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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.
sulphonamides in feed. correct house relative humidity. from long-term intestinal carriers. rigid depopulation and disinfection. older birds are asymptomatic carriers. Signs Dejection. adequate protection. transovarian. feed etc. Inappetance. Huddling near heat. Arizona infection. and is not present in the UK turkey population. 'hardening off'. Paralysis. through faecal contamination of environment. cloudiness in eye. Arizonosis Introduction Caused by the bacterium Arizona hinshawii. Erosions of the cartilage of the hock joint in a duck with chronic Riemerella anatipestifer infection. It affects turkeys.Prevention Good husbandry and hygiene. Cheesy plugs in intestine or caecum. Blindness. Mortality is 10-50% in young birds. Congestion of duodenum. mainly in North America. Autogenous bacterins sometimes used. Transmission is vertical. Nervous signs. Post-mortem lesions Enlarged mottled liver. Unabsorbed yolk sac. Inactivated and attenuated vaccines available in some countries. renamed Salmonella Arizonae. reptiles. 4 . and also horizontal. Foci in lungs. Figure 40. Diarrhoea. rodents. Vent-pasting.
Thickening of atrioventricular valve. Post-mortem lesions Thickening of right-side myocardium. mortality 1-2% but can be 30% at high altitude. Salpingitis. poor ventilation and physiology (oxygen demand. methods as per Salmonella spp. Formerly in-feed medication with nitrofurans was also used. or gentamycin at the hatchery is used in some countries. Morbidity is usually 1-5%. Poor development. Severe muscle congestion. Pulmonary arterial vasoconstriction appears to be the main mechanism of the condition. may be related to type of stock and strain). Recumbency. Lungs and intestines congested. Perihepatitis. The disease has a complex aetiology and is predisposed by reduced ventilation. Ascites is a disease of broiler chickens occurring worldwide but especially at high altitude. General venous congestion. and respiratory disease. inject eggs or poults with antibiotics. high altitude. coli-septicaemia. fumigation of hatching eggs. Progressive weakness and abdominal distension. Signs Sudden deaths in rapidly developing birds. monitor sensitivity. Prevention Eradicate from breeder population. Differentiate from Treatment Injection of streptomycin. 5 . Pericarditis. Dilation of the ventricle. Possibly cyanosis. spectinomycin. Diagnosis Isolation and identification. Ascites Introduction Associated with inadequate supplies of oxygen. Dyspnoea. Ophthalmitis. salmonellosis. good nest and hatchery hygiene.
Drowsiness. especially in young chicks. etc. Differentiate from broiler Sudden Death Syndrome and bacterial endocarditis. penguins. Diagnosis Gross pathology is characteristic. but may be as high as 12%. 6 . Mortality among young affected birds is 5-50%. in which the typical sign is gasping for breath. Microscopic . avoid any genetic tendency. Rapid breathing. Ascites. The infection has an incubation period of 2-5 days. Thirst. A cardiac specific protein (Troponin T) may be measured in the blood. game birds. Pericardial effusion. Prevention Good ventilation (including in incubation and chick transport). Spleen small. Transmission is by inhalation exposure to an environment with a high spore count. Silent gasping. Treatment Improve ventilation. Spores are highly resistant to disinfectants. Sometimes the same organism causes eye lesions or chronic lesions in older birds. waterfowl. Morbidity is usually low. It affects chickens. Liver enlargement. Occasionally similar lesions are produced by other species ofAspergillus or even other fungi such as Penicillium. Nervous signs (rare).cartilage nodules increased in lung. control respiratory disease. Vitamin C (500 ppm) has been reported to be of benefit in South America. The fungus can infect plant material and many species of animals including birds and man. ducks. caused by Aspergillus fumigatus. Signs Acute form: Inappetance. Absidia etc. turkeys. worldwide. there is usually little bird-to-bird transmission. This may offer the ability to identify genetic predisposition. Aspergillosis Introduction A fungal infectious disease. Weakness.
turkeys. The powdery surface is dark green in colour. typically by putting small pieces of affected tissue on Sabouraud agar. The means of transmission is unknown but 7 . Environmental spraying with effective antifungal antiseptic may help reduce challenge. pheasants and occurs in most poultry-producing countries. Brain lesions may be seen in some birds with nervous signs. Amphotericin B and Nystatin have been used in high-value birds. Diagnosis This is usually based on the signs and lesions and microscopic examination for the fungus. See Avian Encephalomyelitis.M. Figure 8. trachea. Avian Encephalomyelitis Egg Drop Introduction Avian encephalomyelitis virus infection in laying bird causes inapparent infection or drops in egg production. hygiene. Growth occurs in 24-48 hours and colonies are powdery green/blue in appearance. plaques in peritoneal cavity. 'Furry' airsacculitis in aspergillosis of an adult duck. Morbidity 5-60%.Abubakar. Wasting. preferably after digestion in 10% potassium hydroxide.Tahir 2 Chronic Forms: Ocular discharge (ocular form only). It affects chickens. good quality litter and feed. It may be confirmed by isolation of the fungus. Thiabendazole or Nystatin has been used in feed. Epidemic tremors for its effect in young birds. Conjunctivitis/keratitis. Treatment Usually none. air sacs. Differentiate from excessive exposure to formalin or vaccinal reactions in day olds and from heat stress in older birds. quail. Prevention Dry. mortality none. may have greenish surface. Post-mortem lesions Yellow to grey nodules or plaques in lungs.
feed. small (5-10%) and lasting no more than 2 weeks. Immunity is usually long lasting. Differentiate from Infectious Bronchitis. EDS76. Dull expression. rising titre to AE virus. attenuated or not. water etc. and quail. and there is serious disease in the progeny (see next section). Imbalance. Predisposed by immunosuppression.The embryo protection test has been used in the past. transmission occurs over about 1-2 weeks. Signs Nervous signs. It has a worldwide distribution. mortality high. Prevention Vaccination of breeders/layers at 9-15 weeks. Virus in faeces may survive 4 weeks or more. Epidemic Tremors Introduction Avian encephalomyelitis is a viral disease of the central nervous system of chickens. Treatment None. The route of infection is transovarian with an incubation period of 1-7 days. some lateral. Diagnosis History. now Elisa is used more commonly. Post-mortem lesions None. Serology . Morbidity 5-60% depending on the immune status of the majority of parents. Signs Drop in egg production. Ataxia and sitting on hocks.probably by faecal contamination of environment. In breeders there may be a drop in hatchability of about 5%. with an oral infection route. lateral transmission is probably by the oral route. turkeys. lentogenic Newcastle disease. Avian Encephalomyelitis. subsequent disease in progeny if breeders. pheasants. incubation >10 days. 8 . Paralysis. Virus in faeces may survive 4 weeks or more. Vertical transmission is very important.
This viral disease can cause exceptionally high mortality. A few recovered birds may develop cataracts weeks after infection. vitamin deficiency (E. ducks. Effectively all 9 . Brain abscess. and isolates are designated sero-type/ species/location/reference number/year/subtype designation(H/N). Fowl One of only two 'Class A' diseases of poultry targeted for emergency disease control measures by OIE. Microscopic . The virus infects chickens. pigeons. 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. Mycotic Encephalitis. The embryo protection test has been used in the past. Post-mortem lesions Gross lesions are mild or absent. The higher the proportion of the chickens dying or showing signs the higher the IVPI. and lack of significant lesions. and/or viral isolation may be carried out if required. neck and wings. attenuated or not. Marek's disease. In addition official control measures disrupt trade in poultry products from affected areas. Enterococcus hirae infection. Prevention Vaccination of breeders at 9-15 weeks. The definitive classification of high pathogenicity is an intravenous pathogenicity test (IVPI) in 6-week-old chickens result of greater than 1. toxicities. especially in turkeys. pheasants. A. Tremor of head. The cause is a virus. Orthomyxovirus type A. partridges. and ostriches.2 . the equivalent of the World Health Organisation for animal diseases. Histopathology is usually diagnostic and IFA. There may be focal white areas in gizzard muscle (inconstant). Immunity is long lasting. riboflavin).nonpurulent diffuse encephalomyelitis with perivascular cuffing. turkeys. EE (especially in pheasant in the Americas). Tremor may be inapparent but is accentuated if chicks are held inverted in the hand. its pathogenicity is variable. quail. Differentiate from Newcastle disease. now Elisa is used more commonly. signs. Avian Influenza-Highly Plague Introduction Pathogenic (HPAI). 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. Treatment None.
air sacs and conjunctiva. reduced feed consumption. trachea. equipment. Diarrhoea (often green). Infections with other pathogens (e. from December 1999. Avirulent in one species may be virulent in others. Nervous signs such as paralysis. Swollen face. Highly pathogenic avian influenza A (HPAI) viruses of the H5 and H7 HA subtypes have been isolated occasionally from free-living birds. and the high mortality that 'low-path' AI can cause in turkeys. can survive 4 days in water at 22°C. Transmission is by direct contact with secretions from infected birds. by acid pH. Cessation of normal flock vocalisation. Mexico and. Drops in egg production. Because of this. More recently outbreaks have occurred in Australia. The route of infection is probably oral initially. over 30 days at 0°C. by oxidising agent and by formalin and iodine compounds. conjunctivitis or severe pneumonia. Pasteurella) may increase mortality. Marked loss of appetite. See current OIE records for up to date information on distribution of HPAI. A serious outbreak occurred in The Netherlands in 2003 with a few linked cases in Belgium and one in Germany. Avian Influenza is a potential zoonosis. Nasal and ocular discharge. drinking water. Ovarian regression or haemorrhage.birds are considered to be at risk of infection. especially faeces. waterfowl. in the years 1983-84. Morbidity is high but mortality usually relatively low. The virus is moderately resistant. Signs Sudden death. Outbreaks due to HPAI were recorded in the Pennsylvania area. 10 . but possibly by the conjunctival or respiratory route and the incubation period is 3-5 days. Coughing. even with 'low pathogenicity' strains. Pakistan. It can result in inapparent infection. The small number of human deaths associated with HPAI appear to have resulted from direct exposure to infected birds on farm or in markets. The virus replicates mainly in respiratory tissues of chickens and turkeys but in the intestinal tract of clinically normal waterfowl. 550%. Apathogenic and mildly pathogenic influenza A viruses occur worldwide. OIE and other bodies are currently examining ways to improve control of LPAI. Depression. Cyanosis of comb/wattles. USA. It can remain viable for long periods in tissues. clothing. It is inactivated by a temperature of 56°C in 3 hours and 60°Cin 30 min. Post-mortem lesions Inflammation of sinuses. Italy). in northern Italy.g. H5 viruses of low pathogenicity may become highly pathogenic usually after circulating in poultry flocks for a time (Pennsylvania. Broken contaminated eggs may infect chicks in the incubator simulating vertical transmission.
21-day interval to re-stocking should be followed. Survivors can be expected to have a high degree of immunity but may harbour virulent virus. disinfection. It has occured in Europe. lesionless carriers of highly pathogenic virus. although it may reduce losses initially. Dehydration. all-in/all-out production. Prevention Hygiene. infectious laryngotracheitis. Muscles congested. Necrosis of skin of comb and wattles. Transmission is by congenital infection from antibody-negative females. However. lateral transmission by faecal-oral route (this declines as the bird ages). but good husbandry. controlled marketing of recovered birds. This condition has until now been seen only in meat-type chickens. HA+. Turkey lesions tend to be less marked than those of chickens. Eradication by slaughter is usual in chickens and turkeys. correct disposal of carcases. Haemorrhage in proventricular and gizzard mucosae and lymphoid tissue of intestinal tract. nutrition and antibiotics may reduce losses. The incubation period is 10-20 weeks. North and South America. Commercial Elisa test kits are now available. DID+. other respiratory infections. isolation. Treatment None. To be effective inactivated vaccines must be the right subtype for the particular situation (H5 will not protect against H7 and vice versa). Minimise contact with wild birds. Congenitally infected birds tend to remain 11 . In outbreaks a regime of slaughter. Subcutaneous oedema of head and neck. Myelocytomatosis Introduction Caused by an avian retrovirus. though there is high mortality of affected birds. cleaning. bleeding and vaccination needles. while ducks may be symptomless. NDV-. Vaccines have been used in recent outbreaks in Mexico and Pakistan. Morbidity is low. Diagnosis A presumptive diagnosis may be made on history and postmortem lesions. Confirmation is by viral isolation in chick embryo. Avian Leukosis (Serotype J). Vaccination is not normally recommended because. with considerable strain-to-strain variation. etc. as with many such tests occasional false positive reactions can occur. The agar gel precipitation test is non-group-specific and is used to confirm any positives. bacterial sinusitis in ducks. quarantine. vaccinated birds may remain carriers if exposed to the infection. fowl cholera. Differentiate from Newcastle disease.
Minimise stress.only 3% produced infected chicks. histology. Loss of weight. Serology . PCR testing of embryonally infected chicks using DNA testing is uniformly positive for blood and faecal samples. Many are asymptomatic. There is also evidence that it is slightly more sensitive than conventional testing. Virus survival is poor but sufficient to allow cross contamination in hatcheries and on farm in rear. lesions.tumours usually contain well-differentiated myelocytes. Prevention Checking of antigen in the albumen is a basis for eradication . Prevent/ reduce cross-infection in hatchery and on farm. Lymphoid Leukosis. 'nonshedders' . shed virus and develop tumours. Splenomegaly and enlarged kidneys also occur. liver. Differentiate from Marek's disease. Most characteristically are chalky white tumours in the bone marrow. 'Shedders' . Emaciation.antibody negative. sacral joint. Two cell types may be found in the same tumour. preferably on separate hatch days and in separate machines. Microscopic . Treatment None. Separation in vaccination. Handle clean lines before infected lines. particularly of the sternum. Enlargement of abdomen. Signs Depression. Critical hatchery practices: Separate infected and uninfected lines.most but not all. age. Post-mortem lesions Liver enlargement. often with tumour foci. Persistent low mortality.80% produce infected chicks. ribs. Diagnosis History. birds with egg antigen will be antibody negative. ultimately identification of virus by isolation and/or PCR.an Elisa test is aviailable to identify antibody positive birds. 12 .
The causative viruses are rapidly inactivated at ambient temperature and on exposure to most disinfectants. Minimise group sizes. erythroblastosis. cytology. Persistent low mortality. other tumours. coligranuloma. Avoid migration errors (birds unintentionally moving between pens). especially in young birds. it may be as short as 6 weeks for some of the other manifestations. Signs Depression. Liver may be very large. Leukosis/Sarkoma Group Introduction Lymphoid Leukosis. osteopetrosis. Emaciation.cells lymphoplastic Diagnosis History. myeloblastosis (see Sero-type J). initially in the bursa. then liver. Microscopic . Differentiate from Marek's disease. Avian Leukosis. There may be increased susceptibility to other infectious diseases due to damage to the immune system. lateral transmission is poor but infection may occur by the faecal-oral route. Delay live vaccine challenges. spleen. myxosarcomas. age. Post-mortem lesions Focal grey to white tumours. Mortality tends to be chronically higher than normal for a prolonged period. kidney etc. It affects chickens worldwide with susceptibility varying considerably among different strains and types of stock . Many are asymptomatic. A complex of viral diseases with various manifestations such as lymphoid leukosis. Egg production is somewhat reduced. Vertical transmission is most important by infection of the egg white in infected breeders (who are long-term carriers). liver or bursa. 13 .egg layers are generally more susceptible to lymphoid leukosis. fibrosarcomas. Morbidity is low but mortality high. Loss of weight. In lymphoid leukosis the incubation period is about 4-6 months.Farm practices: Brood and rear lines separately and maintain separate for as long as possible. lesions. Enlargement of abdomen.
Conjunctivitis. As for many infections. It is caused by a pneumovirus of the Paramyxoviridae family. morbidity is 10-100% and mortality can be 110%. Diffuse lymphoid tumours in an enlarged liver from a mature broiler parent hen. Avian Rhinotracheitis 'Swollen Head Syndrome' Introduction A viral disease of chickens. control arthropods.Treatment None. South America and North America. guinea fowl and possibly pheasants seen in Europe. all-in/all-out production. Snick. Two subgroups have been identified on the basis of the G-protein sequence: A (original UK isolates) and B (original southern Europe isolates). Prevention Good hygiene. Ocular and nasal discharge. vertical transmission is uncertain. Figure 9. Loss of voice. Africa. Dyspnoea. turkeys (see separate summary). The incubation period is 5-7 days. fomites can be important in moving infection between farms. There is rapid lateral transmission with infection by aerosol through the respiratory route. eradication . 14 . weight gain and feed efficiency. This was a case of Myelocytoma Avian Leukosis (Sero-type J). Signs Decreased appetite. Facial and head swelling (though this can occur in other conditions).checking of antigen in the albumen is a basis for eradication (see Sero-type J for details). first isolated from poults in South Africa in 1978.
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.
Histopathology may also be used but the findings are not specific to this condition. 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. 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. 18 . Post-mortem lesions See signs. Must be confirmed by laboratory tests. Drinking water which is well chlorinated should be helpful in reducing challenge by this route. Scabs around eyes and beak. Elisa tests have been developed experimentally. It may be helpful to control other conditions which may be occurring at the same time. Reduced feed intake and blood sugar can precipitate fatty liver and kidney syndrome. Signs Poor growth. in embryos. Good biosecurity. Thickened skin under foot pad. Lung congestion Ovarian regression Yolk peritonitis Pale foci and haemorrhages in pancreas. A RT-PCR test may be used to detect viral RNA in tissues. Pale livers and kidneys in fatty liver and kidney syndrome. Biotin Deficiency. Sudden deaths in fatty liver and kidney syndrome. Leg weakness. Viral particles may be demonstrated in bile. Treatment No specific treatment known. Chondrodystrophy. Allin/all-out production. webbing between toes. Diagnosis Typical signs and lesions. Prevention Thorough cleaning and disinfection after depletion of an affected flock.
bedbugs. especially around vent. Signs Lack of thrift in young birds. Post-mortem lesions Usually none. 19 . Parasites on birds. Differentiate from mites. Diagnosis Identification of the parasites. may be some feather damage and crustiness of skin.naturally present in many raw materials. Differentiate from pantothenic acid deficiency (skin lesions). Treatment Addition of biotin in feed or water. Treatment Malathion powders and pyrethroid sprays where approved for bird application. Prevention Supplementation of diets with biotin . The parasites are 1-6 mm in size and their life cycle takes about 3 weeks. Irritation. response to treatment/prevention.Diagnosis Signs. Drop in egg production. has very low bioavailability. Away from birds adults survive about 4-5 days. Biting Lice Introduction Various species of lice are common external parasites of poultry worldwide. They are spread by direct contact between birds and by litter etc. Lice eggs stuck to feathers. Check flocks regulary for rapidly moving insects at the base of the feathers on the abdomen or around the vent. Scabs around vent. Loss of condition. Loss of vent feathers. lesions. Menocanthus stramineus is the most pathogenic and is said to be capable of causing anaemia in heavy infestations. Crusty clumps of eggs ('nits') may be visible at the base of feathers.
Examine for lice regularly. local history. The condition tends to occur near to rapidly flowing streams. Signs Anaemia in young birds. Biological control using a strain of Bacillus thuringensis has had some success and is preferable to insecticides. The flies transmit leucocytozoonosis and also a filarial parasite in ducks. as the larvae within eggs are not killed by most products. Post-mortem lesions Anaemia. 5 mm long and found in North and South America that are external parasites of birds and mammals. Swarms of flies. Treatment Treatment is difficult. especially in autumn and winter and treat if required. Blackfly Infestation Introduction Grey-black hump-backed flies. Weekly treatments are required. 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. Eggs and larvae survive through the winter to cause new infestations in the following year. 20 .Prevention Avoid direct contact with wild and backyard poultry. Effective removal of all organic material at flock depletion should be practised in all-in/all-out production systems. Diagnosis Anaemia. season. Prevention Similar measures as for mosquito control.
Feathers may be easily pulled (chicken only). turkeys. signs. then sudden death. Diagnosis History. The single most important measure is careful pick-up and removal of all dead birds on a daily basis. and toxin-containing material (pond-mud. antibiotics. weakness. Prevention Preventing access to toxin.Botulism Introduction A condition of chickens. Affected broilers tend to settle with eyes closed when not disturbed. carcases. 21 . wings then neck. 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. especially in hot weather. Post-mortem lesions Possibly no significant lesions. Signs Nervous signs. maggots) is consumed by the birds. Mild enteritis if has been affected for some time. because it rests on the litter. is also quite typical. A soiled beak. mouse toxicology on serum or extract of intestinal contents. supportive treatment if justifiable. The toxin and bacterial spores are relatively stable and may survive for some time in the environment. Differentiate from acute Marek's disease ('Floppy Broiler Syndrome') by histology of the brain. selenium. ducks and other waterfowl occurring worldwide and caused by a bacterial toxin produced byClostridium botulinum mainly types A / C. progressive flaccid paralysis of legs. The toxin is produced in decaying animal (usually carcases) and plant waste. suspect food and stagnant ponds. Toxin may also be produced by the bacteria in the caecum. This will reduce the risk of botulism both in the poultry and in any grazing animals on land where poultry litter is spread. Morbidity is usually low but mortality is high. Maggots or putrid ingesta may be found in the crop. Treatment Remove source of toxin.
Infection is by the oral route. in chronic cases. the cause of Blackhead. Prevention Good litter management and handling. and a four-week prepatent period. Caecal Worm Introduction Heterakis gallinae. Treatment Not usually appropriate. Poor feather cover and caked or wet litter are predisposing factors. leg weakness. Signs Swelling over the keel bone with bruising and discolouration. The meaning of the technical terms relating to parasite life cycle are defined in the glossary. up to 1.5 cm in length that occur in the caecum. 22 . Post-mortem lesions Inflammation of sternal bursa along the keel bone which may. Earthworms may be transport hosts for eggs. give way to scar tissue. and infection withStaphylococcus spp. bacteria. Morbidity may reach more than 50% but the condition is not fatal. They are found worldwide. nematode parasites of poultry and game birds.Breast Blister Introduction A complex condition of chickens and turkeys occurring worldwide associated with trauma. control of leg problems. Heterakis gallinaeeggs and larvae are a transport hosts for Histomonas. are small whitish worms with a pointed tail. Diagnosis Based on lesions. Signs None. Morbidity is high but it is not associated with mortality. There is an incubation period of 2 weeks for eggs to embryonate. or paratenic hosts with partially developed (L2) larvae.
Death from respiratory and cardiac failure. Prevention Avoiding access to earth and earthworms. and the embryonated egg. The egg may be ingested directly by a chicken. possibly with nodule formation. Signs Paralysis. Treatment Flubendazole.Post-mortem lesions Inflammation of caecum. Predisposing factors include heat stress with reduced feed intake and panting. or by an earthworm which is in turn ingested by a chicken. an undeveloped egg as found in fresh faeces. are effective. Calcium Tetany Introduction A metabolic disease of chickens. Routine anthelmintic treatment. 23 . especially broiler parents. Figure 11. Levamisole. The life cycle ofHeterakis showing the location of adults. Diagnosis Adults can be seen in caecal contents at post-mortem examination.
Diagnosis This is made on signs. and response to treatment. Campylobacters are a significant cause of enteritis in man. There is an annual cycle with increased risk of infection in the summer months in some countries. carcase quality and litter quality are better on farms which tend to have Campylobacter-negative stock.Post-mortem lesions Cyanosis. are bacteria that commonly infect a broad range of livestock species. It may be that management that favours dry litter reduces the risk of infection and/or transmission within the flock. The reason for this is unclear. managing birds for maximum uniformity. Campylobacter Infection Introduction Campylobacter spp. In poultry they tend to multiply in large numbers in the hindgut. 24 . Differentiate from IB 793b. Prevention Keep pullet flocks on low calcium diet until 5% production hen/day. lesions. Campylobacter jejuni infection is not currently considered to be pathogenic in poultry though a Campylobacter-like organism is considered to be the cause of 'Vibrionic Hepatitis'. Active ovary with egg in oviduct. Campylobacter jejuni is the commonest species found in poultry. other acute infections and other causes of sudden death. Treatment Provide 5 gm of oyster shell per hen on 3 successive days along with vitamin D in drinking water. Congested lungs. There are indications that plantar pododermatitis. Infected poultry are a potential reservoir of this zoonosis. biofilm or engulfed by protozoa. pets and wild animals. principally in the caecae. All campylobacters are delicate organisms that survive for relatively short periods outside the host unless protected by organic material. lack of other significant lesions.
as well as processing plant technologies to reduce carcase contamination. Samples should be tested as quickly as possible after collection. In practice the success of this will also depend upon the degree of environmental contamination by the organism. 25 . and changing of overalls and boots on entering bird areas. Prevention In principle. sourcing of water from high quality supplies. cloacal swabs or composite faeces. good hand hygiene by stockmen. Research is ongoing on the development of vaccines. Diagnosis Isolation of the organism from caecal contents.Signs None. The organism is sensitive to air so swabs should be collected into transport medium and other samples placed in airtight containers with minimal airspace. Treatment Not required on clinical grounds. housed poultry can be maintained free of Campylobacter infection by consistent application of excellent biosecurity. Post-mortem lesions None. Insects and rodents may act as a means of transfer of the infection from the general environment into the poultry buildings. Key aspects of this include effective sanitation of drinking water. For this reason it may be difficult to stop the spread of infection between houses once it becomes established in one house. phage treatments and competitive exclusion approaches. Many infections are introduced during thinning or other forms of partial depopulation. avoidance of contact with pets and other farmed species.
g. smooth and with a yeasty smell. possibly confused or masked by signs of the primary disease. Ensure good hygiene. Colonies of this fungus appear as white to ivory colour. microscopic examination of a digested smear (heat in 10% potassium hydroxide) to demonstrate the hyphal forms of the yeast in the tissues. Moniliasis. Thrush Introduction A disease of the alimentary tract of chickens. crop. Slow growth. Prevention Avoid excessive use of antibiotics and other stressors. Candida albicans and the condition is seen worldwide. Diagnosis Lesions. 26 . and associated with gizzard erosion. The fungus is resistant to many disinfectants. copper sulphate (1 kg/tonne feed) for 5 days. Morbidity and mortality are usually low. intestine and cloaca. Diarrhoea. Treatment Nystatin (100 ppm in feed) for 7-10 days. oesophagus. Post-mortem lesions White plaques in mouth. Signs Dejection. sodium or calcium proprionate at 1 kg per tonne continually. A finely divided powder of copper sulphate (where approved) at 200gm/tonne continually or to 14-16 weeks in replacement pullets. and sometimes other birds and mammals. proprionic acid. Control of Candida through drinking water is sometimes practised with chlorination (e. histopathology. especially in the crop but sometimes in the proventriculus. or copper sulphate 1gm/2 litre water for 3 days if approved locally. occasionally proventriculus and intestine. Poor appetite. characterised by thickening and white plaques on the mucosa. 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. The cause is a fungal yeast. Raised focal lesions may slough into lumen as caseous material.Candidiasis. turkeys.
Feather-pulling. Beak trimming may be necessary. Differentiate from bacterial dermatitis. Treatment Correct any husbandry problems. This is economical and effective. excessive light intensity or variation (e. anaemia. head. and strain of bird. feed form (mash takes longer to consume than pellets).g. Diagnosis Age.Chlorox. Soluble multivitamins and/ or methionine may be of some benefit in some circumstances. complying with local regulations and any relevant codes of practice. Take care to provide fresh clean feed and water. Generalised anaemia. face. Post-mortem lesions Skin wounding related to particular signs exhibited. nutritional deficiencies. Predisposing factors include overcrowding. distribution of lesions. high temperatures. Cannibalism. through shafts of light in the house). sodium hypochlorite) at 5 ppm. Prevention Proper density and temperature. control ectoparasites. Signs Pecking at feet (especially young chicks) and vents (adult layers and turkey poults 812 days old). tenosynovitis and other diseases affecting mobility. uncontaminated by fungi. post-mortem cannibalism. If so it should be carried out carefully by trained operators. Feather pecking Introduction A complex multifactorial behavioural problem of poultry and game birds seen worldwide. low light level. Morbidity is usually low but mortality is high among affected birds. Provision of a diet that closely matches the nutritional requirements of the stock concerned. 27 . boredom. It should be repeated periodically. wings.
Differentiate from other causes of enteritis.05 mm wide and hair-like in appearance. Post-mortem lesions Enteritis. Hairworms in mucosa of crop. Worm eggs take about 20 days to embryonate with an L1 larvae. about 0. effective cleaning of houses. Some species have earthworms as intermediate hosts. C. seiving intestinal contents. Diagnosis This may be by a combination of macroscopic examination. Infection is by the oral route. Fenbendazole has been shown to have high efficacy . game birds and pigeons ofCapillaria species. Treatment Coumphos has been licensed in some markets. Levamisole. obsignata in the small intestine.Hairworm Infection Introduction Nematode parasitic worms of poultry. Wasting Poor growth. prepatent period about 21-25 days according to species. small intestine or caecum. Signs Diarrhoea. Morbidity and mortality are usually low. The worms are 7-18 mm long.other approved benzimidazoles can be expected also to have activity. Prevention Separation of birds from possible transport and intermediate hosts. Worm eggs in the environment are resistant. Dejection. some are transmitted direct from bird to bird.Capillariasis . contorta in the crop and oesophagus. 28 . or characteristic worm eggs in faeces in patent infections. C.
Signs Affected flocks tend to have poorer than average productivity and uniformity. Treatment Treatment would not be possible if the problem is identified at a final depletion. The condition is caused by infection of. though most of the birds showing toe scrapes will not go on to develop cellulitis. coli. It typically occurs between skin and muscles and between muscles and may be an incidental finding in a range of conditions. which can replicate in the tissues. particularly broiler chickens. Careful flock management with a view to reducing toe wounds has the greatest impact in controlling cellulitis. 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.Cellulitis Introduction Cellulitis is literally an inflammation of connective tissues. Prevention Toe scrapes at 15-25 days of age when feather cover is poor are the most likely predisposing factors. However its main importance is as a cause of condemnation in meat poultry. Many meat inspectors become skilled at detecting subtle differences in skin colour in the affected birds. skin wounds by particular strains of E. but the affected birds are not readily detectable prior to slaughter. 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. Diagnosis Typical lesions. Many affected birds have no other lesions and are reasonably well grown. 29 . Routine monitoring of skin damage at about 25 days of age may be helpful in fostering good practices. In the USA it is called 'Inflammatory Process'. often minor.
If gangrenous dermatitis is a problem then periodic medication may be required. heat (70°C for 1 hour. poor litter quality). Diagnosis Gross lesions. Prior to confirmation that it is in fact a virus it was known as Chicken Anaemia Agent or CAA. Pale birds. and control of other diseases as appropriate. Atrophy of thymus and bursa. Gangrenous dermatitis on feet. Transmission is usually vertical during sero-conversion of a flock in lay. 80°C for 5 minutes) and many disinfectants even for 2 hours at 37°C.Chicken Anaemia Introduction A viral disease of chickens caused by Chicken Anaemia Virus or CAV. chloroform. Discoloured liver and kidney. Inclusion body heptatitis etc. Hypochlorite appears most effective in vitro. demonstration of ongoing sero-conversion in parent flock. may be beneficial. 30 . PCV of 5-15% (normal 27-36%).g.) or poor management (e. Acute mycotic pneumonia. virus may be isolated in lymphoblastoid cell line (MDCC-MSB1). The virus is resistant to pH 2. lateral transmission may result in poor productivity in broilers. Gumboro. Sudden rise in mortality (usually at 13-16 days of age). ether. Mortality is typically 5-10% but may be up to 60% if there are predisposing factors present such as intercurrent disease (Aspergillosis. Signs Poor growth. Post-mortem lesions Pale bone marrow. legs wings or neck. Treatment Good hygiene and management. No clinical signs or effect on egg production or fertility in parent flock during seroconversion.
especially pigeons and robins. Iodophores and formaldehyde are effective disinfecting agents. 15 weeks.Prevention Live vaccines are available for parents. Nasal discharge. caused by Chlamydia psittaci. 31 . Inappetance. Serology: antibodies develop 3-6 weeks after infection. Their use may be restricted to those flocks that have not sero-converted by. Weakness. but occurring probably worldwide. faecal dust and wild bird carriers. other infections may be predisposing factors. Greenish-yellow diarrhoea. Depression. pigeons. Elementary bodies are highly resistant and can survive in dried faeces for many months. ducks. Morbidity is 50-80%. Weight loss. psittacines. Wasting. Signs Respiratory signs. Conjunctivitis. Egg transmission does not occur. man. or IFA. and may be detected by SN. a bacterium of highly variable pathogenicity. Chlamydiosis. Elisa. Production drops in naive laying flocks Post-mortem lesions Vascular congestion. Intercurrent salmonellosis and. They should be used at least 6 weeks prior to collecting eggs for incubation. rarely chickens. Immunity: there is a good response to field challenge (in birds over 4 weeks of age) and to attenuated live vaccines. It is transmitted by contact. say. Fibrinous pericarditis. Psittacosis. mortality 5-40%. Occasional transient ataxia in pigeons. phenolics are less so. Airsacculitis. perhaps. Ornithosis Introduction An infection of turkeys. It is a 'Scheduled Disease' rarely diagnosed in UK. their degree of attenuation is variable.
Necrotic foci in liver. Slipping of Achilles tendon (or perosis). Differentiate from Duck viral hepatitis. Congested lungs and air sacs in the turkey. Distortion of hock. IFA). choline. Fibrinous pneumonia. Live and inactivated vaccines are protective although the former result in carriers and the latter require several applications. folic acid. Slipped Tendon or Perosis Introduction Caused by deficiency of manganese. Perihepatitis. 32 . either singly or in combination (although deficiencies of pyridoxine. Prevention Biosecurity. shortened bones. exclusion of wild birds. Intracytoplasmic inclusions are helpful but confirmation requires demonstration of causal organisms (Giemsa stain. lesions. Diagnosis History. Serology: complement fixation. Lameness. Spleen enlarged and congested. This condition is seen in chickens. Malposition of leg distal to hock. Treatment Tetracycline (200-800 ppm in feed for 3-4 weeks) and/or quinolone medication and supervised slaughter. In embryos parrot beak. zinc. niacin may also be involved). Signs Short legs. Duck septicaemia. signs. ducks and turkeys. In turkeys it may be an inherited deficiency of galactosamine. may rupture in pigeons. Chondrodystrophy. Elisa and gel diffusion. biotin.
while E. This disease is not very common in commercially reared turkeys though most turkey growers receive preventative medication for at least part of their lives. 33 . Prevention Addition of manganese. vitamins. adenoides affects the caecae and rectum. Treatment For flock proceed as for prevention. Depression. infectious synovitis. Five species of Eimeria have been identified that cause lesions in turkeys. Coccidiosis of Turkeys Introduction Infection of turkeys with Eimeria spp. Shallow trochlea. Watery diarrhoea that may occasionally be blood stained or contain clumps of mucus or shed mucosa. ruptured ligaments. E. The contents may be haemorrhagic or be watery with white material shed from the mucosa. rickets. gallopavonis and E. E. meleagrimitis affects the upper small intestine. analysis of feed. correct mineral balance. of which two are associated with significant disease effects. Post-mortem lesions The affected area of intestine shows thickening of the wall and dilation. choline. Tibia and metatarsus bowed. dispersa is found in the small intestine. infectious arthritis. no value to affected bird. Differentiate from twisted leg. Lateral slipping of tendon. Diagnosis Lesions. Signs Huddling.Post-mortem lesions Shortening and thickening of long bones. while E. ruffled feathers. Tucked appearance. Weight loss. meleagridis affect the lower small intestine rectum and caecae.
34 . gamonts). Avoid use of tiamulin in ionophore treated birds. microscopic exam of scrapings (oocysts. meleagrimitis. Turkey caecal coccidiosis caused by E. Differentiate from necrotic enteritis. show some spotty congestion and have abnormal contents due to the sloughed epithelium. The intestines are dilated.Diagnosis Signs. Dosage levels of ionophores may be critical to efficacy and safety. Figure 38. Prevention The ionophore coccidiostats lasalocid and monensin are routinely used in turkey growers. Sulphaquinoxaline). Salinomycin is toxic for turkeys even at very low doses.g. typically to 12 weeks of age. The exudate can range from semi-liquid to solid white cores. adenoides. Exposure of previously unmedicated birds to these compounds can cause toxicity. lesions. Figure 37. Treatment Toltrazuril. Amprolium. Sulphonamides (e. Turkey coccidiosis of the upper small intestine caused by E. Diclazuril is also used for this purpose.
Morbidity is 10-40% and mortality up to 50%. Diagnosis Signs. blood in faeces. Amprolium. 35 . Signs Depression. Vitamins A and K in feed or water. Accumulation of varying quantities of blood and caseous necrotic material in the caecum. of caecal mucosa. Closed eyes.Coccidiosis. Diarrhoea. In some markets the organic arsenical compound 3-Nitro is used as an aid in the control of caecal coccidiosis. mitis (see above). Shuttle programmes with chemicals in the starter diet usually improve control. Inappetance. Treatment Toltrazuril. lesions. histomonosis. E. Sulphonamides. Production less affected than in some of the other forms of coccidiosis. microscopic examination of scrapings. ecchymoses. Post-mortem lesions Petechiae. Recovered birds have good immunity to the same parasite. It is caused by Eimeria tenella and results in lesions in the caecum of chickens worldwide. tenella is more common when 'straight' ionophore programmes are used. Thickening. Vaccines are used mainly in breeders but increasingly in broilers. Differentiate from ulcerative enteritis. Transmission as for E. hygiene. Caecal. Ruffled feathers. Prevention Coccidiostats in feed. vaccination by controlled exposure. E tenella Introduction This was at one time the commonest type of coccidiosis and is certainly the most easily diagnosed.
Coccidiosis. Post-mortem lesions The lesions are minimal and located in the lower small intestine (ileum) which tends to be pale and flaccid with scattered petechiae. secondary bacterial enteritis. Signs Reduced feed conversion efficiency and weight gain.Figure 15. Predisposing factors include exposure to faeces and litter conditions that favour development of the parasite (temperature. The infective agent is found in litter. is caused by the protozoan parasite Eimeria mitis. Diagnosis Mild lesions. The caecal walls are thickened and haemorrhagic and there is a mass of blood in the caecal lumen. faeces and on fomites and birds are infected by the oral route with an incubation period of 2-5 days. The disease occurring is proportional to the amount of infective agent ingested. seen worldwide. Treatment Not usually treated but susceptible to the products used for other forms of intestinal coccidiosis. Moderate Eimeria tenella infection in the caecae of a chicken (Score 3). identification of typical small round oocysts and other stages in fresh scrapings from the small intestine. 36 . The parasite is moderately resistant in the environment and highly resistant to conventional disinfectants. humidity). which colonises the small intestine. May predispose to wet litter. E mitis Introduction This condition of chickens.
37 . Morbidity and mortality are variable. Differentiate from ulcerative enteritis. Vitamins A and K in feed or water. Amprolium. Diarrhoea. Diagnosis Signs. Poor production. hygiene. There is good immunity to the same parasite in recovered birds. Of moderate to high pathogenicity. E brunetti Introduction A relatively rare form of coccidiosis affecting chickens worldwide caused by Eimeria brunetti. This species is not usually included in vaccines for broilers. Coccidiosis. Ileorectal. caecum and rectum. Signs Depression. caecal coccidiosis. Severe necrotising enteritis. Closed eyes. Ruffled feathers. microscopic examination of scrapings. Oocysts in caecum and rectum. it is found in the terminal ileum. May be included in vaccines. Treatment Toltrazuril. vaccination by controlled exposure. blood in faeces. Prevention Coccidiostats in feed. Sulphonamides. extending into caecal tonsils.Prevention Normally controlled by anticoccidials in feed. lesions. Post-mortem lesions Petechiae and thickening of the distal third or more of intestine. Inappetance.
Differentiate from Duck viral hepatitis. microscopic examination of scrapings (usually few or no oocysts. compared to four per oocyst forEimeria. Amprolium. Duck viral enteritis. There is thickening of the intestinal mucosa and there are lines of haemorrhagic spots in the mucosa. Moderate Eimeria brunettiinfection in the terminal ileum and rectum of a chicken. 3 days on. Post-mortem lesions Massive haemorrhage in upper small intestine. Coccidiosis occurs only very rarely in commercially reared ducks in the UK. 3 days on). anatipestifer. anseris is the most important. Depression. Diagnosis Signs. Tucked appearance. Sulphadimidine 30-600gm/100 birds/day.g. large number of merozoites). while in ducksTyzzeria perniciosa is most pathogenic. Vitamins A and K in feed or water. In the goose E. 2 days off. 38 . Signs Sudden death. Treatment Sulphonamides (e. Coccidiosis. Intestinal.Figure 16. lesions. Blood-stained vent. Tyzerria has eight sporocysts in each oocyst. of Ducks and Geese Introduction Young ducks and geese may suffer from Eimeria spp infection.
Post-mortem lesions Enlarged kidneys. 39 .Prevention If required coccidiostats could be used in feed. Diarrhoea . Prevention Good Hygiene.faeces tend to be whitish. Treatment Controlled trials of treatments have not been published. Coccidiosis. Kidneys light grey to greyish pink. Reduced feed intake. Weakness. Hygiene. Diagnosis Lesions. presence of coccidial stages in fresh scrapings of kidney lesions. it can also infect Barbary ducks and swans. Signs Depression. Tiny white foci and petechiae in the kidneys. Kidney Introduction A disease of geese caused by Eimeria truncata that can cause high mortality in geese of 312 weeks of age. however this is not routinely practised.
Amprolium.Coccidiosis. Post-mortem lesions Petechiae and thickening of middle third of intestine. microscopic examination of scrapings. This is one of the less immunogenic species. Mid-intestinal. 40 . Poor absorption of nutrients/pigments. Closed eyes. Blood or pigment in the faeces. acervulina coccidiosis and there may be large numbers of characteristic oocysts in smears. Depigmentation of skin and plasma is especially evident in this form of cocccidiosis and this is commercially important in some markets. E maxima Introduction One of the more common forms of coccidiosis in commercial broilers. hygiene. Treatment Sulphonamides. Inappetance. lesions. non-specific enteritis. Caused by Eimeria maxima. maxima. Diagnosis Signs. contents often orange in colour. Mild to severe enteritis. Morbidity and mortality are variable. Ruffled feathers. Because of the area of intestine affected it tends to have a significant effect on productivity and susceptibility to necrotic enteritis. Signs Depression. Prevention Coccidiostats in feed. Poor production. mucosa tends to be pinker than normal. Vitamins A and K in feed or water. of moderate to high pathogenicity it is seen worldwide. This infection is often associated with E. vaccination. Differentiate from necrotic enteritis. commercial vaccines commonly contain more than one strain of E.
Severe necrotising enteritis.Figure 13. Poor production. Diagnosis Signs. in which the parasite is present in the small intestine and in the caecum. 41 . Deep scrapings necessary to show large schizonts. 'Sausage-like' intestine. Depression. The intestine is slightly thickened and there are scattered haemorrhages in the mucosa when seen from the inside. blood in faeces. Mid-intestinal. Post-mortem lesions Petechiae and thickening. Ruffled feathers. Inappetance. E necatrix Introduction A highly pathogenic form of coccidiosis. Coccidiosis. lesions. caused by Eimeria necatrix. microscopic examination of scrapings Differentiate from necrotic enteritis. Moderate Eimeria maxima infection in the jejunum of a chicken (Score 2). Diarrhoea. The lesions are subtle compared to other forms of coccidiosis. Closed eyes. It occurs in chickens worldwide and has variable morbidity but mortality is high in severely affected birds. Schizonts seen as white spots through the serosa interspersed with petechiae. Oocyts in caecal scrapings. of middle to posterior third or more of small intestine. other types of coccidiosis. Signs Reduced feed consumption.
both alone and in association with other species of coccidia and is caused by Eimeria acervulina. Amprolium. acervulina. Haemorrhages and white spots are visible from the outside of the intestine. Depigmentation. Moderate Eimeria necatrix infection in the jejunum of a chicken (Score 3). In this case the intestine is thickened and can become ballooned and sausage-like. Coccidiosis. Sulphonamides. Inappetance. vaccination. Closed eyes. which is moderately pathogenic. Poor production. It is seen in layers and in broilers. Ruffled feathers. Upper Intestinal. Eimeria mivatiis currently considered not to be a valid species distinct from E. Prevention Coccidiostats in feed. maxima.Treatment Toltrazuril. hygiene. Post-mortem lesions 42 . Figure 14. E acervulina Introduction This is probably the commonest cause of coccidiosis in chickens and occurs worldwide. Diarrhoea. Morbidity is variable and mortality low or absent. commercial vaccines commonly contain more than one strain of E. Vitamins A and K in feed or water. This is one of the less immunogenic species. Signs Depression.
A system of assessing the severity of coccidial challenge by attributing a 'score' is often used. Sulphonamides. Poor absorption of nutrients/pigments. vaccination by controlled exposure. Moderate Eimeria acervulinainfection (score 2) in chicken duodenum. Differentiate from necrotic and non-specific enteritis. hygiene. A detailed description is beyond the scope of this book. Diagnosis Signs. In severe infections they become confluent and cause sloughing of the mucosa. White spots or bands in the mucosa. In milder infections there may be scattered white spots. Immunity is quite short lived (about 30 days) in the absence of continued challenge. Figure 12. restricted to upper third of small intestine . Various publications provide a photographic key to severity of lesion. Petechiae. In general terms a score of 0 indicates no lesions and a score of 4 indicates maximal severity of lesion or death. lesions. Amprolium. Prevention Coccidiostats in feed. in severe the entire surface is pale or denuded of epithelium. Thickening. 43 . in feed or water. Treatment Toltrazuril.the duodenum and part of the ileum. and other lesions. microscopic exam of scrapings.
Omphalitis. Signs Respiratory signs. turkeys. pathology. etc. Poor navel healing. Morbidity varies. It is caused by the bacteriumEscherichia coli and is seen worldwide in chickens. Synovitis. Swollen liver and spleen. Enteritis. or in young birds that are immunologically immature. and via shell membranes/yolk/navel. Arthritis.most strains are rapidly lactose-fermenting producing 44 . water. Granulomata in liver and spleen. Perihepatitis.Colibacillosis. The infectious agent is moderately resistant in the environment. Lesions vary from acute to chronic in the various forms of the disease. Dejection. fomites. but is susceptible to disinfectants and to temperatures of 80°C. with an incubation period of 3-5 days. Colisepticemia Introduction Coli-septicaemia is the commonest infectious disease of farmed poultry. coughing. sneezing. Infection is by the oral or inhalation routes. Omphalitis. Salpingitis. Post-mortem lesions Airsacculitis. Diagnosis Isolation. Cellulitis over the abdomen or in the leg. Peritonitis. It is frequently associated with immunosuppressive diseases such as Infectious Bursal Disease Virus (Gumboro Disease) in chickens or Haemorrhagic Enteritis in turkeys. Aerobic culture yields colonies of 2-5mm on both blood and McConkey agar after 18 hours . Poor growth. sero-typing. mortality is 5-20%. mucosal damage due to viral infections and immunosuppression are predisposing factors. It is most commonly seen following upper respiratory disease (such as Infectious Bronchitis) or Mycoplasmosis. Snick. Pericarditis. Reduced appetite.
Well-nourished embryo and optimal incubation to maximise day-old viability. Pododermatitis Introduction Contact dermatitis affects skin surfaces which have prolonged contact with litter. whereas others progress to deep ulcers so the size. etc. Some lesions are superficial. and in broiler parents. Severe perihepatitis in colibacillosis in a broiler parent chicken. Immunity is not well documented though both autogenous and commercial vaccines have been used. Figure 17. Prevention Good hygiene in handling of hatching eggs. when severe. hatchery hygiene. The liver is almost entirely covered by a substantial layer of fibrin and pus. Hock Burn. tetracyclines. Contact dermatitis is commonly monitored at processing as a means of measuring 'welfare status'. good sanitation of house. the foot pad. Differentiate from acute and chronic infections with Salmonella spp. the breast area.brick-red colonies on McConkey agar. gentamycin or ceftiofur (where hatchery borne). Control of predisposing factors and infections (usually by vaccination). rear surface of the hock and. It is seen in growing broiler chickens and turkeys. stage of resolution and severity of lesion is likely to affect the degree of discomfort or pain suffered. as well as Pseudomonas. neomycin (intestinal activity only). Contact Dermatitis. Staphylococcus spp. 45 . potentiated sulphonamide. flouroquinolones. Treatment Amoxycillin. other enterobacteria such as Proteus. feed and water.
See the discussion in the section on Dysbacteriosis. Signs Blackened skin progressing to erosions and fibrosis on the lower surface of the foot pad. Choice of drinker type (nipple as opposed to bell). stickiness of droppings). Moderate pododermatitis on a foot pad. and. 46 . level of soya bean meal in feed (according to some authors. Figure 18. If severe the foot and hock lesions may contribute to lameness or serve as a portal of entry for secondary infections. Prevention This condition is closely linked to intestinal function as this is the prime determinent of faecal consistency and stickiness. proper insulation in cold climates. Treatment Not applicable. Post-mortem lesions As described under signs.Pododermatitis is often related to high droppings pH. and sometimes in the breast area. Diagnosis Signs and lesions. at the back of the hocks. most importantly. litter moisture. It can be reproduced by adding water to the litter. drinker management. and adequate ventilation to remove moisture are all important.
although bird strains do not infect mammals very well. acervulinaoocyst). Post-mortem lesions Inflammation and thickening of mucosa of crop and oesophagus. Diagnosis Microscopic examination of mucosal scraping. Emaciation. They replicate in the brush border on the surface of epithelial cells. They also differ from coccidia in being poorly host specific. Cryptosporidiosis Introduction Cryptosporidia are related to the coccidia. 47 . Cryptosporidium baileyi can cause respiratory disease in chickens and turkeys.C. but much smaller (typically oocysts are less than ¼ of the size of an E. Routine worming. The same species causes infections of the hindgut and cloacal bursa in chickens. Prevention Effective cleaning of housing. Coumaphos. Signs Anaemia. A further species causes respiratory disease in quail. and vice versa. The oocysts are excreted ready sporulated in the faeces and infection occurs by inhalation and ingestion. White convoluted tracks in the mucosa. turkeys. Treatment Levamisole. Avoidance of access to intermediate hosts.Cropworms Introduction The nematode worms Capillaria spp and Gongylonema ingluvicolainfect the mucosa of the crop and oesophagous of poultry and game birds. and ducks. Some have beetle or earthworms as intermediate hosts. meleagridis also infects both species.
Cough.g. Airsacculitis. 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. Prevention The oocysts of cryptosporidia are extremely resistant to chemical disinfection. Signs Incoordination. Circling. It is becoming increasingly common for water companies to screen water supplies for cryptosporidia because of the human health implications of mammalian strains. Torticollis. coli-septicaemia) there may be benefit in medicating for these. Diarrhoea. There are no effective preventative medicines or feed additives. Post-mortem lesions Sinusitis. Diagnosis Identification of the parasites attached to the epithelium by microscopic examination (smears histopathology acid-fast staining). Treatment Unfortunately there is currently no known effective treatment in poultry. Tremors. 48 . Swollen sinuses. Pneumonia. If other disease processes are complicating the situation (e.Signs Snick. Low weight gain. recumbency.
Post-mortem lesions Necrotic lesions with associated congestion in cerebrum. Treatment 49 . isolation of the fungus. Diagnosis Lesions. resulting in erosions. and cartilage flaps. but it may result from physical damage. Signs Lameness. Microscopically there is necrosis and there may be fissures of articular cartilage and associated osteochondritis. Mycotic lesions in lungs. especially of femoral anti-trochanter but also other leg joints. Reduced breeding performance. Degenerative Joint Disease Introduction A condition of chickens and turkeys seen worldwide. Morbidity and mortality are low but affected birds are more likely to be 'picked upon' and may end up suffering damage and needing to be culled. The cause remains to be confirmed. Post-mortem lesions Damaged epiphyseal articular cartilage. Prevention Use fresh dry litter (avoid old sawdust). air sacs etc. or developmental defects. Treatment None. Diagnosis Gross and microscopic lesions. Rapid growth is a possible predisposing factor.
5mm in diameter. Prevention Avoidance of physical sources of injury to bones and joints. Appropriate management of a segregation pen and early marketing of mildly affected birds may limit losses and improve flock welfare. Diagnosis Signs. round. pheasants. microscopic examination for mites in scrapings.Knemidocoptes spp. Unthriftiness. pigeons etc. The adult females are short legged. Depluming and Scaly Leg Mites Introduction External parasites of adult chickens. Application of mineral or vegetable oil is also beneficial.None available. Post-mortem lesions As described under signs. Signs Cause irritation and the bird pulls feathers. especially during period of rapid growth. Raised thickened scales. up to 0. Exclusion of wild birds from chicken areas is advised as far as possible. It may be best to cull affected birds from small flocks. Treatment Not usually required in commercial poultry. For small flocks dipping the affected parts in a solution of acaricide may be beneficial. Mange lesions on legs and unfeathered parts. Prevention Careful cleaning of buildings during down-time will help reduce the risk of these infections. 50 . There may be a place for growth-control programmes.
Dissecting Aneurysm. genetic condition of turkeys linked to male sex and high growth rate. Haemorrhages in lungs. a tranquilizer. Post-mortem lesions Carcase anaemic. The infective agent. Treatment None currently licensed. Morbidity is around 100% and mortality 0-95%. Reserpine. Aortic Rupture Introduction A complex. Duck Viral Hepatitis Introduction A viral disease of ducks occurring worldwide and previously a scheduled disease in UK. Diagnosis History and lesions. It has been suggested that degenerative changes in the wall of the artery and copper deficiency may be factors. Signs Sudden death with no warning signs. Prevention Limit feed in birds of 16+ weeks. presumably due to a sudden increase in blood pressure. birds found on breast or side. recovered birds carrying the virus for 8 weeks. A longtitudinal split of the abdominal aorta is the most common lesion. A sudden noise or other cause of excitement can lead to an 'outbreak'. Rupture of major blood vessel at base of heart or by the kidneys. Abdominal cavity full of blood. Reserpine in diet of birds of 4+ weeks (no longer licensed in the UK). The disease is transmitted by infected ducks and other waterfowl and spreads rapidly. a picornavirus may also 51 . leg muscles. kidneys. Skin pale. pericardial sac. Aspirin at 250 ppm in feed or water may be of benefit. was included in feed at 1 ppm for 3-5 days to reduce blood pressure. Possibly blood in the mouth.
The disease follows a very acute course with a morbidity of 5-100% and mortality of 5-100%. Influenza and a 'Type II Variant' hepatitis caused by Astrovirus. 0. Post-mortem lesions Liver swollen. fomites and arthropods. Treatment Antiserum. mostly in ornamental collections. Microscopically . in USA since 1967. often in opisthotonus. paddling of legs. Signs Sudden death. All waterfowl are susceptible and the Barbary duck is more susceptible than the Pekin. coccidiosis. 52 . Duck septicaemia (anatipestifer). Death in good condition.focal necrosis. only slightly attenuated vaccine is applied at day old by foot web stab and may be repeated in breeding birds to provide maternal immunity. Recovered birds may carry the virus for a year.5 ml serum of recovered birds given intramuscularly. also the Netherlands and other countries. Duck Virus Enteritis. Prevention Vaccination and/or antiserum. Differentiate from Duck plague (viral enteritis). bile duct proliferation and inflammation. Transmission is by infected birds. rapid deterioration and death. Kidneys and spleen swollen. Newcastle disease. Punctate/diffuse haemorrhages. arching of back. breeder vaccination. Diagnosis History. Fall on side. Live. SN serology. Depression. lesions. A different picornavirus causes a similar condition in North America. isolation in CE (causes stunting of 9 day embryo). Duck Plague Introduction A herpesvirus infection of ducks and geese diagnosed in the UK in 1972.survive for ten weeks in brooders and five weeks in faeces.
53 . Non-specific Bacterial Enteritis Introduction Inflammation of the small intestine associated with wet litter. intranuclear inclusions Differentiate from Duck hepatitis. heart.Signs Sudden deaths. Paresis. but vaccination in face of outbreak is of value. sometimes dysentery. body cavities. Occasionally penile prolapse in the penis in drakes. Ataxia. Haemorrhage in intestine. vent gleet. vaccination if approved by authorities (CE adapted live virus). pericardium. Dehydration. Rapidly spreading disease. Occasionally cyanosis of the bill in the young. excess caecal volume and fermentation. The condition is seen mainly in rapidly growing broiler chickens with good food intake. Thirst. Young ducks may show thymic and bursal lesions. Severe diarrhoea. spleen. Post-mortem lesions Severe enteritis. HA-. probably through interference. Treatment None. Prevention Isolation from waterfowl. Drop egg production. oesophagitis (birds on restricted feed). Dysbacteriosis. Diagnosis Isolation: Duck CAMs 12 day embryos die in 4 days. Photophobia. Closed eyes. liver. is common in countries with restrictions on the use of antimicrobial growth promoters and pressure to reduce therapeutic antimicrobial usage. pasteurellosis. Crusty plaques from oesophagus to bursa (covered by yellowish plaques in later stages). Tremor. coccidiosis.
lesions. England. rather we are dealing with a disruption in the normal flora of the gut. In the autumn of 1976 a distinct egg drop syndrome was first identified in Northern Ireland. often with gas bubbles. Treatment should coincide with good relittering and it is important to provide fresh sanitary drinking water. 127. Diagnosis Signs. Treatment Amoxycillin and tylosin treatment appear to be beneficial. microscopic examination of scrapings from the wall of the small intestine (to exclude coccidiosis and perhaps to assess the bacterial flora). Prevention Competitive exclusion ('normal adult flora') use in day-old chicks reduces the risk of this condition. Spain. Water intake may be increased or irregular. Germany. No single bacterium appears to be responsible. Careful choice of any feed enzymes and their matching with local raw materials can have an impact on substrates made available to intestinal bacteria. Holland. Voluminous caecae. Prophylactic antimicrobial medication may be necessary in some circumstances. It affects chickens and has occurred in Ireland. Post-mortem lesions Excessive fluid content throughout the small intestine. Wet faeces in the rectum. Peru. France. Brazil. Signs Diarrhoea. The cause has been identified as Adenovirus BC14.Dietary changes. Mortality is usually negligible. 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. Good control of coccidiosis. Circumstantial evidence suggests that the main route of transmission is through the eggs (vertical transmission) 54 . especially where treatment is initiated early. Feed acidification may be helpful in some circumstances. feed interruptions and subclinical coccidiosis may be contributory factors. Uruguay. Apparently a similar disease had been seen over a 4-year period in broiler parents in Holland. Argentina. first isolated in Northern Ireland in 1976.
Infectious diseases include Infectious Bronchitis. thin or soft-shelled eggs and shell-less eggs. B 12. Management problems may be involved: inadequate water supply. specifically vitamins E. Cholera. signs/lesions (mainly lack of). Elisa. 55 . Diseases in which egg drop occurs. phosporus. Marek's disease/Leukosis or any infectious disease causing a significant systemic disturbance (CRD. insecticides or nicarbazin. Newcastle disease. oviduct).it may be possible to demonstrate degenerative changes in the epithelial cells of the magnum of the oviduct. selenium. sudden changes of feed. which can be caused by a large number of factors acting individually or in combination. Lack of signs in the birds themselves. intoxication by sulphonamides. Drops may be of 5 to 50% and last for 3-4 weeks.only a slight atrophy of ovary and oviduct. throat swabs. group antigen distinct from classical adenoviruses (white cells. Spread from house to house may take 5-10 weeks. Clinical disease occurs during sexual maturity. Diagnosis History. may be infectious or metabolic. DID. Parasites. Contamination of egg trays at packing stations may play a part in transmission. Lateral transmission from bird to bird is slow and may be prevented or slowed for weeks by netting divisions. The infection is commonly present in ducks and geese but does not cause disease. Diphtheritic Fowl Pox). Serology: HI. Unvaccinated flocks with antibodies before lay do not peak normally. Coryza. It is important to rule out other possible reasons for egg drop. SN. Nutritional deficiency should be considered. Isolation of haemagglutinatin agent in duck eggs or cell culture. Rough. Infectious Laryngotracheitis. as may wildfowl and biting insects. inadequate lighting programme. Post-mortem lesions No specific lesion .followed by latent infection during rear with viral excretion starting shortly before sexual maturity. and D as well as calcium. Histopathology . Avian Encephalomyelitis. Loss of shell pigment. Signs Egg drop at peak or failure to peak. Metabolic diseases include Fatty Liver Syndrome. Poor internal quality. extremes of temperature.
Peripheral vessels congested. and /or trauma. Soluble multivitamins may be recommended as a nonspecific measure. If successive flocks are affected on the same site prophylactic medication ahead of the anticipated problem may be of benefit. 56 . growth plate disease.Treatment None. Prevention Good hygiene at turn-around. Culture of lesions to confirm the bacterium involved. osteomyelitis. Epiphysiolysis Introduction A complex condition of chickens that may be associated with trauma. rickets. Signs Fluid-distended abdomen. Erysipelothrixetc. Post-mortem lesions Right ventricular failure and ascites. Vegetative lesions usually on the right atrioventricular valve. The choice should depend on sensitivity testing of an isolate. Endocarditis Introduction A condition of chickens associated with several bacterial infections such as staphylococci. Diagnosis Differentiate from broiler ascites syndrome by examination of the interior of the heart. Treatment Medication is only likely to be of value in reducing deterioration in birds that are starting to develop lesions. streptococci. Prevention Vaccination with inactivated vaccine prior to lay. bacterial infection.
The natural hosts are wild birds and rodents. Treatment Not applicable. Post-mortem lesions Separation of epiphyses at the growth plate. Paralysis. chickens. 57 . sometimes seen in vivo. These conditions currently only occur from northern South America to North America. Prevention Control of predisposing factors. Signs Nervous symptoms. Ataxia. Horses are also seriously affected. wild birds. May also be asymptomatic. Tremors. histology may be helpful in identifying underlying problems such as rickets or 'FHN'. partridges. turkeys. Post-mortem lesions No gross lesions. Microscopic lesions not pathognomonic.Signs Apparent dislocation at extremities of long bones. Diagnosis Gross inspection. Equine Encephalitis (EEE. often occurs or is identified in the processed carcase. WEE. Paresis. Circling. It is transmitted between birds by pecking and by mosquitoes. VEE) Introduction A viral disease of pheasants. ducks and pigeons having a high morbidity and high mortality. Flaccid neck.
fishmeal and semen and by cannibalism. epicardium. ID by VN. TC. Liver. Erysipelas Introduction A sudden onset infection with the bacterium Erysipelothrix insidiosa (E. water. There is likely to be an increased risk if housing or land has been previously used by pigs or sheep. Depression. in soil. It may be transmitted by faecal carriers for 41 days. rarely in geese. Endocarditis. COFAL. Sudden death. ducks.Diagnosis Isolation in mice. Vaccinate at 5-6 week. Perineal congestion. Treatment None. Joint lesions. muscle. control cannibalism. Swollen snood. especially snood. Sleepiness. Chronic scabby skin. pheasants. Marked catarrhal enteritis. rhusiopathiae) seen in turkeys and increasingly in free-range chickens. It is also seen in some mammals. Prevention Protection from mosquitoes. Haemorrhages in fat. kidney. 58 . The bacterium is fairly resistant to environmental effects or disinfectants and may persist in alkaline soil for years. Post-mortem lesions Carcase congestion. Signs Inappetance. spleen swollen. May be diarrhoea and respiratory signs. and CE.
Sudden drop in egg production. Treatment Penicillin .a combination of the procaine and benzathine salts may be injected. often along with bacterin. Sudden death. Post-mortem lesions Obesity. the demonstration of the organism in stained impression smears from tissues. Prevention Good biosecurity to prevent spread from other susceptible species. and identification. Tetracyclines in feed may also be helpful. 59 . colibacillosis. Signs Overweight typically by 25%. especially caged layers and with a complex set of causes including excessive calories. history. Vaccination or natural infection may cause false positive reactions in the Mycoplasma gallisepticum and M. Diagnosis Lesions.Diagnosis Isolation on blood agar. Death by internal exsanguination after rupture of haematocyst. Headparts pale. vaccine at 16-20 weeks if the condition is enzootic. Liver yellow. Fatty Liver Haemorrhagic Syndrome Introduction A condition occurring worldwide in chickens. salmonellosis. deficiency and stress. synoviae plate tests for a few weeks. Differentiate from pasteurellosis. greasy and soft with numerous haemorrhages. and acute Newcastle disease. mycotoxins. Some birds with pale comb and wattles.
Trichophyton gallinae. of chickens and turkeys. Diagnosis Lesions. Loss of condition. avoid mycotoxins and stress. B 12 and inositol. It is very rare in commercial poultry production. vitamin E. culling affected birds. 60 . Favus Introduction A fungal infection. Thick crusty skin. supplement with choline. Treatment Formalin in petroleum jelly. Prevention Good hygiene of facilities.Treatment Reduce energy intake. isolation. Prevention Feed to avoid obesity. powdery spots and wrinkled crusts and scab on comb and wattles. Signs White. Feather loss. 'Honeycomb' skin. Post-mortem lesions See signs (above).
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. Post-mortem studies of birds culled due to lameness and of birds found dead. It is seen worldwide and was one of the first infectious 61 .Femoral Head Necrosis . highly contagious disease caused by the bacterium Pasteurella multocida in a range of avian species including chickens. E. especially hypophosphataemic. Signs Lameness. spondylolisthesis. Use of a wing for support during walking and hip flexion.FHN Introduction A condition of chickens and turkeys that may be associated with several different bacterial infections e. Pasteurellosis Introduction Fowl Cholera is a serious.g. arthritis. streptococci. rickets. staphylococci. and water fowl. FHN is the commonest infectious cause of lameness in broilers in the UK. Prevention Exclusion of floor eggs and dirty eggs from the hatchery. Post-mortem lesions Degeneration of the epiphyses of long bones with thinning of the cortex and tendency to break when force is applied. coli. Careful attention to mineral and Vitamin D nutrition to avoid subclinical. Differentiate from synovitis.75% of all male broilers placed had lesions in the hip bone. Fowl Cholera. (increasing order of susceptibility). turkeys. indicated that 0. Diagnosis Base on post-mortem lesions and isolation of a causative organism. Predisposing factors include immunosuppresive viruses such as Infectious Bursal Disease Virus and Chicken Anaemia Virus and non-infectious bone pathologies such as hypophosphaetamic rickets.
or limited to haemorrhages at few sites. by Louis Pasteur in 1880. Diagnosis Impression smears. erythromycin. confirmed with biochemical tests. Post-mortem lesions Sometimes none. Swollen joints. septicaemic viral and other bacterial diseases. Focal hepatitis. Diarrhoea. The bacterium is easily destroyed by environmental factors and disinfectants. contaminated soil. ocular and oral discharge.no growth on McConkey). 62 . Swollen and cyanotic wattles and face. necessitating long-term or periodic medication. The route of infection is oral or nasal with transmission via nasal exudate. Predisposing factors include high density and concurrent infections such as respiratory viruses. Differentiate from Erysipelas. Purulent arthritis. Yolk peritonitis. cats. penicillin. The disease often recurs after medication is stopped. Ruffled feathers. The incubation period is usually 5-8 days. Enteritis. equipment. Lameness. Treatment Sulphonamides. Lungs with a consolidated pink 'cooked' appearance in turkeys. tetracyclines. Nasal.diseases to be recognised. The disease can range from acute septicaemia to chronic and localised infections and the morbidity and mortality may be up to 100%. Signs Dejection. Coughing. Cellulitis of face and wattles. Sudden death. Loss of appetite. and possibly pigs. and people. Purulent pneumonia (especially turkeys). streptomycin. but may persist for prolonged periods in soil. isolation (aerobic culture on trypticase soy or blood agar yields colonies up to 3mm in 24 hours . Reservoirs of infection may be present in other species such as rodents. faeces.
63 . Poor egg production. fomites. and mosquitoes (infected for 6 weeks). Morbidity is 1095% and mortality usually low to moderate. Signs Warty. It is transmitted by birds. Pox. The swelling is made up of oedema and purulent exudates (pus). live oral vaccine at 6 weeks. The duration of the disease is about 14 days on an individual bird basis. throat and sometimes trachea. Fowl Pox. Figure 19. Depression. or by the respiratory route. pigeons and canaries worldwide. spreading eruptions and scabs on comb and wattles. and where there are biting insects. turkeys. It is more common in males because of their tendency to fight and cause skin damage.Prevention Biosecurity. The virus persists in the environment for months. bacterins at 8 and 12 weeks. Inappetance. hygiene. Avian Pox Introduction A relatively slow-spreading viral disease characterised by skin lesions and/or plaques in the pharynx and affecting chickens. Caseous deposits in mouth. 0-50%. Infection occurs through skin abrasions and bites. Poor growth. good rodent control. Severe localised Pasteurella infection in the swollen wattle of a 30-week-old male broiler parent chicken.
pharynx. There is good cross-immunity among the different viral strains. Figure 20. Microscopically . be caseous plaques in mouth.intra-cytoplasmic inclusions (Bollinger bodies) with elementary bodies (Borrel bodies). DNA probes. usually with chicken strain by wing web puncture. Turkeys by thigh-stick at 2-3 months. Flocks and individuals still unaffected may be vaccinated. Prevention By vaccination (except canary). check take at 7-10 days post vaccination. It is confirmed by IC inclusions in sections/ scrapings. isolation (pocks on CE CAM) with IC inclusions. Less commonly there may. Differentiate from Trichomoniasis or physical damage to skin. Diagnosis A presumptive diagnosis may be made on history. Treatment None. 64 . trachea and/or nasal cavities. Fowl pox lesions on the wattle of an adult broiler parent chicken. If there is evidence of secondary bacterial infection broad-spectrum antibiotics may be of some benefit. signs and post-mortem lesions.Post-mortem lesions Papules progressing to vesicles then pustules and scabs with distribution described above. Chickens well before production. in the diptheritic form. reproduction in susceptible birds.
early Infectious Bursal Disease Virus infection). usually over wings and breast. spleen. Treatment Sulphaquinoxaline. Loss of appetite. Diagnosis Clinical signs and/or lesions. Post-mortem lesions Patches of gangrenous skin with underlying emphysematous and/or sanguinous cellulitis. It occurs due to invasion of 'normal' wounds by 'normal' bacteria in immunosuppressed birds. Avoid skin trauma and immunosuppression (congenital CAV infection.Gangrenous Dermatitis. Signs Occasionally dejection. penicillin or amoxycillin. Gangrenous skin. wattles. rarely Clostridium noyvi / oedematiens. Morbidity may be up to 50% and mortality is high. Severe cellulitis especially of thighs. sometimes thighs and other parts. 65 . Sudden mortality. occasionally Staphylococcus aureus. especially following congenital Chick Anaemia Virus infection or early Infectious Bursal Disease Virus infection (Gumboro Disease). wings. Immunosuppression is therefore a predisposing factor. Necrotic Dermatitis Introduction A bacterial condition seen in chickens and usually caused byClostridium septicum. Swelling and infarction of the liver. Foci in liver. The spores of Clostridial bacteria are highly resistant in the environment. Recovery of an abundant growth of causative organism in recently dead birds. Prevention Good hygiene and management.
Treatment Flubendazole in feed. Signs Gasping. Gape Introduction Syngamus trachea. Loss of appetite and condition. The condition is seen more commonly in poultry on free range where ground may be contaminated by wild birds e. Prevention Flubendazole. pheasants. turkeys. Dyspnoea. Diagnosis Signs and lesions. Infection is by the oral route with earthworms. There is an 18-20 day prepatent period. a nematode worm parasite of chickens. confirmation of presence of the parasite. Head shaking. from rookeries. Post-mortem lesions Tracheitis. paired parasites up to 2 cm long. slugs and snails acting as transfer hosts but the life cycle may also be direct. Presence of worms.g. by ingestion of embryonated egg or L3.Figure 21. and other game and ornamental birds occurring worldwide. levamisole. Severe gangrenous dermatitis on the upper surface of the wing of a broiler chicken. 66 .
affecting geese and ducks. Loss in condition and weight. Signs Depression. Adults are 2-4 cm long and usually bright red. Gizzard worms . Treatment Levamisole. Prevention Prevention of access to intermediate hosts. benzimidazoles such as flubendazole. Signs Depression. They are more common in free-range birds because of their increased access to intermediate hosts.Geese Introduction A nematode worm parasite. Amidostomum anseris. muscular wall may be sacculated or ruptured. 67 . routine worming. Post-mortem lesions Ulceration. Diagnosis Lesions. Slow growth. confirmation of presence of the worms. necrosis and partial sloughing of gizzard lining. Slow growth. Worms develop to L3 in eggs and infection is by the oral route direct from environment. beetles etc act as intermediate hosts. Grasshoppers. and Histiocephalus are nematode worm parasites of chickens. weevils.Gizzard worms . Loss in condition and weight.Chickens Introduction Cheilospirura. Streptocara. Cheilospirura and Streptocara are seen worldwide but Histiocephalus is restricted to Europe.
Losses are negligible in birds over 5 weeks of age. Swollen eyelids and eye and nasal discharge. Vertical transmission resulting in congenital infection may occur. Derzsy's Disease is caused by a parvovirus distinct from chicken and mammalian parvoviruses. Prevention Rotation of ground on annual basis. Swelling and congestion of liver. Reduced feed intake. Profuse white diarrhoea. Excessive water intake. visualisation of worms.Post-mortem lesions Ulceration. Adults are 2-4 cm long and usually bright red. Goose Parvovirus (Derzsy's Disease) Introduction Goose Parvovirus is a highly contagious condition of geese and young Muscovy ducks. 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. Treatment Levamisole. Reddening of skin. Post-mortem lesions Pale myocardium. The younger the bird affected the more acute the condition and the higher the mortality. Membrane covering tongue. spleen and pancreas. 68 . Diagnosis Lesions. benzimidazoles. muscular wall may be sacculated or ruptured. Signs Prostration and death in acutely affected goslings. Loss of down. necrosis and partial sloughing of gizzard lining.
mycotoxins and viral infections and usually following a course of approximately 3 weeks. Pale comb and wattles. Ascites. Fibrinous perihepatitis. Bone marrow pale with fatty change. Antimicrobials may be of value in reducing the effects of secondary bacterial infections. Haemorrhagic Disease. Carcase anaemia. Haemorrhagic Anaemia Introduction A complex condition of chickens associated with drug toxicities. Morbidity varies. Aplastic Anaemia. mortality is 5-50%. Blood in droppings. Treatment No specific treatment. heart. Prevention Hatching and brooding geese from different parent flocks together should be avoided. 69 . Loss of appetite. serosa and mucosae. Fibrinous pericarditis. Liver yellow. Administration of immune serum has been shown to be effective but may require two doses (day old and around 3 weeks). Poor growth. muscles. Diagnosis Signs and lesions in birds of the appropriate age and species. Signs Dejection. liver. The preferred approach is to immunise breeding birds with an attenuated live vaccine. Post-mortem lesions Haemorrhages in one or more sites: skin. Ideally flocks that have suffered the disease should not be used for breeding as they may become persistent excreters of the infection.
Course 10-21 days. The virulence of the virus varies but morbidity may be 100% and mortality 10-60%. remove sulphonamides. The route of infection is usually oral. and weeks in litter. Serology: DID. 70 . Post-mortem lesions Petechiae in various tissues. Diagnosis Typical lesions. Spleen mottled and enlarged.Diagnosis History. lesions. Treatment Vitamin K. The source of virus is unknown but there is easy lateral spread within flocks. Intestine distended with blood. signs. similar to pheasant Marble Spleen disease. caused by Type II Adenovirus distinct from classical fowl adenovirus and occurring in most turkey-producing areas. Elisa . Microscopic . Drop in feed and water consumption. Diarrhoea. add liver solubles to feed. reticulo-endothelial hyperplasia and intranuclear inclusions. reproduction with filtered contents. Haemorrhagic Enteritis Introduction A viral disease of turkeys. double-immuno-diffusion of splenic extract.spleen shows lymphoid hyperplasia. May induce immunosupression and precipitate respiratory disease or coccidiosis. Prevention Avoid causative factors. Blood from vent of moribund birds. the virus surviving in frozen faeces for months. Signs Sudden deaths.sero-conversion frequently occurs in absence of clinical disease.
Immunity: there is an early age resistance irrespective of maternal antibody status.Treatment Warmth and good management. good hygiene and biosecurity. convalescent serum. and turkeys caused by high environmental temperature. feather cover. some in turkey B-lymphoblastoid cell lines. Immunity to the disease is long lasting. Some are produced in live turkeys. Increased thirst. In this case a loop of intestine has been opened to show the blood. acclimation. Maternal antibody may interfere with vaccination. Prevention All-in/all-out production. Disinfect and 3-4 weeks house rest. high stocking density. Predisposing factors include genetics. Ducks are relatively resistant to heat stress. nicarbazin in feed. drinking water temperature and availability. good management. Turkeys dying with haemorrhagic enteritis commonly have the small intestine distended with blood. Reduced feed consumption. Signs Panting. especially associated with high relative humidity and low air speed.and T-line lymphocytes for up to 5 weeks following exposure. Pathogenic strains can depress both B. Figure 39. oral tetraycline. Heat Stress Introduction A condition seen in chickens. Live vaccines are commonly used in many countries at 4-5 weeks of age. 71 .
Inter-species transmission may occur. pattern of losses. Hexamitiasis Introduction Hexamita meleagridis (pigeons H. if relative humidity is low then wet the roof and fog. Loss in weight. In commercial ducks a related parasiteTetratrichomonas can cause poor growth and drops in egg production. Prostration. Mucoid exudate in nostrils and mouth. evaporative coolers. columbae) is a protozoan parasite of turkeys. Frothy. Inappetance. pigeons. It is transmitted by faeces. Prevention Houses of optimal height and insulation. chirping. Diagnosis Temperature records. carriers. Reduced egg production. and some game birds. Post-mortem lesions Carcases congested. painted white to reflect heat. signs. watery diarrhoea. Later depression. Intestine flabby with some bulbous dilation. Terminal coma and convulsions. Feeding during cooler hours may be beneficial. pheasants. 72 . contains excessive mucus and gas. Reductions in stocking density of meat poultry may be quickly achieved by partial depletion ('thinning'). lesions. Post-mortem lesions Dehydration. fomites. Treatment Cool water. maximise airflow. exclusion of other conditions. Legs and wings outstretched. feed with a reduced protein:energy ratio. Signs Initially birds nervous.
Prevention Depopulation. pheasants and game birds that acts together with facultative bacteria to produce the condition of Blackhead. Progressive depression and emaciation. Blood in faeces (chickens). The effect of antibiotic may be related to the control of secondary bacterial enteritis. Signs Depression. This condition has high morbidity and mortality in turkeys. Inappetance. Within a turkey shed transmission is rapid in spite of the fact that it is difficult to infect birds orally with unprotected parasites. and mixing groups of different ages. It has recently been demonstrated that infection occurs readily via the cloaca when birds are on contaminated litter. scrapings from fresh material. Caecal tonsils congested. significant disease has been seen in breeding chickens and free-range layers. Outwith earth worms orH. presumably introduced with worm eggs. 73 . histomonosis. 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. Furazolidone. Differentiate from transmissible enteritis. hygiene. paratyphoid. and also. if possible. dimetridazole and ipronidazole have been used in the past. gallinae the parasite is easily destroyed. increase ambient temperature. and occasionally chickens. First half of intestine inflamed. Poor growth. Treatment Tetracycline. Histamonosis. Although chickens are relatively resistant to the condition. avoid interspecies mixing. trichomoniasis. all-in/all-out production. dimetridazole. Sulphur-yellow diarrhoea. Blackhead Introduction Histomonas melagridis is a protozoan parasite of turkeys. Cyanosis of head. Diagnosis Lesions. The problem is seen in high-biosecurity facilities. Histomoniasis.
nitrofurans (e. It is a condition caused by an adenovirus. Mortality may reach 60% but more typically 10-30%. grey or green areas. 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. 'Herban)' have been used with some apparent success though controlled trials and formal approval for this purpose are not recorded. The disease is readily reproduced by inoculating birds with a bacteria-free filtrate of a liver extract from an affected bird. Some herbal products based on the essential oils (e. and only nitarsone is approved in the USA. 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. dimetridazole). avoid mixing species. given recent new knowledge on the mechanism of transmission.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. however they may not be present in the early stages.g. usually grey in colour. Hydropericardium-Hepatitis Syndrome.Tahir Post-mortem lesions Enlargement of caeca. Liver may have irregular-round depressed lesions. Having both chickens and turkeys on the same property is likely to increase the risk of this disease in turkeys. concrete floors. nifursol) and arsenicals (e. Diagnosis Lesions.g. Intensive relittering may help reduce the level of infection. Ulcers. caseous cores with yellow. Treatment Historically nitro-imidazoles (e. Arsenicals are less effective in treatment than they are in prevention. scrapings from fresh material. furazolidone.nitarsone) have been used to treat this important disease of poultry.Abubakar. 74 . Use of an anti-histomonas product in feed where such products are approved but due care with respect to residue avoidance would be required.M. especially in chickens. Angara Disease Introduction This condition was first identified in broilers in Pakistan in 1987. Prevention Good sanitation.g.
1% of a 2. Diagnosis Lesions. Lungs oedematous. Formalin-inactivated oil adjuvant vaccines are reported to be highly effective and are used in areas where the condition is endemic. Congestion of the carcase. histopathology. however sometimes free-range poultry consume large stones. Treatment None. Older birds ingest grit to facilitate the grinding activity in the gizzard. and birds of any age can 75 . treatment of drinking water with 0. pale friable liver and kidney. The normal function of the gizzard is to aid in the physical grinding of food materials. Lethargy. This condition usually affects only a small number of birds. Yellow mucoid droppings. Most young commercial poultry consume feeds that have a small particle size. Grit would not be classed as a foreign body. to reduce their particle size to aid digestion. Control of predisposing immunosuppressive diseases may help limit losses. grass.5% iodophor solution) appears to be beneficial. Huddling with ruffled feathers. however if young chicks to do not begin to eat feed properly they often consume litter instead. virology. Post-mortem lesions Excessive straw-coloured fluid distending the pericardium (up to 10 mls). Enlarged. Impaction and Foreign Bodies of Gizzard Introduction The gizzard or crop may become impacted with litter. Impacted gizzards are then found in 'non-starter' type chicks or poults.Signs Sudden increase in mortality.g. Good water sanitation (e. Gizzard activity also acts as a pacemaker of intestinal activity and controls the speed at which food is passed to the small intestine. Prevention The condition typically occurs in areas of high poultry density where multi-age operation is traditional. string etc.
15 days with a morbidity of 1-10% and a mortality of 1-10%. It has a course of 9. The disease was first described in the USA in 1963 and has also been reported in Canada. Daily monitoring of the crop-fill is a useful procedure. This usually happens after maintenance activities have been carred out in the housing. caused by an adenovirus.consume nails. Italy. A foreign body may be found in the interior of the gizzard. Australia. often with severe anaemia. Prevention Good brooding management to encourage early adaptation to the diet and adequate consumption of feed and water. Post-mortem lesions The gizzard is more firm than normal and. Diagnosis Lesions. Nails commonly penetrate the lining of the gizzard. and may penetrate the body wall. Treatment None effective in young birds. Sweep floors after maintenance activities to remove nails and other potentially dangerous foreign bodies. the UK. Infected birds remain carriers for a few weeks. staples etc. 76 . This may extend into the proventriculus and on into the duodeunum. 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. A number of different sero-types have been isolated from disease outbreaks but they may also be isolated from healthy chickens. France and Ireland. Signs Reduced feed intake. Obvious non-starters should be culled in this situation. Inclusion Body Hepatitis Introduction A disease of chickens characterised by acute mortality. and on opening is found to contain a mass of fibrous material. Reduced weight gain.
Post-mortem lesions Liver swollen. pH). Progeny of high health status breeding flocks appear to be at greater risk. Ruffled feathers. Differentiate from Chick anaemia syndrome. Infectious Bursal Disease. SN for individual sero-types. Confirmation is made on finding inclusions in the liver. may be important. perhaps because they have lower levels of maternal antibody. 77 . vibrionic hepatitis. and high temperatures. mottled with petechiae and ecchymoses. yellow. Pallor of comb and wattles. Serology: DID for group antigen. but on the other hand many field cases show eosinophilic inclusions that do not appear to have adenovirus particles.Transmission may be vertical or lateral and may involve fomites. and deficiency of vitamin B12. Microscopically . The virus is generally resistant to disinfectants (ether. Since adenoviruses are commonly found in healthy poultry. Signs Depression. Bursa and spleen small. Curiously. fatty liver syndrome. A form of the disease affecting birds under 3 weeks of age in Australia has been reproduced with serotype 8 adenovirus. The virus grows well in tissue culture (CEK.basophilic intranuclear inclusions. Immunosuppression. Diagnosis A presumptive diagnosis may be made on history and lesions. CEL). Soluble multivitamins may help with the recovery process. Treatment None. many different sero-types have been isolated from different cases. Formaldehyde and iodides work better. Kidneys and bone marrow pale. sulphonamide intoxication. Blood thin. chloroform. for instance due to early IBD challenge or congenital CAV infection. isolation alone does not confirm that they are the cause of a particular problem. Inappetance.
1931). alkalis. dyspnoea. probably the commonest respiratory disease of chickens. The virus. Tracheal oedema. About eight sero-groups are recognised by sero-neutralization. Some birds/viral strains can be carriers to 1 year. Coughing. The cause is a Coronavirus that is antigenically highly variable. Diarrhoea. which may survive 4 weeks in premises. gasping. Poor ventilation and high density are predisposing factors. fomites or aerosol. Typing by haemagglutination-inhibition is also used. Signs Depression. Diuresis. Kidneys and bronchi may be swollen and they and the ureters may have urates. new sero-types continue to emerge.Prevention Quarantine and good sanitary precautions. Morbidity may vary 50-100% and mortality 0-25%. Wet litter. IB Introduction This infection. Tracheitis. the age of the bird. disinfectants (Formal 1% for 3 mins). was first described in the USA (N. Huddling. The infection is highly contagious and spreads rapidly by contact. maternal immunity (young birds). These differences are due to structural differences in the spike proteins (S1 fraction). depending on secondary infections. Newcastle disease). Caseous plugs in bronchi. Post-mortem lesions Mild to moderate respiratory tract inflammation. heat (56°C for 15 mins). prior vaccination. Its affects vary with: the virulence of the virus. Infection is via the conjunctiva or upper respiratory tract with an incubation period of 18-36 hours. prevention of immunosuppression. Airsacculitis. 78 . E. and complicating infections (Mycoplasma. Loss of appetite. Dakota. is sensitive to solvents. coli. Infectious Bronchitis.
flourescent antibody positive and ciliostasis in tracheal organ culture. Treatment Sodium salicylate 1gm/litre (acute phase) where permitted . Poor ventilation and high density are predisposing factors. Definitive diagnosis is based on viral isolation after 3-5 passages in chick embryo.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%.). with typical lesions. Differentiate from Newcastle disease (lentogenic and mesogenic forms). Maternal immunity provides protection for 2-3 weeks. Elisa (both group specific). Signs Sudden death. depending on secondary infections. short duration. Otherwise as for standard IB. IB . Infectious Bronchitis. The virus. possible reactions depending on virulence and particle size. Muscular shivering. Humoral immunity appears 10-14 days post vaccination. Infection is via the conjunctiva or upper respiratory tract with an incubation period of 18-36 hours. Local immunity is first line of defence. Serology: HI. fomites or aerosol. disinfectants (Formal 1% for 3 mins). lesions and serology. The infection spreads rapidly by contact. HA negative. is sensitive to solvents. group specific). 79 . DID (poor sensitivity. SN (type specific). Prevention Live vaccines of appropriate sero-type and attenuation. heat (56°C for 15 mins). which may survive 4 weeks in premises. vaccinal reactions. Avian Influenza and Laryngotracheitis. alkalis.Diagnosis Tentative diagnosis is based on clinical sgns.v. Cellmediated immunity may also be important.antibiotics to control secondary colibacillosis (q. mycoplasmosis. Some birds/viral strains can be carriers for up to 1 year.
In layers the ovules may be intensely congested. ciliostatic in tracheal organ culture. IB Egg-layers Introduction A Coronavirus infection of chickens. Signs Drop in egg production (20-50%). Loss of internal egg quality. Infection is via the conjunctiva or upper respiratory tract. Treatment Sodium salicylate 1gm/litre (acute phase) where permitted . group specific). Rales may or may not be present. The virus is moderately resistant and may survive 4 weeks in premises. Rough shells. DID (poor sensitivity. lesions progress to necrosis and scarring of deep pectorals in convalescence. short duration. The condition has a morbidity of 10-100% and mortality of 0-1%. Other lesions of 'classical' IB may be encountered. CK) only after adaptation Serology: HI. SN (type specific). Prevention Live vaccines of appropriate sero-type and attenuation. fomites or aerosol. cell culture (Vero. Coughing. Elisa (both group specific). possible reactions depending on virulence and particle size. FA. A few birds are carriers up to 49 days post infection.Post-mortem lesions Oedema of pectoral muscles and subcutaneously on abdomen. typical lesions.antibiotics to control secondary colibacillosis (q. Infectious Bronchitis. Soft-shelled eggs. HA-. 80 . There is rapid spread by contact. Diagnosis 3-5 passages in CE allantoic cavity.v. with much antigenic variation. Poor ventilation and high density are predisposing factors. sneezing.).
). Figure 22. Humoral immunity appears 10-14 days post vaccination. Cell-mediated immunity may also be important. HA-. typical lesions. Prevention Live vaccines of appropriate sero-type and attenuation. SN. Maternal immunity provides protection for 2-3 weeks. DID. Local immunity is the first line of defence. 81 .v.Post-mortem lesions Follicles flaccid. Treatment Sodium salicylate 1gm/litre (acute phase) where permitted . FA. Diagnosis 3-5 passages in CE. EDS76. Elisa. although reactions can occur depending on prior immunity. Serology: HI. Differentiate from Egg Drop Syndrome. particle size (if sprayed) and general health status. virulence.antibiotics to control secondary colibacillosis (q. Flaccid ovarian follicles in a broiler parent chicken undergoing challenge with Infectious Bronchitis virus. Yolk in peritoneal cavity (non-specific).
Infectious Bronchitis. Serology: HI. Yolk in peritoneal cavity (non-specific). Prevention Live vaccines of appropriate sero-type and attenuation. Diagnosis 3-5 passages in CE. Local immunity is the first line of defence. Signs Drop in egg production (20-50%). Elisa. Rales may or may not be present. The virus is moderately resistant and may survive 4 weeks in premises. Humoral immunity appears 10-14 days post vaccination. EDS76. FA. Loss of internal egg quality. virulence. Post-mortem lesions Follicles flaccid.). The condition has a morbidity of 10-100% and mortality of 0-1%. There is rapid spread by contact. Soft-shelled eggs. sneezing. Coughing. HA-. with much antigenic variation. typical lesions. Treatment Sodium salicylate 1gm/litre (acute phase) where permitted . IB Egg-layers Introduction A Coronavirus infection of chickens.v. SN. DID. 82 . Infection is via the conjunctiva or upper respiratory tract. A few birds are carriers up to 49 days post infection. fomites or aerosol. Rough shells.antibiotics to control secondary colibacillosis (q. Differentiate from Egg Drop Syndrome. Cell-mediated immunity may also be important. Poor ventilation and high density are predisposing factors. Maternal immunity provides protection for 2-3 weeks. although reactions can occur depending on prior immunity. particle size (if sprayed) and general health status.
with an incubation period of 2-3 days. and affected birds excrete large amounts of virus for about 2 weeks post infection. seen worldwide. the damage caused to the immune system interacts with other pathogens to cause significant effects. especially with sero-type 2). which targets the bursal component of the immune system of chickens. Generally speaking the earlier the damage occurs the more severe the effects. The virus is very resistant. In addition to the direct economic effects of the clinical disease. There is no vertical transmission. Subclinical infection in young chicks results in: deficient immunological response to Newcastle disease. The route of infection is usually oral. 83 . The infective agent is a Birnavirus (Birnaviridae). The disease is highly contagious. susceptibility to Inclusion Body Hepatitis and gangrenous dermatitis and increased susceptibility to CRD. IBD. Infectious Bursal Disease. The age up to which infection can cause serious immunosuppression varies between 14 and 28 days according to the antigen in question. Sero-type 1 only.20% but sometimes up to 60%. Gumboro Introduction A viral disease. but may be via the conjunctiva or respiratory tract.Figure 22. faeces etc. Flaccid ovarian follicles in a broiler parent chicken undergoing challenge with Infectious Bronchitis virus. Morbidity is high with a mortality usually 0. Mealworms and litter mites may harbour the virus for 8 weeks. first identified in the USA in 1962. persisting for months in houses. Marek's disease and Infectious Bronchitis. (Turkeys and ducks show infection only. Signs are most pronounced in birds of 4-6 weeks and White Leghorns are more susceptible than broilers and brown-egg layers.
Diarrhoea with urates in mucus. Diagnosis Clinical disease .History. (previously SN and DID). 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. The normal weight of the bursa in broilers is about 0. Half-life of maternally derived antibodies is 3. Vent pecking. subsequent diagnosis of 'immunosuppression diseases' (especially inclusion body hepatitis and gangrenous dermatitis) is highly suggestive. They are all serotype 1. Inappetance. normal size or reduced in size depending on the stage). Antibiotic medication may be indicated if secondary bacterial infection occurs. Treatment No specific treatment is available. Differentiate clinical disease from: Infectious bronchitis (renal). rapidly proceeds to atrophy.4 days. Huddling under equipment. especially if present prior to 20 days of age. Haemorrhages in skeletal muscle (especially on thighs). Post-mortem lesions Oedematous bursa (may be slightly enlarged. Use of a multivitamin supplement and facilitating access to water may help.1% are highly suggestive.A history of chicks with very low levels of maternal antibody (Fewer than 80% positive in the immunodifusion test at day old. This may be confirmed by demonstrating severe atrophy of the bursa. Cryptosporidiosis of the bursa (rare). Variants: There have been serious problems with early Gumboro disease in chicks with maternal immunity. Dehydration.3% of bodyweight. may have haemorrhages. Elisa vaccination date prediction < 7 days). weights below 0. 84 . Swollen kidneys with urates. Coccidiosis.Signs Depression.5. IBD viruses have been isolated and shown to have significant but not complete cross-protection. Unsteady gait. histopathology. especially in the Delmarva Peninsula in the USA. Haemorrhagic syndrome. Other possible causes of early immunosuppression are severe mycotoxicosis and managment problems leading to severe stress. Tests used are mainly Elisa. Subclinical disease . lesions. Serology: antibodies can be detected as early as 4-7 days after infection and these last for life.
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. and tracing of contacts may indicate sites on which a more rebust vaccination programme is indicated. highly infectious disease of chickens. A strong immunity follows field challenge. Immunity after a live vaccine can be poor if maternal antibody was still high at the time of vaccination. When outbreaks do occur. vaccination of progeny depending on virulence and age of challenge. Infectious Coryza Introduction A usually acute. This shows the anatomical relationship between the bursa. sometimes chronic. occasionally pheasants and guinea-fowl. It is not egg transmitted. 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. Morbidity is high but mortality low if uncomplicated although it may be up to 20%. characterised by catarrhal inflammation of the upper respiratory tract. biosecurity measures may be helpful in limiting the spread between sites. This bursa is from an acutely affected broiler. Figure 23. resulting in increased culling. including passive protection via breeders. turgid and oedematous. Infectious Coryza is caused by the bacterium Haemophilus paragallinarum and is seen in many countries especially in multi-age farms that are never depopulated.Prevention Vaccination. It is enlarged. Carriers are important with transmission via exudates and by direct contact. 85 . especially nasal and sinus mucosae. the rectum and the vent.
Conjunctivitis. Birds recovered from challenge of one serotype are resistant to others. Flouroquinolones are bactericidal and might prevent carriers. Intercurrent respiratory viral and bacterial infections are predisposing factors. Inappetance. Drop in egg production of 10-40%. sulphonamides. preferably in raised CO 2 such as a candle jar. at least two doses are required. Live attenutated strains have been used but are more risky. Serology: HI. tylosin. Loss in condition. Treatment Streptomycin. Differentiate from Mycoplasmosis. 86 . Prevention Stock coryza-free birds on an all-in/all-out production policy.requires X (Haematin) and V (NAD) factors. chronic or localised pasteurellosis and vitamin A deficiency. drying and disinfectants. erythromycin. Dihydrostreptomycin. Commercial bacterins may not fully protect against all field strains but reduce the severity of reactions. identification of the bacteria in a Gram-stained smear from sinus. Confirmation is by isolation and identification . agglutination and IF have all been used but are not routine. while bacterins only protect against homologous strains. Diagnosis A presumptive diagnosis may be made on signs. Caseous material in conjunctiva/sinus. Signs Facial swelling. Tracheitis. DID. Eye-lid adherence. respiratory viruses. Vaccines are used in areas of high incidence. Purulent ocular and nasal discharge. Dyspnoea.The bacterium survives 2-3 days outside the bird but is easily killed by heat. Post-mortem lesions Catarrhal inflammation of nasal passages and sinuses. Bacterin at intervals if history justifies or if multi-age. lesions. Controlled exposure has also been practised. Sneezing. Swollen wattles.
Microscopically . 87 . Nasal discharge (low pathogenicity strains). Signs Dyspnoea.intranuclear inclusions in tracheal epithelium. in severe form may be enough. lesions. PCR. The virus is highly resistant outside host but is susceptible to disinfectants. Differentiate from Newcastle disease. Post-mortem lesions Severe laryngotracheitis. Gasping. Coughing of mucus and blood. severe bronchitis. Keep susceptible stock separate from vaccinated or recovered birds. often with blood in lumen. Fairly slow lateral spread occurs in houses. peafowl and turkeys with a morbidity of 50-100% and a mortality usually 10-20% but sometimes up to 70%. Apply strict biosecurity in moving equipment or materials between these these categories of stock. Drop in egg production. Sera may be examined by VN or Elisa. histology. vaccination. if enzootic or epizootic in an area. antibiotics to control secondary bacterial infection if this is marked.Infectious Laryngotracheitis. Isolation in CE CAMs. Diagnosis Signs. pheasants. Ocular discharge. All-in/allout operation. Recovered and vaccinated birds are long-term carriers. 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. Treatment None. Sinusitis. Movement and mixing of stock and reaching point of lay are predisposing factors. Transmission between farms can occur by airborne particles or fomites. caseous plugs may be present. ILT Introduction A herpesvirus (pathogenicity can vary) infection of chickens. IFA. Prevention Quarantine. after 4 weeks of age.
Diagnosis Typical post-mortem lesions Treatment As appropriate for the underlying disease condition. Post-mortem lesions Telescoping of the bowel. Coccidiosis. Anorexia.Intussusception Introduction A condition of chickens associated with increased intestinal motility. Simulid flies or culicoid midges are intermediate hosts. Careful attention to feeding practices to avoid anticipation of feed arrival if on restricted feeding. usually in the lower small intestine. Survivors may carry infection. The disease has a short course and morbidity and mortality are high. Asia and Africa. Signs Mainly sudden deaths. Prevention Control of coccidiosis and other causes of intestinal inflammation. ducks. Loss of equilibrium. guinea fowl. Leukocytozoonosis Introduction Caused by Leucocytozoon species. 88 . worms and other forms of enteritis are predisposing factors. Signs Sudden onset of depression. protozoan parasites of turkeys. rarely chickens. it may actually protrude at the vent and be cannibalised. Thirst. Different species of this parasite have been reported from North America. Rapid breathing.
Treatment None known. age. Anaemia. gametes in erythrocytes. especially in enlarged spleen. Enlargement of abdomen. lesions. Diagnosis Lesions. Differentiate from Reticuloendotheliosis. schizonts in liver. May be asymptomatic. Lymphoproliferative Disease (LPD) Introduction A Type C retrovirus infection of turkeys with low morbidity and high mortality. disposal of recovered birds. Post-mortem lesions Splenomegaly. cytology. Hepatomegaly. Anaemia. Emaciation. Diagnosis History. Persistent low mortality. Prevention Separation from intermediate hosts. Signs Depression. Microscopically . Loss of weight.megaschizonts in brains of birds with nervous signs. histology and blood smears. liver or bursa. Treatment 89 . Post-mortem lesions Focal tumours.
Post-mortem lesions Enteritis. Treatment Daily cull of affected birds between 14 and 28 days. North and South America and Australia. Diarrhoea. all-in/all-out production. Diarrhoea in older birds may be an effect of on-farm infection.Tahir None. Runting (permanent). Pale shanks in corn. Pancreatic atrophy/fibrosis and pancreatic atrophy (rather variable). Pot-bellied appearance. reoviruses.(maize-) fed birds (often associated with orange intestinal contents and/or faeces). rotavirus etc. 90 . Poor early management (feed and water supply. It is suspected that these viruses can be vertically transmitted and the most severe signs in young birds are associated with this. Eating faeces. Abnormal feathers ('helicopter wings' 'yellow-heads'). Runting/Stunting Introduction A condition of chickens and turkeys that may be associated with several different viruses. in future eradication.M. Prevention Good hygiene. Diagnosis Pathology. direct electron microscope examination of intestinal contents. temperature control) may lead to a similar picture in the absence of specific infection.Abubakar. Signs Uneven growth. Malabsorption Syndrome. for example enteroviruses. Stunting (temporary). Sometimes osteomyelitis and/or rickets. Poor management may contribute to the problem. control arthropods. enterovirus-like particles. Poor feathering. The condition has been seen in Europe.
muscles.Tumours in heart.Tumours of feather follicles. fomites. as well as more longstanding paralysis of legs or wings and eye lesions.poorly digested food enclosed in mucus. good parent nutrition and egg selection and santitation. They are distended with poorly digested feed. seen worldwide.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. The route of infection is usually respiratory and the disease is highly contagious being spread by infective feather-follicle dander. The disease has various manifestations: a) Neurological . tests. both parasitic and bacterial. Infected birds remain viraemic for life. c) Cutaneous . In 'late' Marek's the mortality can extend to 40 weeks of age. A sample of the faeces produced is shown at the bottom of the picture . The virus survives at ambient temperature for a long time (65 weeks) when cell associated 91 . b) Visceral . Figure 24. lungs. Morbidity is 10-50% and mortality up to 100%.Prevention Good broiler farm hygiene. avoidance of intercurrent disease and management problems (such as chilling). Vertical transmission is not considered to be important. Intestines of a young broiler chick suffering from malabsorption syndrome. ovary. etc. Mortality in an affected flock typically continues at a moderate or high rate for quite a few weeks. and rarely turkeys in close association with chickens. Affected birds are more susceptible to other diseases. Marek's disease Introduction Marek's disease is a Herpes virus infection of chickens.
association with other strains (SB1 Sero-type 2) and Rispen's.. Genetics can help by increasing the frequency of the B21 gene that confers increased resistance to Marek's disease challenge. Signs Paralysis of legs. Vision impairment. wings and neck. clinical signs. turkeys. Grey iris or irregular pupil. M. It is inactivated rapidly when frozen and thawed. pigeons and other wild birds. lung.lymphoid infiltration is polymorphic. Loss of weight. It is common practice to use combinations of the different vaccine types in an effort to broaden the protection achieved. distribution of lesions. Microscopically . chronic respiratory disease in chickens. deficiency of Ca/Phosphorus/Vitamin D. gonads. and skeletal muscle.g.Chicken Introduction Infection with Mycoplasma gallisepticum is associated with slow onset. all-in/all-out production. resistant strains. Treatment None. kidney. game birds.and is resistant to some disinfectants (quaternary ammonium and phenol). especially at the start of lay. Prevention Hygiene. heart. Differentiate from Lymphoid leukosis. Skin around feather follicles raised and roughened. age affected. histopathology. Ducks and geese can 92 . Post-mortem lesions Grey-white foci of neoplastic tissue in liver. deficiency of thiamine. vaccination generally with 1500 PFU of HVT at day old (but increasingly by in-ovo application at transfer). Mycoplasma gallisepticum infection. botulism. Thickening of nerve trunks and loss of striation. Chronic Respiratory Disease . spleen. Diagnosis History.
Spread is slow between houses and pens suggesting that aerosols are not normally a major route of transmission. isolation and identification of organism. Slow growth. Diagnosis Lesions. In others it is actually increasing because of more birds in extensive production systems that expose them more to wild birds. Catarrhal inflammation of nasal passages. ART). Survival seems to be improved on hair and feathers. morbidity may be minimal and mortality varies. virulent E. and in lyophilised material. The route of infection is via the conjunctiva or upper respiratory tract with an incubation period of 6-10 days. Occasional encephalopathy and abnormal feathers. sinuses. Inappetance. or by direct contact with birds. In adult birds. though in some countries this infection is now rare in commercial poultry. more commonly in Mycoplasma Broth followed by plating out on Mycoplasma Agar. The infectious agent survives for only a matter of days outwith birds although prolonged survival has been reported in egg yolk and allantoic fluid. Intercurrent infection with respiratory viruses (IB. and inadequate environmental conditions are predisposing factors for clinical disease. The condition occurs worldwide. Pasteurella spp. demonstration of specific DNA (commercial PCR kit available). though infection rates are high. Haemophilus. ND. coli infection). coli. 93 . Culture requires inoculation in mycoplasma-free embryos or. Perihepatitis (especially with secondary E. and to a lesser extent fomites. airborne dust and feathers.become infected when held with infected chickens. Leg problems. Occasionally arthritis. Transmission may be transovarian. subsequent stress may cause recurrence of disease. Pericarditis. exudates. Reduced hatchability and chick viability. aerosols. tenosynovitis and salpingitis in chickens. Suspect colonies may be identified by immuno-flourescence. Fomites appear to a significant factor in transmission between farms. Post-mortem lesions Airsacculitis. serology. trachea and bronchi. Stunting. Nasal and ocular discharge. Recovered birds remain infected for life. Poor productivity. Signs Coughing. In turkeys it is most associated with severe sinusitis (see separate description in the turkey section).
Serology: serum agglutination is the standard screening test. generally as a confirmatory test.g. meleagridis(turkeys). Infectious Sinusitis . or by direct contact with birds. vitamin A deficiency. HI may be used. suspect reactions are examined further by heat inactivation and/or dilution. infection status is important for trade in birds. Live attenuated or naturally mild strains are used in some countries and may be helpful in gradually displacing field strains on multi-age sites. and routine serological monitoring. therefore M. Some inactivated vaccines for other diseases induce 'false positives' in serological testing for 3-8 weeks. hatchingeggs and chicks.-free stock. fluoroquinolones. PCR is possible if it is urgent to determine the flock status. though in many countries this infection is now rare in commercial poultry. In some circumstances preventative medication of known infected flocks may be of benefit. Recovered birds remain infected for life. Suspect flocks should be re-sampled after 2-3 weeks. viral respiratory diseases. 94 . exudates. spiramycin. Morbidity is low to moderate and mortality low. all-in/all-out production. subsequent stress may cause recurrence of disease. and fomites.g. tylosin. biosecurity.g. It is seen worldwide. tetracyclines. other Mycoplasma infections such as M. Elisa is accepted as the primary screening test in some countries. Aspergillosis. The route of infection is via the conjunctiva or upper respiratory tract with an incubation period of 6-10 days.Turkeys Introduction A slow onset chronic respiratory disease of turkeys often with severe sinusitis and associated with Mycoplasma gallisepticuminfection. M. Effort should be made to reduce dust and secondary infections. Productivity in challenged and vaccinated birds is not as good as in M. Treatment Tilmicosin. Mycoplasma gallisepticum infection. aerosols. Transmission may be transovarian. Prevention Eradication of this infection has been the central objective of official poultry health programmes in most countries. Differentiate from Infectious Coryza. These programmes are based on purchase of uninfected chicks.. synoviae and M.
often with inspissated pus. PCR is possible if it is urgent to determine the flock status. Swollen sinuses. Nasal and ocular discharge. Airsacculitis. Stress. Pericarditis. Treatment Tilmicosin. Some inactivated vaccines induce 'false positives' in serological testing. Differentiate from viral respiratory disease. especially Turkey Rhinotracheitis. although prolonged survival has been reported in egg yolk and allantoic fluid.The infectious agent survives for only a matter of days outwith birds. Suspect colonies may be identified by immunofluorescence. Leg problems. These are based on purchase of uninfected poults. more commonly in Mycoplasma Broth followed by plating out on Mycoplasma Agar. HI may also be used. isolation and identification of organism. Slow growth. of swabs taken from the trachea or lesions. Signs Coughing. Inappetance. demonstration of specific DNA (commercial kit available). Post-mortem lesions Swollen infraorbital sinuses. Effort should be made to reduce dust and secondary infections. and in lyophilised material. all-in/allout production. and biosecurity. malnutrition. suspect reactions are examined further by heat inactivation and/or dilution. Serology: serum agglutination is the standard screening test. serology. intercurrent viral disease such as Newcastle disease (even lentogenic) and Turkey Rhinotracheitis are predisposing factors. Diagnosis Lesions. tetracyclines. Culture. Perihepatitis. Prevention Eradication of this infection has been the central objective of official poultry health programmes in most countries. requires inoculation in mycoplasma-free embryos or. 95 . tylosin. Survival seems to be improved on hair and feathers. spiramycin. Stunting. In some circumstances preventative medication of known infected flocks may be of benefit. Suspect flocks should be re-sampled after 2-3 weeks. fluoroquinolones.
Infection occurs via the conjunctiva or upper respiratory tract and transmission among poults may be vertical. perhaps because all affected embryos fail to hatch. Reduced hatchability. and can occur in other poultry and wild bird species. 96 .i. Mycoplasma iowae infection. M.g. ducks (France).Mycoplasma immitans infection Introduction Infection with Mycoplasma immitans is seen in geese. Post-mortem lesions Stunted embryos with hepatitis and enlarged spleens. Prevention As for M. Leg lesions can be shown in inoculated birds but do not seem to occur naturally. some with down abnormality. Introduction Infection with Mycoplasma iowae is seen in turkeys. venereal or horizontal.g. Treatment As for M. Diagnosis Shows cross reaction in IFA to M.g. although DNA homology is only 40%. Signs Embryonic mortality. Signs Swollen sinuses. and partridges (UK). Post-mortem lesions Sinusitis.
Infected eggs result in widespread distribution of infection and increased risk of further vertical transmission. Transmission is venereal in breeders. The infective agent does not survive well outside the bird.m. Mycoplasma meleagridis infection. Leg problems. purchase of M. Introduction A disease of turkeys characterised by respiratory and skeletal problems caused by Mycoplasma meleagridis. Pathogenicity is quite variable. In adult birds though infection rates are high. though up to 25% of infected birds show lesions at slaughter. maintenance of this status by good biosecurity.-free stock. Crooked necks. Treatment Pressure differential dipping has been used where breeder flocks are infected. When the vacuum is released the eggs draw in antibiotic solution which is subsequently absorbed through the shell membranes. Infection is via the conjunctiva or upper respiratory tract with an incubation period of 6-10 days. with transovarian and then lateral spread in meat animals. morbidity may be minimal.i. Infected parents may be asymptomatic. Signs Reduced hatchability.Diagnosis Isolation and identification of the causative organism from dead-in-shell embryos. M. Specialised dip tanks are subjected to negative pressure which partially collapses the air cell of the submerged eggs. For eradication purposes egg injection provides more consistent dosing per egg than does egg dipping. This can increase hatchability by 510% in this situation. it occurs in most turkey-producing countries but is now much rarer in commercial stock. Mortality is low. Stunting. Antibiotics that have been used are tylosin and enrofloxacin. Slow growth. Prevention Eradication of the infection from breeding stock. The organism has also been isolated from raptors. Predisposing factors include stress and viral respiratory infections. Mild respiratory problems. 97 .
tetracyclines. serology. Mycoplasma synoviae infection. demonstration of specific DNA (commercial kit available). Culture requires inoculation in mycoplasma-free embryos or. Infection rates may be very high. Survival of the infectious agent outwith the bird is poor but fomite transmission between farms is important. Spread is generally rapid within and between houses on a farm. Airsacculitis (rarely) seen in adult birds. more commonly in Mycoplasma Broth followed by plating out on Mycoplasma Agar. 98 . Effort should be made to reduce dust and secondary infections. It occurs in most poultry-producing countries. Serology: SAG used routinely . Birds infected from their parents seem to be immuno-tolerant and particularly prone themselves to transmit. fluoroquinolones. Treatment Tylosin. Vaccines are not normally used. Differentiate from Mycoplasma gallisepticum. or lateral via respiratory aerosols and direct contact. Suspect colonies may be identified by immuno-fluorescence. other respiratory viruses. Mycoplasma synoviae. Infected birds do develop some immunity. Infected males are particularly prone to transmit infection and may warrant special attention. spiramycin.Post-mortem lesions Airsacculitis in infected pipped embryos and poults. Infection is via the conjunctiva or upper respiratory tract with a long incubation period. especially in commercial layer flocks. These are based on purchase of uninfected poults.culture used to confirm. Prevention Eradication of this infection is also possible using similar techniques as for Mycoplasma gallisepticum. Transmission may be transovarian. Infectious Synovitis Introduction Infection with Mycoplasma synoviae may be seen in chickens and turkeys in association with synovitis and/or airsacculitis. M. Predisposing factors include stress and viral respiratory infections. Diagnosis Lesions. whilst illness is variable and mortality less than 10%. and biosecurity. In some circumstances preventative medication of known infected flocks may be of benefit. isolation and identification of organism. 11-21 days following contact exposure.s. all-in/all-out production.
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.
usually in less than 48 hours. high levels of most growth promotors and normal levels of ionophore anticoccidials also help. usually of the mid. Ruffled feathers. other debilitating diseases. Inappetance. caused by Clostridium perfringens and characterised by a fibrino-necrotic enteritis. Closed eyes.M.Abubakar. Diagnosis A presumptive diagnosis may be made based on flock history and gross lesions Confirmation is on the observation of abundant rods in smears from affected tissues and a good response to specific medication. Reflux of bile-stained liquid in the crop if upper small intestine affected. in ducks possibly heavy strains. Affected birds tend to be dehydrated and to undergo rapid putrefaction. Sudden death in good condition (ducks). high viscosity diets (often associated with high rye and wheat inclusions in the diet). in drinking water. Intestinal mucosa with diptheritic membrane.small intestine. or Bacitracin in feed (e. Dark coloured diarrhoea. Signs Depression. Immobility.g.Tahir Necrotic Enteritis Introduction An acute or chronic enterotoxemia seen in chickens. Predisposing factors include coccidiosis/coccidiasis. Prevention Penicillin in feed is preventive. neomycin and erythromycin are used in the USA. Spores of the causative organism are highly resistant. Mortality may be 5-50%. Infection occurs by faecal-oral transmission. contaminated feed and/or water. Post-mortem lesions Small intestine (usually middle to distal) thickened and distended. usually around 10%. phenoxymethyl penicillin. diet (high protein). Treatment of ducks is not very successful. 100 ppm).g. Water medication for 3-5 days and in-feed medication for 5-7 days depending on the severity. Treatment Penicillins (e. Probiotics may limit multiplication of bacteria and toxin 102 . turkeys and ducks worldwide. amoxycillin). Intestinal contents may be dark brown with necrotic material.
It is not usually vertical (but chicks may become infected in hatcheries from contaminated shells). Four manifestations have been identified: ND . ND . birds. ND . Signs are typically of disease of the nervous. turkeys. Higher mortality is seen in velogenic disease in unvaccinated stock. Can affect any age. sometimes subclinical. In many countries local regulations or market conditions prevent the routine use of many of these options. the upper has formed a thick crust of necrotic material. The sample at the bottom of the picture is still focal. pigeons and ducks.production.Lentogenic . which is of variable pathogenicity. It is highly virulent for chickens. Transmission is via aerosols.Mesogenic .Neurotropic Velogenic . Figure 25. These viruses have sometimes been used as vaccines in previously immunised birds. The virus involved is Paramyxovirus PMV-1. Affected species include chickens. respiratory or reproductive systems. Severe lesions of necrotic enteritis affecting the small intestine of broilers.Velogenic Viscerotropic (VVND) . Other species can be infected including mammals occasionally (e.sometimes called 'asiatic' or exotic.Mild disease.Mortality and nervous signs in adult. conjunctivitis in man). Newcastle Disease (Paramyxovirus 1) Introduction Paramyxovirus 1 or Newcastle Disease is a highly contagious viral disease affecting poultry of all ages.g. 103 . fomites. visitors and imported psittacines (often asymptomatic). Intestinal lesions are absent. Morbidity is usually high and mortality varies 0-100%. less for turkeys and relatively apathogenic in psittacines. The condition is rarely diagnosed in ducks but is a possible cause of production drops/fertility problems. ND .Acute and fatal in chickens of any age causing neurological and some respiratory signs. Strains can be developed as vaccines.
encephalomalacia. dust etc). pneumovirus infection. HA+. for up to 12 months.tracheal or cloacal. laryngotracheitis. Differentiate from Infectious bronchitis. Sudden Death Depression. encephalomyelitis. It is inactivated by temperatures of 56°C for 3 hours or 60°C for 30 min. acid pH. 104 . rising titre in serology. fumigants and sunlight. Moult. It is confirmed by isolation in CE. post-mortem lesions. the infective dose and the degree of immunity from previous exposure or vaccination. Severe drop in egg production. especially in faeces and can persist in houses (in faeces. and is ether sensitive. Tracheitis. intoxications. Cross-reactions have mainly been with PMV-3. Pathogenicity evaluated by Mean Death Time in embryos. Coughing. Haemorrhage in proventriculus. Necrotic plaques in proventriculus. avian influenza. Diarrhoea. IFA. HI with ND serum or DID (less cross reactions). Diagnosis A presumptive diagnosis may be made on signs. caecal tonsil. middle ear infection/skull osteitis. Intestinal lesions primarily occur in the viscerotropic form. intestine. Nervous signs. However it is quite sensitive to disinfectants. Dyspnoea. haemorrhagic disease. Signs Signs are highly variable and will depend on the nature of the infecting virus (see above). Treatment None. antibiotics to control secondary bacteria. intracerebral or IV pathogenicity in chicks. Post-mortem lesions Airsacculitis. Paralysis. formalin and phenol. Inappetance. Samples . Twisted neck.The virus survives for long periods at ambient temperature. EDS-76. infectious coryza.
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). Figure 28. however. Inactivated vaccines have largely replaced the use of live vaccines in lay but they do not prevent local infections. 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. The LaSota-type vaccine may even repeated at 35-40 days of age if risk is high. In some countries it has been customary to provide antibiotics prophylactically during periods of anticipated vaccinal reaction. It is common to monitor response to vaccination. and is associated with difficulty maintaining brooding temperature and poor management of feeders and drinkers. vaccination. Vaccination programmes should use vaccines of high potency. all-in/all-out production. Mortality peaks at 3-5 days for birds that fail to eat at all. To prevent or reduce vaccinal reactions in young chicks it is important that day old have uniform titres of maternal immunity. whereas it tends to peak between 6-10 days for chicks that begin eating but then cease. and occasionally gasping due to a plug of pus in the lower trachea. which are adequately stored and take into account the local conditions. Use of Mycoplasma gallisepticum free stock under good management reduces the risk of vaccinal reactions.Prevention Quarantine. 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. It is commonest in progeny of young parent flocks (relatively small yolks) or where managers are inexperienced. 105 . Use of spray application is recommended but it needs to be applied with care to achieve good protection with minimal reaction. snicking. Morbidity is up to 10% and mortality close to 100%. HI has been used extensively. These tests do not directly evaluate mucosal immunity. especially in breeding birds by the use of routine serological monitoring. biosecurity. Elisa is now also used. Vaccinal reactions may present as conjunctivitis.
The condition can be reproduced by causing intense exercise of this muscle. good hygiene and biosecurity in brooding areas to minimise early disease challenges. any swelling of the muscle tends to cut off the blood supply. in broiler parent chickens and also in large broiler chickens in various places. Diagnosis Based on post-mortem lesions. bile staining of adjacent tissues. or suffer necrosis. Poor development. age of collection and weight of hatching eggs. Most organs normal.Signs Failure to grow. 106 . It has since been seen in turkeys. Oregon Disease . Prevention Review brooding management.Deep Pectoral Myopathy Introduction This condition is so named because it was first identified in adult breeding turkeys in Oregon State. 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. Without adequate blood supply the tissue of the muscle begins to die. nutrition of young parents. Treatment Correction of management problems. good drinking water hygiene. Gizzard may be impacted with litter. Gall bladder distended. It does not usually cause any mortality or obvious clinical signs and so it is usually identified after slaughter. soluble multivitamin supplementation may help. Differentiate from omphalitis/ yolk sac infection. Because it is enclosed in a relatively unyielding membrane. aspergillosis. It is caused by a reduction in the blood supply to the deep pectoral muscles. Post-mortem lesions Crop empty.
Figure 26. in particular excessive exercise. weighing birds etc). 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. If recent. It may also start to be enclosed in a fibrous capsule. Treatment Not applicable. Diagnosis Lesions. the muscle may be swollen and pale. it may become a healed scar. artificial insemination in breeding turkeys.Signs None. A typical case of the chronic stages deep pectoral myopathy in a broiler chicken. greenish yellow. If the condition is of over 7 days duration the muscle is dry and often shows greenish tinges. The tissue in the centre is dry. It is very difficult to detect affected carcases in standard meat inspection.g. with oedema within it and on its surface. Post-mortem lesions Acute or chronic necrosis of the deep pectoral muscle on one or both sides. This will normally be due to excessive flapping in association with management activities (e. Prevention Avoidance of physical damage of this muscle. and flaking. thinning operations in meat birds. Transillumination of the breast may help identify affected carcases and may be worthwhile if the incidence is high. 107 . If of very long duration. and.
Bordetella aviuminfection. coli infections. Cultures from the trachea of birds showing typical signs are preferred. severe bronchopneumonia. Post-mortem lesions Airsacculitis. The slow-growing bacterium was named in 1994. A range of sero-types have been identified. It is a Gram-negative pleomorphic organism. Most isolates are oxidase positive and galactosidase positive Serology using Elisa tests has been used. tracheitis. This can cause significant losses through condemnations. Diagnosis Clinical signs and lesions. Signs Coughing. The range occurring in turkeys is wider than that seen in chickens. It had been previously isolated in a number of other countries. Confirmation is by isolation of the organism. perhaps through survival of the organism on shell surfaces or shell membranes. In broiler chickens its main importance seems to be as a cause of airsacculitis in apparently healthy flocks that is only identified at slaughter. Growth is more rapid and consistent in an anaerobic jar. Reduced weight gain. preferably as a flock test comparing results before and after the challenge. The infection is common in chickens and turkeys.Ornithobacterium Infection. Important cofactors may include respiratory viral vaccines (Newcastle disease. The organism grows slowly producing tiny colonies on blood agar. Within the poultry house it is likely to be by aerosols. Some uncertainty exists about mechanisms of transmission. age at infection etc. 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. The severity of its effects depends on the pathogenicity of the particular strain and other risk factors such as viral infections. 108 . E. sneezing. and E. direct contact and drinkers. field challenge with respiratory viruses. This was first identified as a new disease syndrome of turkeys in Germany in the early 1990s. It commonly exacerbates respiratory disease caused by pneumovirus infections in turkeys. ventilation problems. Reduced egg production. There is some evidence that hatcheries may play a role in the epidemiology. ORT Introduction Ornithobacterium Infection is an infection of chickens and turkeys with the bacterium Ornithobacterium rhinotracheale(ORT). coli overgrowth may occur. Infectious Bronchitis).
cost etc.it is very sensitive in vitro to a range of chemicals. Figure 27. Some vaccines seem to have difficulty in producing a longlasting serological response to ORT. In the USA in 1998 all strains were sensitive to penicillins and many other microbials. though 54% were sensitive to tetracycline.amoxycillin at 250 ppm in water for 3-7 days or chlortetracycline at 500 ppm for 4-5 days. 109 . Satisfactory disease control depends on good management and biosecurity. Initially in Germany most strains were sensitive to amoxycillin.there are issues relating to availability. regulation. In France and Belgium most strains were sensitive to enrofloxacin. Tilmicosin is also effective at 10-20mg/kg and should be used in the early stages of the disease. Amoxycillin sensitivity remains good. Hygiene .Treatment The sensitivity of ORT to antibiotic is highly variable. ORT is a major problem on multi-age sites. it requires two doses. Preventative medication with the products listed in the previous section may be beneficial in some circumstances. because of the age of slaughter. Severely consolidated lung from an acute ORT infection in 14-week-old turkey growers. neomycin and enrofloxacin. this is unlikely to work in turkeys. The lung is solid and covered by pus/ purulent exudate. chlortetracycline but not to enrofloxacin. also most are sensitive to tiamulin. Vaccination . Some work has been done on live vaccine in the USA. Prevention This is based on good hygiene. therapy and vaccination. Similar lesions may be found in Pasteurellosis. Vaccination of breeder flocks to protect progeny has shown benefits in chickens but. An inactivated vaccine is licensed for broiler parents in Europe. Routine treatment .
Predisposing factors include small body size. Enlarged hocks. Signs Lameness. Birds go off legs. Treatment Not applicable . Gram-variable pleomorphic bacteria have been isolated from affected livers and bones. Birds rest squatting. turkeys and ducks seen worldwide and due to Vitamin D or calcium deficiency. The green discolouration is used to identify carcases that require closer inspection of the other tissues. Cage Fatigue Introduction A condition of chickens. Diagnosis Lesions.Osteomyelitis Complex. Soft-shelled eggs. Turkey Introduction An association has been shown between green discolouration of the livers of turkey growers at slaughter and the occurrence of inflammatory lesions of bones and/or joints. Signs None.only identified at slaughter. 110 . Prevention Unknown. Osteoporosis. high production. Post-mortem lesions Green discolouration of the liver at slaughter. Drop in production. Soft bones and beak.
Drop in egg production. Diagnosis History. Transmission is by wild birds and fomites.Tahir Post-mortem lesions Bones soft and rubbery. Paramyxovirus 2 . Differentiate from Marek's disease.M. place on litter. skeletal size and mineral content at point of lay are critical. Beading and fracture of ribs. 111 . Inappetance. depending on the species affected and whether infection is complicated by other factors and diseases. proper Ca and P levels and ratio. turkeys and passerine cage birds with Paramyxovirus PMV-2 results in disease with variable mortality. bone ash. Prevention Supplementation of vitamin D. lesions. Coughing. Vertical transmission does not usually occur. Post-mortem lesions Not characteristic. Beak soft. Wild birds are believed to be especially important. Signs Depression. Treatment Over-correct ration vitamin D.Abubakar.Yucaipa Disease Introduction An infection of chickens. antioxidants. spondylitis. whereas turkeys are more severely affected. calcium carbonate capsules. signs. In chickens it is usually mild. Epiphyses of long bones enlarged. Parathyroids enlarged. As birds progressively mobilise skeletal calcium for egg production through lay.
The infection is transmitted by birds. Inappetance. Treatment No specific treatment. including wild bird contact and fomites. antibiotics to control secondary bacteria. Diagnosis Isolation in CE. Paramyxovirus-3 Introduction Paramyxovirus PMV-3 infects turkeys. Prevention Quarantine. IFA. IFA. Treatment No specific treatment. Vertical transmission does not usually occur. Post-mortem lesions No specific lesions. HA+. laryngotracheitis. antibiotics to control secondary bacteria. occasionally chickens and psittacine cage birds. HA+. biosecurity. 112 . haemorrhagic disease. High mortality (cage birds). Differentiate from Infectious bronchitis. all-in/all-out production. Coughing. Mortality is usually low in poultry.Diagnosis Isolation in CE. HI with ND serum or DID (less cross reactions). HI with ND serum or DID (less cross reactions). Drop in egg production (turkeys). Loss of shell pigment Nervous symptoms (psittacines). EDS-76. Signs Depression.
HI with ND serum or DID (less cross reactions). The infection is transmitted by birds. all-in/all-out production. Vertical transmission does not usually occur. 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. IFA. all-in/all-out production. Paramyxovirus-6 Introduction Paramyxovirus PMV-6 infection of turkeys. Diagnosis Isolation in CE. antibiotics to control secondary bacteria. including wild bird contact and fomites. The infection is inapparent in ducks and geese. biosecurity.Prevention Quarantine. Mild respiratory signs. HA+. Mortality is 0-5%. In both cases mortality can be high and can be associated with a marked depression in growth. biosecurity. Prevention Quarantine. Treatment No specific treatment. Post-mortem lesions No specific lesions. It is an infectious and transmissible cause of sudden increases in mortality in turkeys between 7 and 28 days of age. A less acute form of the disease appears to produce more of a lingering mortality. Vaccination has been used in turkeys but may not be cost-effective. Signs Reduction in egg production.
114 . Overdistension of crop in young birds because of an interruption in feed supply may predispose. Reduced feed consumption and growth. pale brown. All-in/all-out production. Fluoroquinolone antimicrobials appear to be especially effective. Increasing weakness. Post-mortem lesions Dehydration. Weight loss. To replicate the condition in full it appears to be necessary to include bacteria in the inoculum. multivitamins and milk replacer products are helpful for nutritional support in the acute phase. Pendulous Crop Introduction A complex condition of turkeys and chickens associated with coarse fibrous feed. Diagnosis Signs. Emaciation.5-8% will encourage feed intake and recovery. A highly digestible diet with fat at 7. Treatment A range of antibiotics and arsenicals have been used to control the bacterial component of this condition. Increased water consumption. Effective terminal disinfection. Droppings watery. Muscle atrophy. Caseous cores in bursae (late in the process). huddling. Wet litter. Picking at feed. Prevention Biosecurity to reduce the introduction of new infections into brooding facilities. This syndrome is clearly distinguished from typical viral enteritis in young turkeys because of the high mortality and severe growth depression. eating litter. Signs Initial hyperactivity and increased vocalisation.viruses have been isolated from affected flocks. Good quality diets of a suitable form . lesions.mash and poor quality crumbles increase risk. Liquid intestinal contents. seeking heat.
Emaciation in heavily infected young chicks (Tetrameres). have ulcerations and sometimes mycosis. Diarrhoea. and thickening of mucosa of proventriculus. spiruroid worm parasites of poultry and game birds. Signs Anaemia. haemorrhage. ulceration. Lack of muscle tone. Post-mortem lesions Crop distended with feed. Prevention Remove predisposing factors. if these can be identified. grasshoppers and cockroaches. may be impacted. Diagnosis Signs.Signs Enlargement of crop. Tetrameres and Cyrnea are nematodes. lesions. Post-mortem lesions Inflammation. Proventricular Worms Introduction Dispharynx. including crustaceans. identification of worms. They are found in the mucosa of crop and proventriculus causing mainly inapparent infections. Crop contents semi-liquid and foul smelling. 115 . Diagnosis Macroscopic examination of lesions. Infection is by the oral route on exposure to the intermediate hosts. necrosis. Treatment None.
Differentiate from Duck viral enteritis. Prevention Prevention of access to intermediate hosts. isolation. colibacillosis. wild birds. tuberculosis. adequate protection. rodents and man with the bacterium Yersinia pseudotuberculosis. 116 . The disease has a mortality of 5-75%. coccidiosis. duck viral hepatitis. Post-mortem lesions Miliary lesions in a variety of organs but especially in the liver. Prevention Good husbandry and hygiene. Ruffled feathers. other poultry. Diagnosis Lesions.Treatment Not usually required. Diarrhoea. sulphonamides in feed. Sometimes sudden death. 'hardening off'. Treatment Tetracyclines. Signs Weakness. In peracute disease the only lesion may be enteritis. Pseudotuberculosis Introduction An infection of ducks.
Dehydration. coccidiosis. 117 .Tahir Pullet disease. elimination of other causes. Pancreas chalky. toxin and possibly a virus infection. Catarrhal enteritis. hygiene. Skeletal muscle necrosis. Affected birds have an increase in circulating monocytes in their blood. antibiotics. Prevention Good management. It was commonly reported prior to 1960 but is now rare. Bluecomb. Signs Depression. Avian Monocytosis Introduction A sudden onset condition of chickens early in lay with high morbidity and a mortality of 050%. Diagnosis History. It is associated with hot weather. Differentiate from fowl cholera. Loss of appetite. diet and water supply. Kidneys swollen. mucoid casts in intestine. IBD and typhoid. molasses. multivitamins in water. Treatment Adequate water supply. Post-mortem lesions Dehydration. Watery diarrhoea. Crop distension. Liver swollen with foci.M. capillariasis. water deprivation. Crop distended. Skin cyanosis of head. Dark comb and wattles. vibriosis. Drop in egg production.Abubakar. lesions.
Post-mortem lesions Anaemia. feeds by sucking blood.7 mm. Treatment Pyrethroids. the Northern Fowl Mite spends its entire life cycle on the bird and can multiply more rapidly as a result. Birds restless. Staff complaints . 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. organophosphates. For northern fowl mite it is essential to apply approved insecticides to the affected birds.itching. May cause anaemia and death in young birds. which are external parasites of chickens and turkeys. Dermanyssus gallinae.Red Mite and Northern Fowl Mite Introduction Arachnid mites. Spots on eggs. 118 . Signs Presence of grey to red mites up to 0. Prevention Thorough cleaning. Diagnosis Number and type of mites identified. citrus extracts. cracks. Effective monitoring of mite numbers and implementation of control measures before birds are heavily infested improves control. and good design of new equipment to limit harbourages for red mites. Ornithonyssus bursae. fumigation and insecticide treatment at turnaround. the Common Red Mite. mainly at night and may transmit fowl cholera and other diseases. Loss of condition. crevices etc. vegetable oil and mineralbased products (both liquid sand dusts) have been used to control red mites in the environment. Filling of cracks and crevices. Drop in egg production. in nest boxes. Pale comb and wattles. carbamates.
E. lesions. vaccinal and field strains) and bacteria (Ornithobacterium rhinotracheale. A number of respiratory viruses (Infectious Bronchitis. Lentogenic Newcastle disease virus. temperature. Infected birds may remain carriers for a few weeks. may act as 119 . intranuclear inclusions in liver. CE liver). Respiratory Disease Complex Introduction Respiratory infections in chicken and turkeys are seen worldwide but especially in temperate poultry-producing areas in winter months. Post-mortem lesions Mild catarrhal tracheitis. The virus is generally resistant to disinfectants (ether. The virus grows well in tissue culture (CE kidney.M. Opinions vary as to whether adenovirus can be characterised as a primary respiratory pathogen. ammonia and other gases. It may occur as an exacerbating factor in other types of respiratory disease. and by fomites.Tahir Respiratory Adenovirus Infection. prevention of immunosuppression. Prevention Quarantine and good sanitary precautions. Dust. pH). Signs Mild snick and cough without mortality. formaldehyde and iodides work better.Abubakar. Diagnosis History. coli) may be involved. Treatment None. Avian pneumovirus. at least 12 sero-types have been described and these may be isolated from healthy chickens. chloroform. 'Mild Respiratory Disease' Introduction An adenovirus infection of chickens with a morbidity of 1-10% and a mortality of 1-10%. Transmission may be vertical and lateral. and other factors associated with poor ventilation.
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. Figure 29.predisposing factors. There is also percarditis evident (at top right). mortality 5. Conjunctivitis. Differentiate from Chronic Respiratory Disease (Mycoplasmosis).10%. and have been cut into to reveal a cheesy (caseous) mass of pus. response to environmental changes. carefully applied appropriate viral vaccines. 120 . Pericarditis. Prevention Effective ventilation. of course. If condemned birds are included mortality may be more than 10%. The air sacs are thickened and congested. serology. Airsacculitis.catarrhal to purulent. Nasal exudate. Head swelling. Diagnosis Lesions. Severe airsacculitis of thoracic air sacs in a broiler close to slaughter. sanitation of drinking water. Treatment Antimicrobial treatment of specific bacterial infections. Rattling noises. Morbidity is typically 10-20%. be challenged by some of these pathogens). Signs Snick. Sneezing. Post-mortem lesions Severe tracheitis with variable exudate .
geese. Diagnosis Pathology. turkeys. Transmission is lateral and possibly transovarian. ducks. Both tracheas were congested and the upper sample had mucopurulent material in the lumen. spleen and kidney. chick inoculation. A gradual increase in mortality and poor growth in broilers may be the main signs. Sometimes nodules in intestine and caecae. 121 . Leg weakness. There is an incubation period of 5-15 days. Severe tracheitis is broilers with respiratory disease complex. and the infection can be spread by mosquitoes or in contaminated Marek's disease vaccines.Figure 30. Post-mortem lesions Neoplastic lesions in liver. Reticuloendotheliosis. Signs There may be no obvious signs. and quail with morbidity up to 25%. Sometimes enteritis and proventriculitis (especially in broilers infected with contaminated Marek's disease vaccine). Treatment None. Diarrhoea. Lympoid Tumour Disease Introduction A retrovirus infection of chickens. usually higher in females than males. Marked stunting when Marek's disease vaccine is contaminated.
Rickets (hypocalcaemic) Introduction Vitamin D deficiency or phosphorus/calcium imbalance is seen in chickens. Differentiate from Encephalomalacia. Diagnosis History. proper calcium and phosphorus levels and ratio. Birds go off legs. Beak soft. Epiphyses of long bones enlarged. or Vitamin D or 25-hydroxy vitamin D in drinking water. Post-mortem lesions Bones soft and rubbery. Poor growth. Signs Lameness.Prevention Formal control programmes have not been documented as the condition is sporadic and relatively self-limiting. Prevention Supplementation of vitamin D. Soft bones and beak. Hock swelling. Beading and fracture of ribs. Reduction in bodyweight. turkeys and ducks worldwide. signs. lesions. 122 . Birds rest squatting. antioxidants. Femoral Head Necrosis. Treatment Over-correct ration with three times vitamin D for 2 weeks. Parathyroids enlarged. Growth plates widened and disorganised. Avoidance of contamination of live vaccines is the main control measure practised.
Prevention Supplementation of Vitamin D. Reduction in bodyweight. Intestinal diseases may reduce absorption. Growth plates widened and disorganised. turkeys and duck is seen worldwide. signs. Birds rest squatting. Enlarged hocks.M. Even subclinical levels of this condition can predispose to Femoral Head Necrosis. antioxidants. Epiphyses of long bones enlarged. Soft bones and beak. Treatment Over-correct ration with 3 times vitamin D for 2 weeks. 123 . Signs Lameness. Parathyroids enlarged. This has led feed manufacturers to try various approaches to reduce added phosphorus in diets. Birds go off legs. or vitamin D in drinking water. lesions (analyse Vitamin A or manganese as a guide to premix inclusion). Diagnosis History. Post-mortem lesions Bones soft and rubbery. proper calcium and phosphorus levels and ratio. Some countries have regulations governing the use of phosphorus in fertiliser with a view to reducing water pollution.Abubakar. Beak soft.Tahir Rickets (hypophosphataemic) Introduction Phosphorus deficiency in chickens. Hock swelling. Beading and fracture of ribs. Poor growth.
A. Diagnosis Demonstration of virus (PAGE. Virus may be found in asymptomatic birds.M. dissimilis in turkeys. turkeys. large . except that the adults reside in the small intestine and earthworms are not significant paratenic or transport hosts. guinea fowl. Signs Diarrhoea. Control of secondary bacterial enteritis may require antimicrobial medication. The life cycle is similar to that illustrated in the section on the caecal worm Heterakis. electron microscopy or Elisa on intestinal contents . Use of a good electrolyte solution is beneficial in the acute stage of infection. columbae in pigeons. The route of infection is oral and maximum viral excretion occurs 2-5 days post infection. Prevention Good hygiene in brooding areas. Post-mortem lesions Viruses replicate mainly in the mature villous epithelial cells. galli in fowl. partridges and pigeons. stout white worms up to 12 cms in length. pheasants.submit 6 x .5 g faeces). The route of infection is oral usually by direct ingestion of the embryonated egg and there is a 5-10-week prepatent period. are nematode worm parasites. It is not known if vertical transmission occurs though virus has been occasionally isolated from embryonated eggs. The parasite species vary: A. Treatment No specific treatment for this infection.Tahir Rotavirus Infection Introduction Rotavirus infection is seen in chickens. shorter in young birds. The 124 . Roundworm. seen worldwide. Adult birds can tolerate burdens asymptomatically. and A.Abubakar.Ascaridia Introduction Ascaridia sp.
Prevention Prevention of contamination of feeders and drinkers with faeces. Listlessness. Treatment Flubendazole.parasites may be transported by grasshoppers and earthworms and are resistant to environmental effects. Signs Loss of condition. mainly in young birds. Post-mortem lesions Enteritis. oval smooth-shelled nonembryonated eggs in faeces. Worms up to 12 cm in length in duodenum and ileum. pasture rotation and regular treatment. 125 . Wasting. Figure 31. A collection of mature roundworms (Ascaridia galli) recovered from the small intestine of a layer chicken in rear. Poor growth. especially for young birds. piperazine as locally approved. In the bottom left quadrant there are also some immature worms. Diarrhoea. Diagnosis Macroscopic examination with identification of worms. levamisole.
game birds. Ruptures of ligaments and joints are also occasionally seen. Salmonella Gallinarum. Broiler parents and brown-shell egg layers are especially susceptible. If there is a greenish tinge to the area of swelling it occurred a few days previously.M. The bird may have the hock dropped to the floor. guinea fowls. Signs Severe lameness. sparrows. Infections still occur worldwide in non-commercial poultry but are rare in most commercial systems now. Fowl Typhoid Introduction Disease caused by one of the two poultry-adapted strains ofSalmonella bacteria. Reoviral or staphylococcal arthritis or tenosynovitis may predispose but many cases have no evidence of an inflammatory response. This can cause mortality in birds of any age.Abubakar. Salmonella Gallinarum. Avoidance of physical stresses on the musculoskeletal system through careful handling as well as careful design and layout of equipment. Histology may be helpful in determining if there is an underlying inflammatory process. canaries and bullfinches. Treatment None.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. Affected birds should be culled humanely as soon as they are identified. 126 . Broiler chickens have an avascular area of tendon just above the hock that is the usual site of rupture. Post-mortem lesions The fresh lesion contains a haematoma with the end of the ruptured tendon within or adjacent to it. Diagnosis Signs and lesions are obvious. Chickens are most commonly affected but it also infects turkeys. parrots.
Transmission may be transovarian or horizontal by faecal-oral contamination. McConkey and non-selective agar is advisable. and/or congestion. Thirst. In clinical cases direct plating on Brilliant Green. mortality is increased in stressed or immunocompromised flocks and may be up to 100%. Post-mortem lesions Bronzed enlarged liver with small necrotic foci. Engorgement of kidneys and spleen. Prevention Biosecurity. Reluctance to move. The bacterium is fairly resistant to normal climate. Diagnosis Isolation and identification. pullorum disease and coli-septicaemia. Signs Dejection. Differentiate from Pasteurellosis. LPS-based Elisa assays have been developed but not widely applied commercially. tetracylines. 127 . Inappetance. surviving months. Tube and rapid plate agglutination tests have been the standard serological tests for many years but have only been validated for chickens. Yellow diarrhoea.Morbidity is 10-100%. both live (usually based on the Houghton 9R strain) and bacterins. As with other salmonellae. Enrichment procedures usually rely on selenite broth followed by plating on selective media. egg eating etc. Vaccines for fowl typhoid have been used in some areas. Anaemia. fluoroquinolones. clean chicks. Treatment Amoxycillin. Enteritis of anterior small intestine. recovered birds are resistant to the effects of infection but may remain carriers. potentiated sulponamide. The route of infection is oral or via the navel/yolk. Ruffled feathers. but is susceptible to normal disinfectants. even in adults.
this usually only causes mortality in birds up to 3 weeks of age. Closed eyes. Depression. It affects chickens most commonly. ring doves. sparrows. but also infects turkeys. Ruffled feathers. in young broiler chickens. Transmission may be transovarian or horizontal mainly in young birds and may sometimes be associated with cannibalism. 'Bacillary White Diarrhoea' Introduction Disease caused by one of the two poultry-adapted strains ofSalmonella bacteria. White diarrhoea. The bacterium is fairly resistant to normal climate. 128 . Salmonella Pullorum. It still occurs worldwide in noncommercial poultry but is now rare in most commercial systems. Lameness. Similar lesions can be seen in Pullorum Disease and with other causes of septicaemia in young chicks. guinea fowls. Salmonella Pullorum. Bacterial septicaemia caused by Salmonella Gallinarum. usually brown-shell egg layers. parrots. the one on the right is slightly enlarged.Figure 32. mortality is increased in stressed or immunocompromised flocks and may be up to 100%. pale and shows focal necrosis. ostriches and peafowl. Occasionally it can cause losses in adult birds. Morbidity is 10-80%. surviving months but is susceptible to normal disinfectants. game birds. The liver on the left is normal. The route of infection is oral or via the navel/yolk. Gasping. Pullorum Disease. Loud chirping. Signs Inappetance. Vent pasting.
S. Vaccines are not normally used as they interfere with serological testing and elimination of carriers. Enteritidis andS. Derby. Gallinarum. it may become established on certain farms. Montevideo. Prevention Eradication from breeder flocks. S. Differentiate from Typhoid. Enrichment procedures usually rely on selenite broth followed by plating on selective media. chilling and omphalitis Treatment Amoxycillin. turkeys and ducks worldwide. Splenomegaly. their presence may be significant with respect to carcase contamination as a potential source of human food poisoning. in the environment or in rodent populations. The route of infection is oral and transmission may be vertical as a result of shell contamination. Newport. Diagnosis Isolation and identification. and also other than S. Typhimurium (which are considered separately). fluoroquinolones.Post-mortem lesions Grey nodules in lungs. They infect chickens. McConkey and non-selective agar is advisable. poteniated sulponamide. tetracylines. Urate crystals in ureters. Anatum. Regardless of the initial source of the infection. As with other salmonellae. Caecal cores. gizzard wall and heart. other enterobacteria. Paratyphoid Infections Introduction Salmonellae bacteria other than the species specific sero-typesS. S. liver. Salmonellosis. Even if these infections do not cause clinical disease. Paratyphoid. S. Bredeney are among the more common isolates. paracolon. fomites and feed (especially protein supplements but also poorly stored grain). Certain sero- 129 . recovered birds are resistant to the effects of infection but may remain carriers. Sero-types vary. Intestinal or caecal inflammation. are capable of causing enteritis and septicaemia in young birds. In clinical cases direct plating on Brilliant Green. S. Morbidity is 0-90% and mortality is usually low. Pullorum. but S. Many species are intestinal carriers and infection is spread by faeces.
types are prone to remain resident in particular installations (e.g. Rappaport-Vassiliadis) followed by plating on two selective media will greatly increase sensitivity. Differentiate from Pullorum/Typhoid. applied at sufficient concentrations. Diagnosis Isolation and identification. Enrichment media such as buffered peptone followed by selective broth or semi-solid media (e. Ruffled feathers. chilling. Predisposing factors include nutritional deficiencies. Pericarditis. inadequate water. other enterobacteria. 130 . Treatment Sulphonamides. Vent pasting.g. fluoroquinolones. Post-mortem lesions In acute disease there may be few lesions. Good management. Signs Signs are generally mild compared to host-specific salmonellae. Dehydration. This approach is often used in the heat treatment of feed. Enteritis. Dejection. S. Cheesy cores in caecae. other bacterial infections and ornithosis (in ducks). Focal necrotic intestinal lesions. especially in dry dusty areas. amoxycillin. The bacteria are often persistent in the environment. or absent. Chemotherapy can prolong carrier status in some circumstances. but are susceptible to disinfectants that are suitable for the particular contaminated surfaces and conditions. Foci in liver. Closed eyes. Temperatures of around 80°C are effective in eliminating low to moderate infection if applied for 1-2 minutes. Unabsorbed yolk. Senftenberg in hatcheries). Loss of appetite and thirst. However this has the potential to reveal the presence of salmonellae that are irrelevant to the clinical problem under investigation. tetracyclines. In clinical cases direct plating on Brilliant Green and McConkey agar may be adequate. Diarrhoea. neomycin.
turkeys and ducks cause problems worldwide with morbidity of 0-90% and a low to moderate mortality. many species are intestinal carriers and infection may be carried by faeces. care in avoiding damage to natural flora. Infections in chickens. and. 131 . The bacteria are often persistent in the environment.Prevention Uninfected breeders. S. Predisposing factors include nutritional deficiencies. Typhimurium infections Introduction Salmonella Enteritidis and S. These are the predominant sero-types associated with human disease in most countries. hatcheries and feed mills is required for effective control. applied at sufficient concentrations.Typhimurium has remained relatively stable though the spread of the highly antibiotic-resistant strain DT104 in various farmed species gives some reason for concern. all-in/all-out production. fumigate eggs. competitive exclusion. Infection results in a strong immune response manifest by progressive reduction in excretion of the organism and reduced disease and excretion on subsequent challenge. Enteritidis and S. clean nests. inadequate water and other bacterial infections. breeding and grow-out farms. especially in dry dusty areas. because there are differences in the epidemiology as compared to other salmonellae. elimination of resident infections in hatcheries. Routine monitoring of breeding flocks. secondly. chilling. Vaccines are not generally used for this group of infections. has become much more common in both poultry and humans since the early 80s. Salmonella Enteritidis.Typhimurium are presented separately from other sero-types of Salmonella because. mills. This approach is often used in the heat treatment of feed. Salmonellosis. Vertical transmission may be either by shell contamination or internal transovarian contamination of yolk. fomites and on eggshells. good feed. The prevalence of S. Feed and feed raw material contamination is less common than for other sero-types. The route of infection is oral. but are susceptible to disinfectants that are suitable for the particular contaminated surfaces and conditions. Temperatures of around 80°C are effective in eliminating low to moderate infection if applied for 1-2 minutes. on the one hand. Many infected birds are culled and others are rejected at slaughter. these bacteria are often specifically cited in zoonosis control legislation. especially phage type 4.
It is possible to detect reactions with specific antigens in agglutination tests but competitive and direct Elisa tests are more commonly used today. Cheesy cores in caecae. Differentiate from Pullorum/Typhoid.Signs Dejection. Enrichment media such as buffered peptone followed by selective broth or semi-solid media (e. Early depletion of infected breeding stock is required in some countries such as those of the European Union. other enterobacteria such as E. tetracyclines. care in avoiding damage to natural flora. infection Diagnosis Isolation and identification. clean nests. fumigate eggs.Pullorum serum agglutination tests. Routine monitoring of breeding flocks. Chemotherapy can prolong carrier status in some circumstances. competitive exclusion. In clinical cases direct plating on Brilliant Green and McConkey agar may be adequate. coli. Closed eyes. mills. Foci in liver. Perihepatitis. Enteritis. Vent pasting. all-in/all-out production. Lost of appetite and thirst. Ruffled feathers.E. Diarrhoea. Focal necrotic intestinal lesions. Misshapen ovules in the ovaries in S. amoxycillin. Post-mortem lesions In acute disease there may be few lesions. Unabsorbed yolk. Treatment Sulphonamides. Pericarditis.Enteritidiscauses cross-reactions which may be detected with S. breeding and grow-out farms. good feed. neomycin. Prevention Uninfected breeders. Good management. Stunting in older birds.g. fluoroquinolones in accordance with the sensitivity. elimination of resident infections in hatcheries. S. Infection 132 . hatcheries and feed mills is required for effective control. However this has the potential to reveal the presence of salmonellae that are irrelevant to the clinical problem under investigation. Dehydration. Rappaport-Vassiliadis) followed by plating on two selective media will greatly increase sensitivity.
Damaged vents. Typhimurium infection. May form a multi-layered caseous cast in oviduct or be amorphous. Infection may spread downwards from an infected left abdominal air sac. Enteritidis and S. The oviduct is a hollow tube joining the normally sterile environment of the body cavity with the cloaca. coliand occasionally Salmonella spp. are especially prone to increasing salpingitis. Peritonitis. Vaccines are increasingly being used for S. The control of infection in this area is probably achieved by ciliated epithelium that mostly wafts a carpet of mucus towards the cloaca. Death. Bacteriology of oviduct. both inactivated (bacterins) and attenuated live organisms. Distended abdomen. Post-mortem lesions Slight to marked distension of oviduct with exudate. Diagnosis Use the signs to select birds for culling and post-mortem investigation. It is a complex condition of chickens and ducks associated with various infections including Mycoplasma and bacteria (especially E. Lesions.results in a strong immune response manifest by progressive reduction in excretion of the organism and reduced disease and excretion on subsequent challenge. Salpingitis Introduction Salpingitis is an inflammation of the oviduct. which normally has many millions of potentially pathogenic bacteria.). Anything that damages the epithelium or disturbs normal oviduct motility is likely to increase the likelihood of salpingitis. leaking urates. or may proceed upwards from the cloaca. 133 . Some birds may 'lay' a caseous mass of pus (which may be found in a nest or on the egg belt). Systemic viral infections that cause ovarian regression or damage to the oviduct or cloaca. Signs Sporadic loss of lay.
Diagnosis Clinical examination. Prevention Control any septicaemia earlier in life. possibly associated with tendon injury. exclusion of other problems. immunise effectively against respiratory viral pathogens common in the area. Morbidity is 10-20%. use healthy parent flocks. Shaking or quivering of legs after rising. Post-mortem lesions None. Signs Stand on toes shaking. Prevention Care in transport of brooded poults. releasing poults into larger areas and in handling heavier birds.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. Use of a suitable antimicrobial may be beneficial for birds in the early stages and if associated with efforts to minimise risk factors. Treatment Multivitamins. 134 .
Feed intake. Dehydration. suggesting a viral component. Orange mucoid droppings. This appears to be a multifactorial condition. Signs Tremor. Avoidance of physical 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. Prevention Good sanitation of the brooding house. Minimise stress. Mortality drops off as sharply as it started.Spiking Mortality of Chickens Introduction This is a condition characterised by a sudden increase in mortality in young. Death. and/or carbohydrate absorption are disturbed resulting in a hypoglycaemia. electrolytes and glucose solution to flock. Males are more susceptible than females. Diagnosis Pattern of mortality. Avoidance of interruptions in feed supply. Coma. 135 . typically 7-14day-old. Birds in good condition die after showing neurological signs. Filtered intestinal contents from affected flocks appear to be capable of reproducing the condition. Paralysis. Provide multivitamins. Excess fluid in lower small intestine and caecae. probably because they are growing faster. rapidly growing broiler chickens. Signs and lesions. Post-mortem lesions Mild enteritis. Treatment Leave affected chicks undisturbed.
Necrotic foci. grouse and canaries with morbidity and mortality up to 100%. and egg soiling in chickens. Drops in egg production may be seen in both systemic and intestinal forms Post-mortem lesions Marked splenomegaly. Signs Depression. It has been associated with typhilitis. Mucoid enteritis. Often diarrhoea with excessive urates. ducks. Prevention Control vectors. Brachyspira pilosicoli. Diagnosis Haematology. geese. reduced egg production. Cyanosis. It is transmitted by arthropods. Weakness and progressive paralysis. vaccines in some countries. previously known as Serpulina pilosicoli. The bacterium is poorly resistant outside host but may be carried by Argas persicus for 430 days.g. pheasants.Spirochaetosis Introduction The bacterium Borrelia anserina infects chickens. Argas persicus. Spleen mottled with ecchymotic haemorrhages. e. isolate in chicken eggs or chicks or poults. Treatment Various antibiotics including penicillin. diarrhoea. Thirst. is an intestinal spirochaete that can be associated with inflammation of the large intestine in a broad range of mammals and birds. 136 . Liver enlarged with small haemorrhages. and occasionally by infected faeces. turkey.
Signs Sitting on hock or rumps. The sample on the right is normal. lesions. That on the left shows the typical lesion of spondylolisthesis.Abubakar. 137 . Diagnosis Symptoms. Post-mortem lesions Anterior-posterior rotation of the bodies of the last or penultimate thoracic vertebrae resulting in scoliosis just anterior to the kidney. Kinky-back Introduction A complex condition of broiler chickens with a morbidity of 1-5% and low mortality associated with rapid growth and possibly having a genetic component.Tahir Spondylolisthesis.M. with rotation of the body of the vertebra and the pinching of the spinal column that causes paralysis. May walk backwards. legs extended forward. Prevention Selection for satisfactory conformation in primary breeding. These are cross-sections of the spinal column of 4-5-weekold broilers. Treatment None. Use of wings to help in walking. Figure 33.
and toe trimming may be a portal of entry with subsequent spread via the bloodstream to the typical sites of lesions. 138 . Infection is usually by the respiratory route with an incubation period of 2-3 days seen after artificial infection. Treatment None. Morbidity is usually low and mortality 0-15% though affected birds will often be culled on humane grounds. The type of chick box liners and the feeding papers used in the brooding house can also influence the occurrence of the condition. Wounds. mainly S. Signs Legs splay and chick is unable to stand. Staphylococcosis. Damaged skin due to nutritional deficiencies (such as of biotin) may also be a point of entry. These include good breeder nutrition. Diagnosis Clinical signs. avoidance of excessive hatching egg storage.Abubakar. Post-mortem lesions Gross lesions are not usually evident.M. Bumble Foot Introduction Caused by Staphylococcus bacteria. Staphylococcal Arthritis.Tahir Spraddle Legs or Splay Leg Introduction Occurs in all species in the recent hatchling. Prevention All measures that improve chick vitality at hatching are beneficial in reducing this problem. and careful monitoring of incubation conditions. either accidental or induced by interventions such as beak trimming. aureus and seen in chickens and turkeys worldwide.
especially M.g. Infected joints may have clear exudate with fibrin clots. particularly of parent birds. chronic stress. Recovered birds may have some immunity but vaccination with staphylococci has not been found to be helpful in preventing the disease to date. Lameness. Possibly vaccination against reovirus infection. low stress and prevention of immunosuppression from any cause will all tend to help. in accordance with sensitivity. Post-mortem lesions Tenosynovitis. Low mobility. This may progress to abscess formation in these areas. and by fomites. e. Swollen above the hock and around the hocks and feet. Treatment Antibiotics.. toe clipping). Competitive exclusion with a non-pathogenic Staphylococcushas been shown to be effective (no commercial products yet available based on this technology).Transmission occurs in the hatchery and in the general farm environment. Signs Ruffled feathers. and imunosuppression. Diagnosis Lesions. the hatchery and in any intervention or surgery (processing. trauma. synoviae. most commonly in the plantar area of the foot or just above the hock joint. Differentiate from septicaemia or tenosynovitis due to Colibacillosis.. Mycoplasma spp. Good management. isolation and identification of pathogen. Streptococcus bovis Septicaemia Introduction An infection of ducks with the bacterium Streptococcus bovis. 139 . Salmonella spp. Prevention Good hygiene in the nest. Some sudden deaths from acute septicaemia if very heavy challenge. This condition is a cause of sudden deaths in ducklings of 2-3 weeks of age. Predisposing factors include reovirus infection.
'Flipover' Introduction A condition of broiler chickens of unknown cause. Post-mortem lesions Intestine filled with feed. most are found lying on their back.affected birds respond well to saline injection and will actively seek out salt scattered in the litter. isolation. Prevention Good husbandry and hygiene. Haemorrhages in muscles and kidneys.Signs Sudden deaths. Treatment Amoxycillin. Affected well-grown birds may appear to have died from smothering. 140 . Splenic hyperplasia. possibly metabolic. Sudden Death Syndrome. Leg weakness or incoordination in a few birds. Serum accumulation in lung (may be little if examined shortly after death). Livers heavier than those of pen-mates (as a percentage of bodyweight. It can be induced by lactic acidosis and about 70% of birds affected are males. Lung congestion and oedema. Liver congestion. Diagnosis History. Signs Sudden death in convulsion. extra care in the immediate post-brooding period. The atria of the heart have blood. Sodium deficiency can appear very similar at about the same age . lesions. the ventricles are empty.). Post-mortem lesions Beak cyanosis.
low intensity light. however it may not have a zero withdrawal in commercial egg layers.Diagnosis Birds found on back with lack of other pathology. 141 . Tapeworms. Cestodes Introduction Cestodes are tapeworms that are seen in many species. Check your local regulations. Post-mortem lesions Occupy space in intestine and create small lesions at point of attachment. Treatment Flubendazole is effective at a 60 ppm in diet. Prevention Control the intermediate hosts. Diagnosis Identification of the presence of the worms at post-mortem examination. or birds' access to them. Signs It is doubtful if any signs are produced under most circumstances. feed restriction. lighting programmes. Treatment None possible. use of dawn to dusk simulation and avoidance of disturbance. Prevention Lowering carbohydrate intake (change to mash). they may not be host specific. Most have intermediate invertebrate hosts such as beetles or earthworms.
distal tibia. Tibial Dyschondroplasia. 142 . Lixiscope may identify in vivo as early as 2 weeks of age. turkeys and ducks. TD Introduction A complex condition seen in chickens. Mature tapeworms with their heads (scolices) embedded in the intestine. Differentiate from rickets. modifications of calcium and phosphorus ratios. Vitamin D3 supplementation. Diagnosis Gross pathology.a mass of avascular cartilage with transitional chondrocytes. It may be associated with rapid growth and have a nutritional factor. Post-mortem lesions Plug of cartilage in proximal end of tibia. Microscopically .Figure 34. and proximal metatarsus. Swelling and bowing in the region of the knee joints. chloride levels and acid/base balance. Treatment None. Prevention Genetic selection using the Lixiscope to identify bone phenotype. mild lesions may require histology to distinguish from other problems. Signs There are usually no signs unless the condition is severe. small ovoid lacunae and more matrix than normal. Lameness. in decreasing order of frequency.
Transmission is lateral with birds and faeces. Occasionally paralysis from toxins in the tick saliva. spends little time on host. Transmissible Enteritis. Diagnosis Identification of the presence of the parasites. Emaciation. Post-mortem lesions Anaemia. Treatment Elimination of cracks and crevices in the poultry housing. Skin blemishes. Bluecomb Introduction Some coronaviruses involved in this condition are considered to be bovine coronaviruses (or closely related thereto). Reduced productivity. and is also found on mammals.M. The infection is seen in turkeys and sometimes pheasants. than in commercial poultry in temperate climates.Abubakar. others are avian coronaviruses closely related to infectious bronchitis virus.Tahir Ticks Introduction Argas persicus is an external parasite of poultry and wild birds. with 143 . and may also transmit spirochaetosis and Pasteurella infection. Prevention As for red mite control. It is more common in warm climates. Signs Anaemia. These parasites are more likely to be a problem of small scale poultry production in the tropics. Morbidity is close to 100% and mortality is 5-100%. Weakness. Insecticide sprays in these areas are more likely to be effective than treatment of the 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.
Morbidity is 10-100% and mortality 1. chlorinate drinking water. chlorination of drinking water. possibly involving fomites.Antibiotics are not very effective.30%. Signs Decreased appetite. Eggs depigmented and thin-shelled. Sudden drop in production that lasts 2-3 weeks. vaccination . Loss of voice. Paramyxoviridae. Diagnosis Signs. control respiratory stressors. 147 . Prevention All-in/all-out production. Rapid transmission occurs laterally. Post-mortem lesions Serous rhinitis and tracheitis. control respiratory stressors. Turkey Rhinotracheitis (Adult) Introduction A disease of turkeys caused by the viruses of the Pneumovirus genus. isolation of ciliostatic agent. Ocular and nasal discharge. vertical transmission is uncertain. Serology. Prevention All-in/all-out production.live primer followed by inactivated. Treatment Antibiotics are not very effective. Good drinking water hygiene. maternal antibody may protect.
Rapid transmission occurs laterally.Abubakar. 148 . vertical transmission is uncertain. Loss of voice. Morbidity varies. airsacculitis and perihepatitis. control respiratory stressors. coli infection then pneumonia. weight gain and feed efficiency. If there is secondary E. possibly involving fomites. chlorinate drinking water.30%. Conjunctivitis. Snick. Signs Decreased appetite. Ocular and nasal discharge. mortality is 1-25%. Transmission may be by direct or indirect contact and possibly vertical. Turkey Viral Hepatitis Introduction An infection of turkeys caused by an unidentified virus. serology (using an Elisa test to demonstrate rising titre). maternal antibody may protect. Sinusitis. Prevention All-in/all-out production. Diagnosis Clinical signs. isolation and identification of the ciliostatic virus. Dyspnoea.Tahir Turkey Rhinotracheitis (in rear) Introduction A disease of turkeys caused by the viruses of the Pneumovirus genus. sometimes pus in bronchi. Paramyxoviridae. Birds remain carriers for up to 16 days.M. Morbidity is 10-100% and mortality 1. Post-mortem lesions Serous rhinitis and tracheitis. Treatment Antibiotics are not very effective. Vaccination at day-old seems to be most effective.
Gastrocnemius tendon may slip. 1 mm) coalescing. Twisted leg Introduction A complex condition seen in chickens and turkeys. Focal haemorrhage. Factors involved may include genetics. environment and high growth rate. Depression and sporadic deaths in birds in good condition. Congestion. nutrition. Post-mortem lesions Grey foci (c. Morbidity is 1-20% and mortality is low. bacterial and fungal infections. with good management many birds recover. Treatment None. Various angulations of leg. lesions pathognomonic.Signs Signs are usually subclinical. Signs Lameness.no inclusion bodies. Prevention Good sanitation and management. Diagnosis Isolation in CE. Post-mortem lesions Linear twisting of growth of long bones. Differentiate from histomonosis. Bile staining. Distortion at hock. 149 . Grey to pink foci in the pancreas. Microscopically . Valgus/varus.
Post-mortem lesions Deep ulcers throughout intestine. Predisposing factors include Coccidiosis (especially E. Drooping wings. Partially closed eyes. highly contagious disease of chickens and quail caused by the bacterium Clostridium colinumand characterised by ulcers of the intestines and caecae. greater than 20% is abnormal. The bacterium resists boiling for 3 minutes. E. Retracted neck. Peritonitis (if ulcers penetrate). but mainly ileum and caecae. 150 . Signs Listlessness. Prevention Selection for good conformation in primary breeding. Differentiate from perosis. Treatment None. Changed angulation of tibial condyles. The condition occurs worldwide. necatrix. which may coalesce and may be round or lenticular. Diarrhoea. Pale yellow membranes. Diagnosis Symptoms. arthritis and synovitis. tenella. The route of infection is oral and transmission is from faeces of sick or carrier birds or via flies. lesions. game birds and pigeons may also be affected. Blood in intestine. intertarsal angulation up to 10% is physiological. It can start suddenly and cause high mortality: 100% in quail and 10% in chickens. Turkeys. Watery white faeces (quail). Quail disease Introduction Ulcerative Enteritis is an acute. brunetti). Anaemia. IBDV and overcrowding. Adoption of optimal nutrition and growth patterns for the economic objectives of the production system.. Ruffled feathers. and E. Ulcerative Enteritis.
Morbidity is low. Signs Dejection. 151 . possibly probiotics. Transmission is by faecal contamination. trichomoniasis. Prevention Infection-free birds. Wall of the caecum of a chicken suffering from ulcerative enteritis Vibrionic Hepatitis. penicillin (50-100 ppm in feed). necrotic enteritis. all-in/all-out production. Treatment Streptomycin (44 gm/100 litres water). Necrotic foci in liver. Response to treatment should occur in 48 to 96 hours. and disease is precipitated by stress. Diarrhoea. Diagnosis A presumptive diagnosis may be made on history and lesions. Figure 35. Loss of condition. coccidiosis. Bacitracin. birds remaining carriers for months. amoxycillin. low level antibiotics as per treatment. Treat for coccidiosis if this is a factor. Avian Infectious Hepatitis Introduction An insidious onset disease of chickens caused by Vibrio bacteria. The infective agent is rather resistant to environment and disinfectants. colinum in anaerobic conditions (the agent is often present in pure culture in liver). salmonellosis. Tetracyclines. multivitamins. Differentiate from histomonosis ('Blackhead'). Confirmation is on absence of other diseases and isolation of Cl. Inappetance.
Pale comb and wattles. Scaly comb. Jaundice. Drop in production/weight gain.
Focal hepatic necrosis in 10% of affected. Foci often stellate, or there may be a cauliflower-like 'spotty liver'. Haematocysts under capsule. Swelling of organs. Catarrhal enteritis.
History, lesions, isolation of infective agent from bile. Differentiate from leukosis, histomonosis, ulcerative enteritis, fowl cholera, and typhoid.
Hygiene, depopulate, obtain birds free of disease, contain stressors.
Viral Arthritis is the classic, but by no means the only, manifestation of reovirus infection of chickens; at least 5 sero-types of virus occur. Morbidity is high but mortality is usually low. Transmission is by faecal contamination, and good both laterally and vertically. Birds remain carriers for over 250 days. The virus is resistant to heat, ether, chloroform, pH and environmental factors. Reoviruses vary markedly in pathogenicity and the tissue damaged. Some can cause other disease syndromes such as early chick mortality and malabsorption syndrome. Some strains have shown severe systemic disease including pericarditis in chickens. Others have caused immunosuppression by damaging the cloacal bursa in ducks.
Lameness. Low mobility. Poor growth. Inflammation at hock. Swelling of tendon sheaths. Unthriftiness. Rupture of gastrocnemius tendons.
Swelling and inflammation of digital flexor and metatarsal extensor tendon sheaths. Foot pad swelling. Articular cartilages may be ulcerated. Haemorrhage in tissues. Fibrosis in chronic cases.
Diagnosis may be based on the history, lesions, IFA and rising antibody titre. Isolation may be readily achieved in CE yolk sac and CAM and also cell cultures (CE kidney or liver cells). Serology may be by DID, FAT or Elisa. 'Silent' infections (not associated with obvious disease) are common. Differentiate from mycoplasmosis, salmonellosis, Marek's, Pasteurella, erysipelas.
Vaccination is ideally carried out by administering a live vaccine in rear followed by an inactivated vaccine prior to coming into lay. Most vaccines are based on strain 11/33. Rear birds in all-in/all-out production systems.
Visceral Gout, Nephrosis, Baby Chick Nephropathy
Visceral gout is the deposition of white urates, which are normally excreted as a white cap on well formed faeces, in various tissues. Urates are also often deposited in joints and in the kidney. This condition can occur as an individual problem at any age. Outbreaks are seen in young chicks in the first week of life (baby chick nephropathy) or in flocks suffering kidney damage, or reduced water intake. All poultry species are susceptible. The kidney damage can arise from infection with certain strains of Infectious Bronchtiis virus, exposure to some mycotoxins or inadequate water intake (often because the birds have not adapated to a new type of drinker). Baby Chick Nephropathy can be due to inappropriate egg storage conditions, excessive water loss during incubation or during chick holding/transport, or inadequate water intake during the first few days of life. Very low humidity in brooding will also increase the likelihood of this problem. The timing of mortality is a reasonable guide as to the source of the problem. In Pekin/mallard ducks the condition is almost always due to inadequate water intake, whereas in muscovy ducks it is seen in breeders allowed to continue laying for over 24 weeks without a rest.
Depression. Low feed intake and growth.
Chalky white deposits on pericardium, liver, air sacs, peritoneum. Similar deposits may be present in joints and are usually present in the kidney.
This is based on correcting any management errors and encouraging water intake. Avoid any intentional or unintentional restriction in water intake. Sodium bicarbonate at 1g/litre water is mildly diuretic, however it could be counter-productive if water intake is in any way restricted.
Careful monitoring of the conditions of hatching egg storage and incubation with a view to achieving a standard egg weight loss profile. Humidification of holding rooms and chick transporters may also be beneficial. Humidifiers in chick brooding areas are being used increasingly, especially where whole house hot air brooders are in use. Ample supplies of drinkers should be available and filled with water at house temperature prior to the arrival of the chicks.
Figure 36. Severe visceral gout in a young chick. There are white chalky deposits around the heart (in the pericardium) on all major abdominal organs, including liver, gizzard and intestines, and even in the tissues of the thigh.
antioxidant. Prevention Supplementation of diet with vitamin A. Drowsiness.M. As in the case of other nutritional deficiencies. lesions.Tahir Vitamin A Deficiency. classic signs of deficiency are very rare in commercial poultry fed complete diets. Poor feathering.squamous metaplasia of epithelia. chronic fowl cholera. good quality raw materials. Differentiate from Infectious coryza. Microscopically . Post-mortem lesions Eyelids inflamed and adhered. Nasal and ocular discharge. Signs Poor growth. Excessive urates in kidneys and ureters. feed formulation. 155 . Eyelids stuck shut with thick exudate. Pustules in mouth and pharynx. infectious sinusitis etc. Diagnosis Signs. Treatment Vitamin A in drinking water. Nutritional Roup Introduction Vitamin A deficiency is occasionally seen in chickens and turkeys (insufficient vitamin A during 1-7 weeks of age).Abubakar. Pale comb and wattles.
Some deficiencies induce characteristic microscopic effects. They act in a broad range of metabolic pathways. exclusion of specific diseases. and egg production in the layer. See the separate discussion under Chondrodystrophy and Fatty Liver and Kidney Syndrome. response to supplementation.Abubakar. Most will reduce productivity. Vitamin deficiencies are especially prone to cause problems of hatchability. The embryo is particularly dependent on having adequate supplies of vitamins deposited in the egg. Simple deficiency is now rare as diets are usually well supplemented. because a continuous supply is required.Tahir Vitamin B Deficiencies Introduction The B complex vitamins are water soluble and not stored to any significant extent in the body. including growth in the young animal. Diagnosis Signs. However. If it is suspected that the vitamin premix may not have been included in the ration (or included at too low a level) it 156 . 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.M. damage to the intestine or increased demand for some reason may have an effect.
The balance of vitamins present should be similar to the daily nutritional requirement of the stock concerned. Exudative Diathesis. White streaks in muscle. Staggering. Haemorrhage. Post-mortem lesions Swollen cerebellum with areas of congestion. Falling over. drinking water supplementation with that vitamin is ideal and usually results in a rapid response in birds that are still drinking. Uncontrolled movements. Steatitis. Muscular Dystrophy Introduction A spectrum of diseases of chickens and turkeys. Treatment If a specific vitamin deficiency is suspected. 157 . Encephalomalacia. Muscular dystrophy is seen more frequently in older and mature birds. occasionally ducklings and other birds. Encephalomalacia and exudative diathesis tends to be seen in young birds of 1-5 weeks of age. Prevention Adequate supplementation of the feed with all required vitamins in levels which both support normal productivity but also have enough overage to deal with the increased demands that often occur during periods of disease challenge. less expensive) to analyse feed for a marker substance such as manganese rather than testing for vitamin levels. seen worldwide. Paralysis.may be appropriate (faster. The problem is associated with feed rancidity typically in diets with high fat. Blood-stained or greenish subcutaneous oedema. Signs Imbalance. Good quality multivitamin solutions are beneficial in the supportive care of a range of problems characterised by reduced feed intake. Vitamin E Deficiency. Green wings. characterised by oxidation of various tissues and caused by Vitamin E deficiency. Ventral oedema. Necrosis.
Treatment Vitamin E and/or selenium in feed and/or water. Prevention Proper levels of vitamin E. for example poor hygiene of hatching eggs.Diagnosis Signs. Diarrhoea. consistency) that vary according to the bacteria involved. Pseudomonas. and poor hygiene of setters. Loss of appetite. response to medication. selenium. Staphylococci. It is seen where there is poor breeder farm nest hygiene. toxicities. Closed eyes.coli. turkeys and ducks due to bacterial infection of the navel and yolk sac of newly hatched chicks as a result of contamination before healing of the navel. Swollen abdomen. feed rancidity. Various bacteria may be involved. Signs Dejection. Abnormal yolk sac contents (colour. hatchers or chick boxes. 'bangers'. Disease occurs after an incubation period of 1-3 days. necrotic dermatitis. especially E . antioxidant. 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.Proteus. 158 . good quality raw materials. Broad-spectrum antibiotics where there are extensive skin lesions. Vent pasting. Differentiate from Encephalomyelitis. lesions. histopathology. Yolk Sac Infection. inadequate hatchery hygiene or poor incubation conditions. Morbidity is 1-10% and mortality is high in affected chicks. Post-mortem lesions Enlarged yolk sac with congestion. use of floor eggs. Omphallitis Introduction A condition seen worldwide in chickens.
sanitation of eggs. There should be routine sanitation monitoring of the hatchery. frequent collection. clean nests.g. however the prognosis for chicks showing obvious signs is poor. Treatment Antibiotics in accordance with sensitivity may be beneficial in the acute stages. Prevention Prevention is based on a good programme of hygiene and sanitation from the nest through to the chick box (e. separate incubation of floor eggs etc. most will die before 7 days of age. Multivitamins in the first few days may generally boost ability to fight off mild infections. Differentiate from incubation problems resulting in weak chicks. Confirmation is by isolation and identification of the bacteria involved in the internal lesions. 159 .Diagnosis A presumptive diagnosis is based on the age and typical lesions. exclusion of severely soiled eggs.
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