritional deficiencies (such as of biotin) may also be a point of entry. Prevention All measures that improve chick vitality at hatching are beneficial in reducing this problem. avoidance of excessive hatching egg storage. 138 . Post-mortem lesions Gross lesions are not usually evident. Diagnosis Clinical signs. Staphylococcal Arthritis.Tahir Spraddle Legs or Splay Leg Introduction Occurs in all species in the recent hatchling. either accidental or induced by interventions such as beak trimming.M. Signs Legs splay and chick is unable to stand. mainly S. Bumble Foot Introduction Caused by Staphylococcus bacteria.
g. Competitive exclusion with a non-pathogenic Staphylococcushas been shown to be effective (no commercial products yet available based on this technology). and by fomites. the hatchery and in any intervention or surgery (processing. Recovered birds may have some immunity but vaccination with staphylococci has not been found to be helpful in preventing the disease to date. particularly of parent birds. Swollen above the hock and around the hocks and feet. Predisposing factors include reovirus infection. This may progress to abscess formation in these areas.. Treatment Antibiotics. Mycoplasma spp. Lameness. Possibly vaccination against reovirus infection. Good management. Diagnosis Lesions. Some sudden deaths from acute septicaemia if very heavy challenge. toe clipping). e. Streptococcus bovis Septicaemia Introduction An infection of ducks with the bacterium Streptococcus bovis. 139 . low stress and prevention of immunosuppression from any cause will all tend to help. trauma. and imunosuppression. most commonly in the plantar area of the foot or just above the hock joint. Signs Ruffled feathers. Prevention Good hygiene in the nest. in accordance with sensitivity. Low mobility. Post-mortem lesions Tenosynovitis.. chronic stress. Salmonella spp. Differentiate from septicaemia or tenosynovitis due to Colibacillosis. This condition is a cause of sudden deaths in ducklings of 2-3 weeks of age. Infected joints may have clear exudate with fibrin clots. isolation and identification of pathogen. synoviae.Transmission occurs in the hatchery and in the general farm environment. especially M.
The atria of the heart have blood. Treatment Amoxycillin. Post-mortem lesions Beak cyanosis. Serum accumulation in lung (may be little if examined shortly after death). Leg weakness or incoordination in a few birds.Signs Sudden deaths. Signs Sudden death in convulsion. Livers heavier than those of pen-mates (as a percentage of bodyweight. Sudden Death Syndrome. 140 . Diagnosis History. Post-mortem lesions Intestine filled with feed. It can be induced by lactic acidosis and about 70% of birds affected are males. possibly metabolic. extra care in the immediate post-brooding period. Splenic hyperplasia. lesions. isolation. Liver congestion. the ventricles are empty. Affected well-grown birds may appear to have died from smothering. 'Flipover' Introduction A condition of broiler chickens of unknown cause. Prevention Good husbandry and hygiene.). most are found lying on their back.affected birds respond well to saline injection and will actively seek out salt scattered in the litter. Lung congestion and oedema. Sodium deficiency can appear very similar at about the same age . Haemorrhages in muscles and kidneys.
use of dawn to dusk simulation and avoidance of disturbance. Treatment None possible. Prevention Control the intermediate hosts. Check your local regulations. they may not be host specific. Treatment Flubendazole is effective at a 60 ppm in diet. Prevention Lowering carbohydrate intake (change to mash). feed restriction. 141 .Diagnosis Birds found on back with lack of other pathology. Most have intermediate invertebrate hosts such as beetles or earthworms. Post-mortem lesions Occupy space in intestine and create small lesions at point of attachment. however it may not have a zero withdrawal in commercial egg layers. Cestodes Introduction Cestodes are tapeworms that are seen in many species. Diagnosis Identification of the presence of the worms at post-mortem examination. or birds' access to them. Tapeworms. lighting programmes. Signs It is doubtful if any signs are produced under most circumstances. low intensity light.
chloride levels and acid/base balance. Vitamin D3 supplementation. Prevention Genetic selection using the Lixiscope to identify bone phenotype. Swelling and bowing in the region of the knee joints. Post-mortem lesions Plug of cartilage in proximal end of tibia. in decreasing order of frequency. small ovoid lacunae and more matrix than normal. Microscopically . It may be associated with rapid growth and have a nutritional factor.a mass of avascular cartilage with transitional chondrocytes.Figure 34. Lixiscope may identify in vivo as early as 2 weeks of age. Signs There are usually no signs unless the condition is severe. Tibial Dyschondroplasia. turkeys and ducks. Differentiate from rickets. mild lesions may require histology to distinguish from other problems. modifications of calcium and phosphorus ratios. and proximal metatarsus. Diagnosis Gross pathology. Lameness. TD Introduction A complex condition seen in chickens. Mature tapeworms with their heads (scolices) embedded in the intestine. 142 . Treatment None. distal tibia.
than in commercial poultry in temperate climates. The infection is seen in turkeys and sometimes pheasants. It is more common in warm climates. Transmissible Enteritis.Tahir Ticks Introduction Argas persicus is an external parasite of poultry and wild birds. Weakness. and is also found on mammals. Reduced productivity. Transmission is lateral with birds and faeces. Insecticide sprays in these areas are more likely to be effective than treatment of the birds. Occasionally paralysis from toxins in the tick saliva. others are avian coronaviruses closely related to infectious bronchitis virus.Abubakar. Prevention As for red mite control. Diagnosis Identification of the presence of the parasites. These parasites are more likely to be a problem of small scale poultry production in the tropics. Treatment Elimination of cracks and crevices in the poultry housing. Morbidity is close to 100% and mortality is 5-100%. Signs Anaemia. Post-mortem lesions Anaemia. Bluecomb Introduction Some coronaviruses involved in this condition are considered to be bovine coronaviruses (or closely related thereto). and may also transmit spirochaetosis and Pasteurella infection.M. spends little time on host. Emaciation. with 143 . Skin blemishes.
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.
Eggs depigmented and thin-shelled. Prevention All-in/all-out production. isolation of ciliostatic agent. Turkey Rhinotracheitis (Adult) Introduction A disease of turkeys caused by the viruses of the Pneumovirus genus. Ocular and nasal discharge. maternal antibody may protect. Morbidity is 10-100% and mortality 1. control respiratory stressors. chlorination of drinking water.live primer followed by inactivated. control respiratory stressors. Post-mortem lesions Serous rhinitis and tracheitis. Prevention All-in/all-out production. vertical transmission is uncertain. possibly involving fomites.Antibiotics are not very effective. Serology. Diagnosis Signs. Signs Decreased appetite. 147 . Paramyxoviridae. chlorinate drinking water.30%. Loss of voice. Treatment Antibiotics are not very effective. Rapid transmission occurs laterally. Good drinking water hygiene. vaccination . Sudden drop in production that lasts 2-3 weeks.
Tahir Turkey Rhinotracheitis (in rear) Introduction A disease of turkeys caused by the viruses of the Pneumovirus genus. Dyspnoea. maternal antibody may protect. Turkey Viral Hepatitis Introduction An infection of turkeys caused by an unidentified virus. Transmission may be by direct or indirect contact and possibly vertical. Sinusitis. Morbidity varies. If there is secondary E. Ocular and nasal discharge. sometimes pus in bronchi. possibly involving fomites. Prevention All-in/all-out production. Rapid transmission occurs laterally.M. Paramyxoviridae. Snick. airsacculitis and perihepatitis. control respiratory stressors.30%. mortality is 1-25%. Post-mortem lesions Serous rhinitis and tracheitis. 148 . Vaccination at day-old seems to be most effective. Signs Decreased appetite.Abubakar. coli infection then pneumonia. serology (using an Elisa test to demonstrate rising titre). Morbidity is 10-100% and mortality 1. Loss of voice. Birds remain carriers for up to 16 days. isolation and identification of the ciliostatic virus. chlorinate drinking water. weight gain and feed efficiency. vertical transmission is uncertain. Diagnosis Clinical signs. Conjunctivitis. Treatment Antibiotics are not very effective.
Bile staining. Post-mortem lesions Grey foci (c. Twisted leg Introduction A complex condition seen in chickens and turkeys. Factors involved may include genetics. Valgus/varus. Focal haemorrhage. Morbidity is 1-20% and mortality is low. Signs Lameness. Congestion. Depression and sporadic deaths in birds in good condition. Prevention Good sanitation and management. environment and high growth rate. Post-mortem lesions Linear twisting of growth of long bones. 149 . Various angulations of leg. with good management many birds recover. Gastrocnemius tendon may slip. lesions pathognomonic. Grey to pink foci in the pancreas.no inclusion bodies.Signs Signs are usually subclinical. 1 mm) coalescing. Microscopically . Differentiate from histomonosis. bacterial and fungal infections. nutrition. Diagnosis Isolation in CE. Distortion at hock. Treatment None.
intertarsal angulation up to 10% is physiological. lesions. The condition occurs worldwide. E. brunetti). Anaemia. Treatment None. arthritis and synovitis. Pale yellow membranes. Ruffled feathers. Turkeys. Partially closed eyes. Prevention Selection for good conformation in primary breeding. greater than 20% is abnormal. Quail disease Introduction Ulcerative Enteritis is an acute. Differentiate from perosis. and E.. Signs Listlessness. necatrix. Diarrhoea. but mainly ileum and caecae. Diagnosis Symptoms. highly contagious disease of chickens and quail caused by the bacterium Clostridium colinumand characterised by ulcers of the intestines and caecae. It can start suddenly and cause high mortality: 100% in quail and 10% in chickens. Watery white faeces (quail). tenella. 150 . IBDV and overcrowding. Post-mortem lesions Deep ulcers throughout intestine. Adoption of optimal nutrition and growth patterns for the economic objectives of the production system. The bacterium resists boiling for 3 minutes. game birds and pigeons may also be affected. Drooping wings. Blood in intestine. The route of infection is oral and transmission is from faeces of sick or carrier birds or via flies. which may coalesce and may be round or lenticular. Predisposing factors include Coccidiosis (especially E. Retracted neck. Ulcerative Enteritis. Changed angulation of tibial condyles. Peritonitis (if ulcers penetrate).
Differentiate from histomonosis ('Blackhead'). Signs Dejection. amoxycillin. coccidiosis. birds remaining carriers for months. Wall of the caecum of a chicken suffering from ulcerative enteritis Vibrionic Hepatitis. Morbidity is low. Treatment Streptomycin (44 gm/100 litres water). Bacitracin. salmonellosis. Diagnosis A presumptive diagnosis may be made on history and lesions. Treat for coccidiosis if this is a factor. Loss of condition. low level antibiotics as per treatment. colinum in anaerobic conditions (the agent is often present in pure culture in liver). all-in/all-out production. The infective agent is rather resistant to environment and disinfectants. Prevention Infection-free birds. Avian Infectious Hepatitis Introduction An insidious onset disease of chickens caused by Vibrio bacteria. Figure 35. and disease is precipitated by stress. 151 . possibly probiotics. Transmission is by faecal contamination. Tetracyclines. penicillin (50-100 ppm in feed). necrotic enteritis. Necrotic foci in liver. multivitamins. Response to treatment should occur in 48 to 96 hours. trichomoniasis. Inappetance. Diarrhoea. Confirmation is on absence of other diseases and isolation of Cl.
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.
M. lesions. classic signs of deficiency are very rare in commercial poultry fed complete diets. Pustules in mouth and pharynx. Eyelids stuck shut with thick exudate. Differentiate from Infectious coryza. Pale comb and wattles. Post-mortem lesions Eyelids inflamed and adhered. antioxidant. Excessive urates in kidneys and ureters. Treatment Vitamin A in drinking water. Poor feathering. Prevention Supplementation of diet with vitamin A. good quality raw materials.Tahir Vitamin A Deficiency. Nutritional Roup Introduction Vitamin A deficiency is occasionally seen in chickens and turkeys (insufficient vitamin A during 1-7 weeks of age). Diagnosis Signs. Microscopically . infectious sinusitis etc. As in the case of other nutritional deficiencies.squamous metaplasia of epithelia. chronic fowl cholera. Signs Poor growth. feed formulation. Nasal and ocular discharge. 155 .Abubakar. Drowsiness.
damage to the intestine or increased demand for some reason may have an effect. Most will reduce productivity. exclusion of specific diseases.Abubakar. Diagnosis Signs. including growth in the young animal.M. Simple deficiency is now rare as diets are usually well supplemented. Vitamin deficiencies are especially prone to cause problems of hatchability. 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. See the separate discussion under Chondrodystrophy and Fatty Liver and Kidney Syndrome. and egg production in the layer. The embryo is particularly dependent on having adequate supplies of vitamins deposited in the egg.Tahir Vitamin B Deficiencies Introduction The B complex vitamins are water soluble and not stored to any significant extent in the body. Some deficiencies induce characteristic microscopic effects. They act in a broad range of metabolic pathways. response to supplementation. because a continuous supply is required. However. 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 .
less expensive) to analyse feed for a marker substance such as manganese rather than testing for vitamin levels. Post-mortem lesions Swollen cerebellum with areas of congestion. Encephalomalacia. occasionally ducklings and other birds. Steatitis. The problem is associated with feed rancidity typically in diets with high fat. Exudative Diathesis. Haemorrhage.may be appropriate (faster. Staggering. Ventral oedema. seen worldwide. Signs Imbalance. Falling over. 157 . Treatment If a specific vitamin deficiency is suspected. Vitamin E Deficiency. Muscular dystrophy is seen more frequently in older and mature birds. Necrosis. White streaks in muscle. characterised by oxidation of various tissues and caused by Vitamin E deficiency. Green wings. Paralysis. drinking water supplementation with that vitamin is ideal and usually results in a rapid response in birds that are still drinking. The balance of vitamins present should be similar to the daily nutritional requirement of the stock concerned. Muscular Dystrophy Introduction A spectrum of diseases of chickens and turkeys. Uncontrolled movements. Good quality multivitamin solutions are beneficial in the supportive care of a range of problems characterised by reduced feed intake. 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. Blood-stained or greenish subcutaneous oedema. Encephalomalacia and exudative diathesis tends to be seen in young birds of 1-5 weeks of age.
Loss of appetite. selenium. Omphallitis Introduction A condition seen worldwide in chickens. It is seen where there is poor breeder farm nest hygiene. lesions. 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. consistency) that vary according to the bacteria involved. antioxidant. Prevention Proper levels of vitamin E. 158 . Closed eyes. Differentiate from Encephalomyelitis. turkeys and ducks due to bacterial infection of the navel and yolk sac of newly hatched chicks as a result of contamination before healing of the navel. Signs Dejection. toxicities. Various bacteria may be involved. especially E . Yolk Sac Infection.coli. response to medication. Disease occurs after an incubation period of 1-3 days. Morbidity is 1-10% and mortality is high in affected chicks. inadequate hatchery hygiene or poor incubation conditions. histopathology. hatchers or chick boxes. Swollen abdomen. Vent pasting. necrotic dermatitis. good quality raw materials.Diagnosis Signs. Treatment Vitamin E and/or selenium in feed and/or water. Pseudomonas. for example poor hygiene of hatching eggs. Broad-spectrum antibiotics where there are extensive skin lesions. Post-mortem lesions Enlarged yolk sac with congestion. Staphylococci. Abnormal yolk sac contents (colour. Diarrhoea. and poor hygiene of setters.Proteus. 'bangers'. feed rancidity. use of floor eggs.
clean nests. exclusion of severely soiled eggs. There should be routine sanitation monitoring of the hatchery. most will die before 7 days of age. frequent collection. Multivitamins in the first few days may generally boost ability to fight off mild infections. Confirmation is by isolation and identification of the bacteria involved in the internal lesions. sanitation of eggs. Treatment Antibiotics in accordance with sensitivity may be beneficial in the acute stages. however the prognosis for chicks showing obvious signs is poor. Differentiate from incubation problems resulting in weak chicks. separate incubation of floor eggs etc.Diagnosis A presumptive diagnosis is based on the age and typical lesions. 159 .g. Prevention Prevention is based on a good programme of hygiene and sanitation from the nest through to the chick box (e.
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