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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.
through faecal contamination of environment. Mortality is 10-50% in young birds. 'hardening off'. Congestion of duodenum. mainly in North America. correct house relative humidity. sulphonamides in feed. reptiles. Paralysis. 4 . Foci in lungs. Figure 40. from long-term intestinal carriers. Arizona infection. Cheesy plugs in intestine or caecum. and also horizontal. It affects turkeys. Arizonosis Introduction Caused by the bacterium Arizona hinshawii. feed etc. Vent-pasting. Inappetance. and is not present in the UK turkey population. transovarian. Signs Dejection. cloudiness in eye. renamed Salmonella Arizonae. Blindness. Unabsorbed yolk sac. Diarrhoea. Autogenous bacterins sometimes used. Huddling near heat. older birds are asymptomatic carriers.Prevention Good husbandry and hygiene. rigid depopulation and disinfection. Transmission is vertical. adequate protection. Inactivated and attenuated vaccines available in some countries. Nervous signs. Erosions of the cartilage of the hock joint in a duck with chronic Riemerella anatipestifer infection. rodents. Post-mortem lesions Enlarged mottled liver.
Pericarditis. Lungs and intestines congested. The disease has a complex aetiology and is predisposed by reduced ventilation. or gentamycin at the hatchery is used in some countries. Thickening of atrioventricular valve. Post-mortem lesions Thickening of right-side myocardium. fumigation of hatching eggs. and respiratory disease. Ascites is a disease of broiler chickens occurring worldwide but especially at high altitude. may be related to type of stock and strain). Prevention Eradicate from breeder population. poor ventilation and physiology (oxygen demand. methods as per Salmonella spp. General venous congestion. Recumbency. Poor development. 5 . mortality 1-2% but can be 30% at high altitude. spectinomycin. Ascites Introduction Associated with inadequate supplies of oxygen. Dilation of the ventricle. coli-septicaemia. Diagnosis Isolation and identification. monitor sensitivity. Perihepatitis. Formerly in-feed medication with nitrofurans was also used. Possibly cyanosis. Morbidity is usually 1-5%. Progressive weakness and abdominal distension. Pulmonary arterial vasoconstriction appears to be the main mechanism of the condition. Salpingitis. Signs Sudden deaths in rapidly developing birds. Dyspnoea. Ophthalmitis. Severe muscle congestion. high altitude. good nest and hatchery hygiene. Differentiate from Treatment Injection of streptomycin. salmonellosis. inject eggs or poults with antibiotics.
Thirst. Morbidity is usually low. Vitamin C (500 ppm) has been reported to be of benefit in South America. Prevention Good ventilation (including in incubation and chick transport). in which the typical sign is gasping for breath. The infection has an incubation period of 2-5 days. Treatment Improve ventilation. there is usually little bird-to-bird transmission. Mortality among young affected birds is 5-50%. It affects chickens. etc. Microscopic . Absidia etc. Liver enlargement. turkeys. 6 . control respiratory disease. Diagnosis Gross pathology is characteristic. A cardiac specific protein (Troponin T) may be measured in the blood. waterfowl. Drowsiness.cartilage nodules increased in lung. Rapid breathing. avoid any genetic tendency. Ascites. worldwide. ducks. especially in young chicks. penguins. game birds. Signs Acute form: Inappetance. Weakness. The fungus can infect plant material and many species of animals including birds and man. Spleen small. Transmission is by inhalation exposure to an environment with a high spore count. but may be as high as 12%. Nervous signs (rare). This may offer the ability to identify genetic predisposition. Sometimes the same organism causes eye lesions or chronic lesions in older birds. Differentiate from broiler Sudden Death Syndrome and bacterial endocarditis. Pericardial effusion. Silent gasping. Aspergillosis Introduction A fungal infectious disease. Spores are highly resistant to disinfectants. Occasionally similar lesions are produced by other species ofAspergillus or even other fungi such as Penicillium. caused by Aspergillus fumigatus.
typically by putting small pieces of affected tissue on Sabouraud agar. turkeys. 'Furry' airsacculitis in aspergillosis of an adult duck. trachea. Diagnosis This is usually based on the signs and lesions and microscopic examination for the fungus. It may be confirmed by isolation of the fungus. The powdery surface is dark green in colour. Conjunctivitis/keratitis. mortality none. Prevention Dry. Avian Encephalomyelitis Egg Drop Introduction Avian encephalomyelitis virus infection in laying bird causes inapparent infection or drops in egg production. may have greenish surface. It affects chickens. preferably after digestion in 10% potassium hydroxide.M. quail.Tahir 2 Chronic Forms: Ocular discharge (ocular form only). Wasting. Environmental spraying with effective antifungal antiseptic may help reduce challenge. Epidemic tremors for its effect in young birds. Figure 8. good quality litter and feed. Treatment Usually none. Thiabendazole or Nystatin has been used in feed. hygiene. Morbidity 5-60%. See Avian Encephalomyelitis. pheasants and occurs in most poultry-producing countries. plaques in peritoneal cavity. Amphotericin B and Nystatin have been used in high-value birds. The means of transmission is unknown but 7 .Abubakar. Differentiate from excessive exposure to formalin or vaccinal reactions in day olds and from heat stress in older birds. Brain lesions may be seen in some birds with nervous signs. air sacs. Post-mortem lesions Yellow to grey nodules or plaques in lungs. Growth occurs in 24-48 hours and colonies are powdery green/blue in appearance.
Vertical transmission is very important. subsequent disease in progeny if breeders. Treatment None. attenuated or not. some lateral. small (5-10%) and lasting no more than 2 weeks. now Elisa is used more commonly. Virus in faeces may survive 4 weeks or more. Dull expression. mortality high. Morbidity 5-60% depending on the immune status of the majority of parents. Ataxia and sitting on hocks. turkeys. Avian Encephalomyelitis. Predisposed by immunosuppression.The embryo protection test has been used in the past. EDS76. In breeders there may be a drop in hatchability of about 5%. Signs Nervous signs. transmission occurs over about 1-2 weeks. Signs Drop in egg production. The route of infection is transovarian with an incubation period of 1-7 days. feed. Serology . Diagnosis History. Imbalance. and quail. water etc. Differentiate from Infectious Bronchitis. with an oral infection route. Epidemic Tremors Introduction Avian encephalomyelitis is a viral disease of the central nervous system of chickens. Immunity is usually long lasting. and there is serious disease in the progeny (see next section). It has a worldwide distribution. incubation >10 days. Prevention Vaccination of breeders/layers at 9-15 weeks. lentogenic Newcastle disease. pheasants. rising titre to AE virus. Post-mortem lesions None.probably by faecal contamination of environment. lateral transmission is probably by the oral route. Virus in faeces may survive 4 weeks or more. Paralysis. 8 .
vitamin deficiency (E.nonpurulent diffuse encephalomyelitis with perivascular cuffing. attenuated or not. neck and wings. and isolates are designated sero-type/ species/location/reference number/year/subtype designation(H/N). pheasants. Mycotic Encephalitis. and/or viral isolation may be carried out if required. Brain abscess. and ostriches. the equivalent of the World Health Organisation for animal diseases. Histopathology is usually diagnostic and IFA. Prevention Vaccination of breeders at 9-15 weeks. its pathogenicity is variable. There may be focal white areas in gizzard muscle (inconstant). partridges. turkeys. especially in turkeys. 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. This is a test in which the virus is inoculated into susceptible chickens that are then kept under observation. Diagnosis A presumptive diagnosis is based on the history. toxicities. Immunity is long lasting. Fowl One of only two 'Class A' diseases of poultry targeted for emergency disease control measures by OIE. EE (especially in pheasant in the Americas). Enterococcus hirae infection. A few recovered birds may develop cataracts weeks after infection. The virus infects chickens. This viral disease can cause exceptionally high mortality. Tremor may be inapparent but is accentuated if chicks are held inverted in the hand. ducks. quail. Orthomyxovirus type A. The cause is a virus. Marek's disease. Tremor of head. Microscopic . Differentiate from Newcastle disease. pigeons. now Elisa is used more commonly. 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. In addition official control measures disrupt trade in poultry products from affected areas. Treatment None. The embryo protection test has been used in the past. A. The higher the proportion of the chickens dying or showing signs the higher the IVPI. signs. Avian Influenza-Highly Plague Introduction Pathogenic (HPAI). Effectively all 9 . Post-mortem lesions Gross lesions are mild or absent.2 . riboflavin).
Coughing. Highly pathogenic avian influenza A (HPAI) viruses of the H5 and H7 HA subtypes have been isolated occasionally from free-living birds. drinking water. Drops in egg production. Signs Sudden death. Ovarian regression or haemorrhage. clothing. equipment. Pakistan. The virus replicates mainly in respiratory tissues of chickens and turkeys but in the intestinal tract of clinically normal waterfowl. 550%. The small number of human deaths associated with HPAI appear to have resulted from direct exposure to infected birds on farm or in markets. 10 . Outbreaks due to HPAI were recorded in the Pennsylvania area. It can result in inapparent infection. Avirulent in one species may be virulent in others. See current OIE records for up to date information on distribution of HPAI. Nasal and ocular discharge. in the years 1983-84. More recently outbreaks have occurred in Australia. Apathogenic and mildly pathogenic influenza A viruses occur worldwide. Cyanosis of comb/wattles. Morbidity is high but mortality usually relatively low. especially faeces. Post-mortem lesions Inflammation of sinuses. by acid pH. Broken contaminated eggs may infect chicks in the incubator simulating vertical transmission. by oxidising agent and by formalin and iodine compounds. USA. Diarrhoea (often green). and the high mortality that 'low-path' AI can cause in turkeys. The virus is moderately resistant. Marked loss of appetite. even with 'low pathogenicity' strains. air sacs and conjunctiva. in northern Italy. but possibly by the conjunctival or respiratory route and the incubation period is 3-5 days. A serious outbreak occurred in The Netherlands in 2003 with a few linked cases in Belgium and one in Germany. Mexico and.birds are considered to be at risk of infection. trachea. Cessation of normal flock vocalisation. Because of this.g. OIE and other bodies are currently examining ways to improve control of LPAI. conjunctivitis or severe pneumonia. can survive 4 days in water at 22°C. Depression. It is inactivated by a temperature of 56°C in 3 hours and 60°Cin 30 min. It can remain viable for long periods in tissues. Transmission is by direct contact with secretions from infected birds. Italy). Swollen face. Infections with other pathogens (e. waterfowl. Pasteurella) may increase mortality. The route of infection is probably oral initially. Avian Influenza is a potential zoonosis. reduced feed consumption. over 30 days at 0°C. Nervous signs such as paralysis. H5 viruses of low pathogenicity may become highly pathogenic usually after circulating in poultry flocks for a time (Pennsylvania. from December 1999.
etc. other respiratory infections. lateral transmission by faecal-oral route (this declines as the bird ages). Vaccination is not normally recommended because. controlled marketing of recovered birds. Treatment None. infectious laryngotracheitis. vaccinated birds may remain carriers if exposed to the infection. Minimise contact with wild birds. Muscles congested. Turkey lesions tend to be less marked than those of chickens. Dehydration. fowl cholera. quarantine. Avian Leukosis (Serotype J). bacterial sinusitis in ducks. The incubation period is 10-20 weeks. Necrosis of skin of comb and wattles. NDV-. Transmission is by congenital infection from antibody-negative females. as with many such tests occasional false positive reactions can occur. Diagnosis A presumptive diagnosis may be made on history and postmortem lesions. This condition has until now been seen only in meat-type chickens. In outbreaks a regime of slaughter. Eradication by slaughter is usual in chickens and turkeys. 21-day interval to re-stocking should be followed. Myelocytomatosis Introduction Caused by an avian retrovirus. correct disposal of carcases. cleaning. Prevention Hygiene. disinfection. HA+. bleeding and vaccination needles. isolation. Confirmation is by viral isolation in chick embryo. Differentiate from Newcastle disease. The agar gel precipitation test is non-group-specific and is used to confirm any positives. It has occured in Europe. However. but good husbandry. Vaccines have been used in recent outbreaks in Mexico and Pakistan. To be effective inactivated vaccines must be the right subtype for the particular situation (H5 will not protect against H7 and vice versa). with considerable strain-to-strain variation. though there is high mortality of affected birds. Morbidity is low. Haemorrhage in proventricular and gizzard mucosae and lymphoid tissue of intestinal tract. Congenitally infected birds tend to remain 11 . nutrition and antibiotics may reduce losses. while ducks may be symptomless. North and South America. lesionless carriers of highly pathogenic virus. all-in/all-out production. Subcutaneous oedema of head and neck. Survivors can be expected to have a high degree of immunity but may harbour virulent virus. Commercial Elisa test kits are now available. DID+. although it may reduce losses initially.
age. lesions. 'nonshedders' . Separation in vaccination. Enlargement of abdomen. liver. Critical hatchery practices: Separate infected and uninfected lines.antibody negative. ultimately identification of virus by isolation and/or PCR.an Elisa test is aviailable to identify antibody positive birds. Virus survival is poor but sufficient to allow cross contamination in hatcheries and on farm in rear. Handle clean lines before infected lines. Loss of weight. 12 . often with tumour foci. PCR testing of embryonally infected chicks using DNA testing is uniformly positive for blood and faecal samples. Two cell types may be found in the same tumour. Persistent low mortality. Splenomegaly and enlarged kidneys also occur. Most characteristically are chalky white tumours in the bone marrow. particularly of the sternum. preferably on separate hatch days and in separate machines.most but not all.only 3% produced infected chicks. Diagnosis History. Treatment None. shed virus and develop tumours. Prevention Checking of antigen in the albumen is a basis for eradication .80% produce infected chicks. Signs Depression. ribs. Microscopic .tumours usually contain well-differentiated myelocytes. birds with egg antigen will be antibody negative. Post-mortem lesions Liver enlargement. histology. Serology . Many are asymptomatic. Emaciation. Minimise stress. There is also evidence that it is slightly more sensitive than conventional testing. Differentiate from Marek's disease. 'Shedders' . Prevent/ reduce cross-infection in hatchery and on farm. Lymphoid Leukosis. sacral joint.
Liver may be very large. myxosarcomas. Differentiate from Marek's disease. Delay live vaccine challenges. especially in young birds. Leukosis/Sarkoma Group Introduction Lymphoid Leukosis. Enlargement of abdomen. In lymphoid leukosis the incubation period is about 4-6 months. lateral transmission is poor but infection may occur by the faecal-oral route.egg layers are generally more susceptible to lymphoid leukosis. 13 . The causative viruses are rapidly inactivated at ambient temperature and on exposure to most disinfectants. cytology. spleen. erythroblastosis. Many are asymptomatic.cells lymphoplastic Diagnosis History. osteopetrosis. A complex of viral diseases with various manifestations such as lymphoid leukosis. Avian Leukosis. other tumours. Signs Depression. Loss of weight. There may be increased susceptibility to other infectious diseases due to damage to the immune system. age. myeloblastosis (see Sero-type J). kidney etc. Microscopic . Mortality tends to be chronically higher than normal for a prolonged period. Minimise group sizes. initially in the bursa. lesions. then liver. Avoid migration errors (birds unintentionally moving between pens). it may be as short as 6 weeks for some of the other manifestations. liver or bursa. Persistent low mortality.Farm practices: Brood and rear lines separately and maintain separate for as long as possible. Vertical transmission is most important by infection of the egg white in infected breeders (who are long-term carriers). Post-mortem lesions Focal grey to white tumours. Emaciation. coligranuloma. Morbidity is low but mortality high. It affects chickens worldwide with susceptibility varying considerably among different strains and types of stock . Egg production is somewhat reduced. fibrosarcomas.
Dyspnoea. control arthropods. Two subgroups have been identified on the basis of the G-protein sequence: A (original UK isolates) and B (original southern Europe isolates). It is caused by a pneumovirus of the Paramyxoviridae family. vertical transmission is uncertain. Avian Rhinotracheitis 'Swollen Head Syndrome' Introduction A viral disease of chickens. This was a case of Myelocytoma Avian Leukosis (Sero-type J). Africa. turkeys (see separate summary). Diffuse lymphoid tumours in an enlarged liver from a mature broiler parent hen. morbidity is 10-100% and mortality can be 110%. Snick. Ocular and nasal discharge. South America and North America. weight gain and feed efficiency. As for many infections. Facial and head swelling (though this can occur in other conditions). Loss of voice. Prevention Good hygiene. Conjunctivitis. 14 . Signs Decreased appetite. eradication .checking of antigen in the albumen is a basis for eradication (see Sero-type J for details). all-in/all-out production. There is rapid lateral transmission with infection by aerosol through the respiratory route. The incubation period is 5-7 days. fomites can be important in moving infection between farms. first isolated from poults in South Africa in 1978. Figure 9. guinea fowl and possibly pheasants seen in Europe.Treatment None.
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.
A RT-PCR test may be used to detect viral RNA in tissues. Signs Poor growth. Scabs around eyes and beak. Post-mortem lesions See signs. Pale livers and kidneys in fatty liver and kidney syndrome. Sudden deaths in fatty liver and kidney syndrome. Chondrodystrophy. Must be confirmed by laboratory tests. Histopathology may also be used but the findings are not specific to this condition. Thickened skin under foot pad. Diagnosis Typical signs and lesions. Drinking water which is well chlorinated should be helpful in reducing challenge by this route. Reduced feed intake and blood sugar can precipitate fatty liver and kidney syndrome. Elisa tests have been developed experimentally. 18 . Viral particles may be demonstrated in bile. Biotin Deficiency. Serological tests (agar gel immunodiffusion) may be used to detect either the specific antigen (which is likely to be positive first) or the antibody response to it. Treatment No specific treatment known. Lung congestion Ovarian regression Yolk peritonitis Pale foci and haemorrhages in pancreas. Prevention Thorough cleaning and disinfection after depletion of an affected flock. Allin/all-out production. webbing between toes. Good biosecurity. Leg weakness. It may be helpful to control other conditions which may be occurring at the same time. in embryos. 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.
Crusty clumps of eggs ('nits') may be visible at the base of feathers. may be some feather damage and crustiness of skin. Post-mortem lesions Usually none. Treatment Malathion powders and pyrethroid sprays where approved for bird application. Treatment Addition of biotin in feed or water. Irritation. They are spread by direct contact between birds and by litter etc. Away from birds adults survive about 4-5 days. Diagnosis Identification of the parasites. response to treatment/prevention. Menocanthus stramineus is the most pathogenic and is said to be capable of causing anaemia in heavy infestations. Check flocks regulary for rapidly moving insects at the base of the feathers on the abdomen or around the vent. Drop in egg production. Differentiate from pantothenic acid deficiency (skin lesions). Loss of condition.Diagnosis Signs. Scabs around vent. Loss of vent feathers. Prevention Supplementation of diets with biotin . lesions. Signs Lack of thrift in young birds. has very low bioavailability. Biting Lice Introduction Various species of lice are common external parasites of poultry worldwide. Lice eggs stuck to feathers. 19 .naturally present in many raw materials. bedbugs. The parasites are 1-6 mm in size and their life cycle takes about 3 weeks. Differentiate from mites. especially around vent. Parasites on birds.
season. Biological control using a strain of Bacillus thuringensis has had some success and is preferable to insecticides. Post-mortem lesions Anaemia. Diagnosis Anaemia. 5 mm long and found in North and South America that are external parasites of birds and mammals. Signs Anaemia in young birds.Prevention Avoid direct contact with wild and backyard poultry. 20 . Eggs and larvae survive through the winter to cause new infestations in the following year. Effective removal of all organic material at flock depletion should be practised in all-in/all-out production systems. although these insects can travel up to 15 miles. It is usually necessary to treat twice at a 7-10 day interval to fully control the condition. especially in autumn and winter and treat if required. Swarms of flies. Examine for lice regularly. Weekly treatments are required. Treatment Treatment is difficult. The condition tends to occur near to rapidly flowing streams. Blackfly Infestation Introduction Grey-black hump-backed flies. as the larvae within eggs are not killed by most products. Prevention Similar measures as for mosquito control. The flies transmit leucocytozoonosis and also a filarial parasite in ducks. local history.
Mild enteritis if has been affected for some time. Morbidity is usually low but mortality is high. turkeys. suspect food and stagnant ponds. Prevention Preventing access to toxin. Signs Nervous signs. wings then neck. The toxin and bacterial spores are relatively stable and may survive for some time in the environment. This will reduce the risk of botulism both in the poultry and in any grazing animals on land where poultry litter is spread. selenium. Diagnosis History. The single most important measure is careful pick-up and removal of all dead birds on a daily basis. A soiled beak. carcases. Toxin may also be produced by the bacteria in the caecum. weakness. Affected broilers tend to settle with eyes closed when not disturbed. especially in hot weather.Botulism Introduction A condition of chickens. supportive treatment if justifiable. The toxin is produced in decaying animal (usually carcases) and plant waste. is also quite typical. Treatment Remove source of toxin. then sudden death. Differentiate from acute Marek's disease ('Floppy Broiler Syndrome') by histology of the brain. ducks and other waterfowl occurring worldwide and caused by a bacterial toxin produced byClostridium botulinum mainly types A / C. Post-mortem lesions Possibly no significant lesions. antibiotics. It has also been suggested that poultry carcases lost in litter can be a cause of botulism in cattle grazing land or consuming silage where poultry litter has been spread. and toxin-containing material (pond-mud. signs. because it rests on the litter. maggots) is consumed by the birds. Feathers may be easily pulled (chicken only). progressive flaccid paralysis of legs. mouse toxicology on serum or extract of intestinal contents. 21 . Maggots or putrid ingesta may be found in the crop.
up to 1. Signs Swelling over the keel bone with bruising and discolouration. Morbidity may reach more than 50% but the condition is not fatal. 22 . bacteria. nematode parasites of poultry and game birds. They are found worldwide. and infection withStaphylococcus spp. leg weakness. Post-mortem lesions Inflammation of sternal bursa along the keel bone which may. control of leg problems. The meaning of the technical terms relating to parasite life cycle are defined in the glossary. in chronic cases.Breast Blister Introduction A complex condition of chickens and turkeys occurring worldwide associated with trauma. Heterakis gallinaeeggs and larvae are a transport hosts for Histomonas. Earthworms may be transport hosts for eggs.5 cm in length that occur in the caecum. Signs None. Infection is by the oral route. are small whitish worms with a pointed tail. Morbidity is high but it is not associated with mortality. Treatment Not usually appropriate. the cause of Blackhead. Diagnosis Based on lesions. Caecal Worm Introduction Heterakis gallinae. There is an incubation period of 2 weeks for eggs to embryonate. Prevention Good litter management and handling. and a four-week prepatent period. Poor feather cover and caked or wet litter are predisposing factors. or paratenic hosts with partially developed (L2) larvae. give way to scar tissue.
or by an earthworm which is in turn ingested by a chicken. Figure 11. Death from respiratory and cardiac failure. Levamisole. The egg may be ingested directly by a chicken. and the embryonated egg. are effective. possibly with nodule formation. Prevention Avoiding access to earth and earthworms. Diagnosis Adults can be seen in caecal contents at post-mortem examination. an undeveloped egg as found in fresh faeces. Treatment Flubendazole. 23 . Signs Paralysis. Calcium Tetany Introduction A metabolic disease of chickens. Routine anthelmintic treatment. especially broiler parents. The life cycle ofHeterakis showing the location of adults.Post-mortem lesions Inflammation of caecum. Predisposing factors include heat stress with reduced feed intake and panting.
There is an annual cycle with increased risk of infection in the summer months in some countries. Prevention Keep pullet flocks on low calcium diet until 5% production hen/day. Campylobacter Infection Introduction Campylobacter spp. Treatment Provide 5 gm of oyster shell per hen on 3 successive days along with vitamin D in drinking water. 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'. It may be that management that favours dry litter reduces the risk of infection and/or transmission within the flock. and response to treatment. There are indications that plantar pododermatitis. other acute infections and other causes of sudden death. Differentiate from IB 793b. Diagnosis This is made on signs.Post-mortem lesions Cyanosis. managing birds for maximum uniformity. All campylobacters are delicate organisms that survive for relatively short periods outside the host unless protected by organic material. principally in the caecae. Infected poultry are a potential reservoir of this zoonosis. Congested lungs. lack of other significant lesions. In poultry they tend to multiply in large numbers in the hindgut. are bacteria that commonly infect a broad range of livestock species. carcase quality and litter quality are better on farms which tend to have Campylobacter-negative stock. Active ovary with egg in oviduct. biofilm or engulfed by protozoa. lesions. Campylobacter jejuni is the commonest species found in poultry. 24 . pets and wild animals. The reason for this is unclear. Campylobacters are a significant cause of enteritis in man.
sourcing of water from high quality supplies.Signs None. Insects and rodents may act as a means of transfer of the infection from the general environment into the poultry buildings. Post-mortem lesions None. Samples should be tested as quickly as possible after collection. For this reason it may be difficult to stop the spread of infection between houses once it becomes established in one house. Research is ongoing on the development of vaccines. housed poultry can be maintained free of Campylobacter infection by consistent application of excellent biosecurity. In practice the success of this will also depend upon the degree of environmental contamination by the organism. phage treatments and competitive exclusion approaches. 25 . as well as processing plant technologies to reduce carcase contamination. avoidance of contact with pets and other farmed species. The organism is sensitive to air so swabs should be collected into transport medium and other samples placed in airtight containers with minimal airspace. Many infections are introduced during thinning or other forms of partial depopulation. and changing of overalls and boots on entering bird areas. good hand hygiene by stockmen. cloacal swabs or composite faeces. Key aspects of this include effective sanitation of drinking water. Treatment Not required on clinical grounds. Prevention In principle. Diagnosis Isolation of the organism from caecal contents.
The cause is a fungal yeast. Moniliasis.Candidiasis. Morbidity and mortality are usually low. A finely divided powder of copper sulphate (where approved) at 200gm/tonne continually or to 14-16 weeks in replacement pullets. The fungus is resistant to many disinfectants. Thrush Introduction A disease of the alimentary tract of chickens. 26 . occasionally proventriculus and intestine. turkeys. histopathology. The route of infection is normally oral and the organism is often present in healthy animals with disease occurring secondary to stress and poor hygiene. Colonies of this fungus appear as white to ivory colour. Post-mortem lesions White plaques in mouth. especially in the crop but sometimes in the proventriculus. Raised focal lesions may slough into lumen as caseous material. Slow growth. Prevention Avoid excessive use of antibiotics and other stressors. characterised by thickening and white plaques on the mucosa. or copper sulphate 1gm/2 litre water for 3 days if approved locally. copper sulphate (1 kg/tonne feed) for 5 days. Treatment Nystatin (100 ppm in feed) for 7-10 days. Signs Dejection. Diarrhoea. possibly confused or masked by signs of the primary disease. Diagnosis Lesions. Control of Candida through drinking water is sometimes practised with chlorination (e. Poor appetite. microscopic examination of a digested smear (heat in 10% potassium hydroxide) to demonstrate the hyphal forms of the yeast in the tissues. and associated with gizzard erosion. proprionic acid. intestine and cloaca. and sometimes other birds and mammals. Candida albicans and the condition is seen worldwide.g. oesophagus. Ensure good hygiene. crop. sodium or calcium proprionate at 1 kg per tonne continually. smooth and with a yeasty smell.
Differentiate from bacterial dermatitis. excessive light intensity or variation (e. Morbidity is usually low but mortality is high among affected birds. Cannibalism. Beak trimming may be necessary. Signs Pecking at feet (especially young chicks) and vents (adult layers and turkey poults 812 days old). Generalised anaemia. If so it should be carried out carefully by trained operators. This is economical and effective. distribution of lesions. Soluble multivitamins and/ or methionine may be of some benefit in some circumstances. tenosynovitis and other diseases affecting mobility. anaemia. feed form (mash takes longer to consume than pellets). 27 . and strain of bird. sodium hypochlorite) at 5 ppm. Treatment Correct any husbandry problems. Prevention Proper density and temperature. high temperatures. face. Provision of a diet that closely matches the nutritional requirements of the stock concerned. Predisposing factors include overcrowding. low light level. post-mortem cannibalism. nutritional deficiencies. boredom.g. Take care to provide fresh clean feed and water.Chlorox. head. control ectoparasites. Feather-pulling. Post-mortem lesions Skin wounding related to particular signs exhibited. Feather pecking Introduction A complex multifactorial behavioural problem of poultry and game birds seen worldwide. wings. It should be repeated periodically. complying with local regulations and any relevant codes of practice. through shafts of light in the house). uncontaminated by fungi. Diagnosis Age.
obsignata in the small intestine. Fenbendazole has been shown to have high efficacy . Worm eggs in the environment are resistant. 28 . Wasting Poor growth. some are transmitted direct from bird to bird. effective cleaning of houses.Capillariasis . or characteristic worm eggs in faeces in patent infections. Treatment Coumphos has been licensed in some markets.05 mm wide and hair-like in appearance. small intestine or caecum.Hairworm Infection Introduction Nematode parasitic worms of poultry. game birds and pigeons ofCapillaria species. Morbidity and mortality are usually low.other approved benzimidazoles can be expected also to have activity. seiving intestinal contents. The worms are 7-18 mm long. contorta in the crop and oesophagus. Infection is by the oral route. C. Signs Diarrhoea. Hairworms in mucosa of crop. Post-mortem lesions Enteritis. prepatent period about 21-25 days according to species. Diagnosis This may be by a combination of macroscopic examination. Prevention Separation of birds from possible transport and intermediate hosts. C. Dejection. Levamisole. Differentiate from other causes of enteritis. Worm eggs take about 20 days to embryonate with an L1 larvae. Some species have earthworms as intermediate hosts. about 0.
Many meat inspectors become skilled at detecting subtle differences in skin colour in the affected birds. However its main importance is as a cause of condemnation in meat poultry. Treatment Treatment would not be possible if the problem is identified at a final depletion. coli. Signs Affected flocks tend to have poorer than average productivity and uniformity. It typically occurs between skin and muscles and between muscles and may be an incidental finding in a range of conditions. often minor. Many affected birds have no other lesions and are reasonably well grown. particularly broiler chickens. 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. 29 . Routine monitoring of skin damage at about 25 days of age may be helpful in fostering good practices. skin wounds by particular strains of E. though most of the birds showing toe scrapes will not go on to develop cellulitis. The condition is caused by infection of. Post-mortem lesions Typically it presents as exudate ranging from liquid and pale cream pus to yellowish solid plaques of caseous material under the skin of the abdomen and/or in the leg. Prevention Toe scrapes at 15-25 days of age when feather cover is poor are the most likely predisposing factors. In the USA it is called 'Inflammatory Process'. Diagnosis Typical lesions. which can replicate in the tissues. but the affected birds are not readily detectable prior to slaughter.Cellulitis Introduction Cellulitis is literally an inflammation of connective tissues. Careful flock management with a view to reducing toe wounds has the greatest impact in controlling cellulitis.
Gangrenous dermatitis on feet. legs wings or neck. If gangrenous dermatitis is a problem then periodic medication may be required. Treatment Good hygiene and management. and control of other diseases as appropriate. PCV of 5-15% (normal 27-36%). ether.Chicken Anaemia Introduction A viral disease of chickens caused by Chicken Anaemia Virus or CAV. 30 . Post-mortem lesions Pale bone marrow. No clinical signs or effect on egg production or fertility in parent flock during seroconversion. Inclusion body heptatitis etc. The virus is resistant to pH 2. Sudden rise in mortality (usually at 13-16 days of age). Mortality is typically 5-10% but may be up to 60% if there are predisposing factors present such as intercurrent disease (Aspergillosis. chloroform. Discoloured liver and kidney. Hypochlorite appears most effective in vitro. Prior to confirmation that it is in fact a virus it was known as Chicken Anaemia Agent or CAA. Pale birds. Signs Poor growth.) or poor management (e. Diagnosis Gross lesions. Gumboro. lateral transmission may result in poor productivity in broilers. Atrophy of thymus and bursa.g. 80°C for 5 minutes) and many disinfectants even for 2 hours at 37°C. Transmission is usually vertical during sero-conversion of a flock in lay. virus may be isolated in lymphoblastoid cell line (MDCC-MSB1). may be beneficial. heat (70°C for 1 hour. poor litter quality). Acute mycotic pneumonia. demonstration of ongoing sero-conversion in parent flock.
Conjunctivitis. their degree of attenuation is variable. Egg transmission does not occur. Psittacosis. mortality 5-40%. It is transmitted by contact. phenolics are less so. Production drops in naive laying flocks Post-mortem lesions Vascular congestion. or IFA. Immunity: there is a good response to field challenge (in birds over 4 weeks of age) and to attenuated live vaccines. faecal dust and wild bird carriers. psittacines. Elementary bodies are highly resistant and can survive in dried faeces for many months. Weakness.Prevention Live vaccines are available for parents. ducks. Fibrinous pericarditis. man. Serology: antibodies develop 3-6 weeks after infection. perhaps. rarely chickens. especially pigeons and robins. Occasional transient ataxia in pigeons. Wasting. Ornithosis Introduction An infection of turkeys. They should be used at least 6 weeks prior to collecting eggs for incubation. Inappetance. Chlamydiosis. It is a 'Scheduled Disease' rarely diagnosed in UK. Greenish-yellow diarrhoea. Intercurrent salmonellosis and. other infections may be predisposing factors. but occurring probably worldwide. Their use may be restricted to those flocks that have not sero-converted by. Iodophores and formaldehyde are effective disinfecting agents. Morbidity is 50-80%. Airsacculitis. Depression. Weight loss. 31 . 15 weeks. Signs Respiratory signs. say. Elisa. and may be detected by SN. caused by Chlamydia psittaci. a bacterium of highly variable pathogenicity. pigeons. Nasal discharge.
Chondrodystrophy. Serology: complement fixation. either singly or in combination (although deficiencies of pyridoxine. zinc. Differentiate from Duck viral hepatitis. shortened bones. IFA). Slipped Tendon or Perosis Introduction Caused by deficiency of manganese. niacin may also be involved). folic acid. Fibrinous pneumonia. Prevention Biosecurity. Necrotic foci in liver. biotin. Treatment Tetracycline (200-800 ppm in feed for 3-4 weeks) and/or quinolone medication and supervised slaughter. Intracytoplasmic inclusions are helpful but confirmation requires demonstration of causal organisms (Giemsa stain. choline. exclusion of wild birds. Distortion of hock. 32 . may rupture in pigeons. Live and inactivated vaccines are protective although the former result in carriers and the latter require several applications. Duck septicaemia. Congested lungs and air sacs in the turkey. In embryos parrot beak. ducks and turkeys. Signs Short legs. Lameness. Perihepatitis. Malposition of leg distal to hock. Spleen enlarged and congested. Slipping of Achilles tendon (or perosis). This condition is seen in chickens. signs. Elisa and gel diffusion. lesions. In turkeys it may be an inherited deficiency of galactosamine. Diagnosis History.
correct mineral balance. Watery diarrhoea that may occasionally be blood stained or contain clumps of mucus or shed mucosa. Weight loss. ruptured ligaments. adenoides affects the caecae and rectum. of which two are associated with significant disease effects. Tucked appearance. 33 . E. no value to affected bird. vitamins. Differentiate from twisted leg. choline. infectious synovitis. analysis of feed. infectious arthritis. Tibia and metatarsus bowed. Prevention Addition of manganese. Signs Huddling. Lateral slipping of tendon. Treatment For flock proceed as for prevention. rickets. Coccidiosis of Turkeys Introduction Infection of turkeys with Eimeria spp. while E. meleagridis affect the lower small intestine rectum and caecae. gallopavonis and E. ruffled feathers. Five species of Eimeria have been identified that cause lesions in turkeys.Post-mortem lesions Shortening and thickening of long bones. while E. Post-mortem lesions The affected area of intestine shows thickening of the wall and dilation. meleagrimitis affects the upper small intestine. Shallow trochlea. The contents may be haemorrhagic or be watery with white material shed from the mucosa. E. dispersa is found in the small intestine. This disease is not very common in commercially reared turkeys though most turkey growers receive preventative medication for at least part of their lives. Depression. Diagnosis Lesions.
microscopic exam of scrapings (oocysts. Figure 37. Dosage levels of ionophores may be critical to efficacy and safety. The intestines are dilated. Prevention The ionophore coccidiostats lasalocid and monensin are routinely used in turkey growers. Sulphaquinoxaline). typically to 12 weeks of age. Turkey caecal coccidiosis caused by E. lesions. 34 . Sulphonamides (e. gamonts). adenoides. Turkey coccidiosis of the upper small intestine caused by E. Treatment Toltrazuril. The exudate can range from semi-liquid to solid white cores.g.Diagnosis Signs. Diclazuril is also used for this purpose. Figure 38. Salinomycin is toxic for turkeys even at very low doses. Exposure of previously unmedicated birds to these compounds can cause toxicity. meleagrimitis. show some spotty congestion and have abnormal contents due to the sloughed epithelium. Avoid use of tiamulin in ionophore treated birds. Amprolium. Differentiate from necrotic enteritis.
In some markets the organic arsenical compound 3-Nitro is used as an aid in the control of caecal coccidiosis. Sulphonamides. Post-mortem lesions Petechiae. Recovered birds have good immunity to the same parasite. Ruffled feathers. Prevention Coccidiostats in feed. Treatment Toltrazuril. Morbidity is 10-40% and mortality up to 50%.Coccidiosis. Accumulation of varying quantities of blood and caseous necrotic material in the caecum. Production less affected than in some of the other forms of coccidiosis. histomonosis. Closed eyes. ecchymoses. vaccination by controlled exposure. Diarrhoea. Amprolium. 35 . Differentiate from ulcerative enteritis. Shuttle programmes with chemicals in the starter diet usually improve control. mitis (see above). Inappetance. lesions. Signs Depression. It is caused by Eimeria tenella and results in lesions in the caecum of chickens worldwide. Vitamins A and K in feed or water. E tenella Introduction This was at one time the commonest type of coccidiosis and is certainly the most easily diagnosed. tenella is more common when 'straight' ionophore programmes are used. of caecal mucosa. Vaccines are used mainly in breeders but increasingly in broilers. blood in faeces. Caecal. Transmission as for E. microscopic examination of scrapings. Thickening. hygiene. E. Diagnosis Signs.
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. humidity). is caused by the protozoan parasite Eimeria mitis. E mitis Introduction This condition of chickens. The disease occurring is proportional to the amount of infective agent ingested. seen worldwide. Moderate Eimeria tenella infection in the caecae of a chicken (Score 3). Diagnosis Mild lesions. Predisposing factors include exposure to faeces and litter conditions that favour development of the parasite (temperature. Coccidiosis. The parasite is moderately resistant in the environment and highly resistant to conventional disinfectants. Signs Reduced feed conversion efficiency and weight gain. which colonises the small intestine. Treatment Not usually treated but susceptible to the products used for other forms of intestinal coccidiosis. 36 . The infective agent is found in litter.Figure 15. identification of typical small round oocysts and other stages in fresh scrapings from the small intestine. faeces and on fomites and birds are infected by the oral route with an incubation period of 2-5 days. May predispose to wet litter. secondary bacterial enteritis. The caecal walls are thickened and haemorrhagic and there is a mass of blood in the caecal lumen.
it is found in the terminal ileum. Treatment Toltrazuril. Morbidity and mortality are variable. Of moderate to high pathogenicity. blood in faeces. Inappetance. lesions. This species is not usually included in vaccines for broilers. Post-mortem lesions Petechiae and thickening of the distal third or more of intestine. Severe necrotising enteritis. Prevention Coccidiostats in feed. 37 . E brunetti Introduction A relatively rare form of coccidiosis affecting chickens worldwide caused by Eimeria brunetti. There is good immunity to the same parasite in recovered birds. microscopic examination of scrapings. vaccination by controlled exposure. caecal coccidiosis. Sulphonamides. Ileorectal. May be included in vaccines.Prevention Normally controlled by anticoccidials in feed. Diagnosis Signs. Differentiate from ulcerative enteritis. Poor production. Closed eyes. caecum and rectum. Oocysts in caecum and rectum. Amprolium. Ruffled feathers. Coccidiosis. Diarrhoea. extending into caecal tonsils. Vitamins A and K in feed or water. Signs Depression. hygiene.
Treatment Sulphonamides (e. anseris is the most important. while in ducksTyzzeria perniciosa is most pathogenic. Duck viral enteritis. Intestinal. 3 days on). Amprolium. Coccidiosis. microscopic examination of scrapings (usually few or no oocysts. of Ducks and Geese Introduction Young ducks and geese may suffer from Eimeria spp infection. In the goose E. Tyzerria has eight sporocysts in each oocyst. Tucked appearance.g. lesions. Sulphadimidine 30-600gm/100 birds/day. Moderate Eimeria brunettiinfection in the terminal ileum and rectum of a chicken. Blood-stained vent. Diagnosis Signs.Figure 16. There is thickening of the intestinal mucosa and there are lines of haemorrhagic spots in the mucosa. compared to four per oocyst forEimeria. 38 . Depression. large number of merozoites). Differentiate from Duck viral hepatitis. Post-mortem lesions Massive haemorrhage in upper small intestine. anatipestifer. 2 days off. Signs Sudden death. 3 days on. Vitamins A and K in feed or water. Coccidiosis occurs only very rarely in commercially reared ducks in the UK.
Hygiene. Weakness. Coccidiosis.faeces tend to be whitish. Post-mortem lesions Enlarged kidneys. Kidney Introduction A disease of geese caused by Eimeria truncata that can cause high mortality in geese of 312 weeks of age. Diagnosis Lesions.Prevention If required coccidiostats could be used in feed. Prevention Good Hygiene. Reduced feed intake. presence of coccidial stages in fresh scrapings of kidney lesions. Treatment Controlled trials of treatments have not been published. it can also infect Barbary ducks and swans. Kidneys light grey to greyish pink. 39 . however this is not routinely practised. Signs Depression. Tiny white foci and petechiae in the kidneys. Diarrhoea .
Amprolium. maxima. hygiene. Vitamins A and K in feed or water. Depigmentation of skin and plasma is especially evident in this form of cocccidiosis and this is commercially important in some markets. This is one of the less immunogenic species. Mild to severe enteritis.Coccidiosis. Morbidity and mortality are variable. commercial vaccines commonly contain more than one strain of E. lesions. Diagnosis Signs. Poor production. Prevention Coccidiostats in feed. Poor absorption of nutrients/pigments. Differentiate from necrotic enteritis. Caused by Eimeria maxima. Mid-intestinal. Ruffled feathers. acervulina coccidiosis and there may be large numbers of characteristic oocysts in smears. microscopic examination of scrapings. contents often orange in colour. Signs Depression. of moderate to high pathogenicity it is seen worldwide. Post-mortem lesions Petechiae and thickening of middle third of intestine. Closed eyes. non-specific enteritis. Treatment Sulphonamides. Because of the area of intestine affected it tends to have a significant effect on productivity and susceptibility to necrotic enteritis. Blood or pigment in the faeces. Inappetance. vaccination. 40 . This infection is often associated with E. mucosa tends to be pinker than normal. E maxima Introduction One of the more common forms of coccidiosis in commercial broilers.
microscopic examination of scrapings Differentiate from necrotic enteritis. Schizonts seen as white spots through the serosa interspersed with petechiae. The intestine is slightly thickened and there are scattered haemorrhages in the mucosa when seen from the inside. 41 . The lesions are subtle compared to other forms of coccidiosis. Oocyts in caecal scrapings. Ruffled feathers. Coccidiosis. Depression. in which the parasite is present in the small intestine and in the caecum. blood in faeces. 'Sausage-like' intestine. of middle to posterior third or more of small intestine. Closed eyes. It occurs in chickens worldwide and has variable morbidity but mortality is high in severely affected birds. Moderate Eimeria maxima infection in the jejunum of a chicken (Score 2). Mid-intestinal. Post-mortem lesions Petechiae and thickening. Signs Reduced feed consumption. Diagnosis Signs. Severe necrotising enteritis. Diarrhoea. Deep scrapings necessary to show large schizonts. Inappetance. Poor production. E necatrix Introduction A highly pathogenic form of coccidiosis. other types of coccidiosis. lesions. caused by Eimeria necatrix.Figure 13.
Morbidity is variable and mortality low or absent. maxima. Figure 14. Diarrhoea. acervulina. commercial vaccines commonly contain more than one strain of E. Depigmentation. Moderate Eimeria necatrix infection in the jejunum of a chicken (Score 3). Poor production. Post-mortem lesions 42 .Treatment Toltrazuril. both alone and in association with other species of coccidia and is caused by Eimeria acervulina. hygiene. Eimeria mivatiis currently considered not to be a valid species distinct from E. Prevention Coccidiostats in feed. Amprolium. Ruffled feathers. Coccidiosis. Sulphonamides. This is one of the less immunogenic species. Inappetance. Vitamins A and K in feed or water. Signs Depression. Upper Intestinal. It is seen in layers and in broilers. E acervulina Introduction This is probably the commonest cause of coccidiosis in chickens and occurs worldwide. In this case the intestine is thickened and can become ballooned and sausage-like. which is moderately pathogenic. vaccination. Haemorrhages and white spots are visible from the outside of the intestine. Closed eyes.
in severe the entire surface is pale or denuded of epithelium. restricted to upper third of small intestine . A system of assessing the severity of coccidial challenge by attributing a 'score' is often used. Various publications provide a photographic key to severity of lesion. Petechiae. Figure 12. Moderate Eimeria acervulinainfection (score 2) in chicken duodenum. Treatment Toltrazuril. Immunity is quite short lived (about 30 days) in the absence of continued challenge.the duodenum and part of the ileum. In milder infections there may be scattered white spots. Poor absorption of nutrients/pigments. Thickening. Sulphonamides. A detailed description is beyond the scope of this book. hygiene. White spots or bands in the mucosa. Prevention Coccidiostats in feed. lesions. Amprolium. Differentiate from necrotic and non-specific enteritis. microscopic exam of scrapings. in feed or water. and other lesions. 43 . In general terms a score of 0 indicates no lesions and a score of 4 indicates maximal severity of lesion or death. Diagnosis Signs. vaccination by controlled exposure. In severe infections they become confluent and cause sloughing of the mucosa.
Reduced appetite. Granulomata in liver and spleen. fomites. Poor navel healing. Pericarditis. Poor growth. Snick. sneezing. mucosal damage due to viral infections and immunosuppression are predisposing factors. Post-mortem lesions Airsacculitis. Diagnosis Isolation. turkeys. It is most commonly seen following upper respiratory disease (such as Infectious Bronchitis) or Mycoplasmosis. water. Dejection. Infection is by the oral or inhalation routes. Peritonitis. Omphalitis. pathology. with an incubation period of 3-5 days. or in young birds that are immunologically immature. Colisepticemia Introduction Coli-septicaemia is the commonest infectious disease of farmed poultry.Colibacillosis. Arthritis. etc. Lesions vary from acute to chronic in the various forms of the disease. Synovitis. Cellulitis over the abdomen or in the leg. Signs Respiratory signs. Morbidity varies.most strains are rapidly lactose-fermenting producing 44 . Salpingitis. sero-typing. Enteritis. Swollen liver and spleen. coughing. Omphalitis. The infectious agent is moderately resistant in the environment. It is frequently associated with immunosuppressive diseases such as Infectious Bursal Disease Virus (Gumboro Disease) in chickens or Haemorrhagic Enteritis in turkeys. It is caused by the bacteriumEscherichia coli and is seen worldwide in chickens. and via shell membranes/yolk/navel. but is susceptible to disinfectants and to temperatures of 80°C. Perihepatitis. Aerobic culture yields colonies of 2-5mm on both blood and McConkey agar after 18 hours . mortality is 5-20%.
flouroquinolones. rear surface of the hock and. Prevention Good hygiene in handling of hatching eggs. Hock Burn. Some lesions are superficial. Well-nourished embryo and optimal incubation to maximise day-old viability. gentamycin or ceftiofur (where hatchery borne). whereas others progress to deep ulcers so the size. other enterobacteria such as Proteus. Control of predisposing factors and infections (usually by vaccination). Pododermatitis Introduction Contact dermatitis affects skin surfaces which have prolonged contact with litter.brick-red colonies on McConkey agar. and in broiler parents. hatchery hygiene. Treatment Amoxycillin. the breast area. The liver is almost entirely covered by a substantial layer of fibrin and pus. It is seen in growing broiler chickens and turkeys. as well as Pseudomonas. Contact dermatitis is commonly monitored at processing as a means of measuring 'welfare status'. Contact Dermatitis. good sanitation of house. neomycin (intestinal activity only). when severe. the foot pad. potentiated sulphonamide. Figure 17. feed and water. Immunity is not well documented though both autogenous and commercial vaccines have been used. Differentiate from acute and chronic infections with Salmonella spp. tetracyclines. etc. 45 . Severe perihepatitis in colibacillosis in a broiler parent chicken. stage of resolution and severity of lesion is likely to affect the degree of discomfort or pain suffered. Staphylococcus spp.
It can be reproduced by adding water to the litter. and sometimes in the breast area. Treatment Not applicable. Post-mortem lesions As described under signs. and. proper insulation in cold climates. Diagnosis Signs and lesions. and adequate ventilation to remove moisture are all important. level of soya bean meal in feed (according to some authors. stickiness of droppings). See the discussion in the section on Dysbacteriosis. If severe the foot and hock lesions may contribute to lameness or serve as a portal of entry for secondary infections. Moderate pododermatitis on a foot pad. 46 . Figure 18. litter moisture. drinker management. Prevention This condition is closely linked to intestinal function as this is the prime determinent of faecal consistency and stickiness. Choice of drinker type (nipple as opposed to bell). at the back of the hocks. Signs Blackened skin progressing to erosions and fibrosis on the lower surface of the foot pad.Pododermatitis is often related to high droppings pH. most importantly.
They replicate in the brush border on the surface of epithelial cells. meleagridis also infects both species. Cryptosporidiosis Introduction Cryptosporidia are related to the coccidia. Prevention Effective cleaning of housing. White convoluted tracks in the mucosa. The oocysts are excreted ready sporulated in the faeces and infection occurs by inhalation and ingestion. Post-mortem lesions Inflammation and thickening of mucosa of crop and oesophagus. but much smaller (typically oocysts are less than ¼ of the size of an E. Some have beetle or earthworms as intermediate hosts. Diagnosis Microscopic examination of mucosal scraping. Emaciation. although bird strains do not infect mammals very well.Cropworms Introduction The nematode worms Capillaria spp and Gongylonema ingluvicolainfect the mucosa of the crop and oesophagous of poultry and game birds. Coumaphos. and vice versa. Cryptosporidium baileyi can cause respiratory disease in chickens and turkeys. and ducks. Signs Anaemia. A further species causes respiratory disease in quail. 47 . acervulinaoocyst).C. Treatment Levamisole. Avoidance of access to intermediate hosts. The same species causes infections of the hindgut and cloacal bursa in chickens. turkeys. Routine worming. They also differ from coccidia in being poorly host specific.
It is becoming increasingly common for water companies to screen water supplies for cryptosporidia because of the human health implications of mammalian strains. coli-septicaemia) there may be benefit in medicating for these. Cough. Tremors. 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. Signs Incoordination. Low weight gain. Prevention The oocysts of cryptosporidia are extremely resistant to chemical disinfection.g. Torticollis. Airsacculitis.Signs Snick. If other disease processes are complicating the situation (e. Swollen sinuses. There are no effective preventative medicines or feed additives. 48 . Post-mortem lesions Sinusitis. recumbency. Diarrhoea. Treatment Unfortunately there is currently no known effective treatment in poultry. Diagnosis Identification of the parasites attached to the epithelium by microscopic examination (smears histopathology acid-fast staining). Circling. Pneumonia.
resulting in erosions. but it may result from physical damage. Prevention Use fresh dry litter (avoid old sawdust). air sacs etc. Mycotic lesions in lungs. Post-mortem lesions Damaged epiphyseal articular cartilage. Diagnosis Gross and microscopic lesions. Diagnosis Lesions. 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. Treatment None. isolation of the fungus. and cartilage flaps. Signs Lameness. The cause remains to be confirmed. Degenerative Joint Disease Introduction A condition of chickens and turkeys seen worldwide.Post-mortem lesions Necrotic lesions with associated congestion in cerebrum. Rapid growth is a possible predisposing factor. Microscopically there is necrosis and there may be fissures of articular cartilage and associated osteochondritis. or developmental defects. Reduced breeding performance. especially of femoral anti-trochanter but also other leg joints. Treatment 49 .
Raised thickened scales. Mange lesions on legs and unfeathered parts. There may be a place for growth-control programmes. pheasants. up to 0. Application of mineral or vegetable oil is also beneficial. Prevention Careful cleaning of buildings during down-time will help reduce the risk of these infections. Treatment Not usually required in commercial poultry. pigeons etc. Prevention Avoidance of physical sources of injury to bones and joints.None available. especially during period of rapid growth. Exclusion of wild birds from chicken areas is advised as far as possible. The adult females are short legged.Knemidocoptes spp. For small flocks dipping the affected parts in a solution of acaricide may be beneficial. Post-mortem lesions As described under signs.5mm in diameter. It may be best to cull affected birds from small flocks. 50 . Appropriate management of a segregation pen and early marketing of mildly affected birds may limit losses and improve flock welfare. microscopic examination for mites in scrapings. Signs Cause irritation and the bird pulls feathers. Diagnosis Signs. Depluming and Scaly Leg Mites Introduction External parasites of adult chickens. Unthriftiness. round.
Reserpine in diet of birds of 4+ weeks (no longer licensed in the UK).Dissecting Aneurysm. A longtitudinal split of the abdominal aorta is the most common lesion. recovered birds carrying the virus for 8 weeks. genetic condition of turkeys linked to male sex and high growth rate. leg muscles. Treatment None currently licensed. A sudden noise or other cause of excitement can lead to an 'outbreak'. Reserpine. presumably due to a sudden increase in blood pressure. Duck Viral Hepatitis Introduction A viral disease of ducks occurring worldwide and previously a scheduled disease in UK. Haemorrhages in lungs. Aortic Rupture Introduction A complex. Possibly blood in the mouth. Post-mortem lesions Carcase anaemic. Prevention Limit feed in birds of 16+ weeks. Aspirin at 250 ppm in feed or water may be of benefit. birds found on breast or side. Skin pale. Rupture of major blood vessel at base of heart or by the kidneys. Morbidity is around 100% and mortality 0-95%. Abdominal cavity full of blood. a tranquilizer. a picornavirus may also 51 . It has been suggested that degenerative changes in the wall of the artery and copper deficiency may be factors. Diagnosis History and lesions. The disease is transmitted by infected ducks and other waterfowl and spreads rapidly. pericardial sac. kidneys. The infective agent. was included in feed at 1 ppm for 3-5 days to reduce blood pressure. Signs Sudden death with no warning signs.
Depression. in USA since 1967. 0. fomites and arthropods. often in opisthotonus. mostly in ornamental collections. Microscopically . breeder vaccination. arching of back. Death in good condition.survive for ten weeks in brooders and five weeks in faeces. also the Netherlands and other countries. Punctate/diffuse haemorrhages. Influenza and a 'Type II Variant' hepatitis caused by Astrovirus. Duck Plague Introduction A herpesvirus infection of ducks and geese diagnosed in the UK in 1972. Duck Virus Enteritis. Duck septicaemia (anatipestifer). Treatment Antiserum. Transmission is by infected birds. 52 . coccidiosis. Post-mortem lesions Liver swollen. Recovered birds may carry the virus for a year. 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. SN serology. Newcastle disease. isolation in CE (causes stunting of 9 day embryo). Signs Sudden death. rapid deterioration and death. A different picornavirus causes a similar condition in North America. Fall on side. Live. bile duct proliferation and inflammation.focal necrosis. Differentiate from Duck plague (viral enteritis). Prevention Vaccination and/or antiserum. paddling of legs. lesions. Kidneys and spleen swollen.5 ml serum of recovered birds given intramuscularly. All waterfowl are susceptible and the Barbary duck is more susceptible than the Pekin. The disease follows a very acute course with a morbidity of 5-100% and mortality of 5-100%.
body cavities. 53 . Paresis. spleen. probably through interference. Occasionally cyanosis of the bill in the young. Dysbacteriosis. Rapidly spreading disease. Closed eyes. Young ducks may show thymic and bursal lesions. but vaccination in face of outbreak is of value. Dehydration. pericardium. oesophagitis (birds on restricted feed). Treatment None. Thirst. intranuclear inclusions Differentiate from Duck hepatitis. Post-mortem lesions Severe enteritis. The condition is seen mainly in rapidly growing broiler chickens with good food intake. Photophobia. heart. vaccination if approved by authorities (CE adapted live virus). Haemorrhage in intestine. excess caecal volume and fermentation. HA-. coccidiosis. is common in countries with restrictions on the use of antimicrobial growth promoters and pressure to reduce therapeutic antimicrobial usage. pasteurellosis.Signs Sudden deaths. vent gleet. sometimes dysentery. Drop egg production. liver. Diagnosis Isolation: Duck CAMs 12 day embryos die in 4 days. Non-specific Bacterial Enteritis Introduction Inflammation of the small intestine associated with wet litter. Tremor. Ataxia. Occasionally penile prolapse in the penis in drakes. Prevention Isolation from waterfowl. Severe diarrhoea. Crusty plaques from oesophagus to bursa (covered by yellowish plaques in later stages).
Spain. Peru. Post-mortem lesions Excessive fluid content throughout the small intestine. The cause has been identified as Adenovirus BC14. rather we are dealing with a disruption in the normal flora of the gut. France. Careful choice of any feed enzymes and their matching with local raw materials can have an impact on substrates made available to intestinal bacteria. Egg Drop Syndrome 76 Introduction Egg drop may be defined as a sudden drop in egg production or a failure to achieve a normal peak in production. microscopic examination of scrapings from the wall of the small intestine (to exclude coccidiosis and perhaps to assess the bacterial flora). Water intake may be increased or irregular. Apparently a similar disease had been seen over a 4-year period in broiler parents in Holland. Holland. Voluminous caecae. Circumstantial evidence suggests that the main route of transmission is through the eggs (vertical transmission) 54 .Dietary changes. In the autumn of 1976 a distinct egg drop syndrome was first identified in Northern Ireland. feed interruptions and subclinical coccidiosis may be contributory factors. Feed acidification may be helpful in some circumstances. first isolated in Northern Ireland in 1976. especially where treatment is initiated early. Uruguay. Treatment Amoxycillin and tylosin treatment appear to be beneficial. Wet faeces in the rectum. Argentina. Germany. lesions. Good control of coccidiosis. No single bacterium appears to be responsible. often with gas bubbles. Brazil. Mortality is usually negligible. England. It affects chickens and has occurred in Ireland. 127. Treatment should coincide with good relittering and it is important to provide fresh sanitary drinking water. Diagnosis Signs. Prophylactic antimicrobial medication may be necessary in some circumstances. Signs Diarrhoea. Prevention Competitive exclusion ('normal adult flora') use in day-old chicks reduces the risk of this condition.
and D as well as calcium. sudden changes of feed. Diagnosis History. Signs Egg drop at peak or failure to peak.followed by latent infection during rear with viral excretion starting shortly before sexual maturity. Marek's disease/Leukosis or any infectious disease causing a significant systemic disturbance (CRD. Post-mortem lesions No specific lesion . Unvaccinated flocks with antibodies before lay do not peak normally. as may wildfowl and biting insects. Histopathology . Cholera. Poor internal quality. Contamination of egg trays at packing stations may play a part in transmission. signs/lesions (mainly lack of). Diphtheritic Fowl Pox). Lateral transmission from bird to bird is slow and may be prevented or slowed for weeks by netting divisions. Metabolic diseases include Fatty Liver Syndrome. Infectious Laryngotracheitis. Parasites.only a slight atrophy of ovary and oviduct. Isolation of haemagglutinatin agent in duck eggs or cell culture. Elisa. phosporus. Infectious diseases include Infectious Bronchitis. selenium. insecticides or nicarbazin. thin or soft-shelled eggs and shell-less eggs. Avian Encephalomyelitis. SN. Diseases in which egg drop occurs. B 12. Management problems may be involved: inadequate water supply. intoxication by sulphonamides. specifically vitamins E. It is important to rule out other possible reasons for egg drop. DID. throat swabs. which can be caused by a large number of factors acting individually or in combination. Rough. 55 . Drops may be of 5 to 50% and last for 3-4 weeks. Nutritional deficiency should be considered. The infection is commonly present in ducks and geese but does not cause disease. Coryza. oviduct). Clinical disease occurs during sexual maturity. Lack of signs in the birds themselves. Spread from house to house may take 5-10 weeks. inadequate lighting programme. Newcastle disease. may be infectious or metabolic.it may be possible to demonstrate degenerative changes in the epithelial cells of the magnum of the oviduct. extremes of temperature. Serology: HI. group antigen distinct from classical adenoviruses (white cells. Loss of shell pigment.
Soluble multivitamins may be recommended as a nonspecific measure. bacterial infection. 56 . Peripheral vessels congested. rickets. growth plate disease. Diagnosis Differentiate from broiler ascites syndrome by examination of the interior of the heart. Post-mortem lesions Right ventricular failure and ascites. Treatment Medication is only likely to be of value in reducing deterioration in birds that are starting to develop lesions. Prevention Good hygiene at turn-around. Culture of lesions to confirm the bacterium involved. Vegetative lesions usually on the right atrioventricular valve. and /or trauma. Erysipelothrixetc. The choice should depend on sensitivity testing of an isolate. Epiphysiolysis Introduction A complex condition of chickens that may be associated with trauma. Prevention Vaccination with inactivated vaccine prior to lay. streptococci.Treatment None. osteomyelitis. Signs Fluid-distended abdomen. Endocarditis Introduction A condition of chickens associated with several bacterial infections such as staphylococci. If successive flocks are affected on the same site prophylactic medication ahead of the anticipated problem may be of benefit.
Signs Nervous symptoms. WEE. partridges. Horses are also seriously affected.Signs Apparent dislocation at extremities of long bones. Microscopic lesions not pathognomonic. Equine Encephalitis (EEE. Post-mortem lesions No gross lesions. wild birds. VEE) Introduction A viral disease of pheasants. often occurs or is identified in the processed carcase. May also be asymptomatic. sometimes seen in vivo. Tremors. Circling. Post-mortem lesions Separation of epiphyses at the growth plate. These conditions currently only occur from northern South America to North America. Diagnosis Gross inspection. Paresis. turkeys. Flaccid neck. Treatment Not applicable. Ataxia. ducks and pigeons having a high morbidity and high mortality. Prevention Control of predisposing factors. chickens. histology may be helpful in identifying underlying problems such as rickets or 'FHN'. It is transmitted between birds by pecking and by mosquitoes. The natural hosts are wild birds and rodents. 57 . Paralysis.
Endocarditis. rarely in geese. Signs Inappetance. Erysipelas Introduction A sudden onset infection with the bacterium Erysipelothrix insidiosa (E. pheasants. muscle. It may be transmitted by faecal carriers for 41 days. especially snood. TC. rhusiopathiae) seen in turkeys and increasingly in free-range chickens. ducks. kidney. control cannibalism. 58 . ID by VN. Joint lesions. Swollen snood.Diagnosis Isolation in mice. COFAL. It is also seen in some mammals. in soil. spleen swollen. Chronic scabby skin. fishmeal and semen and by cannibalism. epicardium. Depression. Marked catarrhal enteritis. The bacterium is fairly resistant to environmental effects or disinfectants and may persist in alkaline soil for years. Liver. Sudden death. water. Haemorrhages in fat. May be diarrhoea and respiratory signs. Vaccinate at 5-6 week. Post-mortem lesions Carcase congestion. Perineal congestion. Sleepiness. Prevention Protection from mosquitoes. There is likely to be an increased risk if housing or land has been previously used by pigs or sheep. Treatment None. and CE.
greasy and soft with numerous haemorrhages. Headparts pale. often along with bacterin. Signs Overweight typically by 25%. especially caged layers and with a complex set of causes including excessive calories. history. salmonellosis.a combination of the procaine and benzathine salts may be injected. Tetracyclines in feed may also be helpful. Differentiate from pasteurellosis. 59 . Prevention Good biosecurity to prevent spread from other susceptible species. the demonstration of the organism in stained impression smears from tissues. and identification.Diagnosis Isolation on blood agar. deficiency and stress. vaccine at 16-20 weeks if the condition is enzootic. Sudden drop in egg production. Sudden death. mycotoxins. and acute Newcastle disease. Treatment Penicillin . Post-mortem lesions Obesity. Death by internal exsanguination after rupture of haematocyst. Liver yellow. Diagnosis Lesions. colibacillosis. Some birds with pale comb and wattles. Vaccination or natural infection may cause false positive reactions in the Mycoplasma gallisepticum and M. Fatty Liver Haemorrhagic Syndrome Introduction A condition occurring worldwide in chickens. synoviae plate tests for a few weeks.
culling affected birds. Treatment Formalin in petroleum jelly.Treatment Reduce energy intake. It is very rare in commercial poultry production. Diagnosis Lesions. supplement with choline. vitamin E. 60 . Post-mortem lesions See signs (above). B 12 and inositol. Prevention Good hygiene of facilities. Thick crusty skin. powdery spots and wrinkled crusts and scab on comb and wattles. isolation. Favus Introduction A fungal infection. Trichophyton gallinae. Prevention Feed to avoid obesity. avoid mycotoxins and stress. of chickens and turkeys. Feather loss. 'Honeycomb' skin. Loss of condition. Signs White.
especially hypophosphataemic. FHN is the commonest infectious cause of lameness in broilers in the UK. and water fowl. 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. Differentiate from synovitis. Use of a wing for support during walking and hip flexion. staphylococci. Careful attention to mineral and Vitamin D nutrition to avoid subclinical. Prevention Exclusion of floor eggs and dirty eggs from the hatchery. Fowl Cholera. indicated that 0. coli.75% of all male broilers placed had lesions in the hip bone. streptococci. Post-mortem lesions Degeneration of the epiphyses of long bones with thinning of the cortex and tendency to break when force is applied. rickets.Femoral Head Necrosis . turkeys. It is seen worldwide and was one of the first infectious 61 . Diagnosis Base on post-mortem lesions and isolation of a causative organism. (increasing order of susceptibility). Pasteurellosis Introduction Fowl Cholera is a serious. spondylolisthesis. E. highly contagious disease caused by the bacterium Pasteurella multocida in a range of avian species including chickens.FHN Introduction A condition of chickens and turkeys that may be associated with several different bacterial infections e.g. arthritis. Signs Lameness. Post-mortem studies of birds culled due to lameness and of birds found dead. Predisposing factors include immunosuppresive viruses such as Infectious Bursal Disease Virus and Chicken Anaemia Virus and non-infectious bone pathologies such as hypophosphaetamic rickets.
equipment. The route of infection is oral or nasal with transmission via nasal exudate. ocular and oral discharge. tetracyclines. Enteritis. necessitating long-term or periodic medication. Reservoirs of infection may be present in other species such as rodents. Post-mortem lesions Sometimes none. by Louis Pasteur in 1880. Swollen and cyanotic wattles and face. Swollen joints.no growth on McConkey). streptomycin. Purulent pneumonia (especially turkeys). penicillin. Loss of appetite. and people. Coughing. Diarrhoea. or limited to haemorrhages at few sites. The bacterium is easily destroyed by environmental factors and disinfectants. faeces. Lameness. Diagnosis Impression smears. Differentiate from Erysipelas. Focal hepatitis. erythromycin. Nasal. Lungs with a consolidated pink 'cooked' appearance in turkeys. Yolk peritonitis. cats.diseases to be recognised. 62 . confirmed with biochemical tests. isolation (aerobic culture on trypticase soy or blood agar yields colonies up to 3mm in 24 hours . contaminated soil. but may persist for prolonged periods in soil. Treatment Sulphonamides. Cellulitis of face and wattles. The disease can range from acute septicaemia to chronic and localised infections and the morbidity and mortality may be up to 100%. Predisposing factors include high density and concurrent infections such as respiratory viruses. Sudden death. and possibly pigs. Ruffled feathers. The disease often recurs after medication is stopped. The incubation period is usually 5-8 days. septicaemic viral and other bacterial diseases. Signs Dejection. Purulent arthritis.
turkeys. or by the respiratory route. The virus persists in the environment for months. Fowl Pox. It is transmitted by birds. hygiene. and where there are biting insects. Poor egg production. It is more common in males because of their tendency to fight and cause skin damage. Severe localised Pasteurella infection in the swollen wattle of a 30-week-old male broiler parent chicken. Figure 19. and mosquitoes (infected for 6 weeks). throat and sometimes trachea. bacterins at 8 and 12 weeks. The duration of the disease is about 14 days on an individual bird basis. fomites. pigeons and canaries worldwide. Poor growth. 0-50%. good rodent control. Avian Pox Introduction A relatively slow-spreading viral disease characterised by skin lesions and/or plaques in the pharynx and affecting chickens. Morbidity is 1095% and mortality usually low to moderate. Inappetance. The swelling is made up of oedema and purulent exudates (pus). Infection occurs through skin abrasions and bites. Caseous deposits in mouth. spreading eruptions and scabs on comb and wattles. Pox. 63 . live oral vaccine at 6 weeks. Signs Warty. Depression.Prevention Biosecurity.
pharynx. 64 . reproduction in susceptible birds. Fowl pox lesions on the wattle of an adult broiler parent chicken. Chickens well before production. Prevention By vaccination (except canary). Microscopically . It is confirmed by IC inclusions in sections/ scrapings. Treatment None. Turkeys by thigh-stick at 2-3 months. Figure 20. isolation (pocks on CE CAM) with IC inclusions. usually with chicken strain by wing web puncture. There is good cross-immunity among the different viral strains. signs and post-mortem lesions.Post-mortem lesions Papules progressing to vesicles then pustules and scabs with distribution described above. check take at 7-10 days post vaccination. Diagnosis A presumptive diagnosis may be made on history. If there is evidence of secondary bacterial infection broad-spectrum antibiotics may be of some benefit. trachea and/or nasal cavities. Less commonly there may. Differentiate from Trichomoniasis or physical damage to skin.intra-cytoplasmic inclusions (Bollinger bodies) with elementary bodies (Borrel bodies). DNA probes. be caseous plaques in mouth. in the diptheritic form. Flocks and individuals still unaffected may be vaccinated.
especially following congenital Chick Anaemia Virus infection or early Infectious Bursal Disease Virus infection (Gumboro Disease). Post-mortem lesions Patches of gangrenous skin with underlying emphysematous and/or sanguinous cellulitis. Diagnosis Clinical signs and/or lesions. early Infectious Bursal Disease Virus infection). Swelling and infarction of the liver. Sudden mortality. wings. It occurs due to invasion of 'normal' wounds by 'normal' bacteria in immunosuppressed birds. Necrotic Dermatitis Introduction A bacterial condition seen in chickens and usually caused byClostridium septicum.Gangrenous Dermatitis. spleen. Foci in liver. 65 . Morbidity may be up to 50% and mortality is high. occasionally Staphylococcus aureus. wattles. Recovery of an abundant growth of causative organism in recently dead birds. Signs Occasionally dejection. sometimes thighs and other parts. Treatment Sulphaquinoxaline. usually over wings and breast. The spores of Clostridial bacteria are highly resistant in the environment. Severe cellulitis especially of thighs. rarely Clostridium noyvi / oedematiens. Gangrenous skin. Avoid skin trauma and immunosuppression (congenital CAV infection. Prevention Good hygiene and management. penicillin or amoxycillin. Loss of appetite. Immunosuppression is therefore a predisposing factor.
Loss of appetite and condition. slugs and snails acting as transfer hosts but the life cycle may also be direct. and other game and ornamental birds occurring worldwide. from rookeries.Figure 21. The condition is seen more commonly in poultry on free range where ground may be contaminated by wild birds e. by ingestion of embryonated egg or L3. Presence of worms. confirmation of presence of the parasite. a nematode worm parasite of chickens. Gape Introduction Syngamus trachea. Severe gangrenous dermatitis on the upper surface of the wing of a broiler chicken. Prevention Flubendazole. Signs Gasping. Infection is by the oral route with earthworms. There is an 18-20 day prepatent period. paired parasites up to 2 cm long. Treatment Flubendazole in feed. turkeys. Post-mortem lesions Tracheitis. 66 . levamisole. Diagnosis Signs and lesions. Head shaking. Dyspnoea.g. pheasants.
Geese Introduction A nematode worm parasite. and Histiocephalus are nematode worm parasites of chickens. Grasshoppers. 67 . They are more common in free-range birds because of their increased access to intermediate hosts. Slow growth. Diagnosis Lesions. affecting geese and ducks. Post-mortem lesions Ulceration.Gizzard worms . routine worming. necrosis and partial sloughing of gizzard lining. Cheilospirura and Streptocara are seen worldwide but Histiocephalus is restricted to Europe. benzimidazoles such as flubendazole. Loss in condition and weight. Prevention Prevention of access to intermediate hosts. Loss in condition and weight. Adults are 2-4 cm long and usually bright red. Slow growth. Signs Depression. Treatment Levamisole. Amidostomum anseris.Chickens Introduction Cheilospirura. Gizzard worms . confirmation of presence of the worms. Streptocara. Signs Depression. Worms develop to L3 in eggs and infection is by the oral route direct from environment. muscular wall may be sacculated or ruptured. beetles etc act as intermediate hosts. weevils.
Prevention Rotation of ground on annual basis. Losses are negligible in birds over 5 weeks of age. spleen and pancreas. 68 . benzimidazoles. 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. Post-mortem lesions Pale myocardium. Adults are 2-4 cm long and usually bright red. Swelling and congestion of liver. necrosis and partial sloughing of gizzard lining. Reduced feed intake. visualisation of worms. Treatment Levamisole. Excessive water intake. Derzsy's Disease is caused by a parvovirus distinct from chicken and mammalian parvoviruses. The younger the bird affected the more acute the condition and the higher the mortality. Vertical transmission resulting in congenital infection may occur. Swollen eyelids and eye and nasal discharge. Reddening of skin. muscular wall may be sacculated or ruptured. Signs Prostration and death in acutely affected goslings. Profuse white diarrhoea. Goose Parvovirus (Derzsy's Disease) Introduction Goose Parvovirus is a highly contagious condition of geese and young Muscovy ducks. Membrane covering tongue.Post-mortem lesions Ulceration. Loss of down. Diagnosis Lesions.
heart. Treatment No specific treatment. Diagnosis Signs and lesions in birds of the appropriate age and species. Pale comb and wattles. Carcase anaemia. liver. Poor growth. Fibrinous perihepatitis. Loss of appetite. Haemorrhagic Disease. Bone marrow pale with fatty change. serosa and mucosae. Morbidity varies. Blood in droppings. Liver yellow. The preferred approach is to immunise breeding birds with an attenuated live vaccine. mortality is 5-50%. Signs Dejection. Ascites. Administration of immune serum has been shown to be effective but may require two doses (day old and around 3 weeks). Haemorrhagic Anaemia Introduction A complex condition of chickens associated with drug toxicities. mycotoxins and viral infections and usually following a course of approximately 3 weeks. Fibrinous pericarditis. 69 . Aplastic Anaemia. Antimicrobials may be of value in reducing the effects of secondary bacterial infections. muscles. Prevention Hatching and brooding geese from different parent flocks together should be avoided. Ideally flocks that have suffered the disease should not be used for breeding as they may become persistent excreters of the infection. Post-mortem lesions Haemorrhages in one or more sites: skin.
similar to pheasant Marble Spleen disease. May induce immunosupression and precipitate respiratory disease or coccidiosis. Treatment Vitamin K. Elisa . The source of virus is unknown but there is easy lateral spread within flocks. reticulo-endothelial hyperplasia and intranuclear inclusions. Diagnosis Typical lesions. the virus surviving in frozen faeces for months. Course 10-21 days. 70 . Serology: DID. double-immuno-diffusion of splenic extract. Signs Sudden deaths. Microscopic . remove sulphonamides. Blood from vent of moribund birds. add liver solubles to feed. Drop in feed and water consumption. Haemorrhagic Enteritis Introduction A viral disease of turkeys. reproduction with filtered contents. Diarrhoea.sero-conversion frequently occurs in absence of clinical disease. caused by Type II Adenovirus distinct from classical fowl adenovirus and occurring in most turkey-producing areas. signs. lesions. Intestine distended with blood. Post-mortem lesions Petechiae in various tissues. Prevention Avoid causative factors. and weeks in litter. The route of infection is usually oral.spleen shows lymphoid hyperplasia.Diagnosis History. The virulence of the virus varies but morbidity may be 100% and mortality 10-60%. Spleen mottled and enlarged.
Maternal antibody may interfere with vaccination.and T-line lymphocytes for up to 5 weeks following exposure. Reduced feed consumption. Prevention All-in/all-out production. good hygiene and biosecurity. Disinfect and 3-4 weeks house rest. Predisposing factors include genetics. and turkeys caused by high environmental temperature. feather cover. In this case a loop of intestine has been opened to show the blood. Live vaccines are commonly used in many countries at 4-5 weeks of age.Treatment Warmth and good management. drinking water temperature and availability. nicarbazin in feed. acclimation. especially associated with high relative humidity and low air speed. Immunity: there is an early age resistance irrespective of maternal antibody status. Some are produced in live turkeys. Heat Stress Introduction A condition seen in chickens. some in turkey B-lymphoblastoid cell lines. Signs Panting. Ducks are relatively resistant to heat stress. Increased thirst. Turkeys dying with haemorrhagic enteritis commonly have the small intestine distended with blood. Pathogenic strains can depress both B. high stocking density. oral tetraycline. 71 . convalescent serum. good management. Figure 39. Immunity to the disease is long lasting.
and some game birds. Prostration. if relative humidity is low then wet the roof and fog. In commercial ducks a related parasiteTetratrichomonas can cause poor growth and drops in egg production. evaporative coolers. Post-mortem lesions Carcases congested. Later depression. Post-mortem lesions Dehydration. Reduced egg production. Feeding during cooler hours may be beneficial. Inter-species transmission may occur. It is transmitted by faeces. Frothy. signs. maximise airflow. exclusion of other conditions. Terminal coma and convulsions. columbae) is a protozoan parasite of turkeys. painted white to reflect heat. Loss in weight. Treatment Cool water. Reductions in stocking density of meat poultry may be quickly achieved by partial depletion ('thinning'). Legs and wings outstretched. Mucoid exudate in nostrils and mouth. Diagnosis Temperature records. pigeons. Prevention Houses of optimal height and insulation. Inappetance. 72 . fomites. contains excessive mucus and gas. pheasants. chirping. Hexamitiasis Introduction Hexamita meleagridis (pigeons H. Signs Initially birds nervous. lesions. pattern of losses. carriers. watery diarrhoea. feed with a reduced protein:energy ratio. Intestine flabby with some bulbous dilation.
It has recently been demonstrated that infection occurs readily via the cloaca when birds are on contaminated litter. Treatment Tetracycline. and also. hygiene. Histamonosis. increase ambient temperature. Prevention Depopulation. dimetridazole. gallinae the parasite is easily destroyed. Furazolidone. paratyphoid. Outwith earth worms orH. The problem is seen in high-biosecurity facilities. scrapings from fresh material. avoid interspecies mixing. Blood in faeces (chickens). Caecal tonsils congested. dimetridazole and ipronidazole have been used in the past. Histomoniasis. Within a turkey shed transmission is rapid in spite of the fact that it is difficult to infect birds orally with unprotected parasites. significant disease has been seen in breeding chickens and free-range layers. Blackhead Introduction Histomonas melagridis is a protozoan parasite of turkeys. Differentiate from transmissible enteritis. Cyanosis of head. The parasite is ingested in the ova ofHeterakis worms or as larvae in earthworms or faeces and there is an incubation period of 15-20 days. and occasionally chickens. pheasants and game birds that acts together with facultative bacteria to produce the condition of Blackhead. presumably introduced with worm eggs. Although chickens are relatively resistant to the condition. Sulphur-yellow diarrhoea. trichomoniasis. Poor growth. The effect of antibiotic may be related to the control of secondary bacterial enteritis. Progressive depression and emaciation. 73 . histomonosis. Signs Depression. if possible. First half of intestine inflamed. Inappetance. and mixing groups of different ages. Diagnosis Lesions. This condition has high morbidity and mortality in turkeys. all-in/all-out production.
avoid mixing species. It is a condition caused by an adenovirus. possibly in combination with an RNA virus and immunosuppression caused by Chick Anaemia Virus or Infectious Bursal Disease. Regular worming to help control the intermediate hosts. usually grey in colour. Treatment Historically nitro-imidazoles (e. nifursol) and arsenicals (e. dimetridazole). concrete floors. Intensive relittering may help reduce the level of infection. scrapings from fresh material. Ulcers. furazolidone.g. given recent new knowledge on the mechanism of transmission.Abubakar. nitrofurans (e. At the time of writing no products of these groups are approved for use in the European Union. It affects mainly broilers and broiler parents in rear and has also been seen in pigeons. Diagnosis Lesions. Mortality may reach 60% but more typically 10-30%. however they may not be present in the early stages. The disease is readily reproduced by inoculating birds with a bacteria-free filtrate of a liver extract from an affected bird. Use of an anti-histomonas product in feed where such products are approved but due care with respect to residue avoidance would be required. grey or green areas. Having both chickens and turkeys on the same property is likely to increase the risk of this disease in turkeys.Tahir Post-mortem lesions Enlargement of caeca. and only nitarsone is approved in the USA. especially in chickens. 'Herban)' have been used with some apparent success though controlled trials and formal approval for this purpose are not recorded. Arsenicals are less effective in treatment than they are in prevention.nitarsone) have been used to treat this important disease of poultry. Hydropericardium-Hepatitis Syndrome. Prevention Good sanitation. 74 . Angara Disease Introduction This condition was first identified in broilers in Pakistan in 1987.g.g. Liver may have irregular-round depressed lesions. Some herbal products based on the essential oils (e. caseous cores with yellow.M.g. It spread rapidly in broiler producing areas in that country and the same or a very similar condition has been seen in North and South America.
treatment of drinking water with 0.5% iodophor solution) appears to be beneficial. The normal function of the gizzard is to aid in the physical grinding of food materials. however if young chicks to do not begin to eat feed properly they often consume litter instead. Prevention The condition typically occurs in areas of high poultry density where multi-age operation is traditional. Enlarged.Signs Sudden increase in mortality. Treatment None. Good water sanitation (e. string etc. to reduce their particle size to aid digestion. Congestion of the carcase. Impaction and Foreign Bodies of Gizzard Introduction The gizzard or crop may become impacted with litter. virology. This condition usually affects only a small number of birds. Yellow mucoid droppings. Huddling with ruffled feathers. Formalin-inactivated oil adjuvant vaccines are reported to be highly effective and are used in areas where the condition is endemic. Control of predisposing immunosuppressive diseases may help limit losses. Gizzard activity also acts as a pacemaker of intestinal activity and controls the speed at which food is passed to the small intestine. Impacted gizzards are then found in 'non-starter' type chicks or poults. Most young commercial poultry consume feeds that have a small particle size. grass. Post-mortem lesions Excessive straw-coloured fluid distending the pericardium (up to 10 mls). histopathology. Older birds ingest grit to facilitate the grinding activity in the gizzard. Lungs oedematous. however sometimes free-range poultry consume large stones. Grit would not be classed as a foreign body.1% of a 2. and birds of any age can 75 . Diagnosis Lesions. pale friable liver and kidney.g. Lethargy.
and on opening is found to contain a mass of fibrous material. Obvious non-starters should be culled in this situation. France and Ireland.15 days with a morbidity of 1-10% and a mortality of 1-10%. the UK. often with severe anaemia. Sweep floors after maintenance activities to remove nails and other potentially dangerous foreign bodies.consume nails. staples etc. A number of different sero-types have been isolated from disease outbreaks but they may also be isolated from healthy chickens. caused by an adenovirus. Australia. Diagnosis Lesions. Treatment None effective in young birds. It has a course of 9. The disease was first described in the USA in 1963 and has also been reported in Canada. Nails commonly penetrate the lining of the gizzard. A foreign body may be found in the interior of the gizzard. This may extend into the proventriculus and on into the duodeunum. Prevention Good brooding management to encourage early adaptation to the diet and adequate consumption of feed and water. This usually happens after maintenance activities have been carred out in the housing. Reduced weight gain. Inclusion Body Hepatitis Introduction A disease of chickens characterised by acute mortality. and may penetrate the body wall. Infected birds remain carriers for a few weeks. It allows us to confirm the proportion of chicks consuming feed and can give inexperienced poultry keepers feedback on the effectiveness of their brooding management. Signs Reduced feed intake. 76 . Daily monitoring of the crop-fill is a useful procedure. Post-mortem lesions The gizzard is more firm than normal and. Italy.
and high temperatures. Since adenoviruses are commonly found in healthy poultry. Confirmation is made on finding inclusions in the liver. Curiously. Bursa and spleen small. pH). Immunosuppression. Inappetance. fatty liver syndrome. for instance due to early IBD challenge or congenital CAV infection.Transmission may be vertical or lateral and may involve fomites. Soluble multivitamins may help with the recovery process. Infectious Bursal Disease. CEL). The virus is generally resistant to disinfectants (ether. Kidneys and bone marrow pale. and deficiency of vitamin B12. perhaps because they have lower levels of maternal antibody. Post-mortem lesions Liver swollen. Serology: DID for group antigen. Blood thin. 77 . isolation alone does not confirm that they are the cause of a particular problem. many different sero-types have been isolated from different cases. The virus grows well in tissue culture (CEK. Formaldehyde and iodides work better. Microscopically . Diagnosis A presumptive diagnosis may be made on history and lesions. Pallor of comb and wattles. sulphonamide intoxication.basophilic intranuclear inclusions. Treatment None. Progeny of high health status breeding flocks appear to be at greater risk. Signs Depression. yellow. Differentiate from Chick anaemia syndrome. vibrionic hepatitis. chloroform. mottled with petechiae and ecchymoses. but on the other hand many field cases show eosinophilic inclusions that do not appear to have adenovirus particles. Ruffled feathers. SN for individual sero-types. may be important. A form of the disease affecting birds under 3 weeks of age in Australia has been reproduced with serotype 8 adenovirus.
Typing by haemagglutination-inhibition is also used. Post-mortem lesions Mild to moderate respiratory tract inflammation. About eight sero-groups are recognised by sero-neutralization. dyspnoea. Infectious Bronchitis. The virus. gasping. alkalis. Poor ventilation and high density are predisposing factors. disinfectants (Formal 1% for 3 mins). is sensitive to solvents. Tracheal oedema. The cause is a Coronavirus that is antigenically highly variable. IB Introduction This infection. the age of the bird. E. coli. Diarrhoea. Kidneys and bronchi may be swollen and they and the ureters may have urates. These differences are due to structural differences in the spike proteins (S1 fraction). Caseous plugs in bronchi. which may survive 4 weeks in premises. 1931). Wet litter. depending on secondary infections. new sero-types continue to emerge. Some birds/viral strains can be carriers to 1 year. Airsacculitis. Newcastle disease). Coughing. probably the commonest respiratory disease of chickens. heat (56°C for 15 mins). Morbidity may vary 50-100% and mortality 0-25%. Signs Depression. Dakota. The infection is highly contagious and spreads rapidly by contact. prior vaccination. fomites or aerosol. and complicating infections (Mycoplasma. Loss of appetite.Prevention Quarantine and good sanitary precautions. Infection is via the conjunctiva or upper respiratory tract with an incubation period of 18-36 hours. Its affects vary with: the virulence of the virus. was first described in the USA (N. Diuresis. 78 . Huddling. Tracheitis. maternal immunity (young birds). prevention of immunosuppression.
heat (56°C for 15 mins). Prevention Live vaccines of appropriate sero-type and attenuation. 79 . alkalis. Infectious Bronchitis.antibiotics to control secondary colibacillosis (q. Infection is via the conjunctiva or upper respiratory tract with an incubation period of 18-36 hours. Poor ventilation and high density are predisposing factors. which may survive 4 weeks in premises. Otherwise as for standard IB. Avian Influenza and Laryngotracheitis.). mycoplasmosis. Elisa (both group specific).793b Variant Sudden Death Syndrome in Broiler Parents Introduction A Coronavirus infection of chickens with a morbidity of 50-100% and a mortality 0-25%. DID (poor sensitivity. Muscular shivering. SN (type specific). Definitive diagnosis is based on viral isolation after 3-5 passages in chick embryo.v. The infection spreads rapidly by contact. Treatment Sodium salicylate 1gm/litre (acute phase) where permitted . Signs Sudden death. Differentiate from Newcastle disease (lentogenic and mesogenic forms). is sensitive to solvents. Cellmediated immunity may also be important. vaccinal reactions. depending on secondary infections. possible reactions depending on virulence and particle size. with typical lesions. short duration. Humoral immunity appears 10-14 days post vaccination. Local immunity is first line of defence. IB . disinfectants (Formal 1% for 3 mins). fomites or aerosol. Some birds/viral strains can be carriers for up to 1 year. The virus.Diagnosis Tentative diagnosis is based on clinical sgns. lesions and serology. HA negative. Serology: HI. flourescent antibody positive and ciliostasis in tracheal organ culture. Maternal immunity provides protection for 2-3 weeks. group specific).
The condition has a morbidity of 10-100% and mortality of 0-1%. typical lesions. cell culture (Vero. Prevention Live vaccines of appropriate sero-type and attenuation. Elisa (both group specific). possible reactions depending on virulence and particle size. sneezing. fomites or aerosol. Rales may or may not be present. Other lesions of 'classical' IB may be encountered. Loss of internal egg quality. Coughing. 80 . Signs Drop in egg production (20-50%). IB Egg-layers Introduction A Coronavirus infection of chickens. SN (type specific).Post-mortem lesions Oedema of pectoral muscles and subcutaneously on abdomen. with much antigenic variation. A few birds are carriers up to 49 days post infection. There is rapid spread by contact. Poor ventilation and high density are predisposing factors. Diagnosis 3-5 passages in CE allantoic cavity.).v. Infectious Bronchitis. lesions progress to necrosis and scarring of deep pectorals in convalescence. short duration. Soft-shelled eggs. Rough shells. Treatment Sodium salicylate 1gm/litre (acute phase) where permitted . In layers the ovules may be intensely congested.antibiotics to control secondary colibacillosis (q. CK) only after adaptation Serology: HI. Infection is via the conjunctiva or upper respiratory tract. DID (poor sensitivity. FA. The virus is moderately resistant and may survive 4 weeks in premises. ciliostatic in tracheal organ culture. group specific). HA-.
Maternal immunity provides protection for 2-3 weeks.v. Prevention Live vaccines of appropriate sero-type and attenuation. HA-. FA.). Serology: HI. Diagnosis 3-5 passages in CE. Elisa.Post-mortem lesions Follicles flaccid. Figure 22. SN. particle size (if sprayed) and general health status. typical lesions. Humoral immunity appears 10-14 days post vaccination. Treatment Sodium salicylate 1gm/litre (acute phase) where permitted . Differentiate from Egg Drop Syndrome. EDS76.antibiotics to control secondary colibacillosis (q. DID. 81 . although reactions can occur depending on prior immunity. Flaccid ovarian follicles in a broiler parent chicken undergoing challenge with Infectious Bronchitis virus. Yolk in peritoneal cavity (non-specific). virulence. Local immunity is the first line of defence. Cell-mediated immunity may also be important.
HA-. FA. The condition has a morbidity of 10-100% and mortality of 0-1%.v. 82 . Coughing. IB Egg-layers Introduction A Coronavirus infection of chickens. EDS76. although reactions can occur depending on prior immunity. Post-mortem lesions Follicles flaccid. Rales may or may not be present. Cell-mediated immunity may also be important.). Soft-shelled eggs. Differentiate from Egg Drop Syndrome. The virus is moderately resistant and may survive 4 weeks in premises.antibiotics to control secondary colibacillosis (q. Poor ventilation and high density are predisposing factors. There is rapid spread by contact. Treatment Sodium salicylate 1gm/litre (acute phase) where permitted .Infectious Bronchitis. fomites or aerosol. virulence. SN. Signs Drop in egg production (20-50%). DID. Local immunity is the first line of defence. Rough shells. Maternal immunity provides protection for 2-3 weeks. typical lesions. Serology: HI. Elisa. Prevention Live vaccines of appropriate sero-type and attenuation. Infection is via the conjunctiva or upper respiratory tract. sneezing. Humoral immunity appears 10-14 days post vaccination. Yolk in peritoneal cavity (non-specific). with much antigenic variation. A few birds are carriers up to 49 days post infection. Loss of internal egg quality. Diagnosis 3-5 passages in CE. particle size (if sprayed) and general health status.
first identified in the USA in 1962. susceptibility to Inclusion Body Hepatitis and gangrenous dermatitis and increased susceptibility to CRD. The disease is highly contagious. with an incubation period of 2-3 days. IBD. Morbidity is high with a mortality usually 0. Signs are most pronounced in birds of 4-6 weeks and White Leghorns are more susceptible than broilers and brown-egg layers.20% but sometimes up to 60%. Mealworms and litter mites may harbour the virus for 8 weeks. but may be via the conjunctiva or respiratory tract. the damage caused to the immune system interacts with other pathogens to cause significant effects. The infective agent is a Birnavirus (Birnaviridae). The virus is very resistant. Gumboro Introduction A viral disease. Infectious Bursal Disease. Flaccid ovarian follicles in a broiler parent chicken undergoing challenge with Infectious Bronchitis virus. There is no vertical transmission. Marek's disease and Infectious Bronchitis. The route of infection is usually oral. 83 . Generally speaking the earlier the damage occurs the more severe the effects. In addition to the direct economic effects of the clinical disease. The age up to which infection can cause serious immunosuppression varies between 14 and 28 days according to the antigen in question. especially with sero-type 2). Subclinical infection in young chicks results in: deficient immunological response to Newcastle disease.Figure 22. and affected birds excrete large amounts of virus for about 2 weeks post infection. (Turkeys and ducks show infection only. seen worldwide. persisting for months in houses. faeces etc. which targets the bursal component of the immune system of chickens. Sero-type 1 only.
Inappetance. Swollen kidneys with urates. Other possible causes of early immunosuppression are severe mycotoxicosis and managment problems leading to severe stress.5. normal size or reduced in size depending on the stage). weights below 0. They are all serotype 1. Cryptosporidiosis of the bursa (rare). especially in the Delmarva Peninsula in the USA. especially if present prior to 20 days of age.3% of bodyweight. subsequent diagnosis of 'immunosuppression diseases' (especially inclusion body hepatitis and gangrenous dermatitis) is highly suggestive. may have haemorrhages. lesions. The normal weight of the bursa in broilers is about 0. Unsteady gait. Huddling under equipment. IBD viruses have been isolated and shown to have significant but not complete cross-protection. Coccidiosis. This may be confirmed by demonstrating severe atrophy of the bursa. Half-life of maternally derived antibodies is 3. Differentiate clinical disease from: Infectious bronchitis (renal). Diarrhoea with urates in mucus. Haemorrhages in skeletal muscle (especially on thighs).History. (previously SN and DID). Antibiotic medication may be indicated if secondary bacterial infection occurs. Treatment No specific treatment is available. Vaccination date prediction uses sera taken at day old and a mathematical formula to estimate the age when a target titre appropriate to vaccination will occur. rapidly proceeds to atrophy. Elisa vaccination date prediction < 7 days).A history of chicks with very low levels of maternal antibody (Fewer than 80% positive in the immunodifusion test at day old. Use of a multivitamin supplement and facilitating access to water may help.Signs Depression. Tests used are mainly Elisa. Haemorrhagic syndrome. Dehydration. Post-mortem lesions Oedematous bursa (may be slightly enlarged. histopathology.1% are highly suggestive. 84 . Diagnosis Clinical disease .4 days. Vent pecking. Serology: antibodies can be detected as early as 4-7 days after infection and these last for life. Variants: There have been serious problems with early Gumboro disease in chicks with maternal immunity. Subclinical disease .
resulting in increased culling. 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. Infectious Coryza is caused by the bacterium Haemophilus paragallinarum and is seen in many countries especially in multi-age farms that are never depopulated. 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. A strong immunity follows field challenge.Prevention Vaccination. It is enlarged. This shows the anatomical relationship between the bursa. the rectum and the vent. including passive protection via breeders. characterised by catarrhal inflammation of the upper respiratory tract. vaccination of progeny depending on virulence and age of challenge. turgid and oedematous. Infectious Coryza Introduction A usually acute. Carriers are important with transmission via exudates and by direct contact. sometimes chronic. Figure 23. It is not egg transmitted. When outbreaks do occur. and tracing of contacts may indicate sites on which a more rebust vaccination programme is indicated. Morbidity is high but mortality low if uncomplicated although it may be up to 20%. Immunity after a live vaccine can be poor if maternal antibody was still high at the time of vaccination. occasionally pheasants and guinea-fowl. biosecurity measures may be helpful in limiting the spread between sites. especially nasal and sinus mucosae. highly infectious disease of chickens. This bursa is from an acutely affected broiler. 85 .
Dihydrostreptomycin. Post-mortem lesions Catarrhal inflammation of nasal passages and sinuses. tylosin. Tracheitis.The bacterium survives 2-3 days outside the bird but is easily killed by heat. Vaccines are used in areas of high incidence. DID. 86 . agglutination and IF have all been used but are not routine. at least two doses are required. Prevention Stock coryza-free birds on an all-in/all-out production policy. drying and disinfectants. Treatment Streptomycin. Birds recovered from challenge of one serotype are resistant to others. erythromycin. Swollen wattles. Intercurrent respiratory viral and bacterial infections are predisposing factors. Serology: HI. Eye-lid adherence. lesions. Bacterin at intervals if history justifies or if multi-age.requires X (Haematin) and V (NAD) factors. Purulent ocular and nasal discharge. Loss in condition. chronic or localised pasteurellosis and vitamin A deficiency. Differentiate from Mycoplasmosis. Signs Facial swelling. Dyspnoea. Live attenutated strains have been used but are more risky. sulphonamides. Commercial bacterins may not fully protect against all field strains but reduce the severity of reactions. Controlled exposure has also been practised. Confirmation is by isolation and identification . Inappetance. Caseous material in conjunctiva/sinus. preferably in raised CO 2 such as a candle jar. Diagnosis A presumptive diagnosis may be made on signs. respiratory viruses. Flouroquinolones are bactericidal and might prevent carriers. while bacterins only protect against homologous strains. Sneezing. identification of the bacteria in a Gram-stained smear from sinus. Conjunctivitis. Drop in egg production of 10-40%.
Post-mortem lesions Severe laryngotracheitis. if enzootic or epizootic in an area. peafowl and turkeys with a morbidity of 50-100% and a mortality usually 10-20% but sometimes up to 70%. Gasping. Differentiate from Newcastle disease. Ocular discharge. Keep susceptible stock separate from vaccinated or recovered birds. The virus is highly resistant outside host but is susceptible to disinfectants. in severe form may be enough. vaccination. Prevention Quarantine. Microscopically . Recovered and vaccinated birds are long-term carriers. Transmission between farms can occur by airborne particles or fomites. Treatment None. severe bronchitis. Apply strict biosecurity in moving equipment or materials between these these categories of stock. histology.Infectious Laryngotracheitis. antibiotics to control secondary bacterial infection if this is marked. IFA. Drop in egg production. Diagnosis Signs. Sera may be examined by VN or Elisa. Nasal discharge (low pathogenicity strains). Coughing of mucus and blood.intranuclear inclusions in tracheal epithelium. Signs Dyspnoea. Movement and mixing of stock and reaching point of lay are predisposing factors. Sinusitis. All-in/allout operation. Fairly slow lateral spread occurs in houses. pheasants. ILT Introduction A herpesvirus (pathogenicity can vary) infection of chickens. 87 . after 4 weeks of age. lesions. often with blood in lumen. caseous plugs may be present. 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. PCR. Isolation in CE CAMs.
88 . Careful attention to feeding practices to avoid anticipation of feed arrival if on restricted feeding. Asia and Africa. Coccidiosis. Survivors may carry infection. Signs Sudden onset of depression. guinea fowl. The disease has a short course and morbidity and mortality are high. Post-mortem lesions Telescoping of the bowel. Loss of equilibrium. Thirst. Leukocytozoonosis Introduction Caused by Leucocytozoon species. ducks.Intussusception Introduction A condition of chickens associated with increased intestinal motility. Anorexia. protozoan parasites of turkeys. Simulid flies or culicoid midges are intermediate hosts. it may actually protrude at the vent and be cannibalised. Diagnosis Typical post-mortem lesions Treatment As appropriate for the underlying disease condition. usually in the lower small intestine. Prevention Control of coccidiosis and other causes of intestinal inflammation. Signs Mainly sudden deaths. rarely chickens. Rapid breathing. worms and other forms of enteritis are predisposing factors. Different species of this parasite have been reported from North America.
Diagnosis Lesions. Hepatomegaly. Persistent low mortality. especially in enlarged spleen. Enlargement of abdomen. disposal of recovered birds. Anaemia. May be asymptomatic. Diagnosis History. age. Differentiate from Reticuloendotheliosis. Treatment None known. Lymphoproliferative Disease (LPD) Introduction A Type C retrovirus infection of turkeys with low morbidity and high mortality. Post-mortem lesions Splenomegaly. Emaciation.megaschizonts in brains of birds with nervous signs. lesions. Prevention Separation from intermediate hosts. Microscopically . liver or bursa. Post-mortem lesions Focal tumours. gametes in erythrocytes. histology and blood smears. Anaemia. Treatment 89 . cytology. Loss of weight. Signs Depression. schizonts in liver.
Malabsorption Syndrome. Prevention Good hygiene. Runting/Stunting Introduction A condition of chickens and turkeys that may be associated with several different viruses.(maize-) fed birds (often associated with orange intestinal contents and/or faeces). control arthropods. Pot-bellied appearance. Pancreatic atrophy/fibrosis and pancreatic atrophy (rather variable). Post-mortem lesions Enteritis. rotavirus etc. Poor early management (feed and water supply. direct electron microscope examination of intestinal contents. in future eradication.Tahir None. enterovirus-like particles. Stunting (temporary).Abubakar. Diarrhoea. Abnormal feathers ('helicopter wings' 'yellow-heads'). Diarrhoea in older birds may be an effect of on-farm infection. Treatment Daily cull of affected birds between 14 and 28 days. Sometimes osteomyelitis and/or rickets. Poor feathering. Poor management may contribute to the problem. temperature control) may lead to a similar picture in the absence of specific infection. Eating faeces. North and South America and Australia. It is suspected that these viruses can be vertically transmitted and the most severe signs in young birds are associated with this.M. 90 . all-in/all-out production. Runting (permanent). Diagnosis Pathology. The condition has been seen in Europe. Signs Uneven growth. Pale shanks in corn. reoviruses. for example enteroviruses.
Acute infiltration of the CNS and nerves resulting in 'floppy broiler syndrome' and transient paralysis. From the 1980s and 1990s highly virulent strains have become a problem in North America and Europe. Affected birds are more susceptible to other diseases. The virus survives at ambient temperature for a long time (65 weeks) when cell associated 91 . as well as more longstanding paralysis of legs or wings and eye lesions. A sample of the faeces produced is shown at the bottom of the picture . Intestines of a young broiler chick suffering from malabsorption syndrome.Tumours of feather follicles. lungs. Infected birds remain viraemic for life. tests. They are distended with poorly digested feed. Figure 24. Vertical transmission is not considered to be important. and rarely turkeys in close association with chickens. The disease has various manifestations: a) Neurological . c) Cutaneous . ovary.Tumours in heart.Prevention Good broiler farm hygiene. muscles. fomites. Morbidity is 10-50% and mortality up to 100%. In 'late' Marek's the mortality can extend to 40 weeks of age. avoidance of intercurrent disease and management problems (such as chilling).poorly digested food enclosed in mucus. etc. seen worldwide. The route of infection is usually respiratory and the disease is highly contagious being spread by infective feather-follicle dander. both parasitic and bacterial. Mortality in an affected flock typically continues at a moderate or high rate for quite a few weeks. b) Visceral . Marek's disease Introduction Marek's disease is a Herpes virus infection of chickens. good parent nutrition and egg selection and santitation.
game birds. Differentiate from Lymphoid leukosis. gonads. all-in/all-out production. clinical signs. resistant strains. deficiency of Ca/Phosphorus/Vitamin D. spleen. association with other strains (SB1 Sero-type 2) and Rispen's. distribution of lesions. It is inactivated rapidly when frozen and thawed. deficiency of thiamine. lung. Loss of weight. turkeys. Diagnosis History. Genetics can help by increasing the frequency of the B21 gene that confers increased resistance to Marek's disease challenge. Post-mortem lesions Grey-white foci of neoplastic tissue in liver. Signs Paralysis of legs. chronic respiratory disease in chickens. and skeletal muscle.g.. M. age affected. wings and neck. heart. histopathology. Thickening of nerve trunks and loss of striation. It is common practice to use combinations of the different vaccine types in an effort to broaden the protection achieved. pigeons and other wild birds.and is resistant to some disinfectants (quaternary ammonium and phenol). Treatment None. Ducks and geese can 92 .Chicken Introduction Infection with Mycoplasma gallisepticum is associated with slow onset. especially at the start of lay. Skin around feather follicles raised and roughened. vaccination generally with 1500 PFU of HVT at day old (but increasingly by in-ovo application at transfer). Microscopically . Vision impairment. Prevention Hygiene. Grey iris or irregular pupil.lymphoid infiltration is polymorphic. botulism. Mycoplasma gallisepticum infection. Chronic Respiratory Disease . kidney.
tenosynovitis and salpingitis in chickens. Diagnosis Lesions. Occasionally arthritis. isolation and identification of organism. and in lyophilised material. Stunting. virulent E. Fomites appear to a significant factor in transmission between farms. morbidity may be minimal and mortality varies. coli. Signs Coughing.become infected when held with infected chickens. and to a lesser extent fomites. In others it is actually increasing because of more birds in extensive production systems that expose them more to wild birds. Poor productivity. The infectious agent survives for only a matter of days outwith birds although prolonged survival has been reported in egg yolk and allantoic fluid. 93 . The route of infection is via the conjunctiva or upper respiratory tract with an incubation period of 6-10 days. Slow growth. Leg problems. Transmission may be transovarian. Suspect colonies may be identified by immuno-flourescence. ND. In adult birds. Catarrhal inflammation of nasal passages. Pericarditis. The condition occurs worldwide. Pasteurella spp. aerosols. Nasal and ocular discharge. In turkeys it is most associated with severe sinusitis (see separate description in the turkey section). subsequent stress may cause recurrence of disease. airborne dust and feathers. though in some countries this infection is now rare in commercial poultry. coli infection). Perihepatitis (especially with secondary E. or by direct contact with birds. Culture requires inoculation in mycoplasma-free embryos or. trachea and bronchi. more commonly in Mycoplasma Broth followed by plating out on Mycoplasma Agar. Haemophilus. Spread is slow between houses and pens suggesting that aerosols are not normally a major route of transmission. Recovered birds remain infected for life. demonstration of specific DNA (commercial PCR kit available). Inappetance. ART). and inadequate environmental conditions are predisposing factors for clinical disease. exudates. sinuses. Intercurrent infection with respiratory viruses (IB. Post-mortem lesions Airsacculitis. though infection rates are high. Reduced hatchability and chick viability. serology. Survival seems to be improved on hair and feathers. Occasional encephalopathy and abnormal feathers.
infection status is important for trade in birds. generally as a confirmatory test. hatchingeggs and chicks. These programmes are based on purchase of uninfected chicks.g. tetracyclines. exudates. Live attenuated or naturally mild strains are used in some countries and may be helpful in gradually displacing field strains on multi-age sites. In some circumstances preventative medication of known infected flocks may be of benefit. HI may be used. Elisa is accepted as the primary screening test in some countries. Prevention Eradication of this infection has been the central objective of official poultry health programmes in most countries. subsequent stress may cause recurrence of disease. synoviae and M. Transmission may be transovarian. and routine serological monitoring. Effort should be made to reduce dust and secondary infections. M. Treatment Tilmicosin. Differentiate from Infectious Coryza.g. meleagridis(turkeys). all-in/all-out production. Aspergillosis. though in many countries this infection is now rare in commercial poultry. and fomites. Infectious Sinusitis . Recovered birds remain infected for life. fluoroquinolones. The route of infection is via the conjunctiva or upper respiratory tract with an incubation period of 6-10 days. 94 . viral respiratory diseases. spiramycin. Mycoplasma gallisepticum infection.Turkeys Introduction A slow onset chronic respiratory disease of turkeys often with severe sinusitis and associated with Mycoplasma gallisepticuminfection.Serology: serum agglutination is the standard screening test. suspect reactions are examined further by heat inactivation and/or dilution. Some inactivated vaccines for other diseases induce 'false positives' in serological testing for 3-8 weeks. It is seen worldwide.-free stock. therefore M. or by direct contact with birds. other Mycoplasma infections such as M. Morbidity is low to moderate and mortality low. PCR is possible if it is urgent to determine the flock status. vitamin A deficiency. Suspect flocks should be re-sampled after 2-3 weeks. aerosols.g. biosecurity. tylosin. Productivity in challenged and vaccinated birds is not as good as in M..
intercurrent viral disease such as Newcastle disease (even lentogenic) and Turkey Rhinotracheitis are predisposing factors. demonstration of specific DNA (commercial kit available). Signs Coughing. malnutrition. of swabs taken from the trachea or lesions. often with inspissated pus. Culture. Pericarditis. spiramycin. Suspect colonies may be identified by immunofluorescence. although prolonged survival has been reported in egg yolk and allantoic fluid. In some circumstances preventative medication of known infected flocks may be of benefit. Swollen sinuses. more commonly in Mycoplasma Broth followed by plating out on Mycoplasma Agar. 95 . tetracyclines. all-in/allout production. Some inactivated vaccines induce 'false positives' in serological testing.The infectious agent survives for only a matter of days outwith birds. requires inoculation in mycoplasma-free embryos or. serology. Stress. Serology: serum agglutination is the standard screening test. Post-mortem lesions Swollen infraorbital sinuses. Airsacculitis. especially Turkey Rhinotracheitis. Suspect flocks should be re-sampled after 2-3 weeks. Inappetance. and biosecurity. These are based on purchase of uninfected poults. Diagnosis Lesions. and in lyophilised material. suspect reactions are examined further by heat inactivation and/or dilution. Nasal and ocular discharge. PCR is possible if it is urgent to determine the flock status. Effort should be made to reduce dust and secondary infections. tylosin. Perihepatitis. Survival seems to be improved on hair and feathers. Slow growth. Stunting. Treatment Tilmicosin. Prevention Eradication of this infection has been the central objective of official poultry health programmes in most countries. isolation and identification of organism. Differentiate from viral respiratory disease. fluoroquinolones. HI may also be used. Leg problems.
i.g. Prevention As for M. M. ducks (France).g. Post-mortem lesions Stunted embryos with hepatitis and enlarged spleens. Signs Embryonic mortality. Post-mortem lesions Sinusitis. Diagnosis Shows cross reaction in IFA to M. Reduced hatchability. although DNA homology is only 40%. venereal or horizontal. some with down abnormality. and can occur in other poultry and wild bird species. Mycoplasma iowae infection. Introduction Infection with Mycoplasma iowae is seen in turkeys. Infection occurs via the conjunctiva or upper respiratory tract and transmission among poults may be vertical. 96 .g. perhaps because all affected embryos fail to hatch. Treatment As for M. Signs Swollen sinuses.Mycoplasma immitans infection Introduction Infection with Mycoplasma immitans is seen in geese. Leg lesions can be shown in inoculated birds but do not seem to occur naturally. and partridges (UK).
purchase of M.-free stock. Antibiotics that have been used are tylosin and enrofloxacin. Slow growth. When the vacuum is released the eggs draw in antibiotic solution which is subsequently absorbed through the shell membranes. Transmission is venereal in breeders. Mycoplasma meleagridis infection. Mild respiratory problems. Crooked necks. Predisposing factors include stress and viral respiratory infections. In adult birds though infection rates are high. Mortality is low. The organism has also been isolated from raptors. M. Prevention Eradication of the infection from breeding stock. 97 . For eradication purposes egg injection provides more consistent dosing per egg than does egg dipping. Infected parents may be asymptomatic. Introduction A disease of turkeys characterised by respiratory and skeletal problems caused by Mycoplasma meleagridis. Infection is via the conjunctiva or upper respiratory tract with an incubation period of 6-10 days. though up to 25% of infected birds show lesions at slaughter. Treatment Pressure differential dipping has been used where breeder flocks are infected.m. with transovarian and then lateral spread in meat animals. Pathogenicity is quite variable. Leg problems.Diagnosis Isolation and identification of the causative organism from dead-in-shell embryos. morbidity may be minimal. maintenance of this status by good biosecurity. The infective agent does not survive well outside the bird. This can increase hatchability by 510% in this situation. Signs Reduced hatchability. Infected eggs result in widespread distribution of infection and increased risk of further vertical transmission.i. Specialised dip tanks are subjected to negative pressure which partially collapses the air cell of the submerged eggs. Stunting. it occurs in most turkey-producing countries but is now much rarer in commercial stock.
Prevention Eradication of this infection is also possible using similar techniques as for Mycoplasma gallisepticum. M. Infected birds do develop some immunity. Treatment Tylosin. Infection is via the conjunctiva or upper respiratory tract with a long incubation period. Mycoplasma synoviae. especially in commercial layer flocks. Suspect colonies may be identified by immuno-fluorescence. It occurs in most poultry-producing countries. Transmission may be transovarian. Mycoplasma synoviae infection. 11-21 days following contact exposure.culture used to confirm. Serology: SAG used routinely . isolation and identification of organism. Differentiate from Mycoplasma gallisepticum. These are based on purchase of uninfected poults. In some circumstances preventative medication of known infected flocks may be of benefit. Diagnosis Lesions. Birds infected from their parents seem to be immuno-tolerant and particularly prone themselves to transmit. and biosecurity.s. whilst illness is variable and mortality less than 10%. Effort should be made to reduce dust and secondary infections. demonstration of specific DNA (commercial kit available). 98 . serology. Predisposing factors include stress and viral respiratory infections. Spread is generally rapid within and between houses on a farm. tetracyclines. or lateral via respiratory aerosols and direct contact. more commonly in Mycoplasma Broth followed by plating out on Mycoplasma Agar. other respiratory viruses.Post-mortem lesions Airsacculitis in infected pipped embryos and poults. Airsacculitis (rarely) seen in adult birds. Vaccines are not normally used. Infection rates may be very high. Infected males are particularly prone to transmit infection and may warrant special attention. Infectious Synovitis Introduction Infection with Mycoplasma synoviae may be seen in chickens and turkeys in association with synovitis and/or airsacculitis. all-in/all-out production. Survival of the infectious agent outwith the bird is poor but fomite transmission between farms is important. spiramycin. fluoroquinolones. Culture requires inoculation in mycoplasma-free embryos or.
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.
Closed eyes. Post-mortem lesions Small intestine (usually middle to distal) thickened and distended. in drinking water. Signs Depression. Probiotics may limit multiplication of bacteria and toxin 102 . high viscosity diets (often associated with high rye and wheat inclusions in the diet).Abubakar. Affected birds tend to be dehydrated and to undergo rapid putrefaction. phenoxymethyl penicillin. Predisposing factors include coccidiosis/coccidiasis.g. Immobility. Ruffled feathers. Intestinal mucosa with diptheritic membrane. usually in less than 48 hours. Reflux of bile-stained liquid in the crop if upper small intestine affected. 100 ppm). high levels of most growth promotors and normal levels of ionophore anticoccidials also help. Mortality may be 5-50%. 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. Prevention Penicillin in feed is preventive. neomycin and erythromycin are used in the USA. Treatment Penicillins (e. Intestinal contents may be dark brown with necrotic material. Infection occurs by faecal-oral transmission. Inappetance. usually of the mid. Spores of the causative organism are highly resistant. amoxycillin). in ducks possibly heavy strains. contaminated feed and/or water. usually around 10%. turkeys and ducks worldwide.M. Dark coloured diarrhoea. Sudden death in good condition (ducks). other debilitating diseases.Tahir Necrotic Enteritis Introduction An acute or chronic enterotoxemia seen in chickens.small intestine. or Bacitracin in feed (e. Water medication for 3-5 days and in-feed medication for 5-7 days depending on the severity. Treatment of ducks is not very successful. diet (high protein). caused by Clostridium perfringens and characterised by a fibrino-necrotic enteritis.g.
ND . In many countries local regulations or market conditions prevent the routine use of many of these options. ND .Velogenic Viscerotropic (VVND) . Intestinal lesions are absent. sometimes subclinical. Strains can be developed as vaccines. 103 .Lentogenic . The sample at the bottom of the picture is still focal. The virus involved is Paramyxovirus PMV-1. ND . conjunctivitis in man). Figure 25.Mesogenic . Other species can be infected including mammals occasionally (e. pigeons and ducks. Affected species include chickens. the upper has formed a thick crust of necrotic material. respiratory or reproductive systems.g.Mild disease. Can affect any age. which is of variable pathogenicity.Acute and fatal in chickens of any age causing neurological and some respiratory signs.Neurotropic Velogenic . Severe lesions of necrotic enteritis affecting the small intestine of broilers.Mortality and nervous signs in adult. Signs are typically of disease of the nervous. Morbidity is usually high and mortality varies 0-100%. These viruses have sometimes been used as vaccines in previously immunised birds. Four manifestations have been identified: ND . It is highly virulent for chickens.sometimes called 'asiatic' or exotic. The condition is rarely diagnosed in ducks but is a possible cause of production drops/fertility problems. birds.production. less for turkeys and relatively apathogenic in psittacines. turkeys. Newcastle Disease (Paramyxovirus 1) Introduction Paramyxovirus 1 or Newcastle Disease is a highly contagious viral disease affecting poultry of all ages. Higher mortality is seen in velogenic disease in unvaccinated stock. Transmission is via aerosols. visitors and imported psittacines (often asymptomatic). fomites. It is not usually vertical (but chicks may become infected in hatcheries from contaminated shells).
Pathogenicity evaluated by Mean Death Time in embryos. encephalomyelitis. formalin and phenol. Intestinal lesions primarily occur in the viscerotropic form. It is confirmed by isolation in CE. Necrotic plaques in proventriculus. and is ether sensitive. Dyspnoea. acid pH. Tracheitis. haemorrhagic disease. Cross-reactions have mainly been with PMV-3. Inappetance. the infective dose and the degree of immunity from previous exposure or vaccination. Diagnosis A presumptive diagnosis may be made on signs. dust etc). encephalomalacia. EDS-76. Signs Signs are highly variable and will depend on the nature of the infecting virus (see above). Coughing. middle ear infection/skull osteitis. HA+. HI with ND serum or DID (less cross reactions). Twisted neck. fumigants and sunlight. especially in faeces and can persist in houses (in faeces. Post-mortem lesions Airsacculitis. for up to 12 months.tracheal or cloacal. Nervous signs. rising titre in serology. pneumovirus infection. infectious coryza. laryngotracheitis. Severe drop in egg production. However it is quite sensitive to disinfectants. Moult. IFA. Haemorrhage in proventriculus. antibiotics to control secondary bacteria. Paralysis. Treatment None. caecal tonsil.The virus survives for long periods at ambient temperature. 104 . post-mortem lesions. intestine. Samples . Diarrhoea. intoxications. It is inactivated by temperatures of 56°C for 3 hours or 60°C for 30 min. Sudden Death Depression. intracerebral or IV pathogenicity in chicks. Differentiate from Infectious bronchitis. avian influenza.
It is commonest in progeny of young parent flocks (relatively small yolks) or where managers are inexperienced. The LaSota-type vaccine may even repeated at 35-40 days of age if risk is high. HI has been used extensively. 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). These tests do not directly evaluate mucosal immunity. Vaccinal reactions may present as conjunctivitis. It is common to monitor response to vaccination. In some countries it has been customary to provide antibiotics prophylactically during periods of anticipated vaccinal reaction. whereas it tends to peak between 6-10 days for chicks that begin eating but then cease. Use of spray application is recommended but it needs to be applied with care to achieve good protection with minimal reaction. 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. Vaccination programmes should use vaccines of high potency. all-in/all-out production. vaccination. biosecurity. which are adequately stored and take into account the local conditions. Acute viral infections or heavily contaminated drinking water may have a similar effect to bad management in reducing feed intake. A typical programme may involve Hitchner B1 vaccine at day old followed by LaSota-type vaccine at 14 days. snicking. Use of Mycoplasma gallisepticum free stock under good management reduces the risk of vaccinal reactions. Figure 28. 105 . Inactivated vaccines have largely replaced the use of live vaccines in lay but they do not prevent local infections. Elisa is now also used. and occasionally gasping due to a plug of pus in the lower trachea. and is associated with difficulty maintaining brooding temperature and poor management of feeders and drinkers. To prevent or reduce vaccinal reactions in young chicks it is important that day old have uniform titres of maternal immunity. Mortality peaks at 3-5 days for birds that fail to eat at all. however. Morbidity is up to 10% and mortality close to 100%.Prevention Quarantine. especially in breeding birds by the use of routine serological monitoring.
age of collection and weight of hatching eggs. 106 . Because it is enclosed in a relatively unyielding membrane. in broiler parent chickens and also in large broiler chickens in various places. good hygiene and biosecurity in brooding areas to minimise early disease challenges.Signs Failure to grow. The condition can be reproduced by causing intense exercise of this muscle. Gall bladder distended. Oregon Disease . 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. aspergillosis. Diagnosis Based on post-mortem lesions. It has since been seen in turkeys. Gizzard may be impacted with litter. Most organs normal. Differentiate from omphalitis/ yolk sac infection. Prevention Review brooding management. good drinking water hygiene. or suffer necrosis. any swelling of the muscle tends to cut off the blood supply. Poor development. Without adequate blood supply the tissue of the muscle begins to die. bile staining of adjacent tissues. soluble multivitamin supplementation may help. nutrition of young parents. It does not usually cause any mortality or obvious clinical signs and so it is usually identified after slaughter.Deep Pectoral Myopathy Introduction This condition is so named because it was first identified in adult breeding turkeys in Oregon State. Treatment Correction of management problems. It is caused by a reduction in the blood supply to the deep pectoral muscles.
with oedema within it and on its surface.Signs None. This will normally be due to excessive flapping in association with management activities (e.g. It is very difficult to detect affected carcases in standard meat inspection. and flaking. 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. artificial insemination in breeding turkeys. it may become a healed scar. greenish yellow. The tissue in the centre is dry. Diagnosis Lesions. It may also start to be enclosed in a fibrous capsule. If the condition is of over 7 days duration the muscle is dry and often shows greenish tinges. If recent. Prevention Avoidance of physical damage of this muscle. Post-mortem lesions Acute or chronic necrosis of the deep pectoral muscle on one or both sides. thinning operations in meat birds. and. Figure 26. A typical case of the chronic stages deep pectoral myopathy in a broiler chicken. 107 . weighing birds etc). in particular excessive exercise. Treatment Not applicable. the muscle may be swollen and pale. Transillumination of the breast may help identify affected carcases and may be worthwhile if the incidence is high. If of very long duration.
Most isolates are oxidase positive and galactosidase positive Serology using Elisa tests has been used. Growth is more rapid and consistent in an anaerobic jar. ventilation problems. This can cause significant losses through condemnations. The infection is common in chickens and turkeys. perhaps through survival of the organism on shell surfaces or shell membranes. E. coli overgrowth may occur. Infectious Bronchitis). In broiler chickens its main importance seems to be as a cause of airsacculitis in apparently healthy flocks that is only identified at slaughter. ORT Introduction Ornithobacterium Infection is an infection of chickens and turkeys with the bacterium Ornithobacterium rhinotracheale(ORT). and E. Confirmation is by isolation of the organism. Cultures from the trachea of birds showing typical signs are preferred. Important cofactors may include respiratory viral vaccines (Newcastle disease. The slow-growing bacterium was named in 1994. It had been previously isolated in a number of other countries. age at infection etc. 108 . It is a Gram-negative pleomorphic organism. Post-mortem lesions Airsacculitis. direct contact and drinkers. Within the poultry house it is likely to be by aerosols. preferably as a flock test comparing results before and after the challenge. Reduced egg production. Signs Coughing.Ornithobacterium Infection. severe bronchopneumonia. The organism grows slowly producing tiny colonies on blood agar. The severity of its effects depends on the pathogenicity of the particular strain and other risk factors such as viral infections. Some uncertainty exists about mechanisms of transmission. There is some evidence that hatcheries may play a role in the epidemiology. It commonly exacerbates respiratory disease caused by pneumovirus infections in turkeys. Diagnosis Clinical signs and lesions. The range occurring in turkeys is wider than that seen in chickens. 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. Reduced weight gain. A range of sero-types have been identified. tracheitis. field challenge with respiratory viruses. sneezing. This was first identified as a new disease syndrome of turkeys in Germany in the early 1990s. Bordetella aviuminfection. coli infections.
Some work has been done on live vaccine in the USA. Severely consolidated lung from an acute ORT infection in 14-week-old turkey growers. cost etc. Satisfactory disease control depends on good management and biosecurity. Tilmicosin is also effective at 10-20mg/kg and should be used in the early stages of the disease. Amoxycillin sensitivity remains good. because of the age of slaughter. In France and Belgium most strains were sensitive to enrofloxacin. chlortetracycline but not to enrofloxacin. regulation. ORT is a major problem on multi-age sites. 109 . it requires two doses. also most are sensitive to tiamulin. Similar lesions may be found in Pasteurellosis. Figure 27.there are issues relating to availability. In the USA in 1998 all strains were sensitive to penicillins and many other microbials. Some vaccines seem to have difficulty in producing a longlasting serological response to ORT. Prevention This is based on good hygiene.amoxycillin at 250 ppm in water for 3-7 days or chlortetracycline at 500 ppm for 4-5 days. though 54% were sensitive to tetracycline. neomycin and enrofloxacin. Initially in Germany most strains were sensitive to amoxycillin. this is unlikely to work in turkeys.it is very sensitive in vitro to a range of chemicals. Vaccination . Hygiene . Vaccination of breeder flocks to protect progeny has shown benefits in chickens but.Treatment The sensitivity of ORT to antibiotic is highly variable. An inactivated vaccine is licensed for broiler parents in Europe. The lung is solid and covered by pus/ purulent exudate. Preventative medication with the products listed in the previous section may be beneficial in some circumstances. Routine treatment . therapy and vaccination.
Diagnosis Lesions.Osteomyelitis Complex. Signs Lameness. Soft bones and beak. Post-mortem lesions Green discolouration of the liver at slaughter. Osteoporosis. Gram-variable pleomorphic bacteria have been isolated from affected livers and bones. high production. Cage Fatigue Introduction A condition of chickens. Drop in production. Treatment Not applicable . Signs None.only identified at slaughter. Birds go off legs. 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. Soft-shelled eggs. Birds rest squatting. Enlarged hocks. 110 . turkeys and ducks seen worldwide and due to Vitamin D or calcium deficiency. Predisposing factors include small body size. The green discolouration is used to identify carcases that require closer inspection of the other tissues. Prevention Unknown.
Transmission is by wild birds and fomites. turkeys and passerine cage birds with Paramyxovirus PMV-2 results in disease with variable mortality. Inappetance.Yucaipa Disease Introduction An infection of chickens. Treatment Over-correct ration vitamin D. Beading and fracture of ribs. place on litter. Drop in egg production. Diagnosis History. Coughing. Vertical transmission does not usually occur. signs. Epiphyses of long bones enlarged. In chickens it is usually mild. Post-mortem lesions Not characteristic. proper Ca and P levels and ratio.Tahir Post-mortem lesions Bones soft and rubbery. skeletal size and mineral content at point of lay are critical. antioxidants. Parathyroids enlarged. Beak soft. Signs Depression. lesions. calcium carbonate capsules. As birds progressively mobilise skeletal calcium for egg production through lay. Prevention Supplementation of vitamin D. spondylitis.M. bone ash. Differentiate from Marek's disease. depending on the species affected and whether infection is complicated by other factors and diseases. Paramyxovirus 2 . 111 . Wild birds are believed to be especially important.Abubakar. whereas turkeys are more severely affected.
laryngotracheitis. including wild bird contact and fomites. 112 . High mortality (cage birds). antibiotics to control secondary bacteria. IFA. The infection is transmitted by birds. Post-mortem lesions No specific lesions. Treatment No specific treatment. biosecurity. antibiotics to control secondary bacteria. occasionally chickens and psittacine cage birds. Vertical transmission does not usually occur. HI with ND serum or DID (less cross reactions). HA+. Coughing. Prevention Quarantine.Diagnosis Isolation in CE. all-in/all-out production. Paramyxovirus-3 Introduction Paramyxovirus PMV-3 infects turkeys. Differentiate from Infectious bronchitis. Diagnosis Isolation in CE. haemorrhagic disease. Loss of shell pigment Nervous symptoms (psittacines). Inappetance. Treatment No specific treatment. Signs Depression. EDS-76. HA+. HI with ND serum or DID (less cross reactions). Drop in egg production (turkeys). IFA. Mortality is usually low in poultry.
In both cases mortality can be high and can be associated with a marked depression in growth. Diagnosis Isolation in CE. Vertical transmission does not usually occur. Signs Reduction in egg production. IFA. Treatment No specific treatment. all-in/all-out production. HI with ND serum or DID (less cross reactions). Prevention Quarantine.Prevention Quarantine. A less acute form of the disease appears to produce more of a lingering mortality. all-in/all-out production. including wild bird contact and fomites. Paramyxovirus-6 Introduction Paramyxovirus PMV-6 infection of turkeys. Mild respiratory signs. biosecurity. Vaccination has been used in turkeys but may not be cost-effective. Mortality is 0-5%. The infection is transmitted by birds. A range of 113 . PEMS and Spiking Mortality of Turkeys Introduction Poult Enteritis and Mortality Syndrome (PEMS) was first identified in high density turkey producing areas of the South Eastern USA in 1991. The infection is inapparent in ducks and geese. It is an infectious and transmissible cause of sudden increases in mortality in turkeys between 7 and 28 days of age. HA+. biosecurity. Post-mortem lesions No specific lesions. antibiotics to control secondary bacteria.
Wet litter. Overdistension of crop in young birds because of an interruption in feed supply may predispose. lesions. multivitamins and milk replacer products are helpful for nutritional support in the acute phase. Droppings watery. Picking at feed. Emaciation. All-in/all-out production. Effective terminal disinfection. This syndrome is clearly distinguished from typical viral enteritis in young turkeys because of the high mortality and severe growth depression. Good quality diets of a suitable form . To replicate the condition in full it appears to be necessary to include bacteria in the inoculum. Caseous cores in bursae (late in the process). Reduced feed consumption and growth. Diagnosis Signs.5-8% will encourage feed intake and recovery. Weight loss.mash and poor quality crumbles increase risk. Fluoroquinolone antimicrobials appear to be especially effective. A highly digestible diet with fat at 7. eating litter.viruses have been isolated from affected flocks. pale brown. 114 . Treatment A range of antibiotics and arsenicals have been used to control the bacterial component of this condition. Increasing weakness. Liquid intestinal contents. seeking heat. Post-mortem lesions Dehydration. huddling. Increased water consumption. Prevention Biosecurity to reduce the introduction of new infections into brooding facilities. Pendulous Crop Introduction A complex condition of turkeys and chickens associated with coarse fibrous feed. Muscle atrophy. Signs Initial hyperactivity and increased vocalisation.
have ulcerations and sometimes mycosis. Lack of muscle tone. grasshoppers and cockroaches. Diagnosis Macroscopic examination of lesions. spiruroid worm parasites of poultry and game birds. Emaciation in heavily infected young chicks (Tetrameres). Signs Anaemia.Signs Enlargement of crop. 115 . and thickening of mucosa of proventriculus. Diarrhoea. Post-mortem lesions Crop distended with feed. Proventricular Worms Introduction Dispharynx. They are found in the mucosa of crop and proventriculus causing mainly inapparent infections. if these can be identified. including crustaceans. Prevention Remove predisposing factors. haemorrhage. Treatment None. identification of worms. ulceration. necrosis. Tetrameres and Cyrnea are nematodes. Diagnosis Signs. may be impacted. Post-mortem lesions Inflammation. Crop contents semi-liquid and foul smelling. Infection is by the oral route on exposure to the intermediate hosts. lesions.
Pseudotuberculosis Introduction An infection of ducks. tuberculosis. other poultry. Ruffled feathers. Differentiate from Duck viral enteritis. sulphonamides in feed. Diagnosis Lesions. wild birds. 116 . Signs Weakness. isolation. coccidiosis. duck viral hepatitis. rodents and man with the bacterium Yersinia pseudotuberculosis. Prevention Prevention of access to intermediate hosts. Prevention Good husbandry and hygiene. Diarrhoea.Treatment Not usually required. Post-mortem lesions Miliary lesions in a variety of organs but especially in the liver. Treatment Tetracyclines. Sometimes sudden death. adequate protection. 'hardening off'. The disease has a mortality of 5-75%. colibacillosis. In peracute disease the only lesion may be enteritis.
Loss of appetite. 117 . Pancreas chalky. molasses. diet and water supply. Affected birds have an increase in circulating monocytes in their blood. hygiene. coccidiosis.M. toxin and possibly a virus infection. IBD and typhoid.Tahir Pullet disease. Skin cyanosis of head. vibriosis. water deprivation. Signs Depression. It was commonly reported prior to 1960 but is now rare. Dehydration. Treatment Adequate water supply. mucoid casts in intestine. Crop distended. Liver swollen with foci. It is associated with hot weather. Skeletal muscle necrosis. Bluecomb. Prevention Good management. Avian Monocytosis Introduction A sudden onset condition of chickens early in lay with high morbidity and a mortality of 050%. Watery diarrhoea. lesions. multivitamins in water. Post-mortem lesions Dehydration. Crop distension. Catarrhal enteritis.Abubakar. Differentiate from fowl cholera. elimination of other causes. capillariasis. Dark comb and wattles. Kidneys swollen. Drop in egg production. Diagnosis History. antibiotics.
citrus extracts. Signs Presence of grey to red mites up to 0. and good design of new equipment to limit harbourages for red mites. Effective monitoring of mite numbers and implementation of control measures before birds are heavily infested improves control. organophosphates. Spots on eggs. Prevention Thorough cleaning. Diagnosis Number and type of mites identified. Pale comb and wattles. Ornithonyssus bursae. feeds by sucking blood. For northern fowl mite it is essential to apply approved insecticides to the affected birds. fumigation and insecticide treatment at turnaround. May cause anaemia and death in young birds. Dermanyssus gallinae. 118 .itching. Post-mortem lesions Anaemia. Loss of condition. the Northern Fowl Mite spends its entire life cycle on the bird and can multiply more rapidly as a result. the Common Red Mite. carbamates. Filling of cracks and crevices. Drop in egg production. Birds restless. in nest boxes. which are external parasites of chickens and turkeys. mainly at night and may transmit fowl cholera and other diseases. cracks.Red Mite and Northern Fowl Mite Introduction Arachnid mites. However keep in mind that the majority of the population of Dermanyssus is in the environment so it is necessary to monitor infection levels on feeder tracks. vegetable oil and mineralbased products (both liquid sand dusts) have been used to control red mites in the environment.7 mm. Staff complaints . Treatment Pyrethroids. crevices etc.
Treatment None. chloroform. Infected birds may remain carriers for a few weeks. Prevention Quarantine and good sanitary precautions. lesions. and by fomites. and other factors associated with poor ventilation. intranuclear inclusions in liver. at least 12 sero-types have been described and these may be isolated from healthy chickens. Lentogenic Newcastle disease virus. coli) may be involved. may act as 119 . Avian pneumovirus. formaldehyde and iodides work better. CE liver). Signs Mild snick and cough without mortality. Dust. The virus is generally resistant to disinfectants (ether. The virus grows well in tissue culture (CE kidney. Opinions vary as to whether adenovirus can be characterised as a primary respiratory pathogen.Abubakar. E. Diagnosis History. temperature.Tahir Respiratory Adenovirus Infection. ammonia and other gases. A number of respiratory viruses (Infectious Bronchitis. Post-mortem lesions Mild catarrhal tracheitis. prevention of immunosuppression. It may occur as an exacerbating factor in other types of respiratory disease. Respiratory Disease Complex Introduction Respiratory infections in chicken and turkeys are seen worldwide but especially in temperate poultry-producing areas in winter months. 'Mild Respiratory Disease' Introduction An adenovirus infection of chickens with a morbidity of 1-10% and a mortality of 1-10%. pH).M. vaccinal and field strains) and bacteria (Ornithobacterium rhinotracheale. Transmission may be vertical and lateral.
Severe airsacculitis of thoracic air sacs in a broiler close to slaughter. mortality 5. Airsacculitis. Rattling noises. Diagnosis Lesions. Differentiate from Chronic Respiratory Disease (Mycoplasmosis).catarrhal to purulent. Nasal exudate.predisposing factors. sanitation of drinking water. 120 . Head swelling. If condemned birds are included mortality may be more than 10%. response to environmental changes. Conjunctivitis. Morbidity is typically 10-20%. Pericarditis.10%. Figure 29. 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. Post-mortem lesions Severe tracheitis with variable exudate . carefully applied appropriate viral vaccines. be challenged by some of these pathogens). of course. serology. and have been cut into to reveal a cheesy (caseous) mass of pus. Sneezing. Treatment Antimicrobial treatment of specific bacterial infections. The air sacs are thickened and congested. Signs Snick. Prevention Effective ventilation. There is also percarditis evident (at top right).
Diarrhoea. Lympoid Tumour Disease Introduction A retrovirus infection of chickens. Leg weakness.Figure 30. geese. Treatment None. spleen and kidney. Sometimes enteritis and proventriculitis (especially in broilers infected with contaminated Marek's disease vaccine). Post-mortem lesions Neoplastic lesions in liver. usually higher in females than males. Both tracheas were congested and the upper sample had mucopurulent material in the lumen. ducks. 121 . There is an incubation period of 5-15 days. chick inoculation. turkeys. Sometimes nodules in intestine and caecae. Diagnosis Pathology. A gradual increase in mortality and poor growth in broilers may be the main signs. and quail with morbidity up to 25%. Transmission is lateral and possibly transovarian. Marked stunting when Marek's disease vaccine is contaminated. Severe tracheitis is broilers with respiratory disease complex. and the infection can be spread by mosquitoes or in contaminated Marek's disease vaccines. Reticuloendotheliosis. Signs There may be no obvious signs.
Diagnosis History. Epiphyses of long bones enlarged. signs. Reduction in bodyweight. Parathyroids enlarged. Growth plates widened and disorganised.Prevention Formal control programmes have not been documented as the condition is sporadic and relatively self-limiting. proper calcium and phosphorus levels and ratio. Treatment Over-correct ration with three times vitamin D for 2 weeks. Post-mortem lesions Bones soft and rubbery. Femoral Head Necrosis. Differentiate from Encephalomalacia. Poor growth. or Vitamin D or 25-hydroxy vitamin D in drinking water. Soft bones and beak. Signs Lameness. Beading and fracture of ribs. Birds rest squatting. Beak soft. lesions. Avoidance of contamination of live vaccines is the main control measure practised. turkeys and ducks worldwide. 122 . Birds go off legs. Prevention Supplementation of vitamin D. Hock swelling. Rickets (hypocalcaemic) Introduction Vitamin D deficiency or phosphorus/calcium imbalance is seen in chickens. antioxidants.
Diagnosis History. Some countries have regulations governing the use of phosphorus in fertiliser with a view to reducing water pollution.Abubakar. Epiphyses of long bones enlarged. Parathyroids enlarged. proper calcium and phosphorus levels and ratio. Soft bones and beak. Post-mortem lesions Bones soft and rubbery. Hock swelling. Treatment Over-correct ration with 3 times vitamin D for 2 weeks. Signs Lameness. Poor growth. 123 . or vitamin D in drinking water. Birds rest squatting.M. Prevention Supplementation of Vitamin D. Intestinal diseases may reduce absorption. signs. Even subclinical levels of this condition can predispose to Femoral Head Necrosis.Tahir Rickets (hypophosphataemic) Introduction Phosphorus deficiency in chickens. Beak soft. Enlarged hocks. Reduction in bodyweight. antioxidants. Beading and fracture of ribs. This has led feed manufacturers to try various approaches to reduce added phosphorus in diets. lesions (analyse Vitamin A or manganese as a guide to premix inclusion). turkeys and duck is seen worldwide. Birds go off legs. Growth plates widened and disorganised.
shorter in young birds. stout white worms up to 12 cms in length. Use of a good electrolyte solution is beneficial in the acute stage of infection.Abubakar. Adult birds can tolerate burdens asymptomatically. The parasite species vary: A. are nematode worm parasites. pheasants. It is not known if vertical transmission occurs though virus has been occasionally isolated from embryonated eggs. galli in fowl. The 124 .submit 6 x . Roundworm. Control of secondary bacterial enteritis may require antimicrobial medication. seen worldwide. Virus may be found in asymptomatic birds. and A. The route of infection is oral and maximum viral excretion occurs 2-5 days post infection.Tahir Rotavirus Infection Introduction Rotavirus infection is seen in chickens. Prevention Good hygiene in brooding areas. dissimilis in turkeys. Post-mortem lesions Viruses replicate mainly in the mature villous epithelial cells. A. Diagnosis Demonstration of virus (PAGE. partridges and pigeons. except that the adults reside in the small intestine and earthworms are not significant paratenic or transport hosts. electron microscopy or Elisa on intestinal contents .5 g faeces). turkeys.M. Treatment No specific treatment for this infection.Ascaridia Introduction Ascaridia sp. Signs Diarrhoea. The route of infection is oral usually by direct ingestion of the embryonated egg and there is a 5-10-week prepatent period. The life cycle is similar to that illustrated in the section on the caecal worm Heterakis. large . columbae in pigeons. guinea fowl.
Diarrhoea. 125 . Listlessness. In the bottom left quadrant there are also some immature worms. oval smooth-shelled nonembryonated eggs in faeces. Diagnosis Macroscopic examination with identification of worms. pasture rotation and regular treatment. levamisole. Prevention Prevention of contamination of feeders and drinkers with faeces. mainly in young birds. A collection of mature roundworms (Ascaridia galli) recovered from the small intestine of a layer chicken in rear. Wasting. Post-mortem lesions Enteritis.parasites may be transported by grasshoppers and earthworms and are resistant to environmental effects. Treatment Flubendazole. Worms up to 12 cm in length in duodenum and ileum. Figure 31. especially for young birds. Signs Loss of condition. Poor growth. piperazine as locally approved.
M. Ruptures of ligaments and joints are also occasionally seen. Broiler parents and brown-shell egg layers are especially susceptible. Treatment None. Post-mortem lesions The fresh lesion contains a haematoma with the end of the ruptured tendon within or adjacent to it. Reoviral or staphylococcal arthritis or tenosynovitis may predispose but many cases have no evidence of an inflammatory response. 126 . Signs Severe lameness. Chickens are most commonly affected but it also infects turkeys. Infections still occur worldwide in non-commercial poultry but are rare in most commercial systems now. game birds. Diagnosis Signs and lesions are obvious. If there is a greenish tinge to the area of swelling it occurred a few days previously. Histology may be helpful in determining if there is an underlying inflammatory process. Salmonella Gallinarum.Tahir Ruptured Gastrocnemius Tendon Introduction This is a condition causing severe lameness in roaster type meat chickens and more rarely in turkeys. Prevention Establishment of a steady growth profile. canaries and bullfinches. Salmonella Gallinarum. The bird may have the hock dropped to the floor. Affected birds should be culled humanely as soon as they are identified. sparrows. Fowl Typhoid Introduction Disease caused by one of the two poultry-adapted strains ofSalmonella bacteria. guinea fowls. parrots. Avoidance of physical stresses on the musculoskeletal system through careful handling as well as careful design and layout of equipment. This can cause mortality in birds of any age.Abubakar. Broiler chickens have an avascular area of tendon just above the hock that is the usual site of rupture.
tetracylines. Signs Dejection. McConkey and non-selective agar is advisable. Enteritis of anterior small intestine. Differentiate from Pasteurellosis. both live (usually based on the Houghton 9R strain) and bacterins. 127 . Engorgement of kidneys and spleen. and/or congestion. surviving months. potentiated sulponamide. In clinical cases direct plating on Brilliant Green. even in adults. recovered birds are resistant to the effects of infection but may remain carriers. As with other salmonellae. Reluctance to move. clean chicks. Ruffled feathers. Treatment Amoxycillin. Diagnosis Isolation and identification. Vaccines for fowl typhoid have been used in some areas. Post-mortem lesions Bronzed enlarged liver with small necrotic foci. Tube and rapid plate agglutination tests have been the standard serological tests for many years but have only been validated for chickens. Prevention Biosecurity. fluoroquinolones.Morbidity is 10-100%. Yellow diarrhoea. mortality is increased in stressed or immunocompromised flocks and may be up to 100%. The bacterium is fairly resistant to normal climate. Anaemia. egg eating etc. but is susceptible to normal disinfectants. LPS-based Elisa assays have been developed but not widely applied commercially. Thirst. Inappetance. pullorum disease and coli-septicaemia. Transmission may be transovarian or horizontal by faecal-oral contamination. Enrichment procedures usually rely on selenite broth followed by plating on selective media. The route of infection is oral or via the navel/yolk.
The liver on the left is normal.Figure 32. Pullorum Disease. in young broiler chickens. mortality is increased in stressed or immunocompromised flocks and may be up to 100%. surviving months but is susceptible to normal disinfectants. game birds. Salmonella Pullorum. ring doves. Similar lesions can be seen in Pullorum Disease and with other causes of septicaemia in young chicks. pale and shows focal necrosis. 128 . Ruffled feathers. sparrows. Gasping. Closed eyes. Transmission may be transovarian or horizontal mainly in young birds and may sometimes be associated with cannibalism. this usually only causes mortality in birds up to 3 weeks of age. The bacterium is fairly resistant to normal climate. guinea fowls. Loud chirping. The route of infection is oral or via the navel/yolk. It affects chickens most commonly. but also infects turkeys. Occasionally it can cause losses in adult birds. White diarrhoea. Signs Inappetance. Morbidity is 10-80%. 'Bacillary White Diarrhoea' Introduction Disease caused by one of the two poultry-adapted strains ofSalmonella bacteria. parrots. Bacterial septicaemia caused by Salmonella Gallinarum. Depression. Lameness. Salmonella Pullorum. It still occurs worldwide in noncommercial poultry but is now rare in most commercial systems. ostriches and peafowl. the one on the right is slightly enlarged. Vent pasting. usually brown-shell egg layers.
Caecal cores. Paratyphoid. Many species are intestinal carriers and infection is spread by faeces. are capable of causing enteritis and septicaemia in young birds. Splenomegaly. S. Diagnosis Isolation and identification. Regardless of the initial source of the infection. Derby. fomites and feed (especially protein supplements but also poorly stored grain). Urate crystals in ureters. gizzard wall and heart. Montevideo. Differentiate from Typhoid. S. Typhimurium (which are considered separately). Anatum. Certain sero- 129 . paracolon. They infect chickens. Paratyphoid Infections Introduction Salmonellae bacteria other than the species specific sero-typesS. The route of infection is oral and transmission may be vertical as a result of shell contamination. but S. other enterobacteria. Vaccines are not normally used as they interfere with serological testing and elimination of carriers. Prevention Eradication from breeder flocks. chilling and omphalitis Treatment Amoxycillin. in the environment or in rodent populations. Morbidity is 0-90% and mortality is usually low. S. Newport. Enteritidis andS. In clinical cases direct plating on Brilliant Green. tetracylines. Even if these infections do not cause clinical disease. Gallinarum. turkeys and ducks worldwide. Sero-types vary. Intestinal or caecal inflammation. it may become established on certain farms. S. fluoroquinolones. Pullorum. Enrichment procedures usually rely on selenite broth followed by plating on selective media. McConkey and non-selective agar is advisable. S. and also other than S. their presence may be significant with respect to carcase contamination as a potential source of human food poisoning. As with other salmonellae. poteniated sulponamide. Bredeney are among the more common isolates. Salmonellosis. recovered birds are resistant to the effects of infection but may remain carriers. liver.Post-mortem lesions Grey nodules in lungs.
In clinical cases direct plating on Brilliant Green and McConkey agar may be adequate. Pericarditis. chilling. Differentiate from Pullorum/Typhoid. especially in dry dusty areas. applied at sufficient concentrations. other bacterial infections and ornithosis (in ducks). This approach is often used in the heat treatment of feed. inadequate water. Loss of appetite and thirst. S. Enteritis. However this has the potential to reveal the presence of salmonellae that are irrelevant to the clinical problem under investigation. The bacteria are often persistent in the environment. neomycin. Signs Signs are generally mild compared to host-specific salmonellae. Diarrhoea. fluoroquinolones. Predisposing factors include nutritional deficiencies. Closed eyes. Senftenberg in hatcheries). amoxycillin.g.types are prone to remain resident in particular installations (e.g. Rappaport-Vassiliadis) followed by plating on two selective media will greatly increase sensitivity. Vent pasting. Ruffled feathers. Enrichment media such as buffered peptone followed by selective broth or semi-solid media (e. but are susceptible to disinfectants that are suitable for the particular contaminated surfaces and conditions. other enterobacteria. Chemotherapy can prolong carrier status in some circumstances. Treatment Sulphonamides. Temperatures of around 80°C are effective in eliminating low to moderate infection if applied for 1-2 minutes. Post-mortem lesions In acute disease there may be few lesions. Dehydration. tetracyclines. Good management. Cheesy cores in caecae. Dejection. or absent. Diagnosis Isolation and identification. Foci in liver. Unabsorbed yolk. 130 . Focal necrotic intestinal lesions.
many species are intestinal carriers and infection may be carried by faeces. clean nests. Enteritidis and S. secondly. fumigate eggs. Salmonella Enteritidis. hatcheries and feed mills is required for effective control. these bacteria are often specifically cited in zoonosis control legislation. Many infected birds are culled and others are rejected at slaughter. inadequate water and other bacterial infections. breeding and grow-out farms. Temperatures of around 80°C are effective in eliminating low to moderate infection if applied for 1-2 minutes. The bacteria are often persistent in the environment.Typhimurium are presented separately from other sero-types of Salmonella because. 131 . Routine monitoring of breeding flocks. good feed. Salmonellosis. The prevalence of S. all-in/all-out production. elimination of resident infections in hatcheries. care in avoiding damage to natural flora. Feed and feed raw material contamination is less common than for other sero-types. Predisposing factors include nutritional deficiencies. on the one hand. chilling. especially in dry dusty areas. Vertical transmission may be either by shell contamination or internal transovarian contamination of yolk. This approach is often used in the heat treatment of feed. fomites and on eggshells. mills. and. has become much more common in both poultry and humans since the early 80s.Prevention Uninfected breeders. competitive exclusion. S. Infection results in a strong immune response manifest by progressive reduction in excretion of the organism and reduced disease and excretion on subsequent challenge. Typhimurium infections Introduction Salmonella Enteritidis and S. especially phage type 4. These are the predominant sero-types associated with human disease in most countries. The route of infection is oral. Infections in chickens. Vaccines are not generally used for this group of infections.Typhimurium has remained relatively stable though the spread of the highly antibiotic-resistant strain DT104 in various farmed species gives some reason for concern. but are susceptible to disinfectants that are suitable for the particular contaminated surfaces and conditions. because there are differences in the epidemiology as compared to other salmonellae. turkeys and ducks cause problems worldwide with morbidity of 0-90% and a low to moderate mortality. applied at sufficient concentrations.
breeding and grow-out farms. tetracyclines.g. clean nests. Closed eyes. Treatment Sulphonamides. other enterobacteria such as E. S. Foci in liver. fumigate eggs. Good management. Routine monitoring of breeding flocks. coli.Signs Dejection. good feed. fluoroquinolones in accordance with the sensitivity. neomycin. Stunting in older birds. Cheesy cores in caecae. Post-mortem lesions In acute disease there may be few lesions. mills.Enteritidiscauses cross-reactions which may be detected with S. all-in/all-out production. Lost of appetite and thirst.E. Enteritis. Dehydration. hatcheries and feed mills is required for effective control. Vent pasting. care in avoiding damage to natural flora. Diarrhoea. Misshapen ovules in the ovaries in S. competitive exclusion. It is possible to detect reactions with specific antigens in agglutination tests but competitive and direct Elisa tests are more commonly used today. Rappaport-Vassiliadis) followed by plating on two selective media will greatly increase sensitivity. However this has the potential to reveal the presence of salmonellae that are irrelevant to the clinical problem under investigation. Enrichment media such as buffered peptone followed by selective broth or semi-solid media (e. Focal necrotic intestinal lesions. amoxycillin. Ruffled feathers. Differentiate from Pullorum/Typhoid. Perihepatitis. Pericarditis. elimination of resident infections in hatcheries. In clinical cases direct plating on Brilliant Green and McConkey agar may be adequate. Early depletion of infected breeding stock is required in some countries such as those of the European Union. infection Diagnosis Isolation and identification. Chemotherapy can prolong carrier status in some circumstances. Prevention Uninfected breeders.Pullorum serum agglutination tests. Unabsorbed yolk. Infection 132 .
Some birds may 'lay' a caseous mass of pus (which may be found in a nest or on the egg belt). Lesions. Enteritidis and S. leaking urates. Post-mortem lesions Slight to marked distension of oviduct with exudate. Infection may spread downwards from an infected left abdominal air sac. are especially prone to increasing salpingitis. Vaccines are increasingly being used for S. Damaged vents. Typhimurium infection. Salpingitis Introduction Salpingitis is an inflammation of the oviduct. The control of infection in this area is probably achieved by ciliated epithelium that mostly wafts a carpet of mucus towards the cloaca.). Death. Peritonitis. coliand occasionally Salmonella spp. Bacteriology of oviduct. The oviduct is a hollow tube joining the normally sterile environment of the body cavity with the cloaca. Systemic viral infections that cause ovarian regression or damage to the oviduct or cloaca. Signs Sporadic loss of lay. It is a complex condition of chickens and ducks associated with various infections including Mycoplasma and bacteria (especially E. May form a multi-layered caseous cast in oviduct or be amorphous. Anything that damages the epithelium or disturbs normal oviduct motility is likely to increase the likelihood of salpingitis. both inactivated (bacterins) and attenuated live organisms. 133 . Distended abdomen. or may proceed upwards from the cloaca. Diagnosis Use the signs to select birds for culling and post-mortem investigation. which normally has many millions of potentially pathogenic bacteria.results in a strong immune response manifest by progressive reduction in excretion of the organism and reduced disease and excretion on subsequent challenge.
Treatment Multivitamins. Prevention Control any septicaemia earlier in life.Treatment Birds with well-developed lesions are unlikely to respond to medication. aspirin may be helpful if locally approved. Shaky Leg Syndrome Introduction A condition of turkeys with a course of often 3-4 weeks. 134 . possibly associated with tendon injury. use healthy parent flocks. Morbidity is 10-20%. Prevention Care in transport of brooded poults. Signs Stand on toes shaking. exclusion of other problems. Diagnosis Clinical examination. immunise effectively against respiratory viral pathogens common in the area. Post-mortem lesions None. Use of a suitable antimicrobial may be beneficial for birds in the early stages and if associated with efforts to minimise risk factors. releasing poults into larger areas and in handling heavier birds. Shaking or quivering of legs after rising.
Mortality drops off as sharply as it started. suggesting a viral component. Coma. Orange mucoid droppings. Avoidance of physical stress. Feed intake. Filtered intestinal contents from affected flocks appear to be capable of reproducing the condition. Treatment Leave affected chicks undisturbed. This appears to be a multifactorial condition. Avoidance of interruptions in feed supply. Prevention Good sanitation of the brooding house. typically 7-14day-old. electrolytes and glucose solution to flock. Death. Diagnosis Pattern of mortality. and/or carbohydrate absorption are disturbed resulting in a hypoglycaemia.Spiking Mortality of Chickens Introduction This is a condition characterised by a sudden increase in mortality in young. Birds in good condition die after showing neurological signs. Post-mortem lesions Mild enteritis. rapidly growing broiler chickens. Signs and lesions. Excess fluid in lower small intestine and caecae. probably because they are growing faster. Minimise stress. In order to reproduce the typical condition the affected birds are subject to 4 hours without feed and then a mild physical stress such as spraying with cool water. Signs Tremor. Males are more susceptible than females. Provide multivitamins. Paralysis. 135 . Dehydration.
Often diarrhoea with excessive urates. and occasionally by infected faeces. ducks. grouse and canaries with morbidity and mortality up to 100%. Necrotic foci. Spleen mottled with ecchymotic haemorrhages. It has been associated with typhilitis. Diagnosis Haematology. is an intestinal spirochaete that can be associated with inflammation of the large intestine in a broad range of mammals and birds. Weakness and progressive paralysis. 136 . Mucoid enteritis. vaccines in some countries. Liver enlarged with small haemorrhages. Drops in egg production may be seen in both systemic and intestinal forms Post-mortem lesions Marked splenomegaly. Cyanosis. and egg soiling in chickens. turkey. e. previously known as Serpulina pilosicoli. geese. The bacterium is poorly resistant outside host but may be carried by Argas persicus for 430 days.g.Spirochaetosis Introduction The bacterium Borrelia anserina infects chickens. Brachyspira pilosicoli. isolate in chicken eggs or chicks or poults. Prevention Control vectors. Thirst. Signs Depression. It is transmitted by arthropods. diarrhoea. reduced egg production. pheasants. Treatment Various antibiotics including penicillin. Argas persicus.
Treatment None. lesions. That on the left shows the typical lesion of spondylolisthesis. The sample on the right is normal. Post-mortem lesions Anterior-posterior rotation of the bodies of the last or penultimate thoracic vertebrae resulting in scoliosis just anterior to the kidney. Use of wings to help in walking.M. legs extended forward. Figure 33. Signs Sitting on hock or rumps.Abubakar. 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. Diagnosis Symptoms.Tahir Spondylolisthesis. with rotation of the body of the vertebra and the pinching of the spinal column that causes paralysis. 137 . These are cross-sections of the spinal column of 4-5-weekold broilers. May walk backwards. Prevention Selection for satisfactory conformation in primary breeding.
Staphylococcal Arthritis. Staphylococcosis. aureus and seen in chickens and turkeys worldwide. Morbidity is usually low and mortality 0-15% though affected birds will often be culled on humane grounds. Bumble Foot Introduction Caused by Staphylococcus bacteria. 138 . mainly S. Signs Legs splay and chick is unable to stand.Tahir Spraddle Legs or Splay Leg Introduction Occurs in all species in the recent hatchling. avoidance of excessive hatching egg storage.M. Wounds. Diagnosis Clinical signs. The type of chick box liners and the feeding papers used in the brooding house can also influence the occurrence of the condition.Abubakar. and careful monitoring of incubation conditions. Post-mortem lesions Gross lesions are not usually evident. Damaged skin due to nutritional deficiencies (such as of biotin) may also be a point of entry. Treatment None. These include good breeder nutrition. Infection is usually by the respiratory route with an incubation period of 2-3 days seen after artificial infection. Prevention All measures that improve chick vitality at hatching are beneficial in reducing this problem. and toe trimming may be a portal of entry with subsequent spread via the bloodstream to the typical sites of lesions. either accidental or induced by interventions such as beak trimming.
Low mobility. and imunosuppression. the hatchery and in any intervention or surgery (processing. and by fomites. Salmonella spp. This condition is a cause of sudden deaths in ducklings of 2-3 weeks of age. Differentiate from septicaemia or tenosynovitis due to Colibacillosis. Diagnosis Lesions. Streptococcus bovis Septicaemia Introduction An infection of ducks with the bacterium Streptococcus bovis.g. Treatment Antibiotics. Signs Ruffled feathers.. especially M. This may progress to abscess formation in these areas. e. Recovered birds may have some immunity but vaccination with staphylococci has not been found to be helpful in preventing the disease to date. Competitive exclusion with a non-pathogenic Staphylococcushas been shown to be effective (no commercial products yet available based on this technology). isolation and identification of pathogen. Some sudden deaths from acute septicaemia if very heavy challenge. Prevention Good hygiene in the nest. Predisposing factors include reovirus infection. in accordance with sensitivity. Possibly vaccination against reovirus infection. synoviae. particularly of parent birds. Infected joints may have clear exudate with fibrin clots. Lameness. Good management.Transmission occurs in the hatchery and in the general farm environment. 139 . Swollen above the hock and around the hocks and feet. Mycoplasma spp. trauma. Post-mortem lesions Tenosynovitis. toe clipping). low stress and prevention of immunosuppression from any cause will all tend to help. most commonly in the plantar area of the foot or just above the hock joint. chronic stress..
Affected well-grown birds may appear to have died from smothering. Haemorrhages in muscles and kidneys. isolation. Post-mortem lesions Intestine filled with feed. Sudden Death Syndrome.). Lung congestion and oedema. Post-mortem lesions Beak cyanosis. possibly metabolic. Treatment Amoxycillin. Splenic hyperplasia. extra care in the immediate post-brooding period. Livers heavier than those of pen-mates (as a percentage of bodyweight. the ventricles are empty.affected birds respond well to saline injection and will actively seek out salt scattered in the litter. Serum accumulation in lung (may be little if examined shortly after death). 140 . Liver congestion. Leg weakness or incoordination in a few birds. The atria of the heart have blood. 'Flipover' Introduction A condition of broiler chickens of unknown cause. Prevention Good husbandry and hygiene.Signs Sudden deaths. Diagnosis History. Signs Sudden death in convulsion. most are found lying on their back. lesions. Sodium deficiency can appear very similar at about the same age . It can be induced by lactic acidosis and about 70% of birds affected are males.
feed restriction. or birds' access to them. Signs It is doubtful if any signs are produced under most circumstances. use of dawn to dusk simulation and avoidance of disturbance. Prevention Lowering carbohydrate intake (change to mash). Treatment None possible. Most have intermediate invertebrate hosts such as beetles or earthworms.Diagnosis Birds found on back with lack of other pathology. Tapeworms. Prevention Control the intermediate hosts. 141 . Cestodes Introduction Cestodes are tapeworms that are seen in many species. Check your local regulations. Treatment Flubendazole is effective at a 60 ppm in diet. they may not be host specific. low intensity light. Diagnosis Identification of the presence of the worms at post-mortem examination. lighting programmes. however it may not have a zero withdrawal in commercial egg layers. Post-mortem lesions Occupy space in intestine and create small lesions at point of attachment.
distal tibia. Microscopically . turkeys and ducks. in decreasing order of frequency. Post-mortem lesions Plug of cartilage in proximal end of tibia. small ovoid lacunae and more matrix than normal. modifications of calcium and phosphorus ratios. and proximal metatarsus. Swelling and bowing in the region of the knee joints.a mass of avascular cartilage with transitional chondrocytes. 142 .Figure 34. Diagnosis Gross pathology. It may be associated with rapid growth and have a nutritional factor. Prevention Genetic selection using the Lixiscope to identify bone phenotype. Vitamin D3 supplementation. Differentiate from rickets. Treatment None. Lameness. TD Introduction A complex condition seen in chickens. mild lesions may require histology to distinguish from other problems. Mature tapeworms with their heads (scolices) embedded in the intestine. Tibial Dyschondroplasia. Lixiscope may identify in vivo as early as 2 weeks of age. chloride levels and acid/base balance. Signs There are usually no signs unless the condition is severe.
Weakness. Reduced productivity. Transmission is lateral with birds and faeces. Bluecomb Introduction Some coronaviruses involved in this condition are considered to be bovine coronaviruses (or closely related thereto). Transmissible Enteritis. Skin blemishes. and is also found on mammals.Abubakar. Diagnosis Identification of the presence of the parasites. with 143 . others are avian coronaviruses closely related to infectious bronchitis virus. Post-mortem lesions Anaemia. It is more common in warm climates. Signs Anaemia. spends little time on host. Morbidity is close to 100% and mortality is 5-100%. than in commercial poultry in temperate climates.M. These parasites are more likely to be a problem of small scale poultry production in the tropics. The infection is seen in turkeys and sometimes pheasants. and may also transmit spirochaetosis and Pasteurella infection. Prevention As for red mite control. Insecticide sprays in these areas are more likely to be effective than treatment of the birds. Treatment Elimination of cracks and crevices in the poultry housing. Emaciation. Occasionally paralysis from toxins in the tick saliva.Tahir Ticks Introduction Argas persicus is an external parasite of poultry and wild birds.
rapid spread. The course of the disease is about 2 weeks and birds then remain carriers for months. The viruses survive in frozen faeces for months.
Anorexia. Depression. Frothy diarrhoea. Subnormal body temperature. Darkening of the head. Loss of weight. Huddling.
Dehydration. Emaciation. Enteritis with petechial haemorrhages. Froth ingesta. Sometimes casts. Pancreas chalky. Urates in kidneys/ureters.
Reproduction with filtered contents, isolation in turkey eggs, electron microscopy, immunofluorescence, Elisa. Commercial M4I IB Elisa will detect some infections.
Warmth and good management, antibiotics, milk replacer, potassium chloride. Disinfect and rest houses for 3-4 weeks.
All-in/all-out production, good hygiene and biosecurity, good management.
Trichomoniasis, Canker, Frounce
Trichomonas gallinae is a protozoan parasite of pigeons and doves (canker), raptors (frounce), turkeys and chickens. It has variable pathogenicity. Morbidity is high and mortality varies but may be high. Transmission is via oral secretions in feed and water, and crop milk.
Mouth open. Drooling and repeated swallowing movements. Loss of conditon. Watery eyes in some birds. Nervous symptoms (rare).
Yellow plaques and raised cheesy masses in mouth, pharynx, oesophagus, crop and proventriculus. Raptors may have liver lesions.
Lesions, large numbers of protozoa in secretions. Differentiate from Pox and candidiasis.
Previously approved products included dimetridazole, nithiazide, and enheptin. Organic arsenical compounds (where approved) and some herbal products may be of some benefit in managing this problem in food animals.
Eliminate stagnant water, eliminate known carriers, add no new birds.
A bacterial infection, caused by Mycobacterium avium, of poultry, game birds, cage birds etc. Morbidity and mortality are high. Transmission is via faecal excretion, ingestion, inhalation, offal and fomites. The disease has a slow course through a flock. The bacterium resists heat, cold, water, dryness, pH changes and many disinfectants.
Severe loss of weight with no loss of appetite. Pale comb. Diarrhoea. Lameness. Sporadic deaths.
Grey to yellow nodules attached to intestine. Granulomas in liver, spleen and many other tissues, even bone marrow.
Isolation, acid-fast stain in tissues, TB test. Differentiate from Lymphoid leukosis.
Market after one season, hygiene, cages, elimination of faeces etc.
A condition of turkeys possibly associated with Bordetella avium(previously designated Alkaligenes faecalis) infections. This bacterium usually causes mild respiratory disease in only a proportion of the flocks, and low mortality. It can be synergistic with other respiratory pathogens such as Ornithobacterium,Pasteurella spp, Mycoplasma spp. and pneumoviruses.
Decreased appetite, weight gain and feed efficiency. Loss of voice. Ocular and nasal discharge. Conjunctivitis. Snick. Dyspnoea.
Excessive mucus in nasal passages and trachea. If there is secondary E. coli infection then pneumonia, airsacculitis and perihepatitis.
Clinical signs, isolation of agent.
maternal antibody may protect. Morbidity is 10-100% and mortality 1. Treatment Antibiotics are not very effective. 147 . Signs Decreased appetite. chlorinate drinking water. possibly involving fomites. chlorination of drinking water. control respiratory stressors. Ocular and nasal discharge.Antibiotics are not very effective.live primer followed by inactivated. Sudden drop in production that lasts 2-3 weeks.30%. Serology. Prevention All-in/all-out production. isolation of ciliostatic agent. Eggs depigmented and thin-shelled. Good drinking water hygiene. vertical transmission is uncertain. Diagnosis Signs. Paramyxoviridae. Prevention All-in/all-out production. vaccination . Post-mortem lesions Serous rhinitis and tracheitis. Loss of voice. Turkey Rhinotracheitis (Adult) Introduction A disease of turkeys caused by the viruses of the Pneumovirus genus. Rapid transmission occurs laterally. control respiratory stressors.
sometimes pus in bronchi. If there is secondary E. mortality is 1-25%. 148 . Prevention All-in/all-out production. possibly involving fomites. Turkey Viral Hepatitis Introduction An infection of turkeys caused by an unidentified virus. Diagnosis Clinical signs. Snick. weight gain and feed efficiency. isolation and identification of the ciliostatic virus. Transmission may be by direct or indirect contact and possibly vertical. Rapid transmission occurs laterally.30%. Paramyxoviridae. Birds remain carriers for up to 16 days. Signs Decreased appetite. Post-mortem lesions Serous rhinitis and tracheitis. serology (using an Elisa test to demonstrate rising titre). Sinusitis. Loss of voice. control respiratory stressors. Conjunctivitis. vertical transmission is uncertain. Morbidity varies. coli infection then pneumonia.Tahir Turkey Rhinotracheitis (in rear) Introduction A disease of turkeys caused by the viruses of the Pneumovirus genus. Ocular and nasal discharge. chlorinate drinking water. maternal antibody may protect. Vaccination at day-old seems to be most effective. Treatment Antibiotics are not very effective. Morbidity is 10-100% and mortality 1. airsacculitis and perihepatitis.Abubakar.M. Dyspnoea.
Signs Lameness. Congestion. Post-mortem lesions Grey foci (c. Various angulations of leg.Signs Signs are usually subclinical. nutrition. with good management many birds recover. Morbidity is 1-20% and mortality is low. Grey to pink foci in the pancreas. Depression and sporadic deaths in birds in good condition. Microscopically . Factors involved may include genetics. Valgus/varus. Focal haemorrhage. bacterial and fungal infections. 1 mm) coalescing. Post-mortem lesions Linear twisting of growth of long bones. environment and high growth rate. Distortion at hock. Gastrocnemius tendon may slip. 149 .no inclusion bodies. Bile staining. Treatment None. Twisted leg Introduction A complex condition seen in chickens and turkeys. Differentiate from histomonosis. Diagnosis Isolation in CE. lesions pathognomonic. Prevention Good sanitation and management.
brunetti). Changed angulation of tibial condyles. IBDV and overcrowding. game birds and pigeons may also be affected. Prevention Selection for good conformation in primary breeding. Differentiate from perosis. Post-mortem lesions Deep ulcers throughout intestine. Quail disease Introduction Ulcerative Enteritis is an acute. tenella. Adoption of optimal nutrition and growth patterns for the economic objectives of the production system. Predisposing factors include Coccidiosis (especially E. highly contagious disease of chickens and quail caused by the bacterium Clostridium colinumand characterised by ulcers of the intestines and caecae. Treatment None. necatrix. Watery white faeces (quail). but mainly ileum and caecae. greater than 20% is abnormal. Anaemia. lesions. Retracted neck. intertarsal angulation up to 10% is physiological. Diagnosis Symptoms.. Blood in intestine. Partially closed eyes. 150 . Turkeys. The condition occurs worldwide. and E. The route of infection is oral and transmission is from faeces of sick or carrier birds or via flies. It can start suddenly and cause high mortality: 100% in quail and 10% in chickens. Diarrhoea. The bacterium resists boiling for 3 minutes. Signs Listlessness. Pale yellow membranes. Ulcerative Enteritis. Drooping wings. arthritis and synovitis. Peritonitis (if ulcers penetrate). E. which may coalesce and may be round or lenticular. Ruffled feathers.
possibly probiotics. coccidiosis. Confirmation is on absence of other diseases and isolation of Cl. Transmission is by faecal contamination. Loss of condition. amoxycillin. Bacitracin. The infective agent is rather resistant to environment and disinfectants. penicillin (50-100 ppm in feed). 151 . Figure 35. Diagnosis A presumptive diagnosis may be made on history and lesions. necrotic enteritis. trichomoniasis. Response to treatment should occur in 48 to 96 hours. Prevention Infection-free birds. all-in/all-out production. Signs Dejection. salmonellosis. Avian Infectious Hepatitis Introduction An insidious onset disease of chickens caused by Vibrio bacteria. Tetracyclines. Necrotic foci in liver. colinum in anaerobic conditions (the agent is often present in pure culture in liver). Differentiate from histomonosis ('Blackhead'). Treatment Streptomycin (44 gm/100 litres water). and disease is precipitated by stress. Inappetance. Diarrhoea. low level antibiotics as per treatment. Treat for coccidiosis if this is a factor. Morbidity is low. birds remaining carriers for months. multivitamins. Wall of the caecum of a chicken suffering from ulcerative enteritis Vibrionic Hepatitis.
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.
As in the case of other nutritional deficiencies. Microscopically . Excessive urates in kidneys and ureters. antioxidant.Abubakar. infectious sinusitis etc.Tahir Vitamin A Deficiency. Diagnosis Signs. feed formulation. Signs Poor growth. Pale comb and wattles. good quality raw materials. Treatment Vitamin A in drinking water. Differentiate from Infectious coryza. Pustules in mouth and pharynx. Prevention Supplementation of diet with vitamin A. classic signs of deficiency are very rare in commercial poultry fed complete diets.squamous metaplasia of epithelia.M. Nutritional Roup Introduction Vitamin A deficiency is occasionally seen in chickens and turkeys (insufficient vitamin A during 1-7 weeks of age). Eyelids stuck shut with thick exudate. Nasal and ocular discharge. Post-mortem lesions Eyelids inflamed and adhered. Poor feathering. 155 . chronic fowl cholera. Drowsiness. lesions.
damage to the intestine or increased demand for some reason may have an effect. exclusion of specific diseases. because a continuous supply is required. They act in a broad range of metabolic pathways.M. Most will reduce productivity. including growth in the young animal. The embryo is particularly dependent on having adequate supplies of vitamins deposited in the egg. See the separate discussion under Chondrodystrophy and Fatty Liver and Kidney Syndrome. and egg production in the layer. Diagnosis Signs. Simple deficiency is now rare as diets are usually well supplemented. 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 . Vitamin deficiencies are especially prone to cause problems of hatchability.Tahir Vitamin B Deficiencies Introduction The B complex vitamins are water soluble and not stored to any significant extent in the body.Abubakar. Some deficiencies induce characteristic microscopic effects. response to supplementation. However. Signs These may be summarised: Perosis Curled Toe Paralysis Paralysis/'Stargazing' Dermatitis/Scaly Skin Mouth Lesions Conjunctivitis Anaemia Fatty Liver and Kidney Syndrome Poor Feathering Loose feathers Hatchability problems Embryo with clubbed down Thiamine (B1) Riboflavin (B2) Pantothenic acid Pyridoxine (B6) Niacin Folic Acid Cyanocobalmin (B12) Biotin Post-mortem lesions Usually the gross lesions are non-specific.
Falling over. Staggering. Necrosis. 157 . Exudative Diathesis. drinking water supplementation with that vitamin is ideal and usually results in a rapid response in birds that are still drinking. Encephalomalacia and exudative diathesis tends to be seen in young birds of 1-5 weeks of age. characterised by oxidation of various tissues and caused by Vitamin E deficiency.may be appropriate (faster. Haemorrhage. Uncontrolled movements. Signs Imbalance. Steatitis. The balance of vitamins present should be similar to the daily nutritional requirement of the stock concerned. Good quality multivitamin solutions are beneficial in the supportive care of a range of problems characterised by reduced feed intake. Blood-stained or greenish subcutaneous oedema. Paralysis. Muscular dystrophy is seen more frequently in older and mature birds. The problem is associated with feed rancidity typically in diets with high fat. Encephalomalacia. Green wings. Treatment If a specific vitamin deficiency is suspected. Post-mortem lesions Swollen cerebellum with areas of congestion. 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. seen worldwide. White streaks in muscle. Ventral oedema. occasionally ducklings and other birds. Vitamin E Deficiency. Muscular Dystrophy Introduction A spectrum of diseases of chickens and turkeys. less expensive) to analyse feed for a marker substance such as manganese rather than testing for vitamin levels.
necrotic dermatitis. Pseudomonas. Various bacteria may be involved. Abnormal yolk sac contents (colour.Diagnosis Signs. Signs Dejection. Diarrhoea. Differentiate from Encephalomyelitis. It is seen where there is poor breeder farm nest hygiene. feed rancidity. 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. and poor hygiene of setters.coli. antioxidant. Prevention Proper levels of vitamin E. histopathology. Loss of appetite. response to medication. 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. use of floor eggs. Morbidity is 1-10% and mortality is high in affected chicks. Post-mortem lesions Enlarged yolk sac with congestion. selenium. Disease occurs after an incubation period of 1-3 days.Proteus. good quality raw materials. Treatment Vitamin E and/or selenium in feed and/or water. hatchers or chick boxes. 158 . especially E . for example poor hygiene of hatching eggs. Closed eyes. lesions. inadequate hatchery hygiene or poor incubation conditions. toxicities. Omphallitis Introduction A condition seen worldwide in chickens. Swollen abdomen. consistency) that vary according to the bacteria involved. Staphylococci. Vent pasting. Yolk Sac Infection. 'bangers'. Broad-spectrum antibiotics where there are extensive skin lesions.
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.Diagnosis A presumptive diagnosis is based on the age and typical lesions. Treatment Antibiotics in accordance with sensitivity may be beneficial in the acute stages. clean nests. most will die before 7 days of age.g. frequent collection. Differentiate from incubation problems resulting in weak chicks. separate incubation of floor eggs etc. 159 . exclusion of severely soiled eggs. There should be routine sanitation monitoring of the hatchery. sanitation of eggs. however the prognosis for chicks showing obvious signs is poor. Multivitamins in the first few days may generally boost ability to fight off mild infections.