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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.
adequate protection. Post-mortem lesions Enlarged mottled liver. Blindness. Paralysis. and is not present in the UK turkey population. Erosions of the cartilage of the hock joint in a duck with chronic Riemerella anatipestifer infection. Cheesy plugs in intestine or caecum. transovarian. Vent-pasting. through faecal contamination of environment. correct house relative humidity. Huddling near heat. from long-term intestinal carriers. Arizonosis Introduction Caused by the bacterium Arizona hinshawii. and also horizontal. Nervous signs. Signs Dejection. Inactivated and attenuated vaccines available in some countries. Autogenous bacterins sometimes used. 'hardening off'. Figure 40. renamed Salmonella Arizonae. rodents. Mortality is 10-50% in young birds. rigid depopulation and disinfection. feed etc. It affects turkeys. Unabsorbed yolk sac. Transmission is vertical. mainly in North America. older birds are asymptomatic carriers. reptiles. Diarrhoea. 4 .Prevention Good husbandry and hygiene. Arizona infection. sulphonamides in feed. cloudiness in eye. Congestion of duodenum. Inappetance. Foci in lungs.
Differentiate from Treatment Injection of streptomycin. Formerly in-feed medication with nitrofurans was also used. Perihepatitis. Progressive weakness and abdominal distension. may be related to type of stock and strain). or gentamycin at the hatchery is used in some countries. fumigation of hatching eggs. Recumbency. Possibly cyanosis. Ophthalmitis. Morbidity is usually 1-5%. poor ventilation and physiology (oxygen demand. Pericarditis. spectinomycin. Diagnosis Isolation and identification. 5 . coli-septicaemia. Pulmonary arterial vasoconstriction appears to be the main mechanism of the condition. Dilation of the ventricle. inject eggs or poults with antibiotics. Severe muscle congestion. mortality 1-2% but can be 30% at high altitude. Signs Sudden deaths in rapidly developing birds. General venous congestion. methods as per Salmonella spp. The disease has a complex aetiology and is predisposed by reduced ventilation. good nest and hatchery hygiene. high altitude. Lungs and intestines congested. Salpingitis. Prevention Eradicate from breeder population. Ascites is a disease of broiler chickens occurring worldwide but especially at high altitude. Ascites Introduction Associated with inadequate supplies of oxygen. Dyspnoea. monitor sensitivity. Thickening of atrioventricular valve. Post-mortem lesions Thickening of right-side myocardium. salmonellosis. Poor development. and respiratory disease.
The fungus can infect plant material and many species of animals including birds and man. Microscopic . Aspergillosis Introduction A fungal infectious disease. Mortality among young affected birds is 5-50%. Diagnosis Gross pathology is characteristic. avoid any genetic tendency. Drowsiness. Silent gasping. Treatment Improve ventilation. Vitamin C (500 ppm) has been reported to be of benefit in South America. Ascites. turkeys. penguins. worldwide. Liver enlargement. The infection has an incubation period of 2-5 days. Thirst. It affects chickens. 6 . game birds. A cardiac specific protein (Troponin T) may be measured in the blood. waterfowl. This may offer the ability to identify genetic predisposition. in which the typical sign is gasping for breath. control respiratory disease. Rapid breathing.cartilage nodules increased in lung. Morbidity is usually low. Spores are highly resistant to disinfectants. Weakness. caused by Aspergillus fumigatus. Pericardial effusion. Sometimes the same organism causes eye lesions or chronic lesions in older birds. especially in young chicks. Occasionally similar lesions are produced by other species ofAspergillus or even other fungi such as Penicillium. Differentiate from broiler Sudden Death Syndrome and bacterial endocarditis. Transmission is by inhalation exposure to an environment with a high spore count. Spleen small. etc. but may be as high as 12%. Absidia etc. Nervous signs (rare). Signs Acute form: Inappetance. there is usually little bird-to-bird transmission. ducks. Prevention Good ventilation (including in incubation and chick transport).
Morbidity 5-60%. preferably after digestion in 10% potassium hydroxide.Tahir 2 Chronic Forms: Ocular discharge (ocular form only). The means of transmission is unknown but 7 . Diagnosis This is usually based on the signs and lesions and microscopic examination for the fungus. It affects chickens. 'Furry' airsacculitis in aspergillosis of an adult duck. mortality none. hygiene. Environmental spraying with effective antifungal antiseptic may help reduce challenge. Differentiate from excessive exposure to formalin or vaccinal reactions in day olds and from heat stress in older birds. air sacs.Abubakar. Amphotericin B and Nystatin have been used in high-value birds. Avian Encephalomyelitis Egg Drop Introduction Avian encephalomyelitis virus infection in laying bird causes inapparent infection or drops in egg production. typically by putting small pieces of affected tissue on Sabouraud agar. pheasants and occurs in most poultry-producing countries. Thiabendazole or Nystatin has been used in feed. Conjunctivitis/keratitis. Prevention Dry. Epidemic tremors for its effect in young birds. quail. plaques in peritoneal cavity. Wasting. Figure 8. Growth occurs in 24-48 hours and colonies are powdery green/blue in appearance. may have greenish surface. See Avian Encephalomyelitis. The powdery surface is dark green in colour. good quality litter and feed. Post-mortem lesions Yellow to grey nodules or plaques in lungs. turkeys. It may be confirmed by isolation of the fungus. Treatment Usually none.M. Brain lesions may be seen in some birds with nervous signs. trachea.
some lateral. small (5-10%) and lasting no more than 2 weeks. pheasants. Post-mortem lesions None. lentogenic Newcastle disease. Ataxia and sitting on hocks. Prevention Vaccination of breeders/layers at 9-15 weeks. turkeys. Signs Nervous signs. Differentiate from Infectious Bronchitis. Avian Encephalomyelitis. The route of infection is transovarian with an incubation period of 1-7 days. lateral transmission is probably by the oral route. Imbalance. Dull expression. incubation >10 days. Virus in faeces may survive 4 weeks or more. Epidemic Tremors Introduction Avian encephalomyelitis is a viral disease of the central nervous system of chickens. Serology . Paralysis. EDS76. now Elisa is used more commonly. Treatment None. Vertical transmission is very important. 8 . Virus in faeces may survive 4 weeks or more.probably by faecal contamination of environment. rising titre to AE virus. Signs Drop in egg production. Predisposed by immunosuppression. and quail. water etc. subsequent disease in progeny if breeders. It has a worldwide distribution. and there is serious disease in the progeny (see next section). attenuated or not.The embryo protection test has been used in the past. In breeders there may be a drop in hatchability of about 5%. feed. with an oral infection route. Morbidity 5-60% depending on the immune status of the majority of parents. mortality high. transmission occurs over about 1-2 weeks. Immunity is usually long lasting. Diagnosis History.
toxicities. Effectively all 9 . pigeons.nonpurulent diffuse encephalomyelitis with perivascular cuffing. A few recovered birds may develop cataracts weeks after infection. vitamin deficiency (E. Highly pathogenic forms are usually of the H groups 5 and 7 and may now be identified (if H5 or H7) by the presence of a sequence at the haemagglutinin cleavage site that codes for multiple basic amino acids. and/or viral isolation may be carried out if required. turkeys. Tremor may be inapparent but is accentuated if chicks are held inverted in the hand. Enterococcus hirae infection. Microscopic . Differentiate from Newcastle disease. Histopathology is usually diagnostic and IFA. neck and wings. Avian Influenza-Highly Plague Introduction Pathogenic (HPAI). and isolates are designated sero-type/ species/location/reference number/year/subtype designation(H/N). especially in turkeys. Fowl One of only two 'Class A' diseases of poultry targeted for emergency disease control measures by OIE. ducks. and lack of significant lesions. The definitive classification of high pathogenicity is an intravenous pathogenicity test (IVPI) in 6-week-old chickens result of greater than 1. The embryo protection test has been used in the past. Immunity is long lasting. attenuated or not. The virus infects chickens. now Elisa is used more commonly. Tremor of head. the equivalent of the World Health Organisation for animal diseases. The cause is a virus. Marek's disease. EE (especially in pheasant in the Americas). The higher the proportion of the chickens dying or showing signs the higher the IVPI. This is a test in which the virus is inoculated into susceptible chickens that are then kept under observation. and ostriches. riboflavin). Diagnosis A presumptive diagnosis is based on the history. Mycotic Encephalitis. Treatment None. Prevention Vaccination of breeders at 9-15 weeks. partridges. Brain abscess. This viral disease can cause exceptionally high mortality. signs.2 . Orthomyxovirus type A. In addition official control measures disrupt trade in poultry products from affected areas. its pathogenicity is variable. pheasants. quail. There may be focal white areas in gizzard muscle (inconstant). Post-mortem lesions Gross lesions are mild or absent. A.
reduced feed consumption. Transmission is by direct contact with secretions from infected birds. Coughing. drinking water. Pasteurella) may increase mortality. and the high mortality that 'low-path' AI can cause in turkeys. can survive 4 days in water at 22°C. More recently outbreaks have occurred in Australia. in northern Italy. by oxidising agent and by formalin and iodine compounds. air sacs and conjunctiva. The small number of human deaths associated with HPAI appear to have resulted from direct exposure to infected birds on farm or in markets. but possibly by the conjunctival or respiratory route and the incubation period is 3-5 days. Nasal and ocular discharge. Morbidity is high but mortality usually relatively low. Drops in egg production. Broken contaminated eggs may infect chicks in the incubator simulating vertical transmission. The virus replicates mainly in respiratory tissues of chickens and turkeys but in the intestinal tract of clinically normal waterfowl. over 30 days at 0°C. Mexico and. equipment. Depression. Post-mortem lesions Inflammation of sinuses. Avirulent in one species may be virulent in others. Cyanosis of comb/wattles. Outbreaks due to HPAI were recorded in the Pennsylvania area. See current OIE records for up to date information on distribution of HPAI. Infections with other pathogens (e. even with 'low pathogenicity' strains. from December 1999. clothing. Highly pathogenic avian influenza A (HPAI) viruses of the H5 and H7 HA subtypes have been isolated occasionally from free-living birds. Pakistan. conjunctivitis or severe pneumonia. Italy). A serious outbreak occurred in The Netherlands in 2003 with a few linked cases in Belgium and one in Germany. Cessation of normal flock vocalisation. by acid pH. in the years 1983-84. Signs Sudden death. Apathogenic and mildly pathogenic influenza A viruses occur worldwide. Ovarian regression or haemorrhage. The virus is moderately resistant. especially faeces. Swollen face. OIE and other bodies are currently examining ways to improve control of LPAI.birds are considered to be at risk of infection. 10 . Diarrhoea (often green). H5 viruses of low pathogenicity may become highly pathogenic usually after circulating in poultry flocks for a time (Pennsylvania. Marked loss of appetite. It can result in inapparent infection. Because of this. waterfowl. Avian Influenza is a potential zoonosis. Nervous signs such as paralysis. It can remain viable for long periods in tissues.g. trachea. 550%. It is inactivated by a temperature of 56°C in 3 hours and 60°Cin 30 min. The route of infection is probably oral initially. USA.
It has occured in Europe. Haemorrhage in proventricular and gizzard mucosae and lymphoid tissue of intestinal tract. as with many such tests occasional false positive reactions can occur. Subcutaneous oedema of head and neck. This condition has until now been seen only in meat-type chickens. Prevention Hygiene. Differentiate from Newcastle disease. infectious laryngotracheitis. lateral transmission by faecal-oral route (this declines as the bird ages). Vaccines have been used in recent outbreaks in Mexico and Pakistan. Treatment None. disinfection. bleeding and vaccination needles. Vaccination is not normally recommended because. but good husbandry. fowl cholera. nutrition and antibiotics may reduce losses. Muscles congested. with considerable strain-to-strain variation. HA+. DID+. vaccinated birds may remain carriers if exposed to the infection. all-in/all-out production. Diagnosis A presumptive diagnosis may be made on history and postmortem lesions. 21-day interval to re-stocking should be followed. Survivors can be expected to have a high degree of immunity but may harbour virulent virus. correct disposal of carcases. while ducks may be symptomless. cleaning. Commercial Elisa test kits are now available. other respiratory infections. Confirmation is by viral isolation in chick embryo. although it may reduce losses initially. Eradication by slaughter is usual in chickens and turkeys. bacterial sinusitis in ducks. Turkey lesions tend to be less marked than those of chickens. Necrosis of skin of comb and wattles. isolation. Congenitally infected birds tend to remain 11 . The incubation period is 10-20 weeks. lesionless carriers of highly pathogenic virus. quarantine. controlled marketing of recovered birds. though there is high mortality of affected birds. North and South America. Dehydration. In outbreaks a regime of slaughter. Avian Leukosis (Serotype J). The agar gel precipitation test is non-group-specific and is used to confirm any positives. etc. Transmission is by congenital infection from antibody-negative females. However. To be effective inactivated vaccines must be the right subtype for the particular situation (H5 will not protect against H7 and vice versa). Minimise contact with wild birds. Myelocytomatosis Introduction Caused by an avian retrovirus. NDV-. Morbidity is low.
Enlargement of abdomen. age.80% produce infected chicks. preferably on separate hatch days and in separate machines. 'nonshedders' . often with tumour foci. histology. sacral joint.antibody negative. Signs Depression. 12 .most but not all.only 3% produced infected chicks. Splenomegaly and enlarged kidneys also occur. Treatment None. ultimately identification of virus by isolation and/or PCR. Lymphoid Leukosis.tumours usually contain well-differentiated myelocytes. 'Shedders' . Prevention Checking of antigen in the albumen is a basis for eradication . Separation in vaccination. PCR testing of embryonally infected chicks using DNA testing is uniformly positive for blood and faecal samples. Microscopic . Serology . Differentiate from Marek's disease. Critical hatchery practices: Separate infected and uninfected lines. Diagnosis History. Emaciation. Handle clean lines before infected lines. Persistent low mortality. Loss of weight. lesions. shed virus and develop tumours. birds with egg antigen will be antibody negative. There is also evidence that it is slightly more sensitive than conventional testing. Many are asymptomatic. ribs. liver. Prevent/ reduce cross-infection in hatchery and on farm.an Elisa test is aviailable to identify antibody positive birds. Two cell types may be found in the same tumour. Virus survival is poor but sufficient to allow cross contamination in hatcheries and on farm in rear. particularly of the sternum. Minimise stress. Most characteristically are chalky white tumours in the bone marrow. Post-mortem lesions Liver enlargement.
The causative viruses are rapidly inactivated at ambient temperature and on exposure to most disinfectants. There may be increased susceptibility to other infectious diseases due to damage to the immune system. Many are asymptomatic. myeloblastosis (see Sero-type J). it may be as short as 6 weeks for some of the other manifestations. age. Loss of weight. initially in the bursa. kidney etc. Egg production is somewhat reduced. Morbidity is low but mortality high.Farm practices: Brood and rear lines separately and maintain separate for as long as possible. liver or bursa. lesions. Liver may be very large. coligranuloma. fibrosarcomas. Post-mortem lesions Focal grey to white tumours. Avian Leukosis. cytology. then liver. spleen.egg layers are generally more susceptible to lymphoid leukosis. Differentiate from Marek's disease. lateral transmission is poor but infection may occur by the faecal-oral route. other tumours. Delay live vaccine challenges. 13 . Emaciation. myxosarcomas. Vertical transmission is most important by infection of the egg white in infected breeders (who are long-term carriers). Signs Depression. Avoid migration errors (birds unintentionally moving between pens). It affects chickens worldwide with susceptibility varying considerably among different strains and types of stock . erythroblastosis. especially in young birds. Mortality tends to be chronically higher than normal for a prolonged period. Enlargement of abdomen. Leukosis/Sarkoma Group Introduction Lymphoid Leukosis. Microscopic . A complex of viral diseases with various manifestations such as lymphoid leukosis.cells lymphoplastic Diagnosis History. In lymphoid leukosis the incubation period is about 4-6 months. Minimise group sizes. Persistent low mortality. osteopetrosis.
Snick. South America and North America. The incubation period is 5-7 days. vertical transmission is uncertain. turkeys (see separate summary). As for many infections. It is caused by a pneumovirus of the Paramyxoviridae family. fomites can be important in moving infection between farms. control arthropods. Figure 9. Africa. all-in/all-out production. first isolated from poults in South Africa in 1978. Prevention Good hygiene. This was a case of Myelocytoma Avian Leukosis (Sero-type J). guinea fowl and possibly pheasants seen in Europe. morbidity is 10-100% and mortality can be 110%. Diffuse lymphoid tumours in an enlarged liver from a mature broiler parent hen. Loss of voice.Treatment None.checking of antigen in the albumen is a basis for eradication (see Sero-type J for details). Facial and head swelling (though this can occur in other conditions). weight gain and feed efficiency. 14 . Ocular and nasal discharge. Conjunctivitis. Signs Decreased appetite. Dyspnoea. Avian Rhinotracheitis 'Swollen Head Syndrome' Introduction A viral disease of chickens. There is rapid lateral transmission with infection by aerosol through the respiratory route. eradication . Two subgroups have been identified on the basis of the G-protein sequence: A (original UK isolates) and B (original southern Europe isolates).
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.
Biotin Deficiency. Sudden deaths in fatty liver and kidney syndrome. Viral particles may be demonstrated in bile. in embryos. Lung congestion Ovarian regression Yolk peritonitis Pale foci and haemorrhages in pancreas. It may be helpful to control other conditions which may be occurring at the same time. Thickened skin under foot pad. Drinking water which is well chlorinated should be helpful in reducing challenge by this route. Must be confirmed by laboratory tests. Pale livers and kidneys in fatty liver and kidney syndrome. Diagnosis Typical signs and lesions. 18 . 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. Leg weakness. Post-mortem lesions See signs. Elisa tests have been developed experimentally. Prevention Thorough cleaning and disinfection after depletion of an affected flock. Reduced feed intake and blood sugar can precipitate fatty liver and kidney syndrome. Histopathology may also be used but the findings are not specific to this condition. Including Fatty Liver and Kidney Syndrome Introduction Biotin deficiency has occured in turkeys and chickens in many countries but is now rare in birds consuming properly formulated feeds. Scabs around eyes and beak. Treatment No specific treatment known. Good biosecurity. A RT-PCR test may be used to detect viral RNA in tissues. Signs Poor growth. Chondrodystrophy. Allin/all-out production. webbing between toes.
Crusty clumps of eggs ('nits') may be visible at the base of feathers. Biting Lice Introduction Various species of lice are common external parasites of poultry worldwide. Differentiate from pantothenic acid deficiency (skin lesions). has very low bioavailability. especially around vent. Scabs around vent. Signs Lack of thrift in young birds. bedbugs. Check flocks regulary for rapidly moving insects at the base of the feathers on the abdomen or around the vent. They are spread by direct contact between birds and by litter etc. Differentiate from mites. lesions. Irritation. Diagnosis Identification of the parasites. Treatment Malathion powders and pyrethroid sprays where approved for bird application. Prevention Supplementation of diets with biotin . Loss of condition. Away from birds adults survive about 4-5 days.Diagnosis Signs. Post-mortem lesions Usually none. Drop in egg production.naturally present in many raw materials. Loss of vent feathers. Menocanthus stramineus is the most pathogenic and is said to be capable of causing anaemia in heavy infestations. Lice eggs stuck to feathers. 19 . may be some feather damage and crustiness of skin. The parasites are 1-6 mm in size and their life cycle takes about 3 weeks. response to treatment/prevention. Treatment Addition of biotin in feed or water. Parasites on birds.
Signs Anaemia in young birds. Weekly treatments are required. Swarms of flies. Eggs and larvae survive through the winter to cause new infestations in the following year. especially in autumn and winter and treat if required. It is usually necessary to treat twice at a 7-10 day interval to fully control the condition. local history. Biological control using a strain of Bacillus thuringensis has had some success and is preferable to insecticides. Examine for lice regularly. Prevention Similar measures as for mosquito control. Treatment Treatment is difficult. 20 . Post-mortem lesions Anaemia. as the larvae within eggs are not killed by most products. The condition tends to occur near to rapidly flowing streams. 5 mm long and found in North and South America that are external parasites of birds and mammals.Prevention Avoid direct contact with wild and backyard poultry. Blackfly Infestation Introduction Grey-black hump-backed flies. season. Effective removal of all organic material at flock depletion should be practised in all-in/all-out production systems. The flies transmit leucocytozoonosis and also a filarial parasite in ducks. Diagnosis Anaemia. although these insects can travel up to 15 miles.
then sudden death. The single most important measure is careful pick-up and removal of all dead birds on a daily basis. carcases. and toxin-containing material (pond-mud. maggots) is consumed by the birds. weakness. 21 . Mild enteritis if has been affected for some time. Signs Nervous signs. The toxin is produced in decaying animal (usually carcases) and plant waste. Prevention Preventing access to toxin. Diagnosis History. Toxin may also be produced by the bacteria in the caecum. progressive flaccid paralysis of legs. because it rests on the litter. turkeys. selenium. ducks and other waterfowl occurring worldwide and caused by a bacterial toxin produced byClostridium botulinum mainly types A / C. Feathers may be easily pulled (chicken only). signs. Treatment Remove source of toxin. is also quite typical. Maggots or putrid ingesta may be found in the crop. supportive treatment if justifiable. A soiled beak. 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. wings then neck. mouse toxicology on serum or extract of intestinal contents. Morbidity is usually low but mortality is high. The toxin and bacterial spores are relatively stable and may survive for some time in the environment. Post-mortem lesions Possibly no significant lesions. suspect food and stagnant ponds. antibiotics. This will reduce the risk of botulism both in the poultry and in any grazing animals on land where poultry litter is spread. Affected broilers tend to settle with eyes closed when not disturbed. Differentiate from acute Marek's disease ('Floppy Broiler Syndrome') by histology of the brain.Botulism Introduction A condition of chickens. especially in hot weather.
Post-mortem lesions Inflammation of sternal bursa along the keel bone which may. Earthworms may be transport hosts for eggs. Signs Swelling over the keel bone with bruising and discolouration. Infection is by the oral route. Morbidity is high but it is not associated with mortality. They are found worldwide. 22 . up to 1.5 cm in length that occur in the caecum. Heterakis gallinaeeggs and larvae are a transport hosts for Histomonas. control of leg problems.Breast Blister Introduction A complex condition of chickens and turkeys occurring worldwide associated with trauma. give way to scar tissue. the cause of Blackhead. Poor feather cover and caked or wet litter are predisposing factors. Diagnosis Based on lesions. or paratenic hosts with partially developed (L2) larvae. are small whitish worms with a pointed tail. The meaning of the technical terms relating to parasite life cycle are defined in the glossary. in chronic cases. Caecal Worm Introduction Heterakis gallinae. Prevention Good litter management and handling. There is an incubation period of 2 weeks for eggs to embryonate. leg weakness. Treatment Not usually appropriate. Signs None. Morbidity may reach more than 50% but the condition is not fatal. nematode parasites of poultry and game birds. bacteria. and infection withStaphylococcus spp. and a four-week prepatent period.
an undeveloped egg as found in fresh faeces. Signs Paralysis. Diagnosis Adults can be seen in caecal contents at post-mortem examination. especially broiler parents. Calcium Tetany Introduction A metabolic disease of chickens. Prevention Avoiding access to earth and earthworms. and the embryonated egg. Treatment Flubendazole.Post-mortem lesions Inflammation of caecum. 23 . The egg may be ingested directly by a chicken. possibly with nodule formation. Predisposing factors include heat stress with reduced feed intake and panting. Death from respiratory and cardiac failure. Figure 11. or by an earthworm which is in turn ingested by a chicken. Routine anthelmintic treatment. Levamisole. The life cycle ofHeterakis showing the location of adults. are effective.
Diagnosis This is made on signs. Campylobacter jejuni is the commonest species found in poultry. lesions. 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.Post-mortem lesions Cyanosis. There are indications that plantar pododermatitis. 24 . Active ovary with egg in oviduct. There is an annual cycle with increased risk of infection in the summer months in some countries. Treatment Provide 5 gm of oyster shell per hen on 3 successive days along with vitamin D in drinking water. Infected poultry are a potential reservoir of this zoonosis. Prevention Keep pullet flocks on low calcium diet until 5% production hen/day. In poultry they tend to multiply in large numbers in the hindgut. lack of other significant lesions. biofilm or engulfed by protozoa. The reason for this is unclear. Campylobacters are a significant cause of enteritis in man. pets and wild animals. carcase quality and litter quality are better on farms which tend to have Campylobacter-negative stock. It may be that management that favours dry litter reduces the risk of infection and/or transmission within the flock. other acute infections and other causes of sudden death. are bacteria that commonly infect a broad range of livestock species. principally in the caecae. and response to treatment. Differentiate from IB 793b. All campylobacters are delicate organisms that survive for relatively short periods outside the host unless protected by organic material. Campylobacter Infection Introduction Campylobacter spp. managing birds for maximum uniformity.
Many infections are introduced during thinning or other forms of partial depopulation. For this reason it may be difficult to stop the spread of infection between houses once it becomes established in one house. avoidance of contact with pets and other farmed species. Prevention In principle. Key aspects of this include effective sanitation of drinking water. Diagnosis Isolation of the organism from caecal contents. housed poultry can be maintained free of Campylobacter infection by consistent application of excellent biosecurity. cloacal swabs or composite faeces. Insects and rodents may act as a means of transfer of the infection from the general environment into the poultry buildings. Research is ongoing on the development of vaccines. good hand hygiene by stockmen. Post-mortem lesions None. In practice the success of this will also depend upon the degree of environmental contamination by the organism. Samples should be tested as quickly as possible after collection. Treatment Not required on clinical grounds. 25 . phage treatments and competitive exclusion approaches. sourcing of water from high quality supplies. and changing of overalls and boots on entering bird areas. The organism is sensitive to air so swabs should be collected into transport medium and other samples placed in airtight containers with minimal airspace. as well as processing plant technologies to reduce carcase contamination.Signs None.
microscopic examination of a digested smear (heat in 10% potassium hydroxide) to demonstrate the hyphal forms of the yeast in the tissues. copper sulphate (1 kg/tonne feed) for 5 days. occasionally proventriculus and intestine.Candidiasis. sodium or calcium proprionate at 1 kg per tonne continually. possibly confused or masked by signs of the primary disease. 26 . Prevention Avoid excessive use of antibiotics and other stressors. The fungus is resistant to many disinfectants. Diagnosis Lesions. Raised focal lesions may slough into lumen as caseous material. Slow growth. especially in the crop but sometimes in the proventriculus. Moniliasis. Candida albicans and the condition is seen worldwide. The cause is a fungal yeast. Morbidity and mortality are usually low. Poor appetite. Post-mortem lesions White plaques in mouth. turkeys. 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. Diarrhoea. histopathology. Signs Dejection. oesophagus. smooth and with a yeasty smell. or copper sulphate 1gm/2 litre water for 3 days if approved locally. Thrush Introduction A disease of the alimentary tract of chickens. intestine and cloaca.g. and sometimes other birds and mammals. characterised by thickening and white plaques on the mucosa. A finely divided powder of copper sulphate (where approved) at 200gm/tonne continually or to 14-16 weeks in replacement pullets. and associated with gizzard erosion. Ensure good hygiene. Control of Candida through drinking water is sometimes practised with chlorination (e. Treatment Nystatin (100 ppm in feed) for 7-10 days. proprionic acid. crop. Colonies of this fungus appear as white to ivory colour.
feed form (mash takes longer to consume than pellets). Soluble multivitamins and/ or methionine may be of some benefit in some circumstances. Treatment Correct any husbandry problems. Predisposing factors include overcrowding. tenosynovitis and other diseases affecting mobility. Provision of a diet that closely matches the nutritional requirements of the stock concerned. head. post-mortem cannibalism. sodium hypochlorite) at 5 ppm. anaemia. face. low light level. It should be repeated periodically. 27 . uncontaminated by fungi.Chlorox. Differentiate from bacterial dermatitis. Morbidity is usually low but mortality is high among affected birds. wings. Diagnosis Age. Feather pecking Introduction A complex multifactorial behavioural problem of poultry and game birds seen worldwide. control ectoparasites. high temperatures. excessive light intensity or variation (e. This is economical and effective. Signs Pecking at feet (especially young chicks) and vents (adult layers and turkey poults 812 days old). distribution of lesions.g. and strain of bird. Prevention Proper density and temperature. Generalised anaemia. complying with local regulations and any relevant codes of practice. Feather-pulling. through shafts of light in the house). Post-mortem lesions Skin wounding related to particular signs exhibited. If so it should be carried out carefully by trained operators. nutritional deficiencies. Cannibalism. Beak trimming may be necessary. boredom. Take care to provide fresh clean feed and water.
Wasting Poor growth. Some species have earthworms as intermediate hosts. Infection is by the oral route. Worm eggs take about 20 days to embryonate with an L1 larvae. Treatment Coumphos has been licensed in some markets.other approved benzimidazoles can be expected also to have activity. Diagnosis This may be by a combination of macroscopic examination. C.05 mm wide and hair-like in appearance. obsignata in the small intestine. or characteristic worm eggs in faeces in patent infections. about 0.Capillariasis .Hairworm Infection Introduction Nematode parasitic worms of poultry. Worm eggs in the environment are resistant. game birds and pigeons ofCapillaria species. C. The worms are 7-18 mm long. Levamisole. effective cleaning of houses. small intestine or caecum. Signs Diarrhoea. prepatent period about 21-25 days according to species. Post-mortem lesions Enteritis. Prevention Separation of birds from possible transport and intermediate hosts. Differentiate from other causes of enteritis. Hairworms in mucosa of crop. contorta in the crop and oesophagus. some are transmitted direct from bird to bird. Fenbendazole has been shown to have high efficacy . Morbidity and mortality are usually low. Dejection. seiving intestinal contents. 28 .
Cellulitis Introduction Cellulitis is literally an inflammation of connective tissues. which can replicate in the tissues. The condition is caused by infection of. Signs Affected flocks tend to have poorer than average productivity and uniformity. often minor. However its main importance is as a cause of condemnation in meat poultry. coli. Post-mortem lesions Typically it presents as exudate ranging from liquid and pale cream pus to yellowish solid plaques of caseous material under the skin of the abdomen and/or in the leg. Treatment Treatment would not be possible if the problem is identified at a final depletion. Routine monitoring of skin damage at about 25 days of age may be helpful in fostering good practices. Many meat inspectors become skilled at detecting subtle differences in skin colour in the affected birds. Many affected birds have no other lesions and are reasonably well grown. It typically occurs between skin and muscles and between muscles and may be an incidental finding in a range of conditions. Prevention Toe scrapes at 15-25 days of age when feather cover is poor are the most likely predisposing factors. skin wounds by particular strains of E. but the affected birds are not readily detectable prior to slaughter. Diagnosis Typical lesions. particularly broiler chickens. though most of the birds showing toe scrapes will not go on to develop cellulitis. 29 . In the USA it is called 'Inflammatory Process'. Careful flock management with a view to reducing toe wounds has the greatest impact in controlling cellulitis. If identified at a thinning there may be time for antibacterial treatment to have some benefit for those birds in the early stages of the problem.
Discoloured liver and kidney. No clinical signs or effect on egg production or fertility in parent flock during seroconversion. Inclusion body heptatitis etc. Transmission is usually vertical during sero-conversion of a flock in lay. Acute mycotic pneumonia. The virus is resistant to pH 2. chloroform. 80°C for 5 minutes) and many disinfectants even for 2 hours at 37°C. demonstration of ongoing sero-conversion in parent flock. Sudden rise in mortality (usually at 13-16 days of age). poor litter quality). Gumboro. Gangrenous dermatitis on feet. Mortality is typically 5-10% but may be up to 60% if there are predisposing factors present such as intercurrent disease (Aspergillosis. Post-mortem lesions Pale bone marrow.g. Pale birds. and control of other diseases as appropriate. Signs Poor growth.) or poor management (e. PCV of 5-15% (normal 27-36%). Hypochlorite appears most effective in vitro. 30 . Diagnosis Gross lesions. legs wings or neck. lateral transmission may result in poor productivity in broilers. If gangrenous dermatitis is a problem then periodic medication may be required.Chicken Anaemia Introduction A viral disease of chickens caused by Chicken Anaemia Virus or CAV. Treatment Good hygiene and management. may be beneficial. Prior to confirmation that it is in fact a virus it was known as Chicken Anaemia Agent or CAA. heat (70°C for 1 hour. ether. virus may be isolated in lymphoblastoid cell line (MDCC-MSB1). Atrophy of thymus and bursa.
phenolics are less so. 31 . 15 weeks. Elementary bodies are highly resistant and can survive in dried faeces for many months. They should be used at least 6 weeks prior to collecting eggs for incubation. Nasal discharge. Inappetance. Fibrinous pericarditis. mortality 5-40%. psittacines. Weight loss. faecal dust and wild bird carriers. man. Elisa. other infections may be predisposing factors. Wasting. say. Airsacculitis. It is a 'Scheduled Disease' rarely diagnosed in UK. pigeons. Psittacosis. Ornithosis Introduction An infection of turkeys. Iodophores and formaldehyde are effective disinfecting agents. Weakness. their degree of attenuation is variable. ducks. Greenish-yellow diarrhoea. especially pigeons and robins. Signs Respiratory signs. Chlamydiosis. Morbidity is 50-80%. Conjunctivitis. rarely chickens.Prevention Live vaccines are available for parents. Occasional transient ataxia in pigeons. but occurring probably worldwide. It is transmitted by contact. perhaps. caused by Chlamydia psittaci. Egg transmission does not occur. Production drops in naive laying flocks Post-mortem lesions Vascular congestion. a bacterium of highly variable pathogenicity. Depression. Their use may be restricted to those flocks that have not sero-converted by. Serology: antibodies develop 3-6 weeks after infection. Immunity: there is a good response to field challenge (in birds over 4 weeks of age) and to attenuated live vaccines. or IFA. Intercurrent salmonellosis and. and may be detected by SN.
either singly or in combination (although deficiencies of pyridoxine. Fibrinous pneumonia. This condition is seen in chickens. Differentiate from Duck viral hepatitis. Distortion of hock. Serology: complement fixation. Signs Short legs. Malposition of leg distal to hock. Slipped Tendon or Perosis Introduction Caused by deficiency of manganese. biotin. zinc. Prevention Biosecurity. Chondrodystrophy. Necrotic foci in liver. ducks and turkeys. shortened bones. Spleen enlarged and congested. exclusion of wild birds. signs. Congested lungs and air sacs in the turkey. niacin may also be involved). Live and inactivated vaccines are protective although the former result in carriers and the latter require several applications. Slipping of Achilles tendon (or perosis). Lameness. 32 . In turkeys it may be an inherited deficiency of galactosamine. In embryos parrot beak. Elisa and gel diffusion. Duck septicaemia. may rupture in pigeons. Perihepatitis. Intracytoplasmic inclusions are helpful but confirmation requires demonstration of causal organisms (Giemsa stain. choline. Treatment Tetracycline (200-800 ppm in feed for 3-4 weeks) and/or quinolone medication and supervised slaughter. folic acid. Diagnosis History. lesions. IFA).
choline. Depression. Differentiate from twisted leg. Tibia and metatarsus bowed. correct mineral balance. E. infectious arthritis. E. Post-mortem lesions The affected area of intestine shows thickening of the wall and dilation. Treatment For flock proceed as for prevention. rickets. while E. Coccidiosis of Turkeys Introduction Infection of turkeys with Eimeria spp. Signs Huddling. This disease is not very common in commercially reared turkeys though most turkey growers receive preventative medication for at least part of their lives. Tucked appearance. The contents may be haemorrhagic or be watery with white material shed from the mucosa. Weight loss. gallopavonis and E. infectious synovitis. while E. dispersa is found in the small intestine. vitamins. no value to affected bird. Prevention Addition of manganese. Lateral slipping of tendon. adenoides affects the caecae and rectum. ruffled feathers. Shallow trochlea. Five species of Eimeria have been identified that cause lesions in turkeys.Post-mortem lesions Shortening and thickening of long bones. ruptured ligaments. of which two are associated with significant disease effects. Diagnosis Lesions. meleagridis affect the lower small intestine rectum and caecae. 33 . Watery diarrhoea that may occasionally be blood stained or contain clumps of mucus or shed mucosa. analysis of feed. meleagrimitis affects the upper small intestine.
Amprolium. Treatment Toltrazuril. microscopic exam of scrapings (oocysts. Sulphonamides (e. Differentiate from necrotic enteritis. The exudate can range from semi-liquid to solid white cores. adenoides. Dosage levels of ionophores may be critical to efficacy and safety. gamonts). Turkey caecal coccidiosis caused by E. Figure 37. The intestines are dilated. Figure 38. Exposure of previously unmedicated birds to these compounds can cause toxicity. show some spotty congestion and have abnormal contents due to the sloughed epithelium. Prevention The ionophore coccidiostats lasalocid and monensin are routinely used in turkey growers.g. Sulphaquinoxaline). Avoid use of tiamulin in ionophore treated birds. Salinomycin is toxic for turkeys even at very low doses. 34 . Turkey coccidiosis of the upper small intestine caused by E.Diagnosis Signs. lesions. Diclazuril is also used for this purpose. typically to 12 weeks of age. meleagrimitis.
Vitamins A and K in feed or water. Signs Depression. Vaccines are used mainly in breeders but increasingly in broilers. E tenella Introduction This was at one time the commonest type of coccidiosis and is certainly the most easily diagnosed. Accumulation of varying quantities of blood and caseous necrotic material in the caecum. ecchymoses. Differentiate from ulcerative enteritis. Diagnosis Signs. Treatment Toltrazuril. Caecal. Post-mortem lesions Petechiae. hygiene. 35 . Inappetance. lesions. Thickening. tenella is more common when 'straight' ionophore programmes are used.Coccidiosis. of caecal mucosa. Diarrhoea. Morbidity is 10-40% and mortality up to 50%. Closed eyes. microscopic examination of scrapings. Transmission as for E. In some markets the organic arsenical compound 3-Nitro is used as an aid in the control of caecal coccidiosis. Recovered birds have good immunity to the same parasite. Amprolium. E. Prevention Coccidiostats in feed. Production less affected than in some of the other forms of coccidiosis. Sulphonamides. blood in faeces. Ruffled feathers. Shuttle programmes with chemicals in the starter diet usually improve control. histomonosis. mitis (see above). vaccination by controlled exposure. It is caused by Eimeria tenella and results in lesions in the caecum of chickens worldwide.
Diagnosis Mild lesions. May predispose to wet litter. The infective agent is found in litter. Moderate Eimeria tenella infection in the caecae of a chicken (Score 3). identification of typical small round oocysts and other stages in fresh scrapings from the small intestine. E mitis Introduction This condition of chickens. The disease occurring is proportional to the amount of infective agent ingested. Signs Reduced feed conversion efficiency and weight gain. Predisposing factors include exposure to faeces and litter conditions that favour development of the parasite (temperature. which colonises the small intestine. The parasite is moderately resistant in the environment and highly resistant to conventional disinfectants. humidity). The caecal walls are thickened and haemorrhagic and there is a mass of blood in the caecal lumen. Coccidiosis. seen worldwide. is caused by the protozoan parasite Eimeria mitis. 36 . faeces and on fomites and birds are infected by the oral route with an incubation period of 2-5 days. Treatment Not usually treated but susceptible to the products used for other forms of intestinal coccidiosis. 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.Figure 15. secondary bacterial enteritis.
Ileorectal. vaccination by controlled exposure. extending into caecal tonsils. 37 . Severe necrotising enteritis. Vitamins A and K in feed or water. Post-mortem lesions Petechiae and thickening of the distal third or more of intestine. Oocysts in caecum and rectum. This species is not usually included in vaccines for broilers. Ruffled feathers. Diarrhoea. caecal coccidiosis. blood in faeces.Prevention Normally controlled by anticoccidials in feed. caecum and rectum. Inappetance. Treatment Toltrazuril. hygiene. Coccidiosis. it is found in the terminal ileum. Morbidity and mortality are variable. Closed eyes. Sulphonamides. Of moderate to high pathogenicity. lesions. Diagnosis Signs. Signs Depression. Differentiate from ulcerative enteritis. May be included in vaccines. Poor production. Prevention Coccidiostats in feed. microscopic examination of scrapings. Amprolium. There is good immunity to the same parasite in recovered birds. E brunetti Introduction A relatively rare form of coccidiosis affecting chickens worldwide caused by Eimeria brunetti.
Differentiate from Duck viral hepatitis. compared to four per oocyst forEimeria. There is thickening of the intestinal mucosa and there are lines of haemorrhagic spots in the mucosa. Tucked appearance. Depression. Tyzerria has eight sporocysts in each oocyst. Post-mortem lesions Massive haemorrhage in upper small intestine. anatipestifer. of Ducks and Geese Introduction Young ducks and geese may suffer from Eimeria spp infection. large number of merozoites). anseris is the most important. lesions. Treatment Sulphonamides (e. Blood-stained vent.g. 2 days off. Signs Sudden death. In the goose E. Duck viral enteritis. 3 days on. 3 days on). Diagnosis Signs. Amprolium. Intestinal. Sulphadimidine 30-600gm/100 birds/day.Figure 16. while in ducksTyzzeria perniciosa is most pathogenic. Coccidiosis occurs only very rarely in commercially reared ducks in the UK. 38 . microscopic examination of scrapings (usually few or no oocysts. Coccidiosis. Vitamins A and K in feed or water. Moderate Eimeria brunettiinfection in the terminal ileum and rectum of a chicken.
Reduced feed intake. Kidneys light grey to greyish pink. Diarrhoea . Kidney Introduction A disease of geese caused by Eimeria truncata that can cause high mortality in geese of 312 weeks of age. Signs Depression. Prevention Good Hygiene. however this is not routinely practised. Post-mortem lesions Enlarged kidneys. 39 . Coccidiosis. Tiny white foci and petechiae in the kidneys. Diagnosis Lesions. Hygiene. Treatment Controlled trials of treatments have not been published.Prevention If required coccidiostats could be used in feed.faeces tend to be whitish. it can also infect Barbary ducks and swans. Weakness. presence of coccidial stages in fresh scrapings of kidney lesions.
Differentiate from necrotic enteritis. Diagnosis Signs. vaccination. Caused by Eimeria maxima. microscopic examination of scrapings. Mild to severe enteritis. Mid-intestinal. Post-mortem lesions Petechiae and thickening of middle third of intestine. Blood or pigment in the faeces. hygiene. lesions. Closed eyes. Depigmentation of skin and plasma is especially evident in this form of cocccidiosis and this is commercially important in some markets. acervulina coccidiosis and there may be large numbers of characteristic oocysts in smears. Morbidity and mortality are variable. Signs Depression. commercial vaccines commonly contain more than one strain of E. Inappetance. Poor production. contents often orange in colour. Ruffled feathers. Because of the area of intestine affected it tends to have a significant effect on productivity and susceptibility to necrotic enteritis. of moderate to high pathogenicity it is seen worldwide. Amprolium. Vitamins A and K in feed or water. non-specific enteritis. E maxima Introduction One of the more common forms of coccidiosis in commercial broilers. This infection is often associated with E. Prevention Coccidiostats in feed.Coccidiosis. maxima. Poor absorption of nutrients/pigments. mucosa tends to be pinker than normal. 40 . This is one of the less immunogenic species. Treatment Sulphonamides.
Poor production. caused by Eimeria necatrix. Depression. 41 . microscopic examination of scrapings Differentiate from necrotic enteritis. Schizonts seen as white spots through the serosa interspersed with petechiae. blood in faeces. It occurs in chickens worldwide and has variable morbidity but mortality is high in severely affected birds. The lesions are subtle compared to other forms of coccidiosis. Oocyts in caecal scrapings. E necatrix Introduction A highly pathogenic form of coccidiosis. Severe necrotising enteritis.Figure 13. Post-mortem lesions Petechiae and thickening. Ruffled feathers. Moderate Eimeria maxima infection in the jejunum of a chicken (Score 2). Diarrhoea. other types of coccidiosis. Inappetance. Diagnosis Signs. in which the parasite is present in the small intestine and in the caecum. of middle to posterior third or more of small intestine. lesions. The intestine is slightly thickened and there are scattered haemorrhages in the mucosa when seen from the inside. Coccidiosis. Closed eyes. Deep scrapings necessary to show large schizonts. Mid-intestinal. Signs Reduced feed consumption. 'Sausage-like' intestine.
hygiene. Moderate Eimeria necatrix infection in the jejunum of a chicken (Score 3). E acervulina Introduction This is probably the commonest cause of coccidiosis in chickens and occurs worldwide. Amprolium. Prevention Coccidiostats in feed. which is moderately pathogenic. Upper Intestinal. Coccidiosis. both alone and in association with other species of coccidia and is caused by Eimeria acervulina. vaccination. In this case the intestine is thickened and can become ballooned and sausage-like. Poor production. Depigmentation. Closed eyes. Diarrhoea. This is one of the less immunogenic species. Signs Depression.Treatment Toltrazuril. It is seen in layers and in broilers. Figure 14. Inappetance. maxima. Sulphonamides. Eimeria mivatiis currently considered not to be a valid species distinct from E. Haemorrhages and white spots are visible from the outside of the intestine. Vitamins A and K in feed or water. Ruffled feathers. commercial vaccines commonly contain more than one strain of E. acervulina. Morbidity is variable and mortality low or absent. Post-mortem lesions 42 .
microscopic exam of scrapings. hygiene. Thickening. Diagnosis Signs. vaccination by controlled exposure. Petechiae. In general terms a score of 0 indicates no lesions and a score of 4 indicates maximal severity of lesion or death. lesions. Figure 12. Various publications provide a photographic key to severity of lesion. In milder infections there may be scattered white spots. Poor absorption of nutrients/pigments. Differentiate from necrotic and non-specific enteritis. restricted to upper third of small intestine . In severe infections they become confluent and cause sloughing of the mucosa. Moderate Eimeria acervulinainfection (score 2) in chicken duodenum. Immunity is quite short lived (about 30 days) in the absence of continued challenge. A detailed description is beyond the scope of this book. Sulphonamides. Treatment Toltrazuril. Amprolium. White spots or bands in the mucosa. in severe the entire surface is pale or denuded of epithelium. Prevention Coccidiostats in feed. A system of assessing the severity of coccidial challenge by attributing a 'score' is often used. in feed or water. and other lesions.the duodenum and part of the ileum. 43 .
Snick. Dejection. Aerobic culture yields colonies of 2-5mm on both blood and McConkey agar after 18 hours . Cellulitis over the abdomen or in the leg. Omphalitis. fomites. The infectious agent is moderately resistant in the environment. and via shell membranes/yolk/navel. with an incubation period of 3-5 days. Peritonitis. water. Perihepatitis. Pericarditis. It is frequently associated with immunosuppressive diseases such as Infectious Bursal Disease Virus (Gumboro Disease) in chickens or Haemorrhagic Enteritis in turkeys. Omphalitis. coughing. Post-mortem lesions Airsacculitis. or in young birds that are immunologically immature. sero-typing. but is susceptible to disinfectants and to temperatures of 80°C. Signs Respiratory signs. Synovitis. Infection is by the oral or inhalation routes. Diagnosis Isolation. mortality is 5-20%. Granulomata in liver and spleen. Arthritis. It is most commonly seen following upper respiratory disease (such as Infectious Bronchitis) or Mycoplasmosis. Poor navel healing. Salpingitis. pathology.Colibacillosis. sneezing. It is caused by the bacteriumEscherichia coli and is seen worldwide in chickens. Morbidity varies. turkeys. Poor growth. etc. Swollen liver and spleen. Enteritis. Lesions vary from acute to chronic in the various forms of the disease. Colisepticemia Introduction Coli-septicaemia is the commonest infectious disease of farmed poultry. mucosal damage due to viral infections and immunosuppression are predisposing factors.most strains are rapidly lactose-fermenting producing 44 . Reduced appetite.
whereas others progress to deep ulcers so the size. tetracyclines. 45 . Staphylococcus spp. Contact dermatitis is commonly monitored at processing as a means of measuring 'welfare status'. gentamycin or ceftiofur (where hatchery borne). hatchery hygiene. neomycin (intestinal activity only). Figure 17. Control of predisposing factors and infections (usually by vaccination). Contact Dermatitis. the breast area.brick-red colonies on McConkey agar. as well as Pseudomonas. feed and water. Severe perihepatitis in colibacillosis in a broiler parent chicken. potentiated sulphonamide. Immunity is not well documented though both autogenous and commercial vaccines have been used. Some lesions are superficial. Treatment Amoxycillin. rear surface of the hock and. stage of resolution and severity of lesion is likely to affect the degree of discomfort or pain suffered. when severe. other enterobacteria such as Proteus. the foot pad. Differentiate from acute and chronic infections with Salmonella spp. The liver is almost entirely covered by a substantial layer of fibrin and pus. flouroquinolones. and in broiler parents. It is seen in growing broiler chickens and turkeys. etc. Well-nourished embryo and optimal incubation to maximise day-old viability. Hock Burn. Prevention Good hygiene in handling of hatching eggs. good sanitation of house. Pododermatitis Introduction Contact dermatitis affects skin surfaces which have prolonged contact with litter.
most importantly. If severe the foot and hock lesions may contribute to lameness or serve as a portal of entry for secondary infections. and. Signs Blackened skin progressing to erosions and fibrosis on the lower surface of the foot pad. at the back of the hocks.Pododermatitis is often related to high droppings pH. proper insulation in cold climates. Choice of drinker type (nipple as opposed to bell). It can be reproduced by adding water to the litter. drinker management. and sometimes in the breast area. Diagnosis Signs and lesions. Treatment Not applicable. level of soya bean meal in feed (according to some authors. Prevention This condition is closely linked to intestinal function as this is the prime determinent of faecal consistency and stickiness. Post-mortem lesions As described under signs. litter moisture. and adequate ventilation to remove moisture are all important. Figure 18. stickiness of droppings). See the discussion in the section on Dysbacteriosis. Moderate pododermatitis on a foot pad. 46 .
and vice versa. They also differ from coccidia in being poorly host specific. Post-mortem lesions Inflammation and thickening of mucosa of crop and oesophagus. meleagridis also infects both species. although bird strains do not infect mammals very well. Avoidance of access to intermediate hosts. and ducks. turkeys. They replicate in the brush border on the surface of epithelial cells. The same species causes infections of the hindgut and cloacal bursa in chickens. Cryptosporidium baileyi can cause respiratory disease in chickens and turkeys. Coumaphos. Diagnosis Microscopic examination of mucosal scraping. A further species causes respiratory disease in quail. acervulinaoocyst). Treatment Levamisole. Prevention Effective cleaning of housing. The oocysts are excreted ready sporulated in the faeces and infection occurs by inhalation and ingestion. Emaciation. White convoluted tracks in the mucosa. Some have beetle or earthworms as intermediate hosts. 47 .Cropworms Introduction The nematode worms Capillaria spp and Gongylonema ingluvicolainfect the mucosa of the crop and oesophagous of poultry and game birds.C. Cryptosporidiosis Introduction Cryptosporidia are related to the coccidia. Routine worming. but much smaller (typically oocysts are less than ¼ of the size of an E. Signs Anaemia.
48 . Swollen sinuses. There are no effective preventative medicines or feed additives. Diagnosis Identification of the parasites attached to the epithelium by microscopic examination (smears histopathology acid-fast staining). Prevention The oocysts of cryptosporidia are extremely resistant to chemical disinfection. Circling. recumbency. Treatment Unfortunately there is currently no known effective treatment in poultry.g. Pneumonia. Signs Incoordination. 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. Diarrhoea. coli-septicaemia) there may be benefit in medicating for these. Airsacculitis. Tremors. Cough. If other disease processes are complicating the situation (e. Torticollis. Post-mortem lesions Sinusitis. Low weight gain. It is becoming increasingly common for water companies to screen water supplies for cryptosporidia because of the human health implications of mammalian strains.Signs Snick.
Post-mortem lesions Necrotic lesions with associated congestion in cerebrum. resulting in erosions. but it may result from physical damage. Signs Lameness. or developmental defects. especially of femoral anti-trochanter but also other leg joints. Diagnosis Lesions. Rapid growth is a possible predisposing factor. Diagnosis Gross and microscopic lesions. Prevention Use fresh dry litter (avoid old sawdust). Reduced breeding performance. air sacs etc. isolation of the fungus. Post-mortem lesions Damaged epiphyseal articular cartilage. and cartilage flaps. Microscopically there is necrosis and there may be fissures of articular cartilage and associated osteochondritis. Treatment None. Mycotic lesions in lungs. The cause remains to be confirmed. Treatment 49 . Degenerative Joint Disease Introduction A condition of chickens and turkeys seen worldwide. 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.
There may be a place for growth-control programmes. Raised thickened scales. Prevention Avoidance of physical sources of injury to bones and joints. Treatment Not usually required in commercial poultry. especially during period of rapid growth. Exclusion of wild birds from chicken areas is advised as far as possible. Application of mineral or vegetable oil is also beneficial. Unthriftiness. microscopic examination for mites in scrapings. Prevention Careful cleaning of buildings during down-time will help reduce the risk of these infections.None available. It may be best to cull affected birds from small flocks. The adult females are short legged. Diagnosis Signs. pheasants. round. For small flocks dipping the affected parts in a solution of acaricide may be beneficial. Post-mortem lesions As described under signs. 50 .Knemidocoptes spp.5mm in diameter. Mange lesions on legs and unfeathered parts. Depluming and Scaly Leg Mites Introduction External parasites of adult chickens. pigeons etc. Signs Cause irritation and the bird pulls feathers. up to 0. Appropriate management of a segregation pen and early marketing of mildly affected birds may limit losses and improve flock welfare.
Reserpine in diet of birds of 4+ weeks (no longer licensed in the UK). was included in feed at 1 ppm for 3-5 days to reduce blood pressure. Rupture of major blood vessel at base of heart or by the kidneys. Morbidity is around 100% and mortality 0-95%. a tranquilizer. The infective agent. Diagnosis History and lesions. recovered birds carrying the virus for 8 weeks. a picornavirus may also 51 . A sudden noise or other cause of excitement can lead to an 'outbreak'. It has been suggested that degenerative changes in the wall of the artery and copper deficiency may be factors. pericardial sac. Haemorrhages in lungs. The disease is transmitted by infected ducks and other waterfowl and spreads rapidly. Skin pale. birds found on breast or side. Aortic Rupture Introduction A complex. presumably due to a sudden increase in blood pressure. genetic condition of turkeys linked to male sex and high growth rate. Reserpine. A longtitudinal split of the abdominal aorta is the most common lesion.Dissecting Aneurysm. Prevention Limit feed in birds of 16+ weeks. leg muscles. Abdominal cavity full of blood. Aspirin at 250 ppm in feed or water may be of benefit. kidneys. Possibly blood in the mouth. Post-mortem lesions Carcase anaemic. Signs Sudden death with no warning signs. Duck Viral Hepatitis Introduction A viral disease of ducks occurring worldwide and previously a scheduled disease in UK. Treatment None currently licensed.
Post-mortem lesions Liver swollen. breeder vaccination. Signs Sudden death. The disease follows a very acute course with a morbidity of 5-100% and mortality of 5-100%. Duck Virus Enteritis. Death in good condition. Influenza and a 'Type II Variant' hepatitis caused by Astrovirus. SN serology.focal necrosis. Transmission is by infected birds. coccidiosis. Duck septicaemia (anatipestifer). often in opisthotonus. mostly in ornamental collections. Live. isolation in CE (causes stunting of 9 day embryo). Diagnosis History. only slightly attenuated vaccine is applied at day old by foot web stab and may be repeated in breeding birds to provide maternal immunity. bile duct proliferation and inflammation. All waterfowl are susceptible and the Barbary duck is more susceptible than the Pekin. fomites and arthropods. arching of back. in USA since 1967.5 ml serum of recovered birds given intramuscularly. Fall on side. Differentiate from Duck plague (viral enteritis). Newcastle disease. also the Netherlands and other countries. 52 . rapid deterioration and death. Kidneys and spleen swollen. Prevention Vaccination and/or antiserum.survive for ten weeks in brooders and five weeks in faeces. Depression. Microscopically . A different picornavirus causes a similar condition in North America. Recovered birds may carry the virus for a year. lesions. 0. Punctate/diffuse haemorrhages. paddling of legs. Duck Plague Introduction A herpesvirus infection of ducks and geese diagnosed in the UK in 1972. Treatment Antiserum.
sometimes dysentery. coccidiosis. oesophagitis (birds on restricted feed). is common in countries with restrictions on the use of antimicrobial growth promoters and pressure to reduce therapeutic antimicrobial usage. pasteurellosis. Prevention Isolation from waterfowl. Dysbacteriosis. excess caecal volume and fermentation. Treatment None. Closed eyes. probably through interference. body cavities. Occasionally cyanosis of the bill in the young. Tremor. Haemorrhage in intestine. Rapidly spreading disease. Drop egg production. Dehydration. liver. Ataxia. Severe diarrhoea. Crusty plaques from oesophagus to bursa (covered by yellowish plaques in later stages). vaccination if approved by authorities (CE adapted live virus). Young ducks may show thymic and bursal lesions. Thirst. Diagnosis Isolation: Duck CAMs 12 day embryos die in 4 days. spleen. but vaccination in face of outbreak is of value. pericardium. Photophobia. intranuclear inclusions Differentiate from Duck hepatitis. Occasionally penile prolapse in the penis in drakes. 53 . vent gleet. heart. The condition is seen mainly in rapidly growing broiler chickens with good food intake. Paresis. Post-mortem lesions Severe enteritis. Non-specific Bacterial Enteritis Introduction Inflammation of the small intestine associated with wet litter. HA-.Signs Sudden deaths.
The cause has been identified as Adenovirus BC14. It affects chickens and has occurred in Ireland. Treatment Amoxycillin and tylosin treatment appear to be beneficial. Feed acidification may be helpful in some circumstances. lesions. Peru. Wet faeces in the rectum. England. often with gas bubbles. France. Circumstantial evidence suggests that the main route of transmission is through the eggs (vertical transmission) 54 . Uruguay. Diagnosis Signs. Holland. Prophylactic antimicrobial medication may be necessary in some circumstances. rather we are dealing with a disruption in the normal flora of the gut. feed interruptions and subclinical coccidiosis may be contributory factors. Voluminous caecae.Dietary changes. microscopic examination of scrapings from the wall of the small intestine (to exclude coccidiosis and perhaps to assess the bacterial flora). Good control of coccidiosis. Post-mortem lesions Excessive fluid content throughout the small intestine. especially where treatment is initiated early. 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. first isolated in Northern Ireland in 1976. Water intake may be increased or irregular. Argentina. Treatment should coincide with good relittering and it is important to provide fresh sanitary drinking water. Brazil. Prevention Competitive exclusion ('normal adult flora') use in day-old chicks reduces the risk of this condition. Apparently a similar disease had been seen over a 4-year period in broiler parents in Holland. 127. Careful choice of any feed enzymes and their matching with local raw materials can have an impact on substrates made available to intestinal bacteria. Spain. Germany. Signs Diarrhoea. No single bacterium appears to be responsible. In the autumn of 1976 a distinct egg drop syndrome was first identified in Northern Ireland. Mortality is usually negligible.
SN. group antigen distinct from classical adenoviruses (white cells. signs/lesions (mainly lack of). which can be caused by a large number of factors acting individually or in combination. Avian Encephalomyelitis. Newcastle disease. Parasites. sudden changes of feed. Poor internal quality. The infection is commonly present in ducks and geese but does not cause disease. phosporus. Infectious diseases include Infectious Bronchitis. Diseases in which egg drop occurs. Clinical disease occurs during sexual maturity. Isolation of haemagglutinatin agent in duck eggs or cell culture. Loss of shell pigment. Post-mortem lesions No specific lesion . Lack of signs in the birds themselves. thin or soft-shelled eggs and shell-less eggs. may be infectious or metabolic. Diagnosis History. Unvaccinated flocks with antibodies before lay do not peak normally. Diphtheritic Fowl Pox).followed by latent infection during rear with viral excretion starting shortly before sexual maturity. extremes of temperature. intoxication by sulphonamides. Marek's disease/Leukosis or any infectious disease causing a significant systemic disturbance (CRD. specifically vitamins E. Lateral transmission from bird to bird is slow and may be prevented or slowed for weeks by netting divisions. Serology: HI. Spread from house to house may take 5-10 weeks. Signs Egg drop at peak or failure to peak. Rough. It is important to rule out other possible reasons for egg drop.it may be possible to demonstrate degenerative changes in the epithelial cells of the magnum of the oviduct. throat swabs. Management problems may be involved: inadequate water supply. 55 . Histopathology . Infectious Laryngotracheitis. as may wildfowl and biting insects. insecticides or nicarbazin. B 12. Coryza. Elisa.only a slight atrophy of ovary and oviduct. and D as well as calcium. Metabolic diseases include Fatty Liver Syndrome. inadequate lighting programme. DID. Cholera. Drops may be of 5 to 50% and last for 3-4 weeks. Nutritional deficiency should be considered. Contamination of egg trays at packing stations may play a part in transmission. selenium. oviduct).
Treatment Medication is only likely to be of value in reducing deterioration in birds that are starting to develop lesions. Culture of lesions to confirm the bacterium involved. Post-mortem lesions Right ventricular failure and ascites. rickets. 56 . growth plate disease. The choice should depend on sensitivity testing of an isolate. Endocarditis Introduction A condition of chickens associated with several bacterial infections such as staphylococci. If successive flocks are affected on the same site prophylactic medication ahead of the anticipated problem may be of benefit. Epiphysiolysis Introduction A complex condition of chickens that may be associated with trauma.Treatment None. Prevention Good hygiene at turn-around. Prevention Vaccination with inactivated vaccine prior to lay. Soluble multivitamins may be recommended as a nonspecific measure. bacterial infection. Vegetative lesions usually on the right atrioventricular valve. Diagnosis Differentiate from broiler ascites syndrome by examination of the interior of the heart. Erysipelothrixetc. Peripheral vessels congested. streptococci. osteomyelitis. and /or trauma. Signs Fluid-distended abdomen.
These conditions currently only occur from northern South America to North America. wild birds. Post-mortem lesions Separation of epiphyses at the growth plate. The natural hosts are wild birds and rodents. Treatment Not applicable. May also be asymptomatic. Flaccid neck. WEE. Paralysis. Signs Nervous symptoms. chickens. sometimes seen in vivo. Horses are also seriously affected. Diagnosis Gross inspection. histology may be helpful in identifying underlying problems such as rickets or 'FHN'. Tremors. Microscopic lesions not pathognomonic. Equine Encephalitis (EEE. Prevention Control of predisposing factors. often occurs or is identified in the processed carcase.Signs Apparent dislocation at extremities of long bones. partridges. Circling. 57 . It is transmitted between birds by pecking and by mosquitoes. ducks and pigeons having a high morbidity and high mortality. Ataxia. Paresis. VEE) Introduction A viral disease of pheasants. turkeys. Post-mortem lesions No gross lesions.
Diagnosis Isolation in mice. ducks. and CE. fishmeal and semen and by cannibalism. Chronic scabby skin. rarely in geese. especially snood. COFAL. muscle. It may be transmitted by faecal carriers for 41 days. spleen swollen. Swollen snood. water. Sleepiness. Sudden death. pheasants. 58 . Post-mortem lesions Carcase congestion. Endocarditis. ID by VN. Joint lesions. kidney. May be diarrhoea and respiratory signs. The bacterium is fairly resistant to environmental effects or disinfectants and may persist in alkaline soil for years. in soil. Treatment None. Marked catarrhal enteritis. Prevention Protection from mosquitoes. It is also seen in some mammals. TC. Perineal congestion. There is likely to be an increased risk if housing or land has been previously used by pigs or sheep. rhusiopathiae) seen in turkeys and increasingly in free-range chickens. Erysipelas Introduction A sudden onset infection with the bacterium Erysipelothrix insidiosa (E. Liver. Vaccinate at 5-6 week. Signs Inappetance. Depression. control cannibalism. epicardium. Haemorrhages in fat.
a combination of the procaine and benzathine salts may be injected. often along with bacterin. 59 . Tetracyclines in feed may also be helpful. and acute Newcastle disease. Vaccination or natural infection may cause false positive reactions in the Mycoplasma gallisepticum and M. history. Some birds with pale comb and wattles. Headparts pale. Signs Overweight typically by 25%. especially caged layers and with a complex set of causes including excessive calories. and identification. Treatment Penicillin . Diagnosis Lesions.Diagnosis Isolation on blood agar. colibacillosis. the demonstration of the organism in stained impression smears from tissues. synoviae plate tests for a few weeks. Sudden drop in egg production. Post-mortem lesions Obesity. Liver yellow. Differentiate from pasteurellosis. deficiency and stress. Death by internal exsanguination after rupture of haematocyst. Sudden death. vaccine at 16-20 weeks if the condition is enzootic. Fatty Liver Haemorrhagic Syndrome Introduction A condition occurring worldwide in chickens. mycotoxins. Prevention Good biosecurity to prevent spread from other susceptible species. greasy and soft with numerous haemorrhages. salmonellosis.
Diagnosis Lesions. 60 . supplement with choline. 'Honeycomb' skin. avoid mycotoxins and stress. Feather loss. of chickens and turkeys. Thick crusty skin. Post-mortem lesions See signs (above). Trichophyton gallinae. Loss of condition. isolation. vitamin E. Treatment Formalin in petroleum jelly. Signs White. It is very rare in commercial poultry production. culling affected birds. Prevention Feed to avoid obesity. B 12 and inositol. Favus Introduction A fungal infection.Treatment Reduce energy intake. Prevention Good hygiene of facilities. powdery spots and wrinkled crusts and scab on comb and wattles.
Careful attention to mineral and Vitamin D nutrition to avoid subclinical. (increasing order of susceptibility). staphylococci. indicated that 0. Post-mortem studies of birds culled due to lameness and of birds found dead. Post-mortem lesions Degeneration of the epiphyses of long bones with thinning of the cortex and tendency to break when force is applied.g. Differentiate from synovitis. highly contagious disease caused by the bacterium Pasteurella multocida in a range of avian species including chickens. streptococci. Fowl Cholera. Pasteurellosis Introduction Fowl Cholera is a serious. arthritis. rickets. Signs Lameness.75% of all male broilers placed had lesions in the hip bone. Diagnosis Base on post-mortem lesions and isolation of a causative organism. 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. E. It is seen worldwide and was one of the first infectious 61 . spondylolisthesis. Prevention Exclusion of floor eggs and dirty eggs from the hatchery. FHN is the commonest infectious cause of lameness in broilers in the UK. coli.Femoral Head Necrosis . turkeys. especially hypophosphataemic. Predisposing factors include immunosuppresive viruses such as Infectious Bursal Disease Virus and Chicken Anaemia Virus and non-infectious bone pathologies such as hypophosphaetamic rickets.FHN Introduction A condition of chickens and turkeys that may be associated with several different bacterial infections e. and water fowl. Use of a wing for support during walking and hip flexion.
Lameness. ocular and oral discharge. equipment. Yolk peritonitis. The route of infection is oral or nasal with transmission via nasal exudate. and possibly pigs. Purulent pneumonia (especially turkeys). cats. Lungs with a consolidated pink 'cooked' appearance in turkeys.diseases to be recognised. Treatment Sulphonamides. The disease often recurs after medication is stopped. Signs Dejection. faeces. Post-mortem lesions Sometimes none. Cellulitis of face and wattles.no growth on McConkey). The disease can range from acute septicaemia to chronic and localised infections and the morbidity and mortality may be up to 100%. Sudden death. Swollen joints. penicillin. necessitating long-term or periodic medication. Enteritis. isolation (aerobic culture on trypticase soy or blood agar yields colonies up to 3mm in 24 hours . confirmed with biochemical tests. or limited to haemorrhages at few sites. Diagnosis Impression smears. Predisposing factors include high density and concurrent infections such as respiratory viruses. streptomycin. and people. The bacterium is easily destroyed by environmental factors and disinfectants. Focal hepatitis. contaminated soil. Nasal. Reservoirs of infection may be present in other species such as rodents. Loss of appetite. Coughing. 62 . but may persist for prolonged periods in soil. Ruffled feathers. Purulent arthritis. septicaemic viral and other bacterial diseases. tetracyclines. Diarrhoea. Differentiate from Erysipelas. erythromycin. Swollen and cyanotic wattles and face. The incubation period is usually 5-8 days. by Louis Pasteur in 1880.
spreading eruptions and scabs on comb and wattles. or by the respiratory route. turkeys. Morbidity is 1095% and mortality usually low to moderate. pigeons and canaries worldwide. Infection occurs through skin abrasions and bites. Avian Pox Introduction A relatively slow-spreading viral disease characterised by skin lesions and/or plaques in the pharynx and affecting chickens. Signs Warty.Prevention Biosecurity. The duration of the disease is about 14 days on an individual bird basis. hygiene. Poor egg production. Pox. Inappetance. good rodent control. Figure 19. Fowl Pox. bacterins at 8 and 12 weeks. and where there are biting insects. Severe localised Pasteurella infection in the swollen wattle of a 30-week-old male broiler parent chicken. live oral vaccine at 6 weeks. It is more common in males because of their tendency to fight and cause skin damage. Depression. The swelling is made up of oedema and purulent exudates (pus). Caseous deposits in mouth. The virus persists in the environment for months. It is transmitted by birds. Poor growth. 63 . fomites. 0-50%. throat and sometimes trachea. and mosquitoes (infected for 6 weeks).
Microscopically . be caseous plaques in mouth. in the diptheritic form. Diagnosis A presumptive diagnosis may be made on history. DNA probes. There is good cross-immunity among the different viral strains. signs and post-mortem lesions. Prevention By vaccination (except canary). Flocks and individuals still unaffected may be vaccinated. pharynx.intra-cytoplasmic inclusions (Bollinger bodies) with elementary bodies (Borrel bodies). reproduction in susceptible birds. Fowl pox lesions on the wattle of an adult broiler parent chicken. trachea and/or nasal cavities. 64 . Figure 20. Chickens well before production. Less commonly there may. If there is evidence of secondary bacterial infection broad-spectrum antibiotics may be of some benefit. Differentiate from Trichomoniasis or physical damage to skin. Turkeys by thigh-stick at 2-3 months. usually with chicken strain by wing web puncture. Treatment None. It is confirmed by IC inclusions in sections/ scrapings.Post-mortem lesions Papules progressing to vesicles then pustules and scabs with distribution described above. check take at 7-10 days post vaccination. isolation (pocks on CE CAM) with IC inclusions.
Signs Occasionally dejection. early Infectious Bursal Disease Virus infection). It occurs due to invasion of 'normal' wounds by 'normal' bacteria in immunosuppressed birds. wattles. Treatment Sulphaquinoxaline. Swelling and infarction of the liver. Prevention Good hygiene and management. usually over wings and breast. Foci in liver. Sudden mortality. Severe cellulitis especially of thighs.Gangrenous Dermatitis. occasionally Staphylococcus aureus. Diagnosis Clinical signs and/or lesions. penicillin or amoxycillin. especially following congenital Chick Anaemia Virus infection or early Infectious Bursal Disease Virus infection (Gumboro Disease). Recovery of an abundant growth of causative organism in recently dead birds. The spores of Clostridial bacteria are highly resistant in the environment. spleen. Immunosuppression is therefore a predisposing factor. wings. sometimes thighs and other parts. rarely Clostridium noyvi / oedematiens. Morbidity may be up to 50% and mortality is high. Post-mortem lesions Patches of gangrenous skin with underlying emphysematous and/or sanguinous cellulitis. 65 . Avoid skin trauma and immunosuppression (congenital CAV infection. Gangrenous skin. Loss of appetite. Necrotic Dermatitis Introduction A bacterial condition seen in chickens and usually caused byClostridium septicum.
Prevention Flubendazole. Head shaking.g. paired parasites up to 2 cm long. levamisole. confirmation of presence of the parasite. slugs and snails acting as transfer hosts but the life cycle may also be direct. Severe gangrenous dermatitis on the upper surface of the wing of a broiler chicken. The condition is seen more commonly in poultry on free range where ground may be contaminated by wild birds e. and other game and ornamental birds occurring worldwide. Treatment Flubendazole in feed. a nematode worm parasite of chickens. Diagnosis Signs and lesions. Signs Gasping. turkeys. from rookeries. 66 . by ingestion of embryonated egg or L3. Presence of worms. Infection is by the oral route with earthworms. Loss of appetite and condition. Dyspnoea. There is an 18-20 day prepatent period.Figure 21. pheasants. Gape Introduction Syngamus trachea. Post-mortem lesions Tracheitis.
muscular wall may be sacculated or ruptured. beetles etc act as intermediate hosts. weevils. 67 . routine worming. confirmation of presence of the worms. affecting geese and ducks. Signs Depression.Geese Introduction A nematode worm parasite. Adults are 2-4 cm long and usually bright red.Chickens Introduction Cheilospirura. Prevention Prevention of access to intermediate hosts. Post-mortem lesions Ulceration. benzimidazoles such as flubendazole. Loss in condition and weight. Cheilospirura and Streptocara are seen worldwide but Histiocephalus is restricted to Europe. Worms develop to L3 in eggs and infection is by the oral route direct from environment. Loss in condition and weight. Treatment Levamisole. Amidostomum anseris. Signs Depression. and Histiocephalus are nematode worm parasites of chickens. They are more common in free-range birds because of their increased access to intermediate hosts. Grasshoppers. Streptocara. Slow growth. necrosis and partial sloughing of gizzard lining. Diagnosis Lesions. Slow growth. Gizzard worms .Gizzard worms .
Vertical transmission resulting in congenital infection may occur. The amount of maternal antibody passed from the breeding birds will affect the severity and timing and severity of the condition in the young birds. Losses are negligible in birds over 5 weeks of age. muscular wall may be sacculated or ruptured. The younger the bird affected the more acute the condition and the higher the mortality. Membrane covering tongue. Prevention Rotation of ground on annual basis. Loss of down. Diagnosis Lesions. Signs Prostration and death in acutely affected goslings. Excessive water intake. Swollen eyelids and eye and nasal discharge. Goose Parvovirus (Derzsy's Disease) Introduction Goose Parvovirus is a highly contagious condition of geese and young Muscovy ducks. 68 . spleen and pancreas. benzimidazoles. Reduced feed intake. Treatment Levamisole.Post-mortem lesions Ulceration. Derzsy's Disease is caused by a parvovirus distinct from chicken and mammalian parvoviruses. Adults are 2-4 cm long and usually bright red. Reddening of skin. Post-mortem lesions Pale myocardium. Swelling and congestion of liver. necrosis and partial sloughing of gizzard lining. visualisation of worms. Profuse white diarrhoea.
Morbidity varies. Carcase anaemia. liver. Ascites. Haemorrhagic Anaemia Introduction A complex condition of chickens associated with drug toxicities. Loss of appetite. Blood in droppings. muscles. Antimicrobials may be of value in reducing the effects of secondary bacterial infections. Diagnosis Signs and lesions in birds of the appropriate age and species. Liver yellow. Ideally flocks that have suffered the disease should not be used for breeding as they may become persistent excreters of the infection. Haemorrhagic Disease. Fibrinous perihepatitis. Poor growth. The preferred approach is to immunise breeding birds with an attenuated live vaccine. Treatment No specific treatment. heart. Bone marrow pale with fatty change. Aplastic Anaemia. Signs Dejection. Administration of immune serum has been shown to be effective but may require two doses (day old and around 3 weeks). 69 . mortality is 5-50%. Prevention Hatching and brooding geese from different parent flocks together should be avoided. mycotoxins and viral infections and usually following a course of approximately 3 weeks. serosa and mucosae. Pale comb and wattles. Post-mortem lesions Haemorrhages in one or more sites: skin. Fibrinous pericarditis.
double-immuno-diffusion of splenic extract. the virus surviving in frozen faeces for months. caused by Type II Adenovirus distinct from classical fowl adenovirus and occurring in most turkey-producing areas. Spleen mottled and enlarged. Microscopic . add liver solubles to feed. The virulence of the virus varies but morbidity may be 100% and mortality 10-60%. Drop in feed and water consumption. Elisa . reticulo-endothelial hyperplasia and intranuclear inclusions. signs. and weeks in litter. Blood from vent of moribund birds. Diarrhoea. Prevention Avoid causative factors.Diagnosis History. Treatment Vitamin K. reproduction with filtered contents. similar to pheasant Marble Spleen disease. 70 . The route of infection is usually oral. May induce immunosupression and precipitate respiratory disease or coccidiosis. Serology: DID.spleen shows lymphoid hyperplasia. Haemorrhagic Enteritis Introduction A viral disease of turkeys. Signs Sudden deaths. Intestine distended with blood. remove sulphonamides.sero-conversion frequently occurs in absence of clinical disease. The source of virus is unknown but there is easy lateral spread within flocks. Course 10-21 days. Post-mortem lesions Petechiae in various tissues. lesions. Diagnosis Typical lesions.
Reduced feed consumption.and T-line lymphocytes for up to 5 weeks following exposure. and turkeys caused by high environmental temperature. Signs Panting. Immunity to the disease is long lasting. Increased thirst. especially associated with high relative humidity and low air speed. some in turkey B-lymphoblastoid cell lines. Disinfect and 3-4 weeks house rest. Predisposing factors include genetics. Prevention All-in/all-out production. drinking water temperature and availability.Treatment Warmth and good management. Ducks are relatively resistant to heat stress. Pathogenic strains can depress both B. good management. In this case a loop of intestine has been opened to show the blood. Figure 39. 71 . Live vaccines are commonly used in many countries at 4-5 weeks of age. high stocking density. Some are produced in live turkeys. Heat Stress Introduction A condition seen in chickens. feather cover. oral tetraycline. Turkeys dying with haemorrhagic enteritis commonly have the small intestine distended with blood. convalescent serum. nicarbazin in feed. Maternal antibody may interfere with vaccination. good hygiene and biosecurity. Immunity: there is an early age resistance irrespective of maternal antibody status. acclimation.
Inter-species transmission may occur. In commercial ducks a related parasiteTetratrichomonas can cause poor growth and drops in egg production. columbae) is a protozoan parasite of turkeys. contains excessive mucus and gas. pigeons. fomites. Prevention Houses of optimal height and insulation. pattern of losses. painted white to reflect heat. Feeding during cooler hours may be beneficial. Intestine flabby with some bulbous dilation. and some game birds. Reduced egg production. Later depression. evaporative coolers. Signs Initially birds nervous. pheasants. Treatment Cool water. Hexamitiasis Introduction Hexamita meleagridis (pigeons H. chirping. Post-mortem lesions Dehydration. carriers. Diagnosis Temperature records. signs. 72 . Reductions in stocking density of meat poultry may be quickly achieved by partial depletion ('thinning'). watery diarrhoea. Frothy. if relative humidity is low then wet the roof and fog. Legs and wings outstretched. Inappetance. maximise airflow. Mucoid exudate in nostrils and mouth. It is transmitted by faeces. Post-mortem lesions Carcases congested. feed with a reduced protein:energy ratio. lesions. Loss in weight. exclusion of other conditions. Terminal coma and convulsions. Prostration.
Prevention Depopulation. The effect of antibiotic may be related to the control of secondary bacterial enteritis. Sulphur-yellow diarrhoea. Histomoniasis. Blackhead Introduction Histomonas melagridis is a protozoan parasite of turkeys. It has recently been demonstrated that infection occurs readily via the cloaca when birds are on contaminated litter. Differentiate from transmissible enteritis. Caecal tonsils congested. and also. Inappetance. Outwith earth worms orH. Poor growth. Treatment Tetracycline. histomonosis. First half of intestine inflamed. trichomoniasis. dimetridazole. scrapings from fresh material. Signs Depression. Cyanosis of head. pheasants and game birds that acts together with facultative bacteria to produce the condition of Blackhead. Furazolidone. 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. all-in/all-out production. significant disease has been seen in breeding chickens and free-range layers. This condition has high morbidity and mortality in turkeys. presumably introduced with worm eggs. dimetridazole and ipronidazole have been used in the past. Diagnosis Lesions. Blood in faeces (chickens). and occasionally chickens. hygiene. Histamonosis. Progressive depression and emaciation. avoid interspecies mixing. 73 . increase ambient temperature. paratyphoid. The problem is seen in high-biosecurity facilities. if possible. gallinae the parasite is easily destroyed. Within a turkey shed transmission is rapid in spite of the fact that it is difficult to infect birds orally with unprotected parasites. Although chickens are relatively resistant to the condition. and mixing groups of different ages.
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. Intensive relittering may help reduce the level of infection. usually grey in colour. Some herbal products based on the essential oils (e. The disease is readily reproduced by inoculating birds with a bacteria-free filtrate of a liver extract from an affected bird. given recent new knowledge on the mechanism of transmission.nitarsone) have been used to treat this important disease of poultry. Having both chickens and turkeys on the same property is likely to increase the risk of this disease in turkeys. Hydropericardium-Hepatitis Syndrome. scrapings from fresh material. caseous cores with yellow. however they may not be present in the early stages. Regular worming to help control the intermediate hosts.Tahir Post-mortem lesions Enlargement of caeca. At the time of writing no products of these groups are approved for use in the European Union. It is a condition caused by an adenovirus.g.g. especially in chickens. Mortality may reach 60% but more typically 10-30%. possibly in combination with an RNA virus and immunosuppression caused by Chick Anaemia Virus or Infectious Bursal Disease. Liver may have irregular-round depressed lesions. 'Herban)' have been used with some apparent success though controlled trials and formal approval for this purpose are not recorded. and only nitarsone is approved in the USA. furazolidone. Use of an anti-histomonas product in feed where such products are approved but due care with respect to residue avoidance would be required. nifursol) and arsenicals (e. Prevention Good sanitation. It affects mainly broilers and broiler parents in rear and has also been seen in pigeons. concrete floors. dimetridazole). Diagnosis Lesions. avoid mixing species.Abubakar.g.g. 74 . nitrofurans (e. grey or green areas. Ulcers. Treatment Historically nitro-imidazoles (e. Angara Disease Introduction This condition was first identified in broilers in Pakistan in 1987.M. Arsenicals are less effective in treatment than they are in prevention.
Lethargy. Prevention The condition typically occurs in areas of high poultry density where multi-age operation is traditional. Formalin-inactivated oil adjuvant vaccines are reported to be highly effective and are used in areas where the condition is endemic. Gizzard activity also acts as a pacemaker of intestinal activity and controls the speed at which food is passed to the small intestine. This condition usually affects only a small number of birds. Treatment None. to reduce their particle size to aid digestion. however if young chicks to do not begin to eat feed properly they often consume litter instead. Yellow mucoid droppings. histopathology. Congestion of the carcase.1% of a 2.g. Impacted gizzards are then found in 'non-starter' type chicks or poults. Diagnosis Lesions. however sometimes free-range poultry consume large stones. treatment of drinking water with 0. virology. Most young commercial poultry consume feeds that have a small particle size. and birds of any age can 75 . Enlarged.5% iodophor solution) appears to be beneficial. string etc. grass. Grit would not be classed as a foreign body. Lungs oedematous. Older birds ingest grit to facilitate the grinding activity in the gizzard. The normal function of the gizzard is to aid in the physical grinding of food materials. Post-mortem lesions Excessive straw-coloured fluid distending the pericardium (up to 10 mls). Control of predisposing immunosuppressive diseases may help limit losses. pale friable liver and kidney. Impaction and Foreign Bodies of Gizzard Introduction The gizzard or crop may become impacted with litter. Huddling with ruffled feathers. Good water sanitation (e.Signs Sudden increase in mortality.
Prevention Good brooding management to encourage early adaptation to the diet and adequate consumption of feed and water. Sweep floors after maintenance activities to remove nails and other potentially dangerous foreign bodies. A foreign body may be found in the interior of the gizzard. Treatment None effective in young birds. Infected birds remain carriers for a few weeks. Italy. The disease was first described in the USA in 1963 and has also been reported in Canada. Inclusion Body Hepatitis Introduction A disease of chickens characterised by acute mortality. A number of different sero-types have been isolated from disease outbreaks but they may also be isolated from healthy chickens. and on opening is found to contain a mass of fibrous material. caused by an adenovirus. staples etc. It has a course of 9. often with severe anaemia. Daily monitoring of the crop-fill is a useful procedure. Nails commonly penetrate the lining of the gizzard.consume nails. Australia. 76 . the UK. Signs Reduced feed intake. and may penetrate the body wall. This usually happens after maintenance activities have been carred out in the housing. This may extend into the proventriculus and on into the duodeunum. Diagnosis Lesions. France and Ireland.15 days with a morbidity of 1-10% and a mortality of 1-10%. Reduced weight gain. Post-mortem lesions The gizzard is more firm than normal and. Obvious non-starters should be culled in this situation. It allows us to confirm the proportion of chicks consuming feed and can give inexperienced poultry keepers feedback on the effectiveness of their brooding management.
Soluble multivitamins may help with the recovery process. Confirmation is made on finding inclusions in the liver. for instance due to early IBD challenge or congenital CAV infection. CEL). may be important. Progeny of high health status breeding flocks appear to be at greater risk. Pallor of comb and wattles. Since adenoviruses are commonly found in healthy poultry. Ruffled feathers. A form of the disease affecting birds under 3 weeks of age in Australia has been reproduced with serotype 8 adenovirus.Transmission may be vertical or lateral and may involve fomites. many different sero-types have been isolated from different cases. Immunosuppression. chloroform. perhaps because they have lower levels of maternal antibody. and deficiency of vitamin B12. fatty liver syndrome. and high temperatures. Treatment None. yellow. Inappetance. Bursa and spleen small. Signs Depression. 77 . sulphonamide intoxication. Blood thin. isolation alone does not confirm that they are the cause of a particular problem. Formaldehyde and iodides work better. mottled with petechiae and ecchymoses. Infectious Bursal Disease. Differentiate from Chick anaemia syndrome. pH). but on the other hand many field cases show eosinophilic inclusions that do not appear to have adenovirus particles.basophilic intranuclear inclusions. Serology: DID for group antigen. The virus is generally resistant to disinfectants (ether. The virus grows well in tissue culture (CEK. SN for individual sero-types. Microscopically . vibrionic hepatitis. Post-mortem lesions Liver swollen. Diagnosis A presumptive diagnosis may be made on history and lesions. Curiously. Kidneys and bone marrow pale.
Coughing. About eight sero-groups are recognised by sero-neutralization. was first described in the USA (N. prevention of immunosuppression. Dakota. Tracheitis. 78 . IB Introduction This infection. prior vaccination. Some birds/viral strains can be carriers to 1 year. fomites or aerosol. disinfectants (Formal 1% for 3 mins). Poor ventilation and high density are predisposing factors. The virus. Its affects vary with: the virulence of the virus. Loss of appetite. dyspnoea. Kidneys and bronchi may be swollen and they and the ureters may have urates. Post-mortem lesions Mild to moderate respiratory tract inflammation. Diarrhoea. Infection is via the conjunctiva or upper respiratory tract with an incubation period of 18-36 hours. and complicating infections (Mycoplasma. depending on secondary infections. The cause is a Coronavirus that is antigenically highly variable. Huddling. Tracheal oedema. new sero-types continue to emerge. E. coli. Wet litter. These differences are due to structural differences in the spike proteins (S1 fraction). which may survive 4 weeks in premises. Signs Depression. alkalis. The infection is highly contagious and spreads rapidly by contact. is sensitive to solvents. Airsacculitis. Diuresis. Caseous plugs in bronchi. the age of the bird. Infectious Bronchitis. maternal immunity (young birds). gasping. Typing by haemagglutination-inhibition is also used. Newcastle disease). 1931). Morbidity may vary 50-100% and mortality 0-25%. probably the commonest respiratory disease of chickens. heat (56°C for 15 mins).Prevention Quarantine and good sanitary precautions.
flourescent antibody positive and ciliostasis in tracheal organ culture. IB . Differentiate from Newcastle disease (lentogenic and mesogenic forms). short duration. Prevention Live vaccines of appropriate sero-type and attenuation. with typical lesions. Definitive diagnosis is based on viral isolation after 3-5 passages in chick embryo. Cellmediated immunity may also be important. Humoral immunity appears 10-14 days post vaccination. Serology: HI. group specific). Elisa (both group specific). Infectious Bronchitis. lesions and serology. SN (type specific). vaccinal reactions. The infection spreads rapidly by contact. fomites or aerosol.antibiotics to control secondary colibacillosis (q. Maternal immunity provides protection for 2-3 weeks. The virus. possible reactions depending on virulence and particle size.Diagnosis Tentative diagnosis is based on clinical sgns. Some birds/viral strains can be carriers for up to 1 year. alkalis. Poor ventilation and high density are predisposing factors. heat (56°C for 15 mins). is sensitive to solvents. disinfectants (Formal 1% for 3 mins). which may survive 4 weeks in premises. depending on secondary infections.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%. Muscular shivering.). Treatment Sodium salicylate 1gm/litre (acute phase) where permitted . mycoplasmosis. Infection is via the conjunctiva or upper respiratory tract with an incubation period of 18-36 hours. DID (poor sensitivity. Local immunity is first line of defence.v. 79 . HA negative. Signs Sudden death. Avian Influenza and Laryngotracheitis. Otherwise as for standard IB.
The virus is moderately resistant and may survive 4 weeks in premises. Infectious Bronchitis. Loss of internal egg quality. lesions progress to necrosis and scarring of deep pectorals in convalescence.Post-mortem lesions Oedema of pectoral muscles and subcutaneously on abdomen. HA-. Treatment Sodium salicylate 1gm/litre (acute phase) where permitted . ciliostatic in tracheal organ culture. Elisa (both group specific). sneezing. Infection is via the conjunctiva or upper respiratory tract. typical lesions. A few birds are carriers up to 49 days post infection. cell culture (Vero. Rough shells. Coughing. Rales may or may not be present. possible reactions depending on virulence and particle size. 80 . with much antigenic variation. Poor ventilation and high density are predisposing factors. CK) only after adaptation Serology: HI.v. IB Egg-layers Introduction A Coronavirus infection of chickens. Other lesions of 'classical' IB may be encountered. Soft-shelled eggs. There is rapid spread by contact. short duration. Diagnosis 3-5 passages in CE allantoic cavity. SN (type specific). DID (poor sensitivity.). Prevention Live vaccines of appropriate sero-type and attenuation. In layers the ovules may be intensely congested. Signs Drop in egg production (20-50%). FA.antibiotics to control secondary colibacillosis (q. fomites or aerosol. The condition has a morbidity of 10-100% and mortality of 0-1%. group specific).
). Maternal immunity provides protection for 2-3 weeks. typical lesions. Humoral immunity appears 10-14 days post vaccination. FA. EDS76. HA-.antibiotics to control secondary colibacillosis (q. Elisa. particle size (if sprayed) and general health status. Prevention Live vaccines of appropriate sero-type and attenuation. 81 . virulence. Figure 22. Cell-mediated immunity may also be important. although reactions can occur depending on prior immunity. Diagnosis 3-5 passages in CE. Flaccid ovarian follicles in a broiler parent chicken undergoing challenge with Infectious Bronchitis virus. DID. SN. Serology: HI.Post-mortem lesions Follicles flaccid. Differentiate from Egg Drop Syndrome.v. Yolk in peritoneal cavity (non-specific). Local immunity is the first line of defence. Treatment Sodium salicylate 1gm/litre (acute phase) where permitted .
Coughing. although reactions can occur depending on prior immunity. Prevention Live vaccines of appropriate sero-type and attenuation.Infectious Bronchitis. Serology: HI. Poor ventilation and high density are predisposing factors. HA-. A few birds are carriers up to 49 days post infection. particle size (if sprayed) and general health status.v. Post-mortem lesions Follicles flaccid. DID. The virus is moderately resistant and may survive 4 weeks in premises. Rales may or may not be present. Maternal immunity provides protection for 2-3 weeks. Differentiate from Egg Drop Syndrome. typical lesions. Humoral immunity appears 10-14 days post vaccination. IB Egg-layers Introduction A Coronavirus infection of chickens. Loss of internal egg quality. Diagnosis 3-5 passages in CE. FA. 82 .). Signs Drop in egg production (20-50%). sneezing. Yolk in peritoneal cavity (non-specific). Treatment Sodium salicylate 1gm/litre (acute phase) where permitted . SN. EDS76. Rough shells. There is rapid spread by contact. virulence. fomites or aerosol.antibiotics to control secondary colibacillosis (q. Local immunity is the first line of defence. Cell-mediated immunity may also be important. Infection is via the conjunctiva or upper respiratory tract. Soft-shelled eggs. Elisa. The condition has a morbidity of 10-100% and mortality of 0-1%. with much antigenic variation.
Mealworms and litter mites may harbour the virus for 8 weeks.20% but sometimes up to 60%. but may be via the conjunctiva or respiratory tract. Gumboro Introduction A viral disease. first identified in the USA in 1962. The infective agent is a Birnavirus (Birnaviridae). Generally speaking the earlier the damage occurs the more severe the effects. The disease is highly contagious. In addition to the direct economic effects of the clinical disease. The route of infection is usually oral. The virus is very resistant. (Turkeys and ducks show infection only. Infectious Bursal Disease. especially with sero-type 2).Figure 22. which targets the bursal component of the immune system of chickens. Marek's disease and Infectious Bronchitis. seen worldwide. and affected birds excrete large amounts of virus for about 2 weeks post infection. Subclinical infection in young chicks results in: deficient immunological response to Newcastle disease. IBD. Signs are most pronounced in birds of 4-6 weeks and White Leghorns are more susceptible than broilers and brown-egg layers. the damage caused to the immune system interacts with other pathogens to cause significant effects. susceptibility to Inclusion Body Hepatitis and gangrenous dermatitis and increased susceptibility to CRD. There is no vertical transmission. The age up to which infection can cause serious immunosuppression varies between 14 and 28 days according to the antigen in question. persisting for months in houses. 83 . faeces etc. Morbidity is high with a mortality usually 0. Flaccid ovarian follicles in a broiler parent chicken undergoing challenge with Infectious Bronchitis virus. with an incubation period of 2-3 days. Sero-type 1 only.
Tests used are mainly Elisa. This may be confirmed by demonstrating severe atrophy of the bursa. Other possible causes of early immunosuppression are severe mycotoxicosis and managment problems leading to severe stress. rapidly proceeds to atrophy. They are all serotype 1. Unsteady gait. subsequent diagnosis of 'immunosuppression diseases' (especially inclusion body hepatitis and gangrenous dermatitis) is highly suggestive. Antibiotic medication may be indicated if secondary bacterial infection occurs. Haemorrhagic syndrome. Elisa vaccination date prediction < 7 days). especially in the Delmarva Peninsula in the USA. Coccidiosis. 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.1% are highly suggestive. The normal weight of the bursa in broilers is about 0. Post-mortem lesions Oedematous bursa (may be slightly enlarged.3% of bodyweight.4 days. Vent pecking. IBD viruses have been isolated and shown to have significant but not complete cross-protection.A history of chicks with very low levels of maternal antibody (Fewer than 80% positive in the immunodifusion test at day old. histopathology. Swollen kidneys with urates. normal size or reduced in size depending on the stage). Diagnosis Clinical disease . Serology: antibodies can be detected as early as 4-7 days after infection and these last for life. lesions. especially if present prior to 20 days of age. Variants: There have been serious problems with early Gumboro disease in chicks with maternal immunity. weights below 0.5. Diarrhoea with urates in mucus. Inappetance. Differentiate clinical disease from: Infectious bronchitis (renal). Haemorrhages in skeletal muscle (especially on thighs). Half-life of maternally derived antibodies is 3. may have haemorrhages. Huddling under equipment. (previously SN and DID). Subclinical disease . Dehydration.History. Treatment No specific treatment is available. Use of a multivitamin supplement and facilitating access to water may help. Cryptosporidiosis of the bursa (rare).Signs Depression. 84 .
This shows the anatomical relationship between the bursa. Carriers are important with transmission via exudates and by direct contact. especially nasal and sinus mucosae. biosecurity measures may be helpful in limiting the spread between sites. vaccination of progeny depending on virulence and age of challenge. Figure 23. When outbreaks do occur. It is not egg transmitted. It is enlarged. 85 . characterised by catarrhal inflammation of the upper respiratory tract. Immunity after a live vaccine can be poor if maternal antibody was still high at the time of vaccination. including passive protection via breeders. Infectious Coryza is caused by the bacterium Haemophilus paragallinarum and is seen in many countries especially in multi-age farms that are never depopulated. highly infectious disease of chickens. Infectious Coryza Introduction A usually acute. In most countries breeders are immunised with a live vaccine at 6-8 weeks of age and then re-vaccinated with an oil-based inactivated vaccine at 18 weeks. The 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. turgid and oedematous.Prevention Vaccination. occasionally pheasants and guinea-fowl. This bursa is from an acutely affected broiler. Morbidity is high but mortality low if uncomplicated although it may be up to 20%. A strong immunity follows field challenge. sometimes chronic. the rectum and the vent. and tracing of contacts may indicate sites on which a more rebust vaccination programme is indicated. resulting in increased culling.
Dyspnoea. Diagnosis A presumptive diagnosis may be made on signs. tylosin. Differentiate from Mycoplasmosis. 86 . Swollen wattles. while bacterins only protect against homologous strains. Serology: HI. Treatment Streptomycin. Live attenutated strains have been used but are more risky. Dihydrostreptomycin. lesions. Bacterin at intervals if history justifies or if multi-age. Conjunctivitis.requires X (Haematin) and V (NAD) factors. erythromycin. Signs Facial swelling. Flouroquinolones are bactericidal and might prevent carriers. DID. Vaccines are used in areas of high incidence. Caseous material in conjunctiva/sinus. Sneezing. Controlled exposure has also been practised. at least two doses are required. Post-mortem lesions Catarrhal inflammation of nasal passages and sinuses. Loss in condition. agglutination and IF have all been used but are not routine. Prevention Stock coryza-free birds on an all-in/all-out production policy. Intercurrent respiratory viral and bacterial infections are predisposing factors. Inappetance. drying and disinfectants. respiratory viruses. Confirmation is by isolation and identification . Drop in egg production of 10-40%. Commercial bacterins may not fully protect against all field strains but reduce the severity of reactions. identification of the bacteria in a Gram-stained smear from sinus. sulphonamides. chronic or localised pasteurellosis and vitamin A deficiency. Tracheitis. Purulent ocular and nasal discharge. Birds recovered from challenge of one serotype are resistant to others. Eye-lid adherence. preferably in raised CO 2 such as a candle jar.The bacterium survives 2-3 days outside the bird but is easily killed by heat.
Coughing of mucus and blood. antibiotics to control secondary bacterial infection if this is marked. after 4 weeks of age. All-in/allout operation. The virus is highly resistant outside host but is susceptible to disinfectants. IFA. Drop in egg production.Infectious Laryngotracheitis. Nasal discharge (low pathogenicity strains). Sera may be examined by VN or Elisa. if enzootic or epizootic in an area. pheasants. Transmission between farms can occur by airborne particles or fomites. 87 . Prevention Quarantine. Treatment None. Gasping. in severe form may be enough.intranuclear inclusions in tracheal epithelium. ILT Introduction A herpesvirus (pathogenicity can vary) infection of chickens. Fairly slow lateral spread occurs in houses. Keep susceptible stock separate from vaccinated or recovered birds. Sinusitis. Post-mortem lesions Severe laryngotracheitis. severe bronchitis. Isolation in CE CAMs. Ocular discharge. Microscopically . often with blood in lumen. histology. Recovered and vaccinated birds are long-term carriers. Movement and mixing of stock and reaching point of lay are predisposing factors. PCR. 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. Signs Dyspnoea. vaccination. Diagnosis Signs. Differentiate from Newcastle disease. lesions. peafowl and turkeys with a morbidity of 50-100% and a mortality usually 10-20% but sometimes up to 70%. Apply strict biosecurity in moving equipment or materials between these these categories of stock. caseous plugs may be present.
rarely chickens. Thirst. Rapid breathing. guinea fowl. Prevention Control of coccidiosis and other causes of intestinal inflammation. 88 . worms and other forms of enteritis are predisposing factors. Careful attention to feeding practices to avoid anticipation of feed arrival if on restricted feeding. Signs Mainly sudden deaths. Simulid flies or culicoid midges are intermediate hosts. Loss of equilibrium. Coccidiosis. Diagnosis Typical post-mortem lesions Treatment As appropriate for the underlying disease condition. Different species of this parasite have been reported from North America. The disease has a short course and morbidity and mortality are high. Asia and Africa. Signs Sudden onset of depression. usually in the lower small intestine.Intussusception Introduction A condition of chickens associated with increased intestinal motility. Survivors may carry infection. Anorexia. it may actually protrude at the vent and be cannibalised. Post-mortem lesions Telescoping of the bowel. ducks. Leukocytozoonosis Introduction Caused by Leucocytozoon species. protozoan parasites of turkeys.
Lymphoproliferative Disease (LPD) Introduction A Type C retrovirus infection of turkeys with low morbidity and high mortality. Post-mortem lesions Focal tumours. Post-mortem lesions Splenomegaly. Anaemia. Diagnosis History. Treatment 89 . Persistent low mortality. Differentiate from Reticuloendotheliosis. Anaemia. Diagnosis Lesions. Loss of weight. Signs Depression. age. Prevention Separation from intermediate hosts. Microscopically . lesions. Enlargement of abdomen. schizonts in liver. liver or bursa. especially in enlarged spleen. May be asymptomatic. Treatment None known. histology and blood smears. Hepatomegaly. disposal of recovered birds. cytology.megaschizonts in brains of birds with nervous signs. Emaciation. gametes in erythrocytes.
Sometimes osteomyelitis and/or rickets.(maize-) fed birds (often associated with orange intestinal contents and/or faeces). for example enteroviruses. Poor management may contribute to the problem. 90 . Stunting (temporary). Diarrhoea. temperature control) may lead to a similar picture in the absence of specific infection. The condition has been seen in Europe. Diarrhoea in older birds may be an effect of on-farm infection. in future eradication. enterovirus-like particles. Abnormal feathers ('helicopter wings' 'yellow-heads').Tahir None. Signs Uneven growth. reoviruses. Prevention Good hygiene.Abubakar. Runting/Stunting Introduction A condition of chickens and turkeys that may be associated with several different viruses. Pot-bellied appearance. Treatment Daily cull of affected birds between 14 and 28 days. rotavirus etc. Diagnosis Pathology. Eating faeces. Post-mortem lesions Enteritis. North and South America and Australia.M. direct electron microscope examination of intestinal contents. Pale shanks in corn. Runting (permanent). Poor feathering. Pancreatic atrophy/fibrosis and pancreatic atrophy (rather variable). control arthropods. all-in/all-out production. Poor early management (feed and water supply. Malabsorption Syndrome. It is suspected that these viruses can be vertically transmitted and the most severe signs in young birds are associated with this.
avoidance of intercurrent disease and management problems (such as chilling). as well as more longstanding paralysis of legs or wings and eye lesions. Vertical transmission is not considered to be important. etc.poorly digested food enclosed in mucus. good parent nutrition and egg selection and santitation. seen worldwide. and rarely turkeys in close association with chickens. c) Cutaneous . Intestines of a young broiler chick suffering from malabsorption syndrome. From the 1980s and 1990s highly virulent strains have become a problem in North America and Europe. Morbidity is 10-50% and mortality up to 100%.Tumours of feather follicles. tests.Acute infiltration of the CNS and nerves resulting in 'floppy broiler syndrome' and transient paralysis. Figure 24. Infected birds remain viraemic for life.Prevention Good broiler farm hygiene. In 'late' Marek's the mortality can extend to 40 weeks of age. both parasitic and bacterial. Affected birds are more susceptible to other diseases.Tumours in heart. b) Visceral . lungs. fomites. Mortality in an affected flock typically continues at a moderate or high rate for quite a few weeks. The virus survives at ambient temperature for a long time (65 weeks) when cell associated 91 . The disease has various manifestations: a) Neurological . muscles. ovary. They are distended with poorly digested feed. A sample of the faeces produced is shown at the bottom of the picture . Marek's disease Introduction Marek's disease is a Herpes virus infection of chickens. The route of infection is usually respiratory and the disease is highly contagious being spread by infective feather-follicle dander.
g. Microscopically . resistant strains. heart. Differentiate from Lymphoid leukosis. vaccination generally with 1500 PFU of HVT at day old (but increasingly by in-ovo application at transfer). game birds. Signs Paralysis of legs. Ducks and geese can 92 . especially at the start of lay. gonads. Chronic Respiratory Disease . association with other strains (SB1 Sero-type 2) and Rispen's. Vision impairment. turkeys. deficiency of Ca/Phosphorus/Vitamin D. Diagnosis History. chronic respiratory disease in chickens. botulism. all-in/all-out production. M. Mycoplasma gallisepticum infection. It is inactivated rapidly when frozen and thawed. Loss of weight. Grey iris or irregular pupil. It is common practice to use combinations of the different vaccine types in an effort to broaden the protection achieved. age affected. Skin around feather follicles raised and roughened. clinical signs.. spleen. Thickening of nerve trunks and loss of striation. lung. Genetics can help by increasing the frequency of the B21 gene that confers increased resistance to Marek's disease challenge. histopathology. deficiency of thiamine. and skeletal muscle. kidney. pigeons and other wild birds.lymphoid infiltration is polymorphic. Treatment None. distribution of lesions. Prevention Hygiene.Chicken Introduction Infection with Mycoplasma gallisepticum is associated with slow onset. wings and neck.and is resistant to some disinfectants (quaternary ammonium and phenol). Post-mortem lesions Grey-white foci of neoplastic tissue in liver.
subsequent stress may cause recurrence of disease. though infection rates are high. exudates. Reduced hatchability and chick viability. Pasteurella spp. serology. 93 . The route of infection is via the conjunctiva or upper respiratory tract with an incubation period of 6-10 days. and to a lesser extent fomites. airborne dust and feathers. coli infection). and inadequate environmental conditions are predisposing factors for clinical disease. Haemophilus. aerosols. Diagnosis Lesions. tenosynovitis and salpingitis in chickens. In adult birds. morbidity may be minimal and mortality varies. more commonly in Mycoplasma Broth followed by plating out on Mycoplasma Agar. Perihepatitis (especially with secondary E. coli. demonstration of specific DNA (commercial PCR kit available). Poor productivity. Fomites appear to a significant factor in transmission between farms. trachea and bronchi. Suspect colonies may be identified by immuno-flourescence. The condition occurs worldwide. and in lyophilised material. though in some countries this infection is now rare in commercial poultry. Signs Coughing. Pericarditis. virulent E. Recovered birds remain infected for life. In turkeys it is most associated with severe sinusitis (see separate description in the turkey section). Spread is slow between houses and pens suggesting that aerosols are not normally a major route of transmission. Leg problems. Occasionally arthritis. Inappetance. Post-mortem lesions Airsacculitis. Occasional encephalopathy and abnormal feathers. ART). In others it is actually increasing because of more birds in extensive production systems that expose them more to wild birds. Nasal and ocular discharge. The infectious agent survives for only a matter of days outwith birds although prolonged survival has been reported in egg yolk and allantoic fluid.become infected when held with infected chickens. Slow growth. sinuses. Culture requires inoculation in mycoplasma-free embryos or. isolation and identification of organism. Intercurrent infection with respiratory viruses (IB. Survival seems to be improved on hair and feathers. Catarrhal inflammation of nasal passages. Transmission may be transovarian. ND. Stunting. or by direct contact with birds.
though in many countries this infection is now rare in commercial poultry. meleagridis(turkeys). Elisa is accepted as the primary screening test in some countries. tetracyclines.g. fluoroquinolones. subsequent stress may cause recurrence of disease. and routine serological monitoring. all-in/all-out production. therefore M.g. Differentiate from Infectious Coryza. Infectious Sinusitis . Suspect flocks should be re-sampled after 2-3 weeks. generally as a confirmatory test.Turkeys Introduction A slow onset chronic respiratory disease of turkeys often with severe sinusitis and associated with Mycoplasma gallisepticuminfection. M. biosecurity. Mycoplasma gallisepticum infection. Productivity in challenged and vaccinated birds is not as good as in M. Live attenuated or naturally mild strains are used in some countries and may be helpful in gradually displacing field strains on multi-age sites. infection status is important for trade in birds. Transmission may be transovarian. HI may be used. These programmes are based on purchase of uninfected chicks. suspect reactions are examined further by heat inactivation and/or dilution. hatchingeggs and chicks. and fomites. The route of infection is via the conjunctiva or upper respiratory tract with an incubation period of 6-10 days. or by direct contact with birds. exudates. Recovered birds remain infected for life. vitamin A deficiency. 94 . PCR is possible if it is urgent to determine the flock status.g. viral respiratory diseases. Treatment Tilmicosin.-free stock. Effort should be made to reduce dust and secondary infections. Aspergillosis. synoviae and M. In some circumstances preventative medication of known infected flocks may be of benefit. Prevention Eradication of this infection has been the central objective of official poultry health programmes in most countries. tylosin. spiramycin.Serology: serum agglutination is the standard screening test. Some inactivated vaccines for other diseases induce 'false positives' in serological testing for 3-8 weeks.. Morbidity is low to moderate and mortality low. It is seen worldwide. other Mycoplasma infections such as M. aerosols.
The infectious agent survives for only a matter of days outwith birds. Effort should be made to reduce dust and secondary infections. suspect reactions are examined further by heat inactivation and/or dilution. tetracyclines. of swabs taken from the trachea or lesions. Signs Coughing. and in lyophilised material. Swollen sinuses. Inappetance. In some circumstances preventative medication of known infected flocks may be of benefit. although prolonged survival has been reported in egg yolk and allantoic fluid. spiramycin. more commonly in Mycoplasma Broth followed by plating out on Mycoplasma Agar. fluoroquinolones. tylosin. Perihepatitis. and biosecurity. Diagnosis Lesions. serology. Pericarditis. Suspect colonies may be identified by immunofluorescence. Treatment Tilmicosin. isolation and identification of organism. Prevention Eradication of this infection has been the central objective of official poultry health programmes in most countries. often with inspissated pus. Stress. especially Turkey Rhinotracheitis. Nasal and ocular discharge. These are based on purchase of uninfected poults. Differentiate from viral respiratory disease. Serology: serum agglutination is the standard screening test. demonstration of specific DNA (commercial kit available). HI may also be used. Survival seems to be improved on hair and feathers. requires inoculation in mycoplasma-free embryos or. Suspect flocks should be re-sampled after 2-3 weeks. Stunting. 95 . Culture. Slow growth. Airsacculitis. Some inactivated vaccines induce 'false positives' in serological testing. intercurrent viral disease such as Newcastle disease (even lentogenic) and Turkey Rhinotracheitis are predisposing factors. PCR is possible if it is urgent to determine the flock status. malnutrition. Leg problems. all-in/allout production. Post-mortem lesions Swollen infraorbital sinuses.
ducks (France). although DNA homology is only 40%. Post-mortem lesions Sinusitis.g. Reduced hatchability. Signs Swollen sinuses. some with down abnormality.g. and can occur in other poultry and wild bird species.i. Infection occurs via the conjunctiva or upper respiratory tract and transmission among poults may be vertical. Post-mortem lesions Stunted embryos with hepatitis and enlarged spleens. perhaps because all affected embryos fail to hatch. Prevention As for M. Leg lesions can be shown in inoculated birds but do not seem to occur naturally.Mycoplasma immitans infection Introduction Infection with Mycoplasma immitans is seen in geese. Treatment As for M. Diagnosis Shows cross reaction in IFA to M. Introduction Infection with Mycoplasma iowae is seen in turkeys. Mycoplasma iowae infection. venereal or horizontal. and partridges (UK). 96 . M. Signs Embryonic mortality.g.
m. 97 .Diagnosis Isolation and identification of the causative organism from dead-in-shell embryos.i. Infected parents may be asymptomatic. Infected eggs result in widespread distribution of infection and increased risk of further vertical transmission. The organism has also been isolated from raptors. Leg problems. Infection is via the conjunctiva or upper respiratory tract with an incubation period of 6-10 days. Pathogenicity is quite variable. Antibiotics that have been used are tylosin and enrofloxacin. Slow growth. Specialised dip tanks are subjected to negative pressure which partially collapses the air cell of the submerged eggs. Mycoplasma meleagridis infection. purchase of M. Stunting. though up to 25% of infected birds show lesions at slaughter. Transmission is venereal in breeders. Predisposing factors include stress and viral respiratory infections. M. with transovarian and then lateral spread in meat animals. morbidity may be minimal. Treatment Pressure differential dipping has been used where breeder flocks are infected. For eradication purposes egg injection provides more consistent dosing per egg than does egg dipping.-free stock. Prevention Eradication of the infection from breeding stock. Signs Reduced hatchability. The infective agent does not survive well outside the bird. When the vacuum is released the eggs draw in antibiotic solution which is subsequently absorbed through the shell membranes. Introduction A disease of turkeys characterised by respiratory and skeletal problems caused by Mycoplasma meleagridis. Mortality is low. it occurs in most turkey-producing countries but is now much rarer in commercial stock. In adult birds though infection rates are high. Mild respiratory problems. This can increase hatchability by 510% in this situation. Crooked necks. maintenance of this status by good biosecurity.
98 . Treatment Tylosin. Predisposing factors include stress and viral respiratory infections.culture used to confirm. or lateral via respiratory aerosols and direct contact. Diagnosis Lesions. other respiratory viruses. Infected birds do develop some immunity. Airsacculitis (rarely) seen in adult birds. These are based on purchase of uninfected poults. Birds infected from their parents seem to be immuno-tolerant and particularly prone themselves to transmit. Prevention Eradication of this infection is also possible using similar techniques as for Mycoplasma gallisepticum. Suspect colonies may be identified by immuno-fluorescence. Mycoplasma synoviae. Infection rates may be very high. Infection is via the conjunctiva or upper respiratory tract with a long incubation period. Infected males are particularly prone to transmit infection and may warrant special attention. all-in/all-out production. Spread is generally rapid within and between houses on a farm. Serology: SAG used routinely . especially in commercial layer flocks. spiramycin. Differentiate from Mycoplasma gallisepticum. tetracyclines. In some circumstances preventative medication of known infected flocks may be of benefit. isolation and identification of organism. Survival of the infectious agent outwith the bird is poor but fomite transmission between farms is important. M. demonstration of specific DNA (commercial kit available). Transmission may be transovarian.s. and biosecurity.Post-mortem lesions Airsacculitis in infected pipped embryos and poults. 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. serology. fluoroquinolones. Culture requires inoculation in mycoplasma-free embryos or. whilst illness is variable and mortality less than 10%. 11-21 days following contact exposure. Mycoplasma synoviae infection. Effort should be made to reduce dust and secondary infections. Vaccines are not normally used. It occurs in most poultry-producing countries.
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.
contaminated feed and/or water. Predisposing factors include coccidiosis/coccidiasis. amoxycillin).Abubakar. usually in less than 48 hours. high viscosity diets (often associated with high rye and wheat inclusions in the diet). Affected birds tend to be dehydrated and to undergo rapid putrefaction. Spores of the causative organism are highly resistant. Probiotics may limit multiplication of bacteria and toxin 102 . or Bacitracin in feed (e. Dark coloured diarrhoea. Treatment Penicillins (e.g.g. Post-mortem lesions Small intestine (usually middle to distal) thickened and distended. diet (high protein).Tahir Necrotic Enteritis Introduction An acute or chronic enterotoxemia seen in chickens. neomycin and erythromycin are used in the USA. Water medication for 3-5 days and in-feed medication for 5-7 days depending on the severity. 100 ppm). Closed eyes. Intestinal mucosa with diptheritic membrane. phenoxymethyl penicillin. Sudden death in good condition (ducks). Inappetance. Prevention Penicillin in feed is preventive. Intestinal contents may be dark brown with necrotic material. in ducks possibly heavy strains. usually around 10%. Treatment of ducks is not very successful. caused by Clostridium perfringens and characterised by a fibrino-necrotic enteritis. Reflux of bile-stained liquid in the crop if upper small intestine affected. high levels of most growth promotors and normal levels of ionophore anticoccidials also help.M. Signs Depression.small intestine. Ruffled feathers. 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. in drinking water. Infection occurs by faecal-oral transmission. Immobility. usually of the mid. turkeys and ducks worldwide. other debilitating diseases. Mortality may be 5-50%.
Other species can be infected including mammals occasionally (e.Lentogenic . ND . respiratory or reproductive systems.production. Morbidity is usually high and mortality varies 0-100%. birds. The virus involved is Paramyxovirus PMV-1. Severe lesions of necrotic enteritis affecting the small intestine of broilers.Mild disease. It is not usually vertical (but chicks may become infected in hatcheries from contaminated shells). ND . pigeons and ducks.Neurotropic Velogenic . Strains can be developed as vaccines. less for turkeys and relatively apathogenic in psittacines. Newcastle Disease (Paramyxovirus 1) Introduction Paramyxovirus 1 or Newcastle Disease is a highly contagious viral disease affecting poultry of all ages.Mesogenic . It is highly virulent for chickens. Affected species include chickens. The condition is rarely diagnosed in ducks but is a possible cause of production drops/fertility problems. Figure 25. Can affect any age. conjunctivitis in man). Higher mortality is seen in velogenic disease in unvaccinated stock. The sample at the bottom of the picture is still focal.g. ND . fomites.Velogenic Viscerotropic (VVND) . In many countries local regulations or market conditions prevent the routine use of many of these options. sometimes subclinical. 103 . Intestinal lesions are absent.sometimes called 'asiatic' or exotic. Transmission is via aerosols.Acute and fatal in chickens of any age causing neurological and some respiratory signs. turkeys. Signs are typically of disease of the nervous. These viruses have sometimes been used as vaccines in previously immunised birds. which is of variable pathogenicity. Four manifestations have been identified: ND .Mortality and nervous signs in adult. visitors and imported psittacines (often asymptomatic). the upper has formed a thick crust of necrotic material.
for up to 12 months. Haemorrhage in proventriculus. Tracheitis. Coughing. antibiotics to control secondary bacteria. However it is quite sensitive to disinfectants. Sudden Death Depression. formalin and phenol. pneumovirus infection. Necrotic plaques in proventriculus. infectious coryza. Cross-reactions have mainly been with PMV-3. Samples . HI with ND serum or DID (less cross reactions). intoxications.tracheal or cloacal. rising titre in serology. and is ether sensitive. Dyspnoea. It is inactivated by temperatures of 56°C for 3 hours or 60°C for 30 min. Treatment None. post-mortem lesions. dust etc). encephalomalacia. Severe drop in egg production.The virus survives for long periods at ambient temperature. Differentiate from Infectious bronchitis. encephalomyelitis. intracerebral or IV pathogenicity in chicks. avian influenza. laryngotracheitis. Twisted neck. Post-mortem lesions Airsacculitis. Inappetance. Moult. IFA. the infective dose and the degree of immunity from previous exposure or vaccination. fumigants and sunlight. EDS-76. Paralysis. intestine. Intestinal lesions primarily occur in the viscerotropic form. Pathogenicity evaluated by Mean Death Time in embryos. It is confirmed by isolation in CE. Diagnosis A presumptive diagnosis may be made on signs. HA+. especially in faeces and can persist in houses (in faeces. caecal tonsil. Signs Signs are highly variable and will depend on the nature of the infecting virus (see above). 104 . acid pH. haemorrhagic disease. middle ear infection/skull osteitis. Nervous signs. Diarrhoea.
however. A typical programme may involve Hitchner B1 vaccine at day old followed by LaSota-type vaccine at 14 days. and occasionally gasping due to a plug of pus in the lower trachea. Inactivated vaccines have largely replaced the use of live vaccines in lay but they do not prevent local infections. HI has been used extensively. and is associated with difficulty maintaining brooding temperature and poor management of feeders and drinkers. Figure 28. snicking. Use of spray application is recommended but it needs to be applied with care to achieve good protection with minimal reaction. To prevent or reduce vaccinal reactions in young chicks it is important that day old have uniform titres of maternal immunity. which are adequately stored and take into account the local conditions. vaccination. whereas it tends to peak between 6-10 days for chicks that begin eating but then cease. all-in/all-out production. biosecurity. Mortality peaks at 3-5 days for birds that fail to eat at all. In some countries it has been customary to provide antibiotics prophylactically during periods of anticipated vaccinal reaction. It is common to monitor response to vaccination. 105 . These tests do not directly evaluate mucosal immunity. Vaccinal reactions may present as conjunctivitis. Morbidity is up to 10% and mortality close to 100%. Vaccination programmes should use vaccines of high potency. especially in breeding birds by the use of routine serological monitoring. It is commonest in progeny of young parent flocks (relatively small yolks) or where managers are inexperienced. Acute viral infections or heavily contaminated drinking water may have a similar effect to bad management in reducing feed intake. Elisa is now also used.Prevention Quarantine. The LaSota-type vaccine may even repeated at 35-40 days of age if risk is high. Use of Mycoplasma gallisepticum free stock under good management reduces the risk of vaccinal reactions. 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. 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).
aspergillosis. Oregon Disease . Gizzard may be impacted with litter. bile staining of adjacent tissues. Treatment Correction of management problems.Signs Failure to grow. soluble multivitamin supplementation may help. good drinking water hygiene. Without adequate blood supply the tissue of the muscle begins to die. Diagnosis Based on post-mortem lesions. or suffer necrosis. good hygiene and biosecurity in brooding areas to minimise early disease challenges.Deep Pectoral Myopathy Introduction This condition is so named because it was first identified in adult breeding turkeys in Oregon State. The condition can be reproduced by causing intense exercise of this muscle. It is caused by a reduction in the blood supply to the deep pectoral muscles. age of collection and weight of hatching eggs. Prevention Review brooding management. Poor development. Post-mortem lesions Crop empty. 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. in broiler parent chickens and also in large broiler chickens in various places. 106 . It has since been seen in turkeys. any swelling of the muscle tends to cut off the blood supply. nutrition of young parents. It does not usually cause any mortality or obvious clinical signs and so it is usually identified after slaughter. Gall bladder distended. Because it is enclosed in a relatively unyielding membrane. Most organs normal. Differentiate from omphalitis/ yolk sac infection.
If of very long duration.Signs None. It may also start to be enclosed in a fibrous capsule. 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. Treatment Not applicable. with oedema within it and on its surface. Diagnosis Lesions. thinning operations in meat birds. If the condition is of over 7 days duration the muscle is dry and often shows greenish tinges. Post-mortem lesions Acute or chronic necrosis of the deep pectoral muscle on one or both sides. it may become a healed scar. If recent. 107 . A typical case of the chronic stages deep pectoral myopathy in a broiler chicken. and. Figure 26. It is very difficult to detect affected carcases in standard meat inspection. greenish yellow. Transillumination of the breast may help identify affected carcases and may be worthwhile if the incidence is high. weighing birds etc). the muscle may be swollen and pale. in particular excessive exercise. Prevention Avoidance of physical damage of this muscle. artificial insemination in breeding turkeys. This will normally be due to excessive flapping in association with management activities (e.g. and flaking. The tissue in the centre is dry.
ventilation problems. 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. Cultures from the trachea of birds showing typical signs are preferred. Infectious Bronchitis). There is some evidence that hatcheries may play a role in the epidemiology. tracheitis. E. sneezing. A range of sero-types have been identified. Post-mortem lesions Airsacculitis. Most isolates are oxidase positive and galactosidase positive Serology using Elisa tests has been used. The severity of its effects depends on the pathogenicity of the particular strain and other risk factors such as viral infections. perhaps through survival of the organism on shell surfaces or shell membranes. This can cause significant losses through condemnations. Signs Coughing.Ornithobacterium Infection. In broiler chickens its main importance seems to be as a cause of airsacculitis in apparently healthy flocks that is only identified at slaughter. The range occurring in turkeys is wider than that seen in chickens. and E. 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). The infection is common in chickens and turkeys. The organism grows slowly producing tiny colonies on blood agar. Reduced egg production. It is a Gram-negative pleomorphic organism. Confirmation is by isolation of the organism. Reduced weight gain. Some uncertainty exists about mechanisms of transmission. preferably as a flock test comparing results before and after the challenge. Bordetella aviuminfection. Growth is more rapid and consistent in an anaerobic jar. The slow-growing bacterium was named in 1994. Diagnosis Clinical signs and lesions. It commonly exacerbates respiratory disease caused by pneumovirus infections in turkeys. age at infection etc. It had been previously isolated in a number of other countries. severe bronchopneumonia. Within the poultry house it is likely to be by aerosols. Important cofactors may include respiratory viral vaccines (Newcastle disease. direct contact and drinkers. coli overgrowth may occur. field challenge with respiratory viruses. coli infections.
Prevention This is based on good hygiene. Figure 27. though 54% were sensitive to tetracycline. also most are sensitive to tiamulin. Vaccination of breeder flocks to protect progeny has shown benefits in chickens but. In the USA in 1998 all strains were sensitive to penicillins and many other microbials. Satisfactory disease control depends on good management and biosecurity. Severely consolidated lung from an acute ORT infection in 14-week-old turkey growers. Amoxycillin sensitivity remains good. because of the age of slaughter. Some work has been done on live vaccine in the USA. it requires two doses.amoxycillin at 250 ppm in water for 3-7 days or chlortetracycline at 500 ppm for 4-5 days.Treatment The sensitivity of ORT to antibiotic is highly variable. The lung is solid and covered by pus/ purulent exudate.it is very sensitive in vitro to a range of chemicals. Some vaccines seem to have difficulty in producing a longlasting serological response to ORT. Routine treatment . Preventative medication with the products listed in the previous section may be beneficial in some circumstances.there are issues relating to availability. neomycin and enrofloxacin. Similar lesions may be found in Pasteurellosis. regulation. Initially in Germany most strains were sensitive to amoxycillin. Tilmicosin is also effective at 10-20mg/kg and should be used in the early stages of the disease. Vaccination . cost etc. Hygiene . 109 . this is unlikely to work in turkeys. In France and Belgium most strains were sensitive to enrofloxacin. chlortetracycline but not to enrofloxacin. therapy and vaccination. An inactivated vaccine is licensed for broiler parents in Europe. ORT is a major problem on multi-age sites.
turkeys and ducks seen worldwide and due to Vitamin D or calcium deficiency. Cage Fatigue Introduction A condition of chickens. Prevention Unknown. Soft-shelled eggs. Birds rest squatting. Post-mortem lesions Green discolouration of the liver at slaughter. 110 . Treatment Not applicable .only identified at slaughter. Signs None. Drop in production. Birds go off legs. Gram-variable pleomorphic bacteria have been isolated from affected livers and bones. Signs Lameness. Diagnosis Lesions. high production. Osteoporosis.Osteomyelitis Complex. Soft bones and beak. Predisposing factors include small body size. The green discolouration is used to identify carcases that require closer inspection of the other tissues. Enlarged hocks. 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.
calcium carbonate capsules. Epiphyses of long bones enlarged. Coughing. skeletal size and mineral content at point of lay are critical. Paramyxovirus 2 .M. bone ash. antioxidants.Abubakar.Yucaipa Disease Introduction An infection of chickens.Tahir Post-mortem lesions Bones soft and rubbery. Inappetance. Post-mortem lesions Not characteristic. Diagnosis History. spondylitis. Drop in egg production. In chickens it is usually mild. signs. turkeys and passerine cage birds with Paramyxovirus PMV-2 results in disease with variable mortality. whereas turkeys are more severely affected. Signs Depression. As birds progressively mobilise skeletal calcium for egg production through lay. Beading and fracture of ribs. Beak soft. Parathyroids enlarged. Treatment Over-correct ration vitamin D. Vertical transmission does not usually occur. Wild birds are believed to be especially important. Differentiate from Marek's disease. place on litter. depending on the species affected and whether infection is complicated by other factors and diseases. 111 . lesions. Transmission is by wild birds and fomites. proper Ca and P levels and ratio. Prevention Supplementation of vitamin D.
antibiotics to control secondary bacteria.Diagnosis Isolation in CE. Mortality is usually low in poultry. biosecurity. Inappetance. IFA. Drop in egg production (turkeys). antibiotics to control secondary bacteria. Coughing. HI with ND serum or DID (less cross reactions). Post-mortem lesions No specific lesions. IFA. Treatment No specific treatment. Treatment No specific treatment. 112 . laryngotracheitis. Diagnosis Isolation in CE. Vertical transmission does not usually occur. including wild bird contact and fomites. Signs Depression. The infection is transmitted by birds. all-in/all-out production. haemorrhagic disease. EDS-76. occasionally chickens and psittacine cage birds. High mortality (cage birds). Loss of shell pigment Nervous symptoms (psittacines). Paramyxovirus-3 Introduction Paramyxovirus PMV-3 infects turkeys. HA+. Differentiate from Infectious bronchitis. HI with ND serum or DID (less cross reactions). HA+. Prevention Quarantine.
Paramyxovirus-6 Introduction Paramyxovirus PMV-6 infection of turkeys. A range of 113 . antibiotics to control secondary bacteria. HI with ND serum or DID (less cross reactions). Mild respiratory signs. Mortality is 0-5%. In both cases mortality can be high and can be associated with a marked depression in growth.Prevention Quarantine. Signs Reduction in egg production. Treatment No specific treatment. all-in/all-out production. It is an infectious and transmissible cause of sudden increases in mortality in turkeys between 7 and 28 days of age. biosecurity. biosecurity. Prevention Quarantine. IFA. The infection is inapparent in ducks and geese. PEMS and Spiking Mortality of Turkeys Introduction Poult Enteritis and Mortality Syndrome (PEMS) was first identified in high density turkey producing areas of the South Eastern USA in 1991. Vertical transmission does not usually occur. Vaccination has been used in turkeys but may not be cost-effective. A less acute form of the disease appears to produce more of a lingering mortality. Diagnosis Isolation in CE. The infection is transmitted by birds. Post-mortem lesions No specific lesions. all-in/all-out production. HA+. including wild bird contact and fomites.
Fluoroquinolone antimicrobials appear to be especially effective. seeking heat. Weight loss. Good quality diets of a suitable form . Liquid intestinal contents. All-in/all-out production. Emaciation. Prevention Biosecurity to reduce the introduction of new infections into brooding facilities. Increasing weakness. Droppings watery. Effective terminal disinfection. pale brown. huddling.5-8% will encourage feed intake and recovery. This syndrome is clearly distinguished from typical viral enteritis in young turkeys because of the high mortality and severe growth depression. Muscle atrophy. A highly digestible diet with fat at 7. Overdistension of crop in young birds because of an interruption in feed supply may predispose. Diagnosis Signs. To replicate the condition in full it appears to be necessary to include bacteria in the inoculum. Reduced feed consumption and growth.viruses have been isolated from affected flocks. Wet litter. Increased water consumption. eating litter. lesions. Picking at feed.mash and poor quality crumbles increase risk. Caseous cores in bursae (late in the process). multivitamins and milk replacer products are helpful for nutritional support in the acute phase. 114 . Post-mortem lesions Dehydration. Treatment A range of antibiotics and arsenicals have been used to control the bacterial component of this condition. Signs Initial hyperactivity and increased vocalisation. Pendulous Crop Introduction A complex condition of turkeys and chickens associated with coarse fibrous feed.
Crop contents semi-liquid and foul smelling. have ulcerations and sometimes mycosis. and thickening of mucosa of proventriculus. Emaciation in heavily infected young chicks (Tetrameres). Treatment None. Diarrhoea. lesions. ulceration. Signs Anaemia. Post-mortem lesions Crop distended with feed. They are found in the mucosa of crop and proventriculus causing mainly inapparent infections. Infection is by the oral route on exposure to the intermediate hosts. 115 . including crustaceans. identification of worms. if these can be identified. grasshoppers and cockroaches. Diagnosis Signs. Post-mortem lesions Inflammation. spiruroid worm parasites of poultry and game birds. Tetrameres and Cyrnea are nematodes. Lack of muscle tone. necrosis. Diagnosis Macroscopic examination of lesions. may be impacted. Proventricular Worms Introduction Dispharynx.Signs Enlargement of crop. Prevention Remove predisposing factors. haemorrhage.
other poultry. Pseudotuberculosis Introduction An infection of ducks. duck viral hepatitis. sulphonamides in feed. 'hardening off'. tuberculosis. The disease has a mortality of 5-75%. colibacillosis. Treatment Tetracyclines. In peracute disease the only lesion may be enteritis. Differentiate from Duck viral enteritis. wild birds. Sometimes sudden death. 116 . Diarrhoea. Ruffled feathers. rodents and man with the bacterium Yersinia pseudotuberculosis. Post-mortem lesions Miliary lesions in a variety of organs but especially in the liver. Prevention Good husbandry and hygiene. coccidiosis. isolation. adequate protection. Prevention Prevention of access to intermediate hosts. Diagnosis Lesions.Treatment Not usually required. Signs Weakness.
Avian Monocytosis Introduction A sudden onset condition of chickens early in lay with high morbidity and a mortality of 050%.Tahir Pullet disease. Bluecomb. diet and water supply. Treatment Adequate water supply. It is associated with hot weather. mucoid casts in intestine. antibiotics. Drop in egg production. Prevention Good management. toxin and possibly a virus infection. molasses. water deprivation. Watery diarrhoea. lesions. Crop distended. Diagnosis History. hygiene. Kidneys swollen. Post-mortem lesions Dehydration. vibriosis. Pancreas chalky. coccidiosis.Abubakar. Affected birds have an increase in circulating monocytes in their blood. Signs Depression. IBD and typhoid. Dehydration. Differentiate from fowl cholera. Catarrhal enteritis. Skeletal muscle necrosis. It was commonly reported prior to 1960 but is now rare. capillariasis. Dark comb and wattles. multivitamins in water. Skin cyanosis of head. elimination of other causes. Crop distension. Loss of appetite.M. 117 . Liver swollen with foci.
Ornithonyssus bursae. Pale comb and wattles. Drop in egg production.7 mm. Prevention Thorough cleaning. Loss of condition. vegetable oil and mineralbased products (both liquid sand dusts) have been used to control red mites in the environment. Diagnosis Number and type of mites identified. Spots on eggs. Filling of cracks and crevices. fumigation and insecticide treatment at turnaround. cracks. For northern fowl mite it is essential to apply approved insecticides to the affected birds. Dermanyssus gallinae. Signs Presence of grey to red mites up to 0.itching. which are external parasites of chickens and turkeys. the Northern Fowl Mite spends its entire life cycle on the bird and can multiply more rapidly as a result. 118 . Effective monitoring of mite numbers and implementation of control measures before birds are heavily infested improves control.Red Mite and Northern Fowl Mite Introduction Arachnid mites. organophosphates. Post-mortem lesions Anaemia. the Common Red Mite. carbamates. and good design of new equipment to limit harbourages for red mites. in nest boxes. Treatment Pyrethroids. May cause anaemia and death in young birds. Staff complaints . crevices etc. mainly at night and may transmit fowl cholera and other diseases. 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. citrus extracts. Birds restless. feeds by sucking blood.
Post-mortem lesions Mild catarrhal tracheitis. pH). Opinions vary as to whether adenovirus can be characterised as a primary respiratory pathogen.Abubakar. vaccinal and field strains) and bacteria (Ornithobacterium rhinotracheale. It may occur as an exacerbating factor in other types of respiratory disease. Signs Mild snick and cough without mortality. formaldehyde and iodides work better. lesions. chloroform. The virus is generally resistant to disinfectants (ether. may act as 119 .Tahir Respiratory Adenovirus Infection. CE liver). Dust. The virus grows well in tissue culture (CE kidney. Lentogenic Newcastle disease virus. at least 12 sero-types have been described and these may be isolated from healthy chickens. Prevention Quarantine and good sanitary precautions. Avian pneumovirus. Diagnosis History. Transmission may be vertical and lateral. E. and other factors associated with poor ventilation. temperature. ammonia and other gases.M. coli) may be involved. intranuclear inclusions in liver. Respiratory Disease Complex Introduction Respiratory infections in chicken and turkeys are seen worldwide but especially in temperate poultry-producing areas in winter months. prevention of immunosuppression. Treatment None. Infected birds may remain carriers for a few weeks. and by fomites. A number of respiratory viruses (Infectious Bronchitis. 'Mild Respiratory Disease' Introduction An adenovirus infection of chickens with a morbidity of 1-10% and a mortality of 1-10%.
carefully applied appropriate viral vaccines. Morbidity is typically 10-20%. mortality 5. If condemned birds are included mortality may be more than 10%. of course. be challenged by some of these pathogens). Differentiate from Chronic Respiratory Disease (Mycoplasmosis). Rattling noises.catarrhal to purulent. Airsacculitis. Prevention Effective ventilation. sanitation of drinking water. Pericarditis. Conjunctivitis. Diagnosis Lesions. Nasal exudate. Severe airsacculitis of thoracic air sacs in a broiler close to slaughter. There is also percarditis evident (at top right). and have been cut into to reveal a cheesy (caseous) mass of pus.10%. serology.predisposing factors. The air sacs are thickened and congested. 120 . Given that many flocks are vaccinated it is necessary to establish normal serological response in vaccinated flocks in the absence of disease (some of which may. response to environmental changes. Treatment Antimicrobial treatment of specific bacterial infections. Figure 29. Signs Snick. Sneezing. Post-mortem lesions Severe tracheitis with variable exudate . Head swelling.
A gradual increase in mortality and poor growth in broilers may be the main signs. geese. Marked stunting when Marek's disease vaccine is contaminated. Sometimes nodules in intestine and caecae. Diagnosis Pathology. Leg weakness. Lympoid Tumour Disease Introduction A retrovirus infection of chickens. usually higher in females than males. There is an incubation period of 5-15 days. Both tracheas were congested and the upper sample had mucopurulent material in the lumen. Treatment None. 121 . turkeys. spleen and kidney. Diarrhoea. Post-mortem lesions Neoplastic lesions in liver. Sometimes enteritis and proventriculitis (especially in broilers infected with contaminated Marek's disease vaccine).Figure 30. and quail with morbidity up to 25%. ducks. Reticuloendotheliosis. chick inoculation. Signs There may be no obvious signs. and the infection can be spread by mosquitoes or in contaminated Marek's disease vaccines. Severe tracheitis is broilers with respiratory disease complex. Transmission is lateral and possibly transovarian.
Poor growth. or Vitamin D or 25-hydroxy vitamin D in drinking water. Beak soft. Post-mortem lesions Bones soft and rubbery. Rickets (hypocalcaemic) Introduction Vitamin D deficiency or phosphorus/calcium imbalance is seen in chickens. Birds go off legs. turkeys and ducks worldwide. Avoidance of contamination of live vaccines is the main control measure practised. Birds rest squatting. lesions. signs. antioxidants. Reduction in bodyweight. Hock swelling. proper calcium and phosphorus levels and ratio. Signs Lameness. Growth plates widened and disorganised.Prevention Formal control programmes have not been documented as the condition is sporadic and relatively self-limiting. Soft bones and beak. 122 . Epiphyses of long bones enlarged. Beading and fracture of ribs. Treatment Over-correct ration with three times vitamin D for 2 weeks. Diagnosis History. Parathyroids enlarged. Femoral Head Necrosis. Prevention Supplementation of vitamin D. Differentiate from Encephalomalacia.
turkeys and duck is seen worldwide. 123 . Beading and fracture of ribs. lesions (analyse Vitamin A or manganese as a guide to premix inclusion).Abubakar.Tahir Rickets (hypophosphataemic) Introduction Phosphorus deficiency in chickens. Soft bones and beak. Diagnosis History. Birds rest squatting. Intestinal diseases may reduce absorption.M. Parathyroids enlarged. Signs Lameness. Poor growth. Treatment Over-correct ration with 3 times vitamin D for 2 weeks. Beak soft. Reduction in bodyweight. Some countries have regulations governing the use of phosphorus in fertiliser with a view to reducing water pollution. signs. Hock swelling. This has led feed manufacturers to try various approaches to reduce added phosphorus in diets. antioxidants. Growth plates widened and disorganised. Prevention Supplementation of Vitamin D. or vitamin D in drinking water. Even subclinical levels of this condition can predispose to Femoral Head Necrosis. Birds go off legs. Epiphyses of long bones enlarged. Enlarged hocks. proper calcium and phosphorus levels and ratio. Post-mortem lesions Bones soft and rubbery.
A. shorter in young birds. turkeys. and A.M. Prevention Good hygiene in brooding areas. stout white worms up to 12 cms in length. Adult birds can tolerate burdens asymptomatically.Ascaridia Introduction Ascaridia sp. Diagnosis Demonstration of virus (PAGE. Control of secondary bacterial enteritis may require antimicrobial medication. The life cycle is similar to that illustrated in the section on the caecal worm Heterakis. The route of infection is oral usually by direct ingestion of the embryonated egg and there is a 5-10-week prepatent period. large . dissimilis in turkeys. The route of infection is oral and maximum viral excretion occurs 2-5 days post infection. guinea fowl. except that the adults reside in the small intestine and earthworms are not significant paratenic or transport hosts. pheasants. The 124 . The parasite species vary: A. Post-mortem lesions Viruses replicate mainly in the mature villous epithelial cells. Treatment No specific treatment for this infection. seen worldwide. Roundworm.Abubakar. partridges and pigeons.Tahir Rotavirus Infection Introduction Rotavirus infection is seen in chickens. It is not known if vertical transmission occurs though virus has been occasionally isolated from embryonated eggs.submit 6 x .5 g faeces). electron microscopy or Elisa on intestinal contents . galli in fowl. Use of a good electrolyte solution is beneficial in the acute stage of infection. Signs Diarrhoea. columbae in pigeons. are nematode worm parasites. Virus may be found in asymptomatic birds.
mainly in young birds. oval smooth-shelled nonembryonated eggs in faeces. Figure 31. Prevention Prevention of contamination of feeders and drinkers with faeces. especially for young birds. A collection of mature roundworms (Ascaridia galli) recovered from the small intestine of a layer chicken in rear. 125 . In the bottom left quadrant there are also some immature worms. Post-mortem lesions Enteritis. Diarrhoea. Poor growth. Worms up to 12 cm in length in duodenum and ileum.parasites may be transported by grasshoppers and earthworms and are resistant to environmental effects. pasture rotation and regular treatment. Signs Loss of condition. Wasting. piperazine as locally approved. Treatment Flubendazole. Diagnosis Macroscopic examination with identification of worms. Listlessness. levamisole.
Ruptures of ligaments and joints are also occasionally seen. This can cause mortality in birds of any age. Fowl Typhoid Introduction Disease caused by one of the two poultry-adapted strains ofSalmonella bacteria.M. canaries and bullfinches. Broiler parents and brown-shell egg layers are especially susceptible. Treatment None. Broiler chickens have an avascular area of tendon just above the hock that is the usual site of rupture. Histology may be helpful in determining if there is an underlying inflammatory process. guinea fowls. Salmonella Gallinarum. 126 . The bird may have the hock dropped to the floor. Post-mortem lesions The fresh lesion contains a haematoma with the end of the ruptured tendon within or adjacent to it. parrots. Reoviral or staphylococcal arthritis or tenosynovitis may predispose but many cases have no evidence of an inflammatory response. Affected birds should be culled humanely as soon as they are identified. Signs Severe lameness. If there is a greenish tinge to the area of swelling it occurred a few days previously. Diagnosis Signs and lesions are obvious. Avoidance of physical stresses on the musculoskeletal system through careful handling as well as careful design and layout of equipment.Abubakar. Chickens are most commonly affected but it also infects turkeys. game birds. sparrows. Salmonella Gallinarum. Infections still occur worldwide in non-commercial poultry but are rare in most commercial systems now. Prevention Establishment of a steady growth profile.Tahir Ruptured Gastrocnemius Tendon Introduction This is a condition causing severe lameness in roaster type meat chickens and more rarely in turkeys.
Morbidity is 10-100%. pullorum disease and coli-septicaemia. clean chicks. Thirst. even in adults. The route of infection is oral or via the navel/yolk. Tube and rapid plate agglutination tests have been the standard serological tests for many years but have only been validated for chickens. Post-mortem lesions Bronzed enlarged liver with small necrotic foci. Engorgement of kidneys and spleen. Enteritis of anterior small intestine. but is susceptible to normal disinfectants. Signs Dejection. Yellow diarrhoea. Reluctance to move. Prevention Biosecurity. McConkey and non-selective agar is advisable. tetracylines. surviving months. LPS-based Elisa assays have been developed but not widely applied commercially. recovered birds are resistant to the effects of infection but may remain carriers. mortality is increased in stressed or immunocompromised flocks and may be up to 100%. Anaemia. Enrichment procedures usually rely on selenite broth followed by plating on selective media. As with other salmonellae. Transmission may be transovarian or horizontal by faecal-oral contamination. and/or congestion. both live (usually based on the Houghton 9R strain) and bacterins. Ruffled feathers. egg eating etc. In clinical cases direct plating on Brilliant Green. fluoroquinolones. Diagnosis Isolation and identification. Vaccines for fowl typhoid have been used in some areas. Differentiate from Pasteurellosis. The bacterium is fairly resistant to normal climate. 127 . Inappetance. potentiated sulponamide. Treatment Amoxycillin.
usually brown-shell egg layers.Figure 32. Transmission may be transovarian or horizontal mainly in young birds and may sometimes be associated with cannibalism. Morbidity is 10-80%. The route of infection is oral or via the navel/yolk. Gasping. Occasionally it can cause losses in adult birds. Salmonella Pullorum. White diarrhoea. Bacterial septicaemia caused by Salmonella Gallinarum. game birds. Ruffled feathers. mortality is increased in stressed or immunocompromised flocks and may be up to 100%. Closed eyes. Depression. Similar lesions can be seen in Pullorum Disease and with other causes of septicaemia in young chicks. Signs Inappetance. Salmonella Pullorum. ring doves. 'Bacillary White Diarrhoea' Introduction Disease caused by one of the two poultry-adapted strains ofSalmonella bacteria. pale and shows focal necrosis. Vent pasting. this usually only causes mortality in birds up to 3 weeks of age. guinea fowls. sparrows. ostriches and peafowl. in young broiler chickens. parrots. The bacterium is fairly resistant to normal climate. The liver on the left is normal. It still occurs worldwide in noncommercial poultry but is now rare in most commercial systems. Lameness. It affects chickens most commonly. Pullorum Disease. but also infects turkeys. Loud chirping. surviving months but is susceptible to normal disinfectants. the one on the right is slightly enlarged. 128 .
Sero-types vary. Vaccines are not normally used as they interfere with serological testing and elimination of carriers. Bredeney are among the more common isolates. Enrichment procedures usually rely on selenite broth followed by plating on selective media. fomites and feed (especially protein supplements but also poorly stored grain). paracolon. S. The route of infection is oral and transmission may be vertical as a result of shell contamination. liver. Pullorum. Prevention Eradication from breeder flocks. Diagnosis Isolation and identification. S. are capable of causing enteritis and septicaemia in young birds. In clinical cases direct plating on Brilliant Green. As with other salmonellae.Post-mortem lesions Grey nodules in lungs. other enterobacteria. Caecal cores. Urate crystals in ureters. chilling and omphalitis Treatment Amoxycillin. Many species are intestinal carriers and infection is spread by faeces. S. S. Gallinarum. their presence may be significant with respect to carcase contamination as a potential source of human food poisoning. Certain sero- 129 . Newport. turkeys and ducks worldwide. it may become established on certain farms. gizzard wall and heart. Montevideo. fluoroquinolones. Splenomegaly. Anatum. poteniated sulponamide. but S. recovered birds are resistant to the effects of infection but may remain carriers. Intestinal or caecal inflammation. McConkey and non-selective agar is advisable. Even if these infections do not cause clinical disease. Salmonellosis. Typhimurium (which are considered separately). Paratyphoid. Enteritidis andS. Morbidity is 0-90% and mortality is usually low. in the environment or in rodent populations. Paratyphoid Infections Introduction Salmonellae bacteria other than the species specific sero-typesS. tetracylines. Regardless of the initial source of the infection. Derby. and also other than S. S. Differentiate from Typhoid. They infect chickens.
or absent. The bacteria are often persistent in the environment. Post-mortem lesions In acute disease there may be few lesions. Unabsorbed yolk. Dejection.types are prone to remain resident in particular installations (e. amoxycillin. Enrichment media such as buffered peptone followed by selective broth or semi-solid media (e. Diarrhoea. In clinical cases direct plating on Brilliant Green and McConkey agar may be adequate. Foci in liver. other bacterial infections and ornithosis (in ducks). Closed eyes. Loss of appetite and thirst. Diagnosis Isolation and identification. Temperatures of around 80°C are effective in eliminating low to moderate infection if applied for 1-2 minutes. fluoroquinolones. However this has the potential to reveal the presence of salmonellae that are irrelevant to the clinical problem under investigation.g. Senftenberg in hatcheries). neomycin. Pericarditis. tetracyclines. Rappaport-Vassiliadis) followed by plating on two selective media will greatly increase sensitivity. inadequate water. other enterobacteria. Predisposing factors include nutritional deficiencies. applied at sufficient concentrations.g. Dehydration. Good management. but are susceptible to disinfectants that are suitable for the particular contaminated surfaces and conditions. S. Chemotherapy can prolong carrier status in some circumstances. This approach is often used in the heat treatment of feed. Differentiate from Pullorum/Typhoid. Ruffled feathers. chilling. Enteritis. 130 . Vent pasting. Treatment Sulphonamides. Cheesy cores in caecae. Signs Signs are generally mild compared to host-specific salmonellae. Focal necrotic intestinal lesions. especially in dry dusty areas.
secondly. fumigate eggs. has become much more common in both poultry and humans since the early 80s. Typhimurium infections Introduction Salmonella Enteritidis and S. clean nests.Prevention Uninfected breeders. Enteritidis and S. Salmonellosis. and. Salmonella Enteritidis.Typhimurium has remained relatively stable though the spread of the highly antibiotic-resistant strain DT104 in various farmed species gives some reason for concern. care in avoiding damage to natural flora. Temperatures of around 80°C are effective in eliminating low to moderate infection if applied for 1-2 minutes. Infection results in a strong immune response manifest by progressive reduction in excretion of the organism and reduced disease and excretion on subsequent challenge. Feed and feed raw material contamination is less common than for other sero-types. good feed. fomites and on eggshells. all-in/all-out production. Infections in chickens. S. especially phage type 4. Many infected birds are culled and others are rejected at slaughter. applied at sufficient concentrations. because there are differences in the epidemiology as compared to other salmonellae. but are susceptible to disinfectants that are suitable for the particular contaminated surfaces and conditions. Vaccines are not generally used for this group of infections. competitive exclusion. Predisposing factors include nutritional deficiencies. The route of infection is oral. mills. inadequate water and other bacterial infections. these bacteria are often specifically cited in zoonosis control legislation. on the one hand. many species are intestinal carriers and infection may be carried by faeces.Typhimurium are presented separately from other sero-types of Salmonella because. breeding and grow-out farms. hatcheries and feed mills is required for effective control. 131 . Vertical transmission may be either by shell contamination or internal transovarian contamination of yolk. chilling. especially in dry dusty areas. Routine monitoring of breeding flocks. These are the predominant sero-types associated with human disease in most countries. turkeys and ducks cause problems worldwide with morbidity of 0-90% and a low to moderate mortality. The bacteria are often persistent in the environment. This approach is often used in the heat treatment of feed. elimination of resident infections in hatcheries. The prevalence of S.
Closed eyes. Foci in liver. all-in/all-out production. Ruffled feathers. Cheesy cores in caecae. good feed. In clinical cases direct plating on Brilliant Green and McConkey agar may be adequate. hatcheries and feed mills is required for effective control.Pullorum serum agglutination tests.g. Misshapen ovules in the ovaries in S. Routine monitoring of breeding flocks. Infection 132 . Post-mortem lesions In acute disease there may be few lesions.Signs Dejection. coli. Chemotherapy can prolong carrier status in some circumstances. other enterobacteria such as E. infection Diagnosis Isolation and identification. S. tetracyclines. Unabsorbed yolk. amoxycillin. fumigate eggs. However this has the potential to reveal the presence of salmonellae that are irrelevant to the clinical problem under investigation. Treatment Sulphonamides. It is possible to detect reactions with specific antigens in agglutination tests but competitive and direct Elisa tests are more commonly used today. Pericarditis. neomycin. Early depletion of infected breeding stock is required in some countries such as those of the European Union. Focal necrotic intestinal lesions. Stunting in older birds. breeding and grow-out farms. Rappaport-Vassiliadis) followed by plating on two selective media will greatly increase sensitivity. Differentiate from Pullorum/Typhoid. Good management. competitive exclusion. care in avoiding damage to natural flora. Diarrhoea. clean nests. Perihepatitis.E. Enrichment media such as buffered peptone followed by selective broth or semi-solid media (e. Prevention Uninfected breeders. mills.Enteritidiscauses cross-reactions which may be detected with S. Vent pasting. Lost of appetite and thirst. Enteritis. fluoroquinolones in accordance with the sensitivity. Dehydration. elimination of resident infections in hatcheries.
133 . The oviduct is a hollow tube joining the normally sterile environment of the body cavity with the cloaca. Enteritidis and S. Signs Sporadic loss of lay. both inactivated (bacterins) and attenuated live organisms. leaking urates. are especially prone to increasing salpingitis. Systemic viral infections that cause ovarian regression or damage to the oviduct or cloaca. Infection may spread downwards from an infected left abdominal air sac.). It is a complex condition of chickens and ducks associated with various infections including Mycoplasma and bacteria (especially E. Death. May form a multi-layered caseous cast in oviduct or be amorphous. Lesions. Typhimurium infection. or may proceed upwards from the cloaca. Distended abdomen.results in a strong immune response manifest by progressive reduction in excretion of the organism and reduced disease and excretion on subsequent challenge. coliand occasionally Salmonella spp. Peritonitis. Diagnosis Use the signs to select birds for culling and post-mortem investigation. Damaged vents. Bacteriology of oviduct. Vaccines are increasingly being used for S. The control of infection in this area is probably achieved by ciliated epithelium that mostly wafts a carpet of mucus towards the cloaca. Some birds may 'lay' a caseous mass of pus (which may be found in a nest or on the egg belt). Post-mortem lesions Slight to marked distension of oviduct with exudate. Salpingitis Introduction Salpingitis is an inflammation of the oviduct. which normally has many millions of potentially pathogenic bacteria. Anything that damages the epithelium or disturbs normal oviduct motility is likely to increase the likelihood of salpingitis.
Shaking or quivering of legs after rising. immunise effectively against respiratory viral pathogens common in the area. Post-mortem lesions None. Signs Stand on toes shaking. use healthy parent flocks.Treatment Birds with well-developed lesions are unlikely to respond to medication. Morbidity is 10-20%. Treatment Multivitamins. Prevention Control any septicaemia earlier in life. Use of a suitable antimicrobial may be beneficial for birds in the early stages and if associated with efforts to minimise risk factors. aspirin may be helpful if locally approved. Shaky Leg Syndrome Introduction A condition of turkeys with a course of often 3-4 weeks. exclusion of other problems. 134 . possibly associated with tendon injury. Prevention Care in transport of brooded poults. Diagnosis Clinical examination. releasing poults into larger areas and in handling heavier birds.
Dehydration. Excess fluid in lower small intestine and caecae. Coma. typically 7-14day-old.Spiking Mortality of Chickens Introduction This is a condition characterised by a sudden increase in mortality in young. electrolytes and glucose solution to flock. Provide multivitamins. and/or carbohydrate absorption are disturbed resulting in a hypoglycaemia. 135 . Filtered intestinal contents from affected flocks appear to be capable of reproducing the condition. Signs and lesions. Death. In order to reproduce the typical condition the affected birds are subject to 4 hours without feed and then a mild physical stress such as spraying with cool water. Paralysis. Birds in good condition die after showing neurological signs. Orange mucoid droppings. Avoidance of physical stress. suggesting a viral component. Prevention Good sanitation of the brooding house. Feed intake. Diagnosis Pattern of mortality. Minimise stress. Post-mortem lesions Mild enteritis. Avoidance of interruptions in feed supply. Mortality drops off as sharply as it started. Treatment Leave affected chicks undisturbed. This appears to be a multifactorial condition. Signs Tremor. rapidly growing broiler chickens. Males are more susceptible than females. probably because they are growing faster.
isolate in chicken eggs or chicks or poults. Drops in egg production may be seen in both systemic and intestinal forms Post-mortem lesions Marked splenomegaly. ducks. and egg soiling in chickens. The bacterium is poorly resistant outside host but may be carried by Argas persicus for 430 days. and occasionally by infected faeces. Diagnosis Haematology. diarrhoea. It has been associated with typhilitis. Weakness and progressive paralysis. previously known as Serpulina pilosicoli.Spirochaetosis Introduction The bacterium Borrelia anserina infects chickens. Spleen mottled with ecchymotic haemorrhages. Brachyspira pilosicoli. Cyanosis. It is transmitted by arthropods. Argas persicus. vaccines in some countries. geese. Liver enlarged with small haemorrhages.g. reduced egg production. Often diarrhoea with excessive urates. Necrotic foci. grouse and canaries with morbidity and mortality up to 100%. Thirst. Signs Depression. pheasants. 136 . Prevention Control vectors. is an intestinal spirochaete that can be associated with inflammation of the large intestine in a broad range of mammals and birds. Treatment Various antibiotics including penicillin. Mucoid enteritis. turkey. e.
Prevention Selection for satisfactory conformation in primary breeding. Figure 33. Diagnosis Symptoms. Signs Sitting on hock or rumps. legs extended forward. May walk backwards. That on the left shows the typical lesion of spondylolisthesis. lesions. The sample on the right is normal. Treatment None.M. Use of wings to help in walking. 137 . Post-mortem lesions Anterior-posterior rotation of the bodies of the last or penultimate thoracic vertebrae resulting in scoliosis just anterior to the kidney. with rotation of the body of the vertebra and the pinching of the spinal column that causes paralysis.Tahir Spondylolisthesis. 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.Abubakar. These are cross-sections of the spinal column of 4-5-weekold broilers.
Staphylococcosis. Infection is usually by the respiratory route with an incubation period of 2-3 days seen after artificial infection. Post-mortem lesions Gross lesions are not usually evident. either accidental or induced by interventions such as beak trimming. mainly S.Tahir Spraddle Legs or Splay Leg Introduction Occurs in all species in the recent hatchling. These include good breeder nutrition. Damaged skin due to nutritional deficiencies (such as of biotin) may also be a point of entry. and toe trimming may be a portal of entry with subsequent spread via the bloodstream to the typical sites of lesions. 138 . Signs Legs splay and chick is unable to stand. Staphylococcal Arthritis. Prevention All measures that improve chick vitality at hatching are beneficial in reducing this problem. Bumble Foot Introduction Caused by Staphylococcus bacteria.M. Morbidity is usually low and mortality 0-15% though affected birds will often be culled on humane grounds. Wounds. Diagnosis Clinical signs.Abubakar. avoidance of excessive hatching egg storage. aureus and seen in chickens and turkeys worldwide. The type of chick box liners and the feeding papers used in the brooding house can also influence the occurrence of the condition. and careful monitoring of incubation conditions. Treatment None.
Streptococcus bovis Septicaemia Introduction An infection of ducks with the bacterium Streptococcus bovis. Low mobility. Mycoplasma spp. Signs Ruffled feathers. Some sudden deaths from acute septicaemia if very heavy challenge. isolation and identification of pathogen. chronic stress.. This condition is a cause of sudden deaths in ducklings of 2-3 weeks of age. low stress and prevention of immunosuppression from any cause will all tend to help. trauma. Prevention Good hygiene in the nest. Lameness. Infected joints may have clear exudate with fibrin clots. the hatchery and in any intervention or surgery (processing. especially M. Possibly vaccination against reovirus infection. e. This may progress to abscess formation in these areas. Differentiate from septicaemia or tenosynovitis due to Colibacillosis. particularly of parent birds..g. and by fomites. Diagnosis Lesions. in accordance with sensitivity. and imunosuppression. Swollen above the hock and around the hocks and feet.Transmission occurs in the hatchery and in the general farm environment. 139 . Predisposing factors include reovirus infection. Salmonella spp. Post-mortem lesions Tenosynovitis. toe clipping). Treatment Antibiotics. Competitive exclusion with a non-pathogenic Staphylococcushas been shown to be effective (no commercial products yet available based on this technology). Recovered birds may have some immunity but vaccination with staphylococci has not been found to be helpful in preventing the disease to date. Good management. most commonly in the plantar area of the foot or just above the hock joint. synoviae.
the ventricles are empty. 140 .). Prevention Good husbandry and hygiene. Haemorrhages in muscles and kidneys. Treatment Amoxycillin.affected birds respond well to saline injection and will actively seek out salt scattered in the litter. Leg weakness or incoordination in a few birds. possibly metabolic. Sodium deficiency can appear very similar at about the same age . Splenic hyperplasia. most are found lying on their back. Affected well-grown birds may appear to have died from smothering.Signs Sudden deaths. The atria of the heart have blood. Lung congestion and oedema. 'Flipover' Introduction A condition of broiler chickens of unknown cause. Sudden Death Syndrome. Post-mortem lesions Intestine filled with feed. Diagnosis History. Post-mortem lesions Beak cyanosis. lesions. Serum accumulation in lung (may be little if examined shortly after death). Livers heavier than those of pen-mates (as a percentage of bodyweight. extra care in the immediate post-brooding period. Signs Sudden death in convulsion. It can be induced by lactic acidosis and about 70% of birds affected are males. Liver congestion. isolation.
low intensity light. or birds' access to them. Check your local regulations. they may not be host specific. Signs It is doubtful if any signs are produced under most circumstances. Most have intermediate invertebrate hosts such as beetles or earthworms. lighting programmes. Prevention Control the intermediate hosts. Tapeworms. Treatment Flubendazole is effective at a 60 ppm in diet. 141 . Prevention Lowering carbohydrate intake (change to mash). however it may not have a zero withdrawal in commercial egg layers. Cestodes Introduction Cestodes are tapeworms that are seen in many species.Diagnosis Birds found on back with lack of other pathology. Treatment None possible. use of dawn to dusk simulation and avoidance of disturbance. feed restriction. Post-mortem lesions Occupy space in intestine and create small lesions at point of attachment. Diagnosis Identification of the presence of the worms at post-mortem examination.
Differentiate from rickets.a mass of avascular cartilage with transitional chondrocytes. Post-mortem lesions Plug of cartilage in proximal end of tibia. Mature tapeworms with their heads (scolices) embedded in the intestine. Lameness. Swelling and bowing in the region of the knee joints. distal tibia. Tibial Dyschondroplasia. Diagnosis Gross pathology. Microscopically . and proximal metatarsus. small ovoid lacunae and more matrix than normal. chloride levels and acid/base balance. Vitamin D3 supplementation. Treatment None. Signs There are usually no signs unless the condition is severe. Prevention Genetic selection using the Lixiscope to identify bone phenotype. mild lesions may require histology to distinguish from other problems. It may be associated with rapid growth and have a nutritional factor. modifications of calcium and phosphorus ratios. turkeys and ducks.Figure 34. 142 . Lixiscope may identify in vivo as early as 2 weeks of age. TD Introduction A complex condition seen in chickens. in decreasing order of frequency.
Transmissible Enteritis. spends little time on host. others are avian coronaviruses closely related to infectious bronchitis virus. The infection is seen in turkeys and sometimes pheasants. than in commercial poultry in temperate climates. Signs Anaemia. Diagnosis Identification of the presence of the parasites.M. Bluecomb Introduction Some coronaviruses involved in this condition are considered to be bovine coronaviruses (or closely related thereto). Reduced productivity.Abubakar. These parasites are more likely to be a problem of small scale poultry production in the tropics. and may also transmit spirochaetosis and Pasteurella infection. Weakness. and is also found on mammals.Tahir Ticks Introduction Argas persicus is an external parasite of poultry and wild birds. Occasionally paralysis from toxins in the tick saliva. Skin blemishes. Morbidity is close to 100% and mortality is 5-100%. Insecticide sprays in these areas are more likely to be effective than treatment of the birds. with 143 . Transmission is lateral with birds and faeces. It is more common in warm climates. Emaciation. Prevention As for red mite control. Post-mortem lesions Anaemia. Treatment Elimination of cracks and crevices in the poultry housing.
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.
chlorinate drinking water. Turkey Rhinotracheitis (Adult) Introduction A disease of turkeys caused by the viruses of the Pneumovirus genus. Morbidity is 10-100% and mortality 1. chlorination of drinking water.Antibiotics are not very effective. Prevention All-in/all-out production. control respiratory stressors. isolation of ciliostatic agent. Loss of voice. Treatment Antibiotics are not very effective. 147 . Signs Decreased appetite. Ocular and nasal discharge. Eggs depigmented and thin-shelled. Prevention All-in/all-out production.live primer followed by inactivated. vaccination . Rapid transmission occurs laterally. maternal antibody may protect. control respiratory stressors. Post-mortem lesions Serous rhinitis and tracheitis. vertical transmission is uncertain.30%. Diagnosis Signs. Serology. possibly involving fomites. Paramyxoviridae. Good drinking water hygiene. Sudden drop in production that lasts 2-3 weeks.
Morbidity is 10-100% and mortality 1. Dyspnoea. Signs Decreased appetite. Diagnosis Clinical signs. Sinusitis. Turkey Viral Hepatitis Introduction An infection of turkeys caused by an unidentified virus.M. Transmission may be by direct or indirect contact and possibly vertical. Ocular and nasal discharge. Morbidity varies.Abubakar. Post-mortem lesions Serous rhinitis and tracheitis. coli infection then pneumonia.30%. airsacculitis and perihepatitis.Tahir Turkey Rhinotracheitis (in rear) Introduction A disease of turkeys caused by the viruses of the Pneumovirus genus. Treatment Antibiotics are not very effective. Birds remain carriers for up to 16 days. control respiratory stressors. chlorinate drinking water. possibly involving fomites. Loss of voice. Conjunctivitis. If there is secondary E. isolation and identification of the ciliostatic virus. vertical transmission is uncertain. serology (using an Elisa test to demonstrate rising titre). Prevention All-in/all-out production. Paramyxoviridae. Snick. Vaccination at day-old seems to be most effective. 148 . Rapid transmission occurs laterally. maternal antibody may protect. weight gain and feed efficiency. mortality is 1-25%. sometimes pus in bronchi.
Signs Signs are usually subclinical. Twisted leg Introduction A complex condition seen in chickens and turkeys. Distortion at hock. Morbidity is 1-20% and mortality is low.no inclusion bodies. Gastrocnemius tendon may slip. Depression and sporadic deaths in birds in good condition. Post-mortem lesions Grey foci (c. with good management many birds recover. Post-mortem lesions Linear twisting of growth of long bones. Valgus/varus. Signs Lameness. Prevention Good sanitation and management. Diagnosis Isolation in CE. environment and high growth rate. Factors involved may include genetics. lesions pathognomonic. Grey to pink foci in the pancreas. nutrition. Treatment None. Various angulations of leg. Congestion. bacterial and fungal infections. Differentiate from histomonosis. 149 . Bile staining. 1 mm) coalescing. Focal haemorrhage. Microscopically .
game birds and pigeons may also be affected. E. Diagnosis Symptoms. highly contagious disease of chickens and quail caused by the bacterium Clostridium colinumand characterised by ulcers of the intestines and caecae. Ulcerative Enteritis. Retracted neck. lesions. Predisposing factors include Coccidiosis (especially E. intertarsal angulation up to 10% is physiological.. IBDV and overcrowding. Changed angulation of tibial condyles. Blood in intestine. It can start suddenly and cause high mortality: 100% in quail and 10% in chickens. Differentiate from perosis. Partially closed eyes. and E. Turkeys. necatrix. Prevention Selection for good conformation in primary breeding. Post-mortem lesions Deep ulcers throughout intestine. Quail disease Introduction Ulcerative Enteritis is an acute. The bacterium resists boiling for 3 minutes. The route of infection is oral and transmission is from faeces of sick or carrier birds or via flies. greater than 20% is abnormal. Watery white faeces (quail). Adoption of optimal nutrition and growth patterns for the economic objectives of the production system. arthritis and synovitis. tenella. Treatment None. Anaemia. brunetti). Ruffled feathers. Signs Listlessness. Drooping wings. Diarrhoea. Peritonitis (if ulcers penetrate). but mainly ileum and caecae. which may coalesce and may be round or lenticular. The condition occurs worldwide. 150 . Pale yellow membranes.
Treatment Streptomycin (44 gm/100 litres water). Avian Infectious Hepatitis Introduction An insidious onset disease of chickens caused by Vibrio bacteria. Inappetance. Diagnosis A presumptive diagnosis may be made on history and lesions. Transmission is by faecal contamination. Wall of the caecum of a chicken suffering from ulcerative enteritis Vibrionic Hepatitis. Confirmation is on absence of other diseases and isolation of Cl. penicillin (50-100 ppm in feed). Treat for coccidiosis if this is a factor. Signs Dejection. Necrotic foci in liver. all-in/all-out production. trichomoniasis. Tetracyclines. Loss of condition. Prevention Infection-free birds. colinum in anaerobic conditions (the agent is often present in pure culture in liver). coccidiosis. 151 . possibly probiotics. amoxycillin. Figure 35. salmonellosis. low level antibiotics as per treatment. and disease is precipitated by stress. Differentiate from histomonosis ('Blackhead'). Bacitracin. Response to treatment should occur in 48 to 96 hours. birds remaining carriers for months. Morbidity is low. The infective agent is rather resistant to environment and disinfectants. necrotic enteritis. multivitamins. Diarrhoea.
Pale comb and wattles. Scaly comb. Jaundice. Drop in production/weight gain.
Focal hepatic necrosis in 10% of affected. Foci often stellate, or there may be a cauliflower-like 'spotty liver'. Haematocysts under capsule. Swelling of organs. Catarrhal enteritis.
History, lesions, isolation of infective agent from bile. Differentiate from leukosis, histomonosis, ulcerative enteritis, fowl cholera, and typhoid.
Hygiene, depopulate, obtain birds free of disease, contain stressors.
Viral Arthritis is the classic, but by no means the only, manifestation of reovirus infection of chickens; at least 5 sero-types of virus occur. Morbidity is high but mortality is usually low. Transmission is by faecal contamination, and good both laterally and vertically. Birds remain carriers for over 250 days. The virus is resistant to heat, ether, chloroform, pH and environmental factors. Reoviruses vary markedly in pathogenicity and the tissue damaged. Some can cause other disease syndromes such as early chick mortality and malabsorption syndrome. Some strains have shown severe systemic disease including pericarditis in chickens. Others have caused immunosuppression by damaging the cloacal bursa in ducks.
Lameness. Low mobility. Poor growth. Inflammation at hock. Swelling of tendon sheaths. Unthriftiness. Rupture of gastrocnemius tendons.
Swelling and inflammation of digital flexor and metatarsal extensor tendon sheaths. Foot pad swelling. Articular cartilages may be ulcerated. Haemorrhage in tissues. Fibrosis in chronic cases.
Diagnosis may be based on the history, lesions, IFA and rising antibody titre. Isolation may be readily achieved in CE yolk sac and CAM and also cell cultures (CE kidney or liver cells). Serology may be by DID, FAT or Elisa. 'Silent' infections (not associated with obvious disease) are common. Differentiate from mycoplasmosis, salmonellosis, Marek's, Pasteurella, erysipelas.
Vaccination is ideally carried out by administering a live vaccine in rear followed by an inactivated vaccine prior to coming into lay. Most vaccines are based on strain 11/33. Rear birds in all-in/all-out production systems.
Visceral Gout, Nephrosis, Baby Chick Nephropathy
Visceral gout is the deposition of white urates, which are normally excreted as a white cap on well formed faeces, in various tissues. Urates are also often deposited in joints and in the kidney. This condition can occur as an individual problem at any age. Outbreaks are seen in young chicks in the first week of life (baby chick nephropathy) or in flocks suffering kidney damage, or reduced water intake. All poultry species are susceptible. The kidney damage can arise from infection with certain strains of Infectious Bronchtiis virus, exposure to some mycotoxins or inadequate water intake (often because the birds have not adapated to a new type of drinker). Baby Chick Nephropathy can be due to inappropriate egg storage conditions, excessive water loss during incubation or during chick holding/transport, or inadequate water intake during the first few days of life. Very low humidity in brooding will also increase the likelihood of this problem. The timing of mortality is a reasonable guide as to the source of the problem. In Pekin/mallard ducks the condition is almost always due to inadequate water intake, whereas in muscovy ducks it is seen in breeders allowed to continue laying for over 24 weeks without a rest.
Depression. Low feed intake and growth.
Chalky white deposits on pericardium, liver, air sacs, peritoneum. Similar deposits may be present in joints and are usually present in the kidney.
This is based on correcting any management errors and encouraging water intake. Avoid any intentional or unintentional restriction in water intake. Sodium bicarbonate at 1g/litre water is mildly diuretic, however it could be counter-productive if water intake is in any way restricted.
Careful monitoring of the conditions of hatching egg storage and incubation with a view to achieving a standard egg weight loss profile. Humidification of holding rooms and chick transporters may also be beneficial. Humidifiers in chick brooding areas are being used increasingly, especially where whole house hot air brooders are in use. Ample supplies of drinkers should be available and filled with water at house temperature prior to the arrival of the chicks.
Figure 36. Severe visceral gout in a young chick. There are white chalky deposits around the heart (in the pericardium) on all major abdominal organs, including liver, gizzard and intestines, and even in the tissues of the thigh.
antioxidant. Poor feathering. Microscopically . chronic fowl cholera.M. Differentiate from Infectious coryza.Abubakar. Eyelids stuck shut with thick exudate.Tahir Vitamin A Deficiency. Excessive urates in kidneys and ureters. 155 . Diagnosis Signs. feed formulation. Nutritional Roup Introduction Vitamin A deficiency is occasionally seen in chickens and turkeys (insufficient vitamin A during 1-7 weeks of age). As in the case of other nutritional deficiencies. Signs Poor growth. Treatment Vitamin A in drinking water.squamous metaplasia of epithelia. Nasal and ocular discharge. Post-mortem lesions Eyelids inflamed and adhered. Drowsiness. Pale comb and wattles. Prevention Supplementation of diet with vitamin A. lesions. classic signs of deficiency are very rare in commercial poultry fed complete diets. good quality raw materials. infectious sinusitis etc. Pustules in mouth and pharynx.
Simple deficiency is now rare as diets are usually well supplemented. response to supplementation.M. Vitamin deficiencies are especially prone to cause problems of hatchability. Some deficiencies induce characteristic microscopic effects. Signs These may be summarised: Perosis Curled Toe Paralysis Paralysis/'Stargazing' Dermatitis/Scaly Skin Mouth Lesions Conjunctivitis Anaemia Fatty Liver and Kidney Syndrome Poor Feathering Loose feathers Hatchability problems Embryo with clubbed down Thiamine (B1) Riboflavin (B2) Pantothenic acid Pyridoxine (B6) Niacin Folic Acid Cyanocobalmin (B12) Biotin Post-mortem lesions Usually the gross lesions are non-specific. including growth in the young animal.Abubakar. However. Diagnosis Signs. The embryo is particularly dependent on having adequate supplies of vitamins deposited in the egg. because a continuous supply is required. See the separate discussion under Chondrodystrophy and Fatty Liver and Kidney Syndrome. They act in a broad range of metabolic pathways. exclusion of specific diseases. If it is suspected that the vitamin premix may not have been included in the ration (or included at too low a level) it 156 .Tahir Vitamin B Deficiencies Introduction The B complex vitamins are water soluble and not stored to any significant extent in the body. damage to the intestine or increased demand for some reason may have an effect. Most will reduce productivity. and egg production in the layer.
Paralysis. White streaks in muscle. Green wings. Falling over. Staggering. Necrosis. 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. Encephalomalacia. seen worldwide. Muscular dystrophy is seen more frequently in older and mature birds. 157 .may be appropriate (faster. Post-mortem lesions Swollen cerebellum with areas of congestion. Steatitis. characterised by oxidation of various tissues and caused by Vitamin E deficiency. Ventral oedema. Good quality multivitamin solutions are beneficial in the supportive care of a range of problems characterised by reduced feed intake. Vitamin E Deficiency. drinking water supplementation with that vitamin is ideal and usually results in a rapid response in birds that are still drinking. Exudative Diathesis. occasionally ducklings and other birds. Encephalomalacia and exudative diathesis tends to be seen in young birds of 1-5 weeks of age. Blood-stained or greenish subcutaneous oedema. Treatment If a specific vitamin deficiency is suspected. Haemorrhage. Signs Imbalance. Prevention Adequate supplementation of the feed with all required vitamins in levels which both support normal productivity but also have enough overage to deal with the increased demands that often occur during periods of disease challenge. less expensive) to analyse feed for a marker substance such as manganese rather than testing for vitamin levels. The problem is associated with feed rancidity typically in diets with high fat. Uncontrolled movements.
and poor hygiene of setters. Pseudomonas. Prevention Proper levels of vitamin E. feed rancidity. 158 . Abnormal yolk sac contents (colour. 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. 'bangers'. inadequate hatchery hygiene or poor incubation conditions. histopathology. Yolk Sac Infection.coli. Broad-spectrum antibiotics where there are extensive skin lesions. for example poor hygiene of hatching eggs. lesions. Disease occurs after an incubation period of 1-3 days. Staphylococci. selenium. Diarrhoea. especially E . Treatment Vitamin E and/or selenium in feed and/or water. necrotic dermatitis. turkeys and ducks due to bacterial infection of the navel and yolk sac of newly hatched chicks as a result of contamination before healing of the navel. Vent pasting. antioxidant.Proteus. hatchers or chick boxes. Swollen abdomen.Diagnosis Signs. Various bacteria may be involved. Loss of appetite. It is seen where there is poor breeder farm nest hygiene. Omphallitis Introduction A condition seen worldwide in chickens. consistency) that vary according to the bacteria involved. Closed eyes. response to medication. use of floor eggs. Differentiate from Encephalomyelitis. Signs Dejection. toxicities. Post-mortem lesions Enlarged yolk sac with congestion. Morbidity is 1-10% and mortality is high in affected chicks. good quality raw materials.
sanitation of eggs. most will die before 7 days of age. There should be routine sanitation monitoring of the hatchery. however the prognosis for chicks showing obvious signs is poor. clean nests. Prevention Prevention is based on a good programme of hygiene and sanitation from the nest through to the chick box (e. Confirmation is by isolation and identification of the bacteria involved in the internal lesions. 159 . exclusion of severely soiled eggs. frequent collection. Treatment Antibiotics in accordance with sensitivity may be beneficial in the acute stages.g. Differentiate from incubation problems resulting in weak chicks. separate incubation of floor eggs etc. Multivitamins in the first few days may generally boost ability to fight off mild infections.Diagnosis A presumptive diagnosis is based on the age and typical lesions.
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