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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.
'hardening off'. rodents. mainly in North America. Nervous signs. Autogenous bacterins sometimes used. and also horizontal. It affects turkeys. from long-term intestinal carriers. renamed Salmonella Arizonae. Blindness. correct house relative humidity. Congestion of duodenum. Figure 40. Diarrhoea. sulphonamides in feed. Paralysis. through faecal contamination of environment. Signs Dejection. Inactivated and attenuated vaccines available in some countries. cloudiness in eye. Arizonosis Introduction Caused by the bacterium Arizona hinshawii. Post-mortem lesions Enlarged mottled liver. Mortality is 10-50% in young birds. Unabsorbed yolk sac. transovarian. Erosions of the cartilage of the hock joint in a duck with chronic Riemerella anatipestifer infection. rigid depopulation and disinfection. Foci in lungs. Transmission is vertical. Vent-pasting. Cheesy plugs in intestine or caecum. Huddling near heat. 4 .Prevention Good husbandry and hygiene. reptiles. Arizona infection. Inappetance. older birds are asymptomatic carriers. and is not present in the UK turkey population. feed etc. adequate protection.
methods as per Salmonella spp. monitor sensitivity. salmonellosis. high altitude. The disease has a complex aetiology and is predisposed by reduced ventilation. Pericarditis. spectinomycin. Lungs and intestines congested. Dilation of the ventricle. Morbidity is usually 1-5%. Signs Sudden deaths in rapidly developing birds. Poor development. mortality 1-2% but can be 30% at high altitude. 5 . Salpingitis. Severe muscle congestion. Ascites is a disease of broiler chickens occurring worldwide but especially at high altitude. Possibly cyanosis. fumigation of hatching eggs. Ophthalmitis. may be related to type of stock and strain). Progressive weakness and abdominal distension. and respiratory disease. Perihepatitis. Diagnosis Isolation and identification. Dyspnoea. Formerly in-feed medication with nitrofurans was also used. Prevention Eradicate from breeder population. inject eggs or poults with antibiotics. coli-septicaemia. Thickening of atrioventricular valve. Post-mortem lesions Thickening of right-side myocardium. good nest and hatchery hygiene. Recumbency. Ascites Introduction Associated with inadequate supplies of oxygen. Pulmonary arterial vasoconstriction appears to be the main mechanism of the condition. General venous congestion. Differentiate from Treatment Injection of streptomycin. or gentamycin at the hatchery is used in some countries. poor ventilation and physiology (oxygen demand.
Absidia etc. Drowsiness. but may be as high as 12%. Silent gasping. Treatment Improve ventilation. Mortality among young affected birds is 5-50%. Diagnosis Gross pathology is characteristic. Prevention Good ventilation (including in incubation and chick transport). Nervous signs (rare). The infection has an incubation period of 2-5 days. Ascites. caused by Aspergillus fumigatus. Morbidity is usually low. avoid any genetic tendency. Spores are highly resistant to disinfectants. in which the typical sign is gasping for breath. Spleen small. The fungus can infect plant material and many species of animals including birds and man. control respiratory disease. A cardiac specific protein (Troponin T) may be measured in the blood. Rapid breathing. Microscopic . It affects chickens. Occasionally similar lesions are produced by other species ofAspergillus or even other fungi such as Penicillium. Signs Acute form: Inappetance. there is usually little bird-to-bird transmission. This may offer the ability to identify genetic predisposition. Sometimes the same organism causes eye lesions or chronic lesions in older birds. etc. worldwide. Weakness. Aspergillosis Introduction A fungal infectious disease. Differentiate from broiler Sudden Death Syndrome and bacterial endocarditis. 6 . Thirst. penguins. Liver enlargement. game birds. waterfowl. Pericardial effusion. ducks. Transmission is by inhalation exposure to an environment with a high spore count. especially in young chicks. turkeys.cartilage nodules increased in lung. Vitamin C (500 ppm) has been reported to be of benefit in South America.
Post-mortem lesions Yellow to grey nodules or plaques in lungs. Environmental spraying with effective antifungal antiseptic may help reduce challenge.Abubakar. Differentiate from excessive exposure to formalin or vaccinal reactions in day olds and from heat stress in older birds. It may be confirmed by isolation of the fungus. plaques in peritoneal cavity. Treatment Usually none. turkeys. air sacs. mortality none.Tahir 2 Chronic Forms: Ocular discharge (ocular form only). may have greenish surface. The means of transmission is unknown but 7 . 'Furry' airsacculitis in aspergillosis of an adult duck. It affects chickens.M. preferably after digestion in 10% potassium hydroxide. pheasants and occurs in most poultry-producing countries. quail. Amphotericin B and Nystatin have been used in high-value birds. See Avian Encephalomyelitis. The powdery surface is dark green in colour. Thiabendazole or Nystatin has been used in feed. Figure 8. hygiene. Morbidity 5-60%. Avian Encephalomyelitis Egg Drop Introduction Avian encephalomyelitis virus infection in laying bird causes inapparent infection or drops in egg production. good quality litter and feed. Brain lesions may be seen in some birds with nervous signs. Wasting. Prevention Dry. Diagnosis This is usually based on the signs and lesions and microscopic examination for the fungus. Growth occurs in 24-48 hours and colonies are powdery green/blue in appearance. Epidemic tremors for its effect in young birds. typically by putting small pieces of affected tissue on Sabouraud agar. trachea. Conjunctivitis/keratitis.
mortality high. transmission occurs over about 1-2 weeks. Virus in faeces may survive 4 weeks or more. now Elisa is used more commonly. EDS76. Signs Nervous signs. subsequent disease in progeny if breeders. small (5-10%) and lasting no more than 2 weeks. with an oral infection route. pheasants. Imbalance. Differentiate from Infectious Bronchitis. Treatment None. Serology . water etc. and quail. Prevention Vaccination of breeders/layers at 9-15 weeks. Epidemic Tremors Introduction Avian encephalomyelitis is a viral disease of the central nervous system of chickens. The route of infection is transovarian with an incubation period of 1-7 days. It has a worldwide distribution. Paralysis. rising titre to AE virus.probably by faecal contamination of environment.The embryo protection test has been used in the past. Vertical transmission is very important. Dull expression. Avian Encephalomyelitis. and there is serious disease in the progeny (see next section). attenuated or not. turkeys. feed. Ataxia and sitting on hocks. incubation >10 days. some lateral. Post-mortem lesions None. Immunity is usually long lasting. lentogenic Newcastle disease. lateral transmission is probably by the oral route. Signs Drop in egg production. Morbidity 5-60% depending on the immune status of the majority of parents. 8 . In breeders there may be a drop in hatchability of about 5%. Predisposed by immunosuppression. Diagnosis History. Virus in faeces may survive 4 weeks or more.
Prevention Vaccination of breeders at 9-15 weeks. Diagnosis A presumptive diagnosis is based on the history. Brain abscess. and isolates are designated sero-type/ species/location/reference number/year/subtype designation(H/N). The cause is a virus. vitamin deficiency (E. now Elisa is used more commonly. Orthomyxovirus type A. Microscopic . In addition official control measures disrupt trade in poultry products from affected areas. There may be focal white areas in gizzard muscle (inconstant). partridges. The higher the proportion of the chickens dying or showing signs the higher the IVPI. turkeys. and/or viral isolation may be carried out if required. Immunity is long lasting. especially in turkeys. Effectively all 9 . riboflavin). 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. Marek's disease.nonpurulent diffuse encephalomyelitis with perivascular cuffing. Tremor may be inapparent but is accentuated if chicks are held inverted in the hand. Enterococcus hirae infection. Treatment None. Avian Influenza-Highly Plague Introduction Pathogenic (HPAI). The virus infects chickens. and ostriches. its pathogenicity is variable. A. pigeons. Tremor of head. Post-mortem lesions Gross lesions are mild or absent. Histopathology is usually diagnostic and IFA. EE (especially in pheasant in the Americas). neck and wings. quail. The definitive classification of high pathogenicity is an intravenous pathogenicity test (IVPI) in 6-week-old chickens result of greater than 1. ducks. toxicities. This is a test in which the virus is inoculated into susceptible chickens that are then kept under observation. and lack of significant lesions. attenuated or not. the equivalent of the World Health Organisation for animal diseases. A few recovered birds may develop cataracts weeks after infection. This viral disease can cause exceptionally high mortality. The embryo protection test has been used in the past. Fowl One of only two 'Class A' diseases of poultry targeted for emergency disease control measures by OIE. signs. pheasants. Differentiate from Newcastle disease. Mycotic Encephalitis.2 .
in the years 1983-84. equipment. Swollen face. reduced feed consumption. especially faeces. The virus is moderately resistant. 10 . trachea. Outbreaks due to HPAI were recorded in the Pennsylvania area. and the high mortality that 'low-path' AI can cause in turkeys. by acid pH. H5 viruses of low pathogenicity may become highly pathogenic usually after circulating in poultry flocks for a time (Pennsylvania. conjunctivitis or severe pneumonia. The small number of human deaths associated with HPAI appear to have resulted from direct exposure to infected birds on farm or in markets. Pakistan. The route of infection is probably oral initially. by oxidising agent and by formalin and iodine compounds. air sacs and conjunctiva.g. Avirulent in one species may be virulent in others. Post-mortem lesions Inflammation of sinuses. Marked loss of appetite. clothing. Morbidity is high but mortality usually relatively low. See current OIE records for up to date information on distribution of HPAI. Because of this. It can remain viable for long periods in tissues. A serious outbreak occurred in The Netherlands in 2003 with a few linked cases in Belgium and one in Germany. Broken contaminated eggs may infect chicks in the incubator simulating vertical transmission. Italy). in northern Italy. Drops in egg production. Mexico and. USA. Pasteurella) may increase mortality. Diarrhoea (often green). It is inactivated by a temperature of 56°C in 3 hours and 60°Cin 30 min. can survive 4 days in water at 22°C. over 30 days at 0°C. The virus replicates mainly in respiratory tissues of chickens and turkeys but in the intestinal tract of clinically normal waterfowl. More recently outbreaks have occurred in Australia. waterfowl. even with 'low pathogenicity' strains. Apathogenic and mildly pathogenic influenza A viruses occur worldwide.birds are considered to be at risk of infection. Transmission is by direct contact with secretions from infected birds. Avian Influenza is a potential zoonosis. Signs Sudden death. from December 1999. Highly pathogenic avian influenza A (HPAI) viruses of the H5 and H7 HA subtypes have been isolated occasionally from free-living birds. Cyanosis of comb/wattles. but possibly by the conjunctival or respiratory route and the incubation period is 3-5 days. Nervous signs such as paralysis. It can result in inapparent infection. 550%. OIE and other bodies are currently examining ways to improve control of LPAI. Cessation of normal flock vocalisation. drinking water. Nasal and ocular discharge. Depression. Infections with other pathogens (e. Ovarian regression or haemorrhage. Coughing.
This condition has until now been seen only in meat-type chickens. Avian Leukosis (Serotype J). as with many such tests occasional false positive reactions can occur. Turkey lesions tend to be less marked than those of chickens. isolation. other respiratory infections. with considerable strain-to-strain variation. The incubation period is 10-20 weeks. vaccinated birds may remain carriers if exposed to the infection. while ducks may be symptomless. To be effective inactivated vaccines must be the right subtype for the particular situation (H5 will not protect against H7 and vice versa). Commercial Elisa test kits are now available. all-in/all-out production. 21-day interval to re-stocking should be followed. Subcutaneous oedema of head and neck. disinfection. cleaning. Confirmation is by viral isolation in chick embryo. North and South America. correct disposal of carcases. quarantine. Necrosis of skin of comb and wattles. Muscles congested. Dehydration. lateral transmission by faecal-oral route (this declines as the bird ages). Eradication by slaughter is usual in chickens and turkeys. nutrition and antibiotics may reduce losses. although it may reduce losses initially. Differentiate from Newcastle disease. Congenitally infected birds tend to remain 11 . DID+. Diagnosis A presumptive diagnosis may be made on history and postmortem lesions. lesionless carriers of highly pathogenic virus. bacterial sinusitis in ducks. Morbidity is low. In outbreaks a regime of slaughter. Treatment None. but good husbandry. etc. though there is high mortality of affected birds. However. It has occured in Europe. Vaccines have been used in recent outbreaks in Mexico and Pakistan. Minimise contact with wild birds. HA+. controlled marketing of recovered birds. infectious laryngotracheitis. Haemorrhage in proventricular and gizzard mucosae and lymphoid tissue of intestinal tract. The agar gel precipitation test is non-group-specific and is used to confirm any positives. Vaccination is not normally recommended because. fowl cholera. Myelocytomatosis Introduction Caused by an avian retrovirus. Transmission is by congenital infection from antibody-negative females. Survivors can be expected to have a high degree of immunity but may harbour virulent virus. NDV-. bleeding and vaccination needles. Prevention Hygiene.
80% produce infected chicks. Differentiate from Marek's disease. histology. sacral joint. Most characteristically are chalky white tumours in the bone marrow. Splenomegaly and enlarged kidneys also occur. Persistent low mortality.tumours usually contain well-differentiated myelocytes. Virus survival is poor but sufficient to allow cross contamination in hatcheries and on farm in rear. Enlargement of abdomen. lesions. There is also evidence that it is slightly more sensitive than conventional testing. Prevent/ reduce cross-infection in hatchery and on farm. Lymphoid Leukosis. liver. 'nonshedders' . ultimately identification of virus by isolation and/or PCR. PCR testing of embryonally infected chicks using DNA testing is uniformly positive for blood and faecal samples. Two cell types may be found in the same tumour. Post-mortem lesions Liver enlargement. Signs Depression.antibody negative. Critical hatchery practices: Separate infected and uninfected lines. preferably on separate hatch days and in separate machines. Treatment None.most but not all. particularly of the sternum.only 3% produced infected chicks. Prevention Checking of antigen in the albumen is a basis for eradication . shed virus and develop tumours.an Elisa test is aviailable to identify antibody positive birds. Many are asymptomatic. Separation in vaccination. 'Shedders' . Handle clean lines before infected lines. Emaciation. birds with egg antigen will be antibody negative. Minimise stress. Loss of weight. Serology . 12 . often with tumour foci. age. ribs. Diagnosis History. Microscopic .
Emaciation. myxosarcomas. Post-mortem lesions Focal grey to white tumours. coligranuloma. erythroblastosis. Avian Leukosis. then liver. it may be as short as 6 weeks for some of the other manifestations. kidney etc. Signs Depression. spleen. Persistent low mortality. Differentiate from Marek's disease. other tumours. The causative viruses are rapidly inactivated at ambient temperature and on exposure to most disinfectants. Microscopic . Egg production is somewhat reduced. 13 . Vertical transmission is most important by infection of the egg white in infected breeders (who are long-term carriers). myeloblastosis (see Sero-type J). especially in young birds. Minimise group sizes.egg layers are generally more susceptible to lymphoid leukosis. In lymphoid leukosis the incubation period is about 4-6 months. fibrosarcomas. It affects chickens worldwide with susceptibility varying considerably among different strains and types of stock . Mortality tends to be chronically higher than normal for a prolonged period. Liver may be very large. Many are asymptomatic. lateral transmission is poor but infection may occur by the faecal-oral route. cytology. Enlargement of abdomen.cells lymphoplastic Diagnosis History. A complex of viral diseases with various manifestations such as lymphoid leukosis. Morbidity is low but mortality high. osteopetrosis. Delay live vaccine challenges.Farm practices: Brood and rear lines separately and maintain separate for as long as possible. Avoid migration errors (birds unintentionally moving between pens). Loss of weight. liver or bursa. age. There may be increased susceptibility to other infectious diseases due to damage to the immune system. Leukosis/Sarkoma Group Introduction Lymphoid Leukosis. lesions. initially in the bursa.
It is caused by a pneumovirus of the Paramyxoviridae family. Figure 9. weight gain and feed efficiency. 14 . guinea fowl and possibly pheasants seen in Europe. morbidity is 10-100% and mortality can be 110%. turkeys (see separate summary). all-in/all-out production. Africa. vertical transmission is uncertain. Facial and head swelling (though this can occur in other conditions). control arthropods. Dyspnoea. Two subgroups have been identified on the basis of the G-protein sequence: A (original UK isolates) and B (original southern Europe isolates). Signs Decreased appetite. This was a case of Myelocytoma Avian Leukosis (Sero-type J). Conjunctivitis. Avian Rhinotracheitis 'Swollen Head Syndrome' Introduction A viral disease of chickens. Ocular and nasal discharge. The incubation period is 5-7 days. eradication . Diffuse lymphoid tumours in an enlarged liver from a mature broiler parent hen. Snick. As for many infections. Loss of voice. Prevention Good hygiene. South America and North America. first isolated from poults in South Africa in 1978.checking of antigen in the albumen is a basis for eradication (see Sero-type J for details).Treatment None. There is rapid lateral transmission with infection by aerosol through the respiratory route. fomites can be important in moving infection between farms.
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.
Pale livers and kidneys in fatty liver and kidney syndrome. Prevention Thorough cleaning and disinfection after depletion of an affected flock. Good biosecurity. Allin/all-out production. Post-mortem lesions See signs. 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. Elisa tests have been developed experimentally. Thickened skin under foot pad. A RT-PCR test may be used to detect viral RNA in tissues. Sudden deaths in fatty liver and kidney syndrome. Treatment No specific treatment known. Scabs around eyes and beak. 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. Viral particles may be demonstrated in bile. Histopathology may also be used but the findings are not specific to this condition. It may be helpful to control other conditions which may be occurring at the same time. in embryos. Drinking water which is well chlorinated should be helpful in reducing challenge by this route. Signs Poor growth. Diagnosis Typical signs and lesions. Lung congestion Ovarian regression Yolk peritonitis Pale foci and haemorrhages in pancreas. 18 . Biotin Deficiency. Chondrodystrophy. Leg weakness. webbing between toes. Must be confirmed by laboratory tests. Reduced feed intake and blood sugar can precipitate fatty liver and kidney syndrome.
lesions. Drop in egg production. Prevention Supplementation of diets with biotin . Parasites on birds. Scabs around vent. Differentiate from mites. especially around vent. may be some feather damage and crustiness of skin. The parasites are 1-6 mm in size and their life cycle takes about 3 weeks. Loss of condition. Crusty clumps of eggs ('nits') may be visible at the base of feathers. Lice eggs stuck to feathers. Signs Lack of thrift in young birds. Treatment Addition of biotin in feed or water.naturally present in many raw materials. Menocanthus stramineus is the most pathogenic and is said to be capable of causing anaemia in heavy infestations. has very low bioavailability. Post-mortem lesions Usually none. response to treatment/prevention. They are spread by direct contact between birds and by litter etc. Away from birds adults survive about 4-5 days. Diagnosis Identification of the parasites. bedbugs. Loss of vent feathers.Diagnosis Signs. 19 . Irritation. Differentiate from pantothenic acid deficiency (skin lesions). Check flocks regulary for rapidly moving insects at the base of the feathers on the abdomen or around the vent. Treatment Malathion powders and pyrethroid sprays where approved for bird application. Biting Lice Introduction Various species of lice are common external parasites of poultry worldwide.
The condition tends to occur near to rapidly flowing streams.Prevention Avoid direct contact with wild and backyard poultry. Eggs and larvae survive through the winter to cause new infestations in the following year. Prevention Similar measures as for mosquito control. Examine for lice regularly. Treatment Treatment is difficult. local history. although these insects can travel up to 15 miles. Diagnosis Anaemia. Effective removal of all organic material at flock depletion should be practised in all-in/all-out production systems. especially in autumn and winter and treat if required. 20 . It is usually necessary to treat twice at a 7-10 day interval to fully control the condition. The flies transmit leucocytozoonosis and also a filarial parasite in ducks. Blackfly Infestation Introduction Grey-black hump-backed flies. Swarms of flies. Post-mortem lesions Anaemia. 5 mm long and found in North and South America that are external parasites of birds and mammals. Biological control using a strain of Bacillus thuringensis has had some success and is preferable to insecticides. season. as the larvae within eggs are not killed by most products. Weekly treatments are required. Signs Anaemia in young birds.
Morbidity is usually low but mortality is high. suspect food and stagnant ponds. Toxin may also be produced by the bacteria in the caecum. weakness. This will reduce the risk of botulism both in the poultry and in any grazing animals on land where poultry litter is spread. Affected broilers tend to settle with eyes closed when not disturbed.Botulism Introduction A condition of chickens. Maggots or putrid ingesta may be found in the crop. then sudden death. Treatment Remove source of toxin. Mild enteritis if has been affected for some time. antibiotics. The toxin and bacterial spores are relatively stable and may survive for some time in the environment. is also quite typical. Differentiate from acute Marek's disease ('Floppy Broiler Syndrome') by histology of the brain. because it rests on the litter. maggots) is consumed by the birds. 21 . wings then neck. selenium. Prevention Preventing access to toxin. supportive treatment if justifiable. Feathers may be easily pulled (chicken only). and toxin-containing material (pond-mud. Diagnosis History. The single most important measure is careful pick-up and removal of all dead birds on a daily basis. Signs Nervous signs. ducks and other waterfowl occurring worldwide and caused by a bacterial toxin produced byClostridium botulinum mainly types A / C. mouse toxicology on serum or extract of intestinal contents. especially in hot weather. carcases. The toxin is produced in decaying animal (usually carcases) and plant waste. Post-mortem lesions Possibly no significant lesions. progressive flaccid paralysis of legs. 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. signs. A soiled beak. turkeys.
They are found worldwide. 22 . nematode parasites of poultry and game birds.5 cm in length that occur in the caecum. bacteria. up to 1. or paratenic hosts with partially developed (L2) larvae. control of leg problems. leg weakness. Diagnosis Based on lesions. Heterakis gallinaeeggs and larvae are a transport hosts for Histomonas.Breast Blister Introduction A complex condition of chickens and turkeys occurring worldwide associated with trauma. Poor feather cover and caked or wet litter are predisposing factors. Morbidity is high but it is not associated with mortality. The meaning of the technical terms relating to parasite life cycle are defined in the glossary. give way to scar tissue. and a four-week prepatent period. Infection is by the oral route. and infection withStaphylococcus spp. the cause of Blackhead. Earthworms may be transport hosts for eggs. are small whitish worms with a pointed tail. Prevention Good litter management and handling. Post-mortem lesions Inflammation of sternal bursa along the keel bone which may. in chronic cases. There is an incubation period of 2 weeks for eggs to embryonate. Signs Swelling over the keel bone with bruising and discolouration. Treatment Not usually appropriate. Morbidity may reach more than 50% but the condition is not fatal. Signs None. Caecal Worm Introduction Heterakis gallinae.
The life cycle ofHeterakis showing the location of adults. especially broiler parents. or by an earthworm which is in turn ingested by a chicken. Diagnosis Adults can be seen in caecal contents at post-mortem examination. possibly with nodule formation. Death from respiratory and cardiac failure. an undeveloped egg as found in fresh faeces. Figure 11. Predisposing factors include heat stress with reduced feed intake and panting. Prevention Avoiding access to earth and earthworms. Treatment Flubendazole. 23 . Routine anthelmintic treatment. are effective. Levamisole. and the embryonated egg. The egg may be ingested directly by a chicken. Signs Paralysis. Calcium Tetany Introduction A metabolic disease of chickens.Post-mortem lesions Inflammation of caecum.
lesions. Prevention Keep pullet flocks on low calcium diet until 5% production hen/day. There is an annual cycle with increased risk of infection in the summer months in some countries. Differentiate from IB 793b. Infected poultry are a potential reservoir of this zoonosis. pets and wild animals. 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'. Campylobacters are a significant cause of enteritis in man. Campylobacter Infection Introduction Campylobacter spp. lack of other significant lesions.Post-mortem lesions Cyanosis. principally in the caecae. 24 . are bacteria that commonly infect a broad range of livestock species. other acute infections and other causes of sudden death. 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. Diagnosis This is made on signs. carcase quality and litter quality are better on farms which tend to have Campylobacter-negative stock. In poultry they tend to multiply in large numbers in the hindgut. and response to treatment. Active ovary with egg in oviduct. managing birds for maximum uniformity. Congested lungs. biofilm or engulfed by protozoa. Campylobacter jejuni is the commonest species found in poultry. Treatment Provide 5 gm of oyster shell per hen on 3 successive days along with vitamin D in drinking water. All campylobacters are delicate organisms that survive for relatively short periods outside the host unless protected by organic material. There are indications that plantar pododermatitis.
25 . sourcing of water from high quality supplies. good hand hygiene by stockmen. Key aspects of this include effective sanitation of drinking water. cloacal swabs or composite faeces. Research is ongoing on the development of vaccines. and changing of overalls and boots on entering bird areas. housed poultry can be maintained free of Campylobacter infection by consistent application of excellent biosecurity. Post-mortem lesions None. For this reason it may be difficult to stop the spread of infection between houses once it becomes established in one house.Signs None. Prevention In principle. Many infections are introduced during thinning or other forms of partial depopulation. In practice the success of this will also depend upon the degree of environmental contamination by the organism. Samples should be tested as quickly as possible after collection. as well as processing plant technologies to reduce carcase contamination. avoidance of contact with pets and other farmed species. Treatment Not required on clinical grounds. Diagnosis Isolation of the organism from caecal contents. Insects and rodents may act as a means of transfer of the infection from the general environment into the poultry buildings. The organism is sensitive to air so swabs should be collected into transport medium and other samples placed in airtight containers with minimal airspace. phage treatments and competitive exclusion approaches.
turkeys. Diarrhoea. Moniliasis. Slow growth. copper sulphate (1 kg/tonne feed) for 5 days. characterised by thickening and white plaques on the mucosa. especially in the crop but sometimes in the proventriculus.g. Colonies of this fungus appear as white to ivory colour. possibly confused or masked by signs of the primary disease. Morbidity and mortality are usually low. The cause is a fungal yeast. Thrush Introduction A disease of the alimentary tract of chickens. oesophagus. sodium or calcium proprionate at 1 kg per tonne continually. and sometimes other birds and mammals. 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. Diagnosis Lesions. or copper sulphate 1gm/2 litre water for 3 days if approved locally. Raised focal lesions may slough into lumen as caseous material. The fungus is resistant to many disinfectants. Ensure good hygiene.Candidiasis. Control of Candida through drinking water is sometimes practised with chlorination (e. crop. Poor appetite. Post-mortem lesions White plaques in mouth. occasionally proventriculus and intestine. proprionic acid. 26 . histopathology. Prevention Avoid excessive use of antibiotics and other stressors. intestine and cloaca. and associated with gizzard erosion. A finely divided powder of copper sulphate (where approved) at 200gm/tonne continually or to 14-16 weeks in replacement pullets. microscopic examination of a digested smear (heat in 10% potassium hydroxide) to demonstrate the hyphal forms of the yeast in the tissues. Treatment Nystatin (100 ppm in feed) for 7-10 days. Signs Dejection. smooth and with a yeasty smell. Candida albicans and the condition is seen worldwide.
Predisposing factors include overcrowding. Morbidity is usually low but mortality is high among affected birds. Signs Pecking at feet (especially young chicks) and vents (adult layers and turkey poults 812 days old). Take care to provide fresh clean feed and water. and strain of bird. high temperatures. It should be repeated periodically. control ectoparasites. through shafts of light in the house). boredom. uncontaminated by fungi. nutritional deficiencies. tenosynovitis and other diseases affecting mobility. Beak trimming may be necessary. anaemia. feed form (mash takes longer to consume than pellets). complying with local regulations and any relevant codes of practice. Feather-pulling. Cannibalism. wings. Treatment Correct any husbandry problems. face. Post-mortem lesions Skin wounding related to particular signs exhibited. head. Provision of a diet that closely matches the nutritional requirements of the stock concerned. Differentiate from bacterial dermatitis. Prevention Proper density and temperature. post-mortem cannibalism.Chlorox. Feather pecking Introduction A complex multifactorial behavioural problem of poultry and game birds seen worldwide. excessive light intensity or variation (e. 27 . sodium hypochlorite) at 5 ppm. Soluble multivitamins and/ or methionine may be of some benefit in some circumstances. If so it should be carried out carefully by trained operators. distribution of lesions. low light level. Generalised anaemia.g. Diagnosis Age. This is economical and effective.
effective cleaning of houses. seiving intestinal contents. Diagnosis This may be by a combination of macroscopic examination. C. C. Hairworms in mucosa of crop. game birds and pigeons ofCapillaria species. The worms are 7-18 mm long. about 0. Infection is by the oral route. Morbidity and mortality are usually low. Prevention Separation of birds from possible transport and intermediate hosts. Worm eggs take about 20 days to embryonate with an L1 larvae. Levamisole. Worm eggs in the environment are resistant.Hairworm Infection Introduction Nematode parasitic worms of poultry. Dejection. small intestine or caecum. Some species have earthworms as intermediate hosts. Treatment Coumphos has been licensed in some markets. prepatent period about 21-25 days according to species.other approved benzimidazoles can be expected also to have activity. obsignata in the small intestine.Capillariasis . some are transmitted direct from bird to bird. contorta in the crop and oesophagus. or characteristic worm eggs in faeces in patent infections. Wasting Poor growth. Differentiate from other causes of enteritis. Signs Diarrhoea. Fenbendazole has been shown to have high efficacy . 28 . Post-mortem lesions Enteritis.05 mm wide and hair-like in appearance.
Signs Affected flocks tend to have poorer than average productivity and uniformity. though most of the birds showing toe scrapes will not go on to develop cellulitis. Many affected birds have no other lesions and are reasonably well grown. Many meat inspectors become skilled at detecting subtle differences in skin colour in the affected birds. 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. coli. but the affected birds are not readily detectable prior to slaughter. Prevention Toe scrapes at 15-25 days of age when feather cover is poor are the most likely predisposing factors. often minor. It typically occurs between skin and muscles and between muscles and may be an incidental finding in a range of conditions. In the USA it is called 'Inflammatory Process'. Routine monitoring of skin damage at about 25 days of age may be helpful in fostering good practices. Diagnosis Typical lesions. 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. skin wounds by particular strains of E. particularly broiler chickens. The condition is caused by infection of. 29 . Treatment Treatment would not be possible if the problem is identified at a final depletion. Careful flock management with a view to reducing toe wounds has the greatest impact in controlling cellulitis.Cellulitis Introduction Cellulitis is literally an inflammation of connective tissues. which can replicate in the tissues. However its main importance is as a cause of condemnation in meat poultry.
demonstration of ongoing sero-conversion in parent flock. ether. heat (70°C for 1 hour.) or poor management (e. Acute mycotic pneumonia. Transmission is usually vertical during sero-conversion of a flock in lay. No clinical signs or effect on egg production or fertility in parent flock during seroconversion. Prior to confirmation that it is in fact a virus it was known as Chicken Anaemia Agent or CAA. lateral transmission may result in poor productivity in broilers. 80°C for 5 minutes) and many disinfectants even for 2 hours at 37°C. Hypochlorite appears most effective in vitro. Sudden rise in mortality (usually at 13-16 days of age). may be beneficial. Signs Poor growth. Treatment Good hygiene and management. Pale birds. PCV of 5-15% (normal 27-36%).g. The virus is resistant to pH 2.Chicken Anaemia Introduction A viral disease of chickens caused by Chicken Anaemia Virus or CAV. Gangrenous dermatitis on feet. Gumboro. If gangrenous dermatitis is a problem then periodic medication may be required. Inclusion body heptatitis etc. poor litter quality). Atrophy of thymus and bursa. 30 . chloroform. legs wings or neck. Discoloured liver and kidney. Post-mortem lesions Pale bone marrow. Mortality is typically 5-10% but may be up to 60% if there are predisposing factors present such as intercurrent disease (Aspergillosis. and control of other diseases as appropriate. Diagnosis Gross lesions. virus may be isolated in lymphoblastoid cell line (MDCC-MSB1).
other infections may be predisposing factors. Morbidity is 50-80%. Weakness. phenolics are less so. caused by Chlamydia psittaci. It is transmitted by contact. man. or IFA. rarely chickens. Ornithosis Introduction An infection of turkeys. Serology: antibodies develop 3-6 weeks after infection. Egg transmission does not occur. Depression. Greenish-yellow diarrhoea. It is a 'Scheduled Disease' rarely diagnosed in UK. 31 . Nasal discharge. Conjunctivitis. Signs Respiratory signs. Iodophores and formaldehyde are effective disinfecting agents. Weight loss.Prevention Live vaccines are available for parents. pigeons. Immunity: there is a good response to field challenge (in birds over 4 weeks of age) and to attenuated live vaccines. Wasting. Inappetance. 15 weeks. Fibrinous pericarditis. but occurring probably worldwide. especially pigeons and robins. Airsacculitis. Elisa. Occasional transient ataxia in pigeons. They should be used at least 6 weeks prior to collecting eggs for incubation. Psittacosis. and may be detected by SN. Intercurrent salmonellosis and. psittacines. mortality 5-40%. perhaps. Their use may be restricted to those flocks that have not sero-converted by. ducks. say. Elementary bodies are highly resistant and can survive in dried faeces for many months. their degree of attenuation is variable. faecal dust and wild bird carriers. a bacterium of highly variable pathogenicity. Production drops in naive laying flocks Post-mortem lesions Vascular congestion. Chlamydiosis.
lesions. may rupture in pigeons. This condition is seen in chickens. exclusion of wild birds. Signs Short legs. Slipping of Achilles tendon (or perosis). Intracytoplasmic inclusions are helpful but confirmation requires demonstration of causal organisms (Giemsa stain. Differentiate from Duck viral hepatitis. Spleen enlarged and congested. Duck septicaemia. Live and inactivated vaccines are protective although the former result in carriers and the latter require several applications. niacin may also be involved). Necrotic foci in liver. Prevention Biosecurity. Slipped Tendon or Perosis Introduction Caused by deficiency of manganese. Perihepatitis. Lameness. Fibrinous pneumonia. folic acid. zinc. Congested lungs and air sacs in the turkey. Malposition of leg distal to hock. ducks and turkeys. Chondrodystrophy. In turkeys it may be an inherited deficiency of galactosamine. choline. Diagnosis History. Serology: complement fixation. Elisa and gel diffusion. either singly or in combination (although deficiencies of pyridoxine. Treatment Tetracycline (200-800 ppm in feed for 3-4 weeks) and/or quinolone medication and supervised slaughter. biotin. shortened bones. In embryos parrot beak. 32 . signs. IFA). Distortion of hock.
while E. Shallow trochlea. Differentiate from twisted leg. ruptured ligaments. 33 . while E. Coccidiosis of Turkeys Introduction Infection of turkeys with Eimeria spp. choline. E. of which two are associated with significant disease effects. This disease is not very common in commercially reared turkeys though most turkey growers receive preventative medication for at least part of their lives. no value to affected bird. E. Treatment For flock proceed as for prevention. Weight loss. dispersa is found in the small intestine. Prevention Addition of manganese. gallopavonis and E. Lateral slipping of tendon. adenoides affects the caecae and rectum. Tibia and metatarsus bowed. Tucked appearance. infectious synovitis. ruffled feathers. analysis of feed. Five species of Eimeria have been identified that cause lesions in turkeys. infectious arthritis. Diagnosis Lesions.Post-mortem lesions Shortening and thickening of long bones. rickets. correct mineral balance. meleagridis affect the lower small intestine rectum and caecae. meleagrimitis affects the upper small intestine. Post-mortem lesions The affected area of intestine shows thickening of the wall and dilation. vitamins. Signs Huddling. Watery diarrhoea that may occasionally be blood stained or contain clumps of mucus or shed mucosa. Depression. The contents may be haemorrhagic or be watery with white material shed from the mucosa.
The exudate can range from semi-liquid to solid white cores. Avoid use of tiamulin in ionophore treated birds. Figure 37. Sulphaquinoxaline). show some spotty congestion and have abnormal contents due to the sloughed epithelium. 34 . typically to 12 weeks of age. microscopic exam of scrapings (oocysts. Treatment Toltrazuril. Diclazuril is also used for this purpose.g. The intestines are dilated. Dosage levels of ionophores may be critical to efficacy and safety. Amprolium. Prevention The ionophore coccidiostats lasalocid and monensin are routinely used in turkey growers. lesions. Exposure of previously unmedicated birds to these compounds can cause toxicity. gamonts). Turkey caecal coccidiosis caused by E. Salinomycin is toxic for turkeys even at very low doses. adenoides. meleagrimitis.Diagnosis Signs. Sulphonamides (e. Figure 38. Differentiate from necrotic enteritis. Turkey coccidiosis of the upper small intestine caused by E.
Recovered birds have good immunity to the same parasite. Vaccines are used mainly in breeders but increasingly in broilers. It is caused by Eimeria tenella and results in lesions in the caecum of chickens worldwide. vaccination by controlled exposure. Diarrhoea. Morbidity is 10-40% and mortality up to 50%. Signs Depression. Ruffled feathers. Prevention Coccidiostats in feed. Vitamins A and K in feed or water. microscopic examination of scrapings. Accumulation of varying quantities of blood and caseous necrotic material in the caecum. Thickening. hygiene. Treatment Toltrazuril. of caecal mucosa.Coccidiosis. Differentiate from ulcerative enteritis. mitis (see above). tenella is more common when 'straight' ionophore programmes are used. Sulphonamides. blood in faeces. Closed eyes. lesions. Post-mortem lesions Petechiae. Amprolium. Diagnosis Signs. E tenella Introduction This was at one time the commonest type of coccidiosis and is certainly the most easily diagnosed. 35 . Shuttle programmes with chemicals in the starter diet usually improve control. ecchymoses. Production less affected than in some of the other forms of coccidiosis. Inappetance. In some markets the organic arsenical compound 3-Nitro is used as an aid in the control of caecal coccidiosis. Transmission as for E. Caecal. histomonosis. E.
seen worldwide. The infective agent is found in litter. secondary bacterial enteritis. 36 . The disease occurring is proportional to the amount of infective agent ingested. humidity). faeces and on fomites and birds are infected by the oral route with an incubation period of 2-5 days. identification of typical small round oocysts and other stages in fresh scrapings from the small intestine. Treatment Not usually treated but susceptible to the products used for other forms of intestinal coccidiosis. E mitis Introduction This condition of chickens. 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. May predispose to wet litter. Diagnosis Mild lesions. Coccidiosis. Moderate Eimeria tenella infection in the caecae of a chicken (Score 3). The caecal walls are thickened and haemorrhagic and there is a mass of blood in the caecal lumen. which colonises the small intestine. is caused by the protozoan parasite Eimeria mitis.Figure 15. The parasite is moderately resistant in the environment and highly resistant to conventional disinfectants. Predisposing factors include exposure to faeces and litter conditions that favour development of the parasite (temperature. Signs Reduced feed conversion efficiency and weight gain.
extending into caecal tonsils. Signs Depression. 37 . May be included in vaccines. Closed eyes. Poor production. hygiene. Severe necrotising enteritis. Diagnosis Signs. caecal coccidiosis. Ileorectal. Inappetance. Amprolium. vaccination by controlled exposure. Differentiate from ulcerative enteritis. Vitamins A and K in feed or water. Ruffled feathers.Prevention Normally controlled by anticoccidials in feed. E brunetti Introduction A relatively rare form of coccidiosis affecting chickens worldwide caused by Eimeria brunetti. Coccidiosis. Of moderate to high pathogenicity. Post-mortem lesions Petechiae and thickening of the distal third or more of intestine. blood in faeces. There is good immunity to the same parasite in recovered birds. Oocysts in caecum and rectum. lesions. caecum and rectum. Morbidity and mortality are variable. Diarrhoea. microscopic examination of scrapings. Sulphonamides. it is found in the terminal ileum. Treatment Toltrazuril. This species is not usually included in vaccines for broilers. Prevention Coccidiostats in feed.
Coccidiosis occurs only very rarely in commercially reared ducks in the UK. Sulphadimidine 30-600gm/100 birds/day. Tucked appearance. Tyzerria has eight sporocysts in each oocyst. 38 . anatipestifer. Blood-stained vent. lesions. compared to four per oocyst forEimeria.g. 3 days on). 2 days off. anseris is the most important. while in ducksTyzzeria perniciosa is most pathogenic. microscopic examination of scrapings (usually few or no oocysts. of Ducks and Geese Introduction Young ducks and geese may suffer from Eimeria spp infection. Vitamins A and K in feed or water. Coccidiosis. Signs Sudden death. Amprolium. Post-mortem lesions Massive haemorrhage in upper small intestine. 3 days on.Figure 16. large number of merozoites). Duck viral enteritis. Depression. In the goose E. Differentiate from Duck viral hepatitis. Diagnosis Signs. Intestinal. Moderate Eimeria brunettiinfection in the terminal ileum and rectum of a chicken. Treatment Sulphonamides (e. There is thickening of the intestinal mucosa and there are lines of haemorrhagic spots in the mucosa.
39 . Post-mortem lesions Enlarged kidneys. Treatment Controlled trials of treatments have not been published. Kidney Introduction A disease of geese caused by Eimeria truncata that can cause high mortality in geese of 312 weeks of age. Weakness. Reduced feed intake. however this is not routinely practised. Coccidiosis. Diagnosis Lesions. Signs Depression. it can also infect Barbary ducks and swans.Prevention If required coccidiostats could be used in feed.faeces tend to be whitish. Kidneys light grey to greyish pink. Prevention Good Hygiene. Hygiene. Diarrhoea . presence of coccidial stages in fresh scrapings of kidney lesions. Tiny white foci and petechiae in the kidneys.
This is one of the less immunogenic species. Poor production. non-specific enteritis. commercial vaccines commonly contain more than one strain of E. mucosa tends to be pinker than normal. E maxima Introduction One of the more common forms of coccidiosis in commercial broilers. Ruffled feathers. Mid-intestinal. Differentiate from necrotic enteritis. Poor absorption of nutrients/pigments. 40 . Depigmentation of skin and plasma is especially evident in this form of cocccidiosis and this is commercially important in some markets. hygiene. Prevention Coccidiostats in feed. Amprolium. This infection is often associated with E.Coccidiosis. lesions. Inappetance. Diagnosis Signs. Because of the area of intestine affected it tends to have a significant effect on productivity and susceptibility to necrotic enteritis. microscopic examination of scrapings. Mild to severe enteritis. Post-mortem lesions Petechiae and thickening of middle third of intestine. Signs Depression. vaccination. acervulina coccidiosis and there may be large numbers of characteristic oocysts in smears. Blood or pigment in the faeces. Treatment Sulphonamides. maxima. Caused by Eimeria maxima. Morbidity and mortality are variable. of moderate to high pathogenicity it is seen worldwide. Closed eyes. contents often orange in colour. Vitamins A and K in feed or water.
Figure 13. Closed eyes. Depression. Mid-intestinal. Severe necrotising enteritis. Ruffled feathers. Poor production. other types of coccidiosis. It occurs in chickens worldwide and has variable morbidity but mortality is high in severely affected birds. 41 . Deep scrapings necessary to show large schizonts. in which the parasite is present in the small intestine and in the caecum. lesions. Moderate Eimeria maxima infection in the jejunum of a chicken (Score 2). 'Sausage-like' intestine. E necatrix Introduction A highly pathogenic form of coccidiosis. The lesions are subtle compared to other forms of coccidiosis. Post-mortem lesions Petechiae and thickening. of middle to posterior third or more of small intestine. Inappetance. Signs Reduced feed consumption. Schizonts seen as white spots through the serosa interspersed with petechiae. microscopic examination of scrapings Differentiate from necrotic enteritis. The intestine is slightly thickened and there are scattered haemorrhages in the mucosa when seen from the inside. Diarrhoea. Oocyts in caecal scrapings. Coccidiosis. blood in faeces. caused by Eimeria necatrix. Diagnosis Signs.
hygiene. which is moderately pathogenic. Figure 14. Haemorrhages and white spots are visible from the outside of the intestine.Treatment Toltrazuril. Eimeria mivatiis currently considered not to be a valid species distinct from E. vaccination. Upper Intestinal. Amprolium. Sulphonamides. It is seen in layers and in broilers. Depigmentation. Poor production. Closed eyes. E acervulina Introduction This is probably the commonest cause of coccidiosis in chickens and occurs worldwide. This is one of the less immunogenic species. Signs Depression. Ruffled feathers. commercial vaccines commonly contain more than one strain of E. Coccidiosis. maxima. Inappetance. Diarrhoea. Prevention Coccidiostats in feed. In this case the intestine is thickened and can become ballooned and sausage-like. Post-mortem lesions 42 . Moderate Eimeria necatrix infection in the jejunum of a chicken (Score 3). Morbidity is variable and mortality low or absent. both alone and in association with other species of coccidia and is caused by Eimeria acervulina. Vitamins A and K in feed or water. acervulina.
Figure 12. Poor absorption of nutrients/pigments. Petechiae. Sulphonamides. in severe the entire surface is pale or denuded of epithelium.the duodenum and part of the ileum. A detailed description is beyond the scope of this book. In milder infections there may be scattered white spots. In general terms a score of 0 indicates no lesions and a score of 4 indicates maximal severity of lesion or death. microscopic exam of scrapings. Various publications provide a photographic key to severity of lesion. hygiene. Thickening. 43 . Differentiate from necrotic and non-specific enteritis. restricted to upper third of small intestine . Amprolium. in feed or water. White spots or bands in the mucosa. and other lesions. A system of assessing the severity of coccidial challenge by attributing a 'score' is often used. lesions. Treatment Toltrazuril. Moderate Eimeria acervulinainfection (score 2) in chicken duodenum. Diagnosis Signs. In severe infections they become confluent and cause sloughing of the mucosa. vaccination by controlled exposure. Prevention Coccidiostats in feed. Immunity is quite short lived (about 30 days) in the absence of continued challenge.
Snick. Infection is by the oral or inhalation routes. and via shell membranes/yolk/navel. Reduced appetite. Enteritis. Dejection. Pericarditis. Perihepatitis. Arthritis. or in young birds that are immunologically immature. Poor growth. Signs Respiratory signs. Omphalitis. etc. Swollen liver and spleen. pathology. Morbidity varies. but is susceptible to disinfectants and to temperatures of 80°C. Granulomata in liver and spleen.most strains are rapidly lactose-fermenting producing 44 . Post-mortem lesions Airsacculitis. coughing. It is frequently associated with immunosuppressive diseases such as Infectious Bursal Disease Virus (Gumboro Disease) in chickens or Haemorrhagic Enteritis in turkeys. Diagnosis Isolation. sero-typing. mucosal damage due to viral infections and immunosuppression are predisposing factors. Colisepticemia Introduction Coli-septicaemia is the commonest infectious disease of farmed poultry. Peritonitis. Lesions vary from acute to chronic in the various forms of the disease. Salpingitis. sneezing. Omphalitis. mortality is 5-20%. turkeys. It is caused by the bacteriumEscherichia coli and is seen worldwide in chickens. Poor navel healing. It is most commonly seen following upper respiratory disease (such as Infectious Bronchitis) or Mycoplasmosis. fomites. Synovitis. Cellulitis over the abdomen or in the leg.Colibacillosis. with an incubation period of 3-5 days. water. The infectious agent is moderately resistant in the environment. Aerobic culture yields colonies of 2-5mm on both blood and McConkey agar after 18 hours .
stage of resolution and severity of lesion is likely to affect the degree of discomfort or pain suffered. Pododermatitis Introduction Contact dermatitis affects skin surfaces which have prolonged contact with litter.brick-red colonies on McConkey agar. gentamycin or ceftiofur (where hatchery borne). Staphylococcus spp. Contact dermatitis is commonly monitored at processing as a means of measuring 'welfare status'. rear surface of the hock and. as well as Pseudomonas. when severe. whereas others progress to deep ulcers so the size. flouroquinolones. Differentiate from acute and chronic infections with Salmonella spp. the foot pad. potentiated sulphonamide. 45 . and in broiler parents. feed and water. Some lesions are superficial. other enterobacteria such as Proteus. Treatment Amoxycillin. hatchery hygiene. Contact Dermatitis. Well-nourished embryo and optimal incubation to maximise day-old viability. Immunity is not well documented though both autogenous and commercial vaccines have been used. The liver is almost entirely covered by a substantial layer of fibrin and pus. good sanitation of house. Hock Burn. the breast area. Control of predisposing factors and infections (usually by vaccination). Figure 17. Prevention Good hygiene in handling of hatching eggs. etc. tetracyclines. neomycin (intestinal activity only). It is seen in growing broiler chickens and turkeys. Severe perihepatitis in colibacillosis in a broiler parent chicken.
most importantly. It can be reproduced by adding water to the litter. and. drinker management. Post-mortem lesions As described under signs. Figure 18. See the discussion in the section on Dysbacteriosis.Pododermatitis is often related to high droppings pH. Signs Blackened skin progressing to erosions and fibrosis on the lower surface of the foot pad. 46 . Treatment Not applicable. level of soya bean meal in feed (according to some authors. If severe the foot and hock lesions may contribute to lameness or serve as a portal of entry for secondary infections. litter moisture. Prevention This condition is closely linked to intestinal function as this is the prime determinent of faecal consistency and stickiness. Moderate pododermatitis on a foot pad. Choice of drinker type (nipple as opposed to bell). stickiness of droppings). at the back of the hocks. and sometimes in the breast area. proper insulation in cold climates. and adequate ventilation to remove moisture are all important. Diagnosis Signs and lesions.
The oocysts are excreted ready sporulated in the faeces and infection occurs by inhalation and ingestion. Cryptosporidium baileyi can cause respiratory disease in chickens and turkeys.Cropworms Introduction The nematode worms Capillaria spp and Gongylonema ingluvicolainfect the mucosa of the crop and oesophagous of poultry and game birds. meleagridis also infects both species. turkeys. Diagnosis Microscopic examination of mucosal scraping. but much smaller (typically oocysts are less than ¼ of the size of an E. A further species causes respiratory disease in quail. White convoluted tracks in the mucosa. Signs Anaemia. They also differ from coccidia in being poorly host specific. Coumaphos. Some have beetle or earthworms as intermediate hosts. They replicate in the brush border on the surface of epithelial cells. although bird strains do not infect mammals very well. 47 . Avoidance of access to intermediate hosts. acervulinaoocyst). Treatment Levamisole. Prevention Effective cleaning of housing. and ducks. The same species causes infections of the hindgut and cloacal bursa in chickens. Emaciation. and vice versa.C. Post-mortem lesions Inflammation and thickening of mucosa of crop and oesophagus. Cryptosporidiosis Introduction Cryptosporidia are related to the coccidia. Routine worming.
Signs Incoordination.g. Pneumonia. Low weight gain. Post-mortem lesions Sinusitis. It is becoming increasingly common for water companies to screen water supplies for cryptosporidia because of the human health implications of mammalian strains. 48 . Circling. There are no effective preventative medicines or feed additives. Treatment Unfortunately there is currently no known effective treatment in poultry. Tremors. recumbency.Signs Snick. If other disease processes are complicating the situation (e. Diagnosis Identification of the parasites attached to the epithelium by microscopic examination (smears histopathology acid-fast staining). Cough. Swollen sinuses. Torticollis. Diarrhoea. 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. coli-septicaemia) there may be benefit in medicating for these. Prevention The oocysts of cryptosporidia are extremely resistant to chemical disinfection. Airsacculitis.
Diagnosis Gross and microscopic lesions. Post-mortem lesions Damaged epiphyseal articular cartilage. Diagnosis Lesions. especially of femoral anti-trochanter but also other leg joints. The cause remains to be confirmed. 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. isolation of the fungus. but it may result from physical damage. Signs Lameness. Prevention Use fresh dry litter (avoid old sawdust). Reduced breeding performance. and cartilage flaps. Treatment 49 . resulting in erosions. air sacs etc. Mycotic lesions in lungs. Treatment None.Post-mortem lesions Necrotic lesions with associated congestion in cerebrum. Microscopically there is necrosis and there may be fissures of articular cartilage and associated osteochondritis. Degenerative Joint Disease Introduction A condition of chickens and turkeys seen worldwide. Rapid growth is a possible predisposing factor. or developmental defects.
For small flocks dipping the affected parts in a solution of acaricide may be beneficial. 50 . Raised thickened scales. pigeons etc. pheasants. Unthriftiness. especially during period of rapid growth.None available. It may be best to cull affected birds from small flocks. up to 0. Signs Cause irritation and the bird pulls feathers. Application of mineral or vegetable oil is also beneficial.Knemidocoptes spp. Prevention Avoidance of physical sources of injury to bones and joints. microscopic examination for mites in scrapings. Appropriate management of a segregation pen and early marketing of mildly affected birds may limit losses and improve flock welfare. round. Prevention Careful cleaning of buildings during down-time will help reduce the risk of these infections.5mm in diameter. Depluming and Scaly Leg Mites Introduction External parasites of adult chickens. Exclusion of wild birds from chicken areas is advised as far as possible. Diagnosis Signs. Mange lesions on legs and unfeathered parts. Treatment Not usually required in commercial poultry. The adult females are short legged. There may be a place for growth-control programmes. Post-mortem lesions As described under signs.
Possibly blood in the mouth. A sudden noise or other cause of excitement can lead to an 'outbreak'. Treatment None currently licensed. a tranquilizer. leg muscles. It has been suggested that degenerative changes in the wall of the artery and copper deficiency may be factors. Aortic Rupture Introduction A complex.Dissecting Aneurysm. Duck Viral Hepatitis Introduction A viral disease of ducks occurring worldwide and previously a scheduled disease in UK. The infective agent. Post-mortem lesions Carcase anaemic. Reserpine in diet of birds of 4+ weeks (no longer licensed in the UK). pericardial sac. Haemorrhages in lungs. The disease is transmitted by infected ducks and other waterfowl and spreads rapidly. Rupture of major blood vessel at base of heart or by the kidneys. Morbidity is around 100% and mortality 0-95%. genetic condition of turkeys linked to male sex and high growth rate. A longtitudinal split of the abdominal aorta is the most common lesion. Prevention Limit feed in birds of 16+ weeks. kidneys. Diagnosis History and lesions. recovered birds carrying the virus for 8 weeks. a picornavirus may also 51 . presumably due to a sudden increase in blood pressure. Aspirin at 250 ppm in feed or water may be of benefit. Skin pale. was included in feed at 1 ppm for 3-5 days to reduce blood pressure. Abdominal cavity full of blood. Signs Sudden death with no warning signs. birds found on breast or side. Reserpine.
Depression. Signs Sudden death. Newcastle disease. Kidneys and spleen swollen. bile duct proliferation and inflammation. rapid deterioration and death. Influenza and a 'Type II Variant' hepatitis caused by Astrovirus. All waterfowl are susceptible and the Barbary duck is more susceptible than the Pekin. The disease follows a very acute course with a morbidity of 5-100% and mortality of 5-100%. arching of back. Live.survive for ten weeks in brooders and five weeks in faeces. SN serology. isolation in CE (causes stunting of 9 day embryo). Duck Virus Enteritis. Treatment Antiserum. Prevention Vaccination and/or antiserum. Duck Plague Introduction A herpesvirus infection of ducks and geese diagnosed in the UK in 1972. Recovered birds may carry the virus for a year. Diagnosis History. fomites and arthropods. paddling of legs. A different picornavirus causes a similar condition in North America. often in opisthotonus. Differentiate from Duck plague (viral enteritis). mostly in ornamental collections. Microscopically . Post-mortem lesions Liver swollen.focal necrosis. Fall on side. Duck septicaemia (anatipestifer). lesions. 52 . 0. Punctate/diffuse haemorrhages. in USA since 1967.5 ml serum of recovered birds given intramuscularly. Transmission is by infected birds. coccidiosis. breeder vaccination. Death in good condition. only slightly attenuated vaccine is applied at day old by foot web stab and may be repeated in breeding birds to provide maternal immunity. also the Netherlands and other countries.
oesophagitis (birds on restricted feed). Occasionally penile prolapse in the penis in drakes. Non-specific Bacterial Enteritis Introduction Inflammation of the small intestine associated with wet litter. 53 . Ataxia. Dehydration. vent gleet. Tremor. Thirst. vaccination if approved by authorities (CE adapted live virus). Paresis. Dysbacteriosis. Young ducks may show thymic and bursal lesions. pasteurellosis. Rapidly spreading disease. Closed eyes. Crusty plaques from oesophagus to bursa (covered by yellowish plaques in later stages). coccidiosis. Haemorrhage in intestine. Post-mortem lesions Severe enteritis. Prevention Isolation from waterfowl. HA-. Diagnosis Isolation: Duck CAMs 12 day embryos die in 4 days. heart.Signs Sudden deaths. Drop egg production. pericardium. sometimes dysentery. liver. intranuclear inclusions Differentiate from Duck hepatitis. probably through interference. is common in countries with restrictions on the use of antimicrobial growth promoters and pressure to reduce therapeutic antimicrobial usage. spleen. excess caecal volume and fermentation. Severe diarrhoea. Photophobia. Treatment None. The condition is seen mainly in rapidly growing broiler chickens with good food intake. body cavities. Occasionally cyanosis of the bill in the young. but vaccination in face of outbreak is of value.
Treatment Amoxycillin and tylosin treatment appear to be beneficial. Water intake may be increased or irregular. No single bacterium appears to be responsible. lesions. 127. especially where treatment is initiated early. Apparently a similar disease had been seen over a 4-year period in broiler parents in Holland. France. Brazil. Prevention Competitive exclusion ('normal adult flora') use in day-old chicks reduces the risk of this condition. Wet faeces in the rectum. 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. Prophylactic antimicrobial medication may be necessary in some circumstances. Treatment should coincide with good relittering and it is important to provide fresh sanitary drinking water. first isolated in Northern Ireland in 1976. Mortality is usually negligible. Spain. Circumstantial evidence suggests that the main route of transmission is through the eggs (vertical transmission) 54 . often with gas bubbles. Holland. Feed acidification may be helpful in some circumstances. Peru. Good control of coccidiosis. Voluminous caecae. Diagnosis Signs. 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. England. Careful choice of any feed enzymes and their matching with local raw materials can have an impact on substrates made available to intestinal bacteria. Post-mortem lesions Excessive fluid content throughout the small intestine. Uruguay. The cause has been identified as Adenovirus BC14. It affects chickens and has occurred in Ireland. Argentina.Dietary changes. microscopic examination of scrapings from the wall of the small intestine (to exclude coccidiosis and perhaps to assess the bacterial flora). Signs Diarrhoea. Germany. feed interruptions and subclinical coccidiosis may be contributory factors.
inadequate lighting programme. Cholera. Diphtheritic Fowl Pox). oviduct). intoxication by sulphonamides. The infection is commonly present in ducks and geese but does not cause disease. selenium. signs/lesions (mainly lack of). which can be caused by a large number of factors acting individually or in combination. Coryza. group antigen distinct from classical adenoviruses (white cells. Nutritional deficiency should be considered. extremes of temperature. Post-mortem lesions No specific lesion . Lateral transmission from bird to bird is slow and may be prevented or slowed for weeks by netting divisions. Infectious Laryngotracheitis.it may be possible to demonstrate degenerative changes in the epithelial cells of the magnum of the oviduct. Metabolic diseases include Fatty Liver Syndrome.only a slight atrophy of ovary and oviduct. Newcastle disease. Infectious diseases include Infectious Bronchitis. Spread from house to house may take 5-10 weeks. as may wildfowl and biting insects. sudden changes of feed. Unvaccinated flocks with antibodies before lay do not peak normally. Rough. Lack of signs in the birds themselves. Avian Encephalomyelitis. Elisa. Serology: HI. Diagnosis History. Contamination of egg trays at packing stations may play a part in transmission. and D as well as calcium. Histopathology . Isolation of haemagglutinatin agent in duck eggs or cell culture. Signs Egg drop at peak or failure to peak. thin or soft-shelled eggs and shell-less eggs. Loss of shell pigment. may be infectious or metabolic. insecticides or nicarbazin. phosporus. Drops may be of 5 to 50% and last for 3-4 weeks. throat swabs. Marek's disease/Leukosis or any infectious disease causing a significant systemic disturbance (CRD. specifically vitamins E.followed by latent infection during rear with viral excretion starting shortly before sexual maturity. Clinical disease occurs during sexual maturity. Diseases in which egg drop occurs. Poor internal quality. DID. B 12. 55 . It is important to rule out other possible reasons for egg drop. Management problems may be involved: inadequate water supply. SN. Parasites.
56 . Endocarditis Introduction A condition of chickens associated with several bacterial infections such as staphylococci.Treatment None. rickets. osteomyelitis. Peripheral vessels congested. Culture of lesions to confirm the bacterium involved. Treatment Medication is only likely to be of value in reducing deterioration in birds that are starting to develop lesions. bacterial infection. 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. Post-mortem lesions Right ventricular failure and ascites. Prevention Good hygiene at turn-around. Signs Fluid-distended abdomen. growth plate disease. The choice should depend on sensitivity testing of an isolate. and /or trauma. Prevention Vaccination with inactivated vaccine prior to lay. streptococci. Vegetative lesions usually on the right atrioventricular valve. Diagnosis Differentiate from broiler ascites syndrome by examination of the interior of the heart. Epiphysiolysis Introduction A complex condition of chickens that may be associated with trauma. Erysipelothrixetc.
57 . Equine Encephalitis (EEE. Post-mortem lesions Separation of epiphyses at the growth plate. histology may be helpful in identifying underlying problems such as rickets or 'FHN'. WEE. Diagnosis Gross inspection. May also be asymptomatic. turkeys. Signs Nervous symptoms. VEE) Introduction A viral disease of pheasants. These conditions currently only occur from northern South America to North America. Horses are also seriously affected. Flaccid neck. often occurs or is identified in the processed carcase. It is transmitted between birds by pecking and by mosquitoes. Prevention Control of predisposing factors. Microscopic lesions not pathognomonic. Paresis. wild birds. ducks and pigeons having a high morbidity and high mortality. Ataxia. Post-mortem lesions No gross lesions. Treatment Not applicable. The natural hosts are wild birds and rodents. partridges. Tremors. Circling. chickens.Signs Apparent dislocation at extremities of long bones. sometimes seen in vivo. Paralysis.
Liver. Depression. ducks. Vaccinate at 5-6 week. Sudden death. and CE. spleen swollen. especially snood. Signs Inappetance. Post-mortem lesions Carcase congestion. 58 . Haemorrhages in fat. pheasants. There is likely to be an increased risk if housing or land has been previously used by pigs or sheep. Swollen snood. Perineal congestion. The bacterium is fairly resistant to environmental effects or disinfectants and may persist in alkaline soil for years. kidney. ID by VN. TC. water. COFAL. rhusiopathiae) seen in turkeys and increasingly in free-range chickens. May be diarrhoea and respiratory signs. Endocarditis. Chronic scabby skin. Joint lesions. fishmeal and semen and by cannibalism.Diagnosis Isolation in mice. Sleepiness. Prevention Protection from mosquitoes. muscle. Marked catarrhal enteritis. It may be transmitted by faecal carriers for 41 days. control cannibalism. rarely in geese. It is also seen in some mammals. Treatment None. in soil. Erysipelas Introduction A sudden onset infection with the bacterium Erysipelothrix insidiosa (E. epicardium.
the demonstration of the organism in stained impression smears from tissues. greasy and soft with numerous haemorrhages. vaccine at 16-20 weeks if the condition is enzootic. synoviae plate tests for a few weeks. Headparts pale. history. Signs Overweight typically by 25%. Sudden drop in egg production. Post-mortem lesions Obesity. Liver yellow. Sudden death. deficiency and stress. Treatment Penicillin . 59 . Death by internal exsanguination after rupture of haematocyst. Vaccination or natural infection may cause false positive reactions in the Mycoplasma gallisepticum and M. Diagnosis Lesions. Fatty Liver Haemorrhagic Syndrome Introduction A condition occurring worldwide in chickens. Some birds with pale comb and wattles. especially caged layers and with a complex set of causes including excessive calories. salmonellosis. Tetracyclines in feed may also be helpful. colibacillosis. Differentiate from pasteurellosis. mycotoxins.Diagnosis Isolation on blood agar. and acute Newcastle disease.a combination of the procaine and benzathine salts may be injected. Prevention Good biosecurity to prevent spread from other susceptible species. and identification. often along with bacterin.
supplement with choline. Signs White. Thick crusty skin. Prevention Feed to avoid obesity. Loss of condition. vitamin E. B 12 and inositol. Trichophyton gallinae. Favus Introduction A fungal infection. powdery spots and wrinkled crusts and scab on comb and wattles. Treatment Formalin in petroleum jelly.Treatment Reduce energy intake. avoid mycotoxins and stress. It is very rare in commercial poultry production. Diagnosis Lesions. culling affected birds. of chickens and turkeys. Prevention Good hygiene of facilities. 'Honeycomb' skin. Post-mortem lesions See signs (above). 60 . isolation. Feather loss.
Pasteurellosis Introduction Fowl Cholera is a serious.FHN Introduction A condition of chickens and turkeys that may be associated with several different bacterial infections e. Predisposing factors include immunosuppresive viruses such as Infectious Bursal Disease Virus and Chicken Anaemia Virus and non-infectious bone pathologies such as hypophosphaetamic rickets. FHN is the commonest infectious cause of lameness in broilers in the UK. Differentiate from synovitis. highly contagious disease caused by the bacterium Pasteurella multocida in a range of avian species including chickens. staphylococci. and water fowl. rickets. E. indicated that 0. Signs Lameness. coli. Fowl Cholera. Post-mortem lesions Degeneration of the epiphyses of long bones with thinning of the cortex and tendency to break when force is applied.g. especially hypophosphataemic. (increasing order of susceptibility).75% of all male broilers placed had lesions in the hip bone. Careful attention to mineral and Vitamin D nutrition to avoid subclinical. 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. streptococci. It is seen worldwide and was one of the first infectious 61 . Prevention Exclusion of floor eggs and dirty eggs from the hatchery. Diagnosis Base on post-mortem lesions and isolation of a causative organism. spondylolisthesis.Femoral Head Necrosis . Use of a wing for support during walking and hip flexion. turkeys. arthritis. Post-mortem studies of birds culled due to lameness and of birds found dead.
ocular and oral discharge. confirmed with biochemical tests. The disease can range from acute septicaemia to chronic and localised infections and the morbidity and mortality may be up to 100%. Ruffled feathers. Coughing. Purulent arthritis. erythromycin. The bacterium is easily destroyed by environmental factors and disinfectants.diseases to be recognised. and possibly pigs. streptomycin. tetracyclines. Enteritis. Predisposing factors include high density and concurrent infections such as respiratory viruses. isolation (aerobic culture on trypticase soy or blood agar yields colonies up to 3mm in 24 hours . The disease often recurs after medication is stopped. septicaemic viral and other bacterial diseases. Swollen and cyanotic wattles and face. 62 .no growth on McConkey). Reservoirs of infection may be present in other species such as rodents. Nasal. Differentiate from Erysipelas. Diarrhoea. Signs Dejection. faeces. cats. Loss of appetite. necessitating long-term or periodic medication. Lameness. and people. contaminated soil. Lungs with a consolidated pink 'cooked' appearance in turkeys. but may persist for prolonged periods in soil. Diagnosis Impression smears. or limited to haemorrhages at few sites. Swollen joints. Post-mortem lesions Sometimes none. by Louis Pasteur in 1880. Focal hepatitis. equipment. Yolk peritonitis. penicillin. Purulent pneumonia (especially turkeys). Cellulitis of face and wattles. The incubation period is usually 5-8 days. Treatment Sulphonamides. Sudden death. The route of infection is oral or nasal with transmission via nasal exudate.
Pox. It is transmitted by birds. and where there are biting insects. hygiene. The duration of the disease is about 14 days on an individual bird basis. Fowl Pox.Prevention Biosecurity. 63 . Infection occurs through skin abrasions and bites. turkeys. Poor egg production. The swelling is made up of oedema and purulent exudates (pus). 0-50%. good rodent control. Inappetance. and mosquitoes (infected for 6 weeks). Avian Pox Introduction A relatively slow-spreading viral disease characterised by skin lesions and/or plaques in the pharynx and affecting chickens. Severe localised Pasteurella infection in the swollen wattle of a 30-week-old male broiler parent chicken. pigeons and canaries worldwide. The virus persists in the environment for months. Caseous deposits in mouth. or by the respiratory route. spreading eruptions and scabs on comb and wattles. Morbidity is 1095% and mortality usually low to moderate. bacterins at 8 and 12 weeks. Depression. live oral vaccine at 6 weeks. Poor growth. throat and sometimes trachea. fomites. It is more common in males because of their tendency to fight and cause skin damage. Signs Warty. Figure 19.
Figure 20. Less commonly there may. Treatment None. Chickens well before production. check take at 7-10 days post vaccination. Differentiate from Trichomoniasis or physical damage to skin. usually with chicken strain by wing web puncture. It is confirmed by IC inclusions in sections/ scrapings. signs and post-mortem lesions. isolation (pocks on CE CAM) with IC inclusions. Turkeys by thigh-stick at 2-3 months. Microscopically . Fowl pox lesions on the wattle of an adult broiler parent chicken.intra-cytoplasmic inclusions (Bollinger bodies) with elementary bodies (Borrel bodies). Flocks and individuals still unaffected may be vaccinated. be caseous plaques in mouth. DNA probes. trachea and/or nasal cavities.Post-mortem lesions Papules progressing to vesicles then pustules and scabs with distribution described above. Diagnosis A presumptive diagnosis may be made on history. 64 . Prevention By vaccination (except canary). There is good cross-immunity among the different viral strains. in the diptheritic form. reproduction in susceptible birds. pharynx. If there is evidence of secondary bacterial infection broad-spectrum antibiotics may be of some benefit.
The spores of Clostridial bacteria are highly resistant in the environment. wattles. sometimes thighs and other parts. Avoid skin trauma and immunosuppression (congenital CAV infection. wings. Foci in liver. spleen. Recovery of an abundant growth of causative organism in recently dead birds. especially following congenital Chick Anaemia Virus infection or early Infectious Bursal Disease Virus infection (Gumboro Disease). Sudden mortality. Loss of appetite. occasionally Staphylococcus aureus. Gangrenous skin. 65 . usually over wings and breast.Gangrenous Dermatitis. Diagnosis Clinical signs and/or lesions. It occurs due to invasion of 'normal' wounds by 'normal' bacteria in immunosuppressed birds. Necrotic Dermatitis Introduction A bacterial condition seen in chickens and usually caused byClostridium septicum. Treatment Sulphaquinoxaline. penicillin or amoxycillin. Post-mortem lesions Patches of gangrenous skin with underlying emphysematous and/or sanguinous cellulitis. Severe cellulitis especially of thighs. Morbidity may be up to 50% and mortality is high. Swelling and infarction of the liver. Prevention Good hygiene and management. Signs Occasionally dejection. rarely Clostridium noyvi / oedematiens. early Infectious Bursal Disease Virus infection). Immunosuppression is therefore a predisposing factor.
Diagnosis Signs and lesions. Gape Introduction Syngamus trachea. Head shaking. Treatment Flubendazole in feed. Prevention Flubendazole. Loss of appetite and condition. turkeys. slugs and snails acting as transfer hosts but the life cycle may also be direct. Signs Gasping. The condition is seen more commonly in poultry on free range where ground may be contaminated by wild birds e. from rookeries. a nematode worm parasite of chickens. levamisole. and other game and ornamental birds occurring worldwide. by ingestion of embryonated egg or L3. 66 . There is an 18-20 day prepatent period. Post-mortem lesions Tracheitis. confirmation of presence of the parasite.Figure 21. Severe gangrenous dermatitis on the upper surface of the wing of a broiler chicken.g. Presence of worms. paired parasites up to 2 cm long. Dyspnoea. Infection is by the oral route with earthworms. pheasants.
They are more common in free-range birds because of their increased access to intermediate hosts. weevils.Geese Introduction A nematode worm parasite. Streptocara. Worms develop to L3 in eggs and infection is by the oral route direct from environment. muscular wall may be sacculated or ruptured. benzimidazoles such as flubendazole. necrosis and partial sloughing of gizzard lining. Adults are 2-4 cm long and usually bright red. Cheilospirura and Streptocara are seen worldwide but Histiocephalus is restricted to Europe. 67 . Signs Depression. affecting geese and ducks. and Histiocephalus are nematode worm parasites of chickens. Grasshoppers. Slow growth. Treatment Levamisole. Loss in condition and weight. Post-mortem lesions Ulceration. beetles etc act as intermediate hosts. Loss in condition and weight. Slow growth.Gizzard worms . routine worming. Signs Depression. Prevention Prevention of access to intermediate hosts. Gizzard worms . Diagnosis Lesions. Amidostomum anseris.Chickens Introduction Cheilospirura. confirmation of presence of the worms.
Reduced feed intake. Loss of down. visualisation of worms. Signs Prostration and death in acutely affected goslings. spleen and pancreas. benzimidazoles. The amount of maternal antibody passed from the breeding birds will affect the severity and timing and severity of the condition in the young birds. Adults are 2-4 cm long and usually bright red. Reddening of skin. The younger the bird affected the more acute the condition and the higher the mortality. 68 . Diagnosis Lesions. muscular wall may be sacculated or ruptured. Post-mortem lesions Pale myocardium. Swelling and congestion of liver. Losses are negligible in birds over 5 weeks of age. Prevention Rotation of ground on annual basis. Vertical transmission resulting in congenital infection may occur. Derzsy's Disease is caused by a parvovirus distinct from chicken and mammalian parvoviruses. Goose Parvovirus (Derzsy's Disease) Introduction Goose Parvovirus is a highly contagious condition of geese and young Muscovy ducks. Profuse white diarrhoea. Excessive water intake. Membrane covering tongue.Post-mortem lesions Ulceration. Treatment Levamisole. Swollen eyelids and eye and nasal discharge. necrosis and partial sloughing of gizzard lining.
Ideally flocks that have suffered the disease should not be used for breeding as they may become persistent excreters of the infection. mycotoxins and viral infections and usually following a course of approximately 3 weeks. Aplastic Anaemia. Poor growth. Bone marrow pale with fatty change. Diagnosis Signs and lesions in birds of the appropriate age and species. Liver yellow. serosa and mucosae. Signs Dejection. Prevention Hatching and brooding geese from different parent flocks together should be avoided. Carcase anaemia. Pale comb and wattles. Haemorrhagic Anaemia Introduction A complex condition of chickens associated with drug toxicities. Fibrinous perihepatitis. mortality is 5-50%. Morbidity varies. 69 . heart. Blood in droppings. Treatment No specific treatment. The preferred approach is to immunise breeding birds with an attenuated live vaccine. Post-mortem lesions Haemorrhages in one or more sites: skin. Administration of immune serum has been shown to be effective but may require two doses (day old and around 3 weeks). Loss of appetite. muscles. Ascites. Haemorrhagic Disease. Fibrinous pericarditis. liver. Antimicrobials may be of value in reducing the effects of secondary bacterial infections.
Post-mortem lesions Petechiae in various tissues. May induce immunosupression and precipitate respiratory disease or coccidiosis. signs. Signs Sudden deaths. Spleen mottled and enlarged. similar to pheasant Marble Spleen disease. Haemorrhagic Enteritis Introduction A viral disease of turkeys. Elisa . 70 . The route of infection is usually oral. lesions. Diagnosis Typical lesions. Blood from vent of moribund birds. double-immuno-diffusion of splenic extract. add liver solubles to feed. Drop in feed and water consumption. Microscopic . reproduction with filtered contents. Course 10-21 days.sero-conversion frequently occurs in absence of clinical disease. Treatment Vitamin K. Serology: DID. remove sulphonamides. caused by Type II Adenovirus distinct from classical fowl adenovirus and occurring in most turkey-producing areas. Prevention Avoid causative factors. Diarrhoea. and weeks in litter. The source of virus is unknown but there is easy lateral spread within flocks.Diagnosis History. Intestine distended with blood. the virus surviving in frozen faeces for months. The virulence of the virus varies but morbidity may be 100% and mortality 10-60%.spleen shows lymphoid hyperplasia. reticulo-endothelial hyperplasia and intranuclear inclusions.
feather cover.Treatment Warmth and good management.and T-line lymphocytes for up to 5 weeks following exposure. Predisposing factors include genetics. Prevention All-in/all-out production. Immunity to the disease is long lasting. Figure 39. oral tetraycline. Immunity: there is an early age resistance irrespective of maternal antibody status. Ducks are relatively resistant to heat stress. good hygiene and biosecurity. convalescent serum. good management. high stocking density. Turkeys dying with haemorrhagic enteritis commonly have the small intestine distended with blood. and turkeys caused by high environmental temperature. 71 . In this case a loop of intestine has been opened to show the blood. Pathogenic strains can depress both B. drinking water temperature and availability. Signs Panting. Maternal antibody may interfere with vaccination. Some are produced in live turkeys. Increased thirst. nicarbazin in feed. especially associated with high relative humidity and low air speed. Disinfect and 3-4 weeks house rest. Live vaccines are commonly used in many countries at 4-5 weeks of age. Reduced feed consumption. Heat Stress Introduction A condition seen in chickens. some in turkey B-lymphoblastoid cell lines. acclimation.
Signs Initially birds nervous. feed with a reduced protein:energy ratio. Inter-species transmission may occur. Terminal coma and convulsions. Legs and wings outstretched. pattern of losses. painted white to reflect heat. pheasants. columbae) is a protozoan parasite of turkeys. Mucoid exudate in nostrils and mouth. Later depression. chirping. Frothy. Post-mortem lesions Carcases congested. watery diarrhoea. Prostration. contains excessive mucus and gas. exclusion of other conditions. Reductions in stocking density of meat poultry may be quickly achieved by partial depletion ('thinning'). lesions. Treatment Cool water. if relative humidity is low then wet the roof and fog. pigeons. Feeding during cooler hours may be beneficial. Reduced egg production. evaporative coolers. carriers. Inappetance. signs. Intestine flabby with some bulbous dilation. Loss in weight. Prevention Houses of optimal height and insulation. Diagnosis Temperature records. 72 . and some game birds. Post-mortem lesions Dehydration. In commercial ducks a related parasiteTetratrichomonas can cause poor growth and drops in egg production. maximise airflow. It is transmitted by faeces. Hexamitiasis Introduction Hexamita meleagridis (pigeons H. fomites.
Within a turkey shed transmission is rapid in spite of the fact that it is difficult to infect birds orally with unprotected parasites. Signs Depression. Prevention Depopulation. and mixing groups of different ages. histomonosis. Sulphur-yellow diarrhoea. Treatment Tetracycline. increase ambient temperature. and occasionally chickens. Histomoniasis. pheasants and game birds that acts together with facultative bacteria to produce the condition of Blackhead. Furazolidone. dimetridazole. The effect of antibiotic may be related to the control of secondary bacterial enteritis. Caecal tonsils congested. avoid interspecies mixing. Blackhead Introduction Histomonas melagridis is a protozoan parasite of turkeys. and also. significant disease has been seen in breeding chickens and free-range layers. Histamonosis. trichomoniasis. Differentiate from transmissible enteritis. The problem is seen in high-biosecurity facilities. Cyanosis of head. paratyphoid. if possible. 73 . Inappetance. It has recently been demonstrated that infection occurs readily via the cloaca when birds are on contaminated litter. The parasite is ingested in the ova ofHeterakis worms or as larvae in earthworms or faeces and there is an incubation period of 15-20 days. Diagnosis Lesions. Poor growth. Progressive depression and emaciation. presumably introduced with worm eggs. all-in/all-out production. gallinae the parasite is easily destroyed. This condition has high morbidity and mortality in turkeys. scrapings from fresh material. First half of intestine inflamed. hygiene. Although chickens are relatively resistant to the condition. dimetridazole and ipronidazole have been used in the past. Outwith earth worms orH. Blood in faeces (chickens).
Some herbal products based on the essential oils (e. Liver may have irregular-round depressed lesions. dimetridazole).nitarsone) have been used to treat this important disease of poultry. Ulcers. Mortality may reach 60% but more typically 10-30%. Arsenicals are less effective in treatment than they are in prevention. It is a condition caused by an adenovirus. Regular worming to help control the intermediate hosts. and only nitarsone is approved in the USA. avoid mixing species.g. Use of an anti-histomonas product in feed where such products are approved but due care with respect to residue avoidance would be required. caseous cores with yellow.g. Treatment Historically nitro-imidazoles (e. 74 . nifursol) and arsenicals (e. 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. Diagnosis Lesions.Tahir Post-mortem lesions Enlargement of caeca. Angara Disease Introduction This condition was first identified in broilers in Pakistan in 1987. scrapings from fresh material. grey or green areas. furazolidone. possibly in combination with an RNA virus and immunosuppression caused by Chick Anaemia Virus or Infectious Bursal Disease. The disease is readily reproduced by inoculating birds with a bacteria-free filtrate of a liver extract from an affected bird. usually grey in colour.g.g. At the time of writing no products of these groups are approved for use in the European Union. given recent new knowledge on the mechanism of transmission. nitrofurans (e. Prevention Good sanitation.Abubakar. It affects mainly broilers and broiler parents in rear and has also been seen in pigeons. concrete floors. 'Herban)' have been used with some apparent success though controlled trials and formal approval for this purpose are not recorded. Hydropericardium-Hepatitis Syndrome.M. Intensive relittering may help reduce the level of infection. Having both chickens and turkeys on the same property is likely to increase the risk of this disease in turkeys. especially in chickens.
Lungs oedematous. Post-mortem lesions Excessive straw-coloured fluid distending the pericardium (up to 10 mls). This condition usually affects only a small number of birds. Impacted gizzards are then found in 'non-starter' type chicks or poults. Grit would not be classed as a foreign body. however sometimes free-range poultry consume large stones. Yellow mucoid droppings. Congestion of the carcase. grass. Control of predisposing immunosuppressive diseases may help limit losses. histopathology.g. and birds of any age can 75 . however if young chicks to do not begin to eat feed properly they often consume litter instead. string etc. Huddling with ruffled feathers. Older birds ingest grit to facilitate the grinding activity in the gizzard. Prevention The condition typically occurs in areas of high poultry density where multi-age operation is traditional.5% iodophor solution) appears to be beneficial. Formalin-inactivated oil adjuvant vaccines are reported to be highly effective and are used in areas where the condition is endemic. Enlarged. pale friable liver and kidney. Diagnosis Lesions. The normal function of the gizzard is to aid in the physical grinding of food materials. Impaction and Foreign Bodies of Gizzard Introduction The gizzard or crop may become impacted with litter. Treatment None. virology.Signs Sudden increase in mortality. treatment of drinking water with 0. Good water sanitation (e. Lethargy.1% of a 2. Most young commercial poultry consume feeds that have a small particle size. Gizzard activity also acts as a pacemaker of intestinal activity and controls the speed at which food is passed to the small intestine. to reduce their particle size to aid digestion.
The disease was first described in the USA in 1963 and has also been reported in Canada. A foreign body may be found in the interior of the gizzard. the UK. Post-mortem lesions The gizzard is more firm than normal and. This usually happens after maintenance activities have been carred out in the housing. Prevention Good brooding management to encourage early adaptation to the diet and adequate consumption of feed and water. Daily monitoring of the crop-fill is a useful procedure. and on opening is found to contain a mass of fibrous material. Signs Reduced feed intake. Australia. Treatment None effective in young birds. Italy. 76 .consume nails. 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. France and Ireland. This may extend into the proventriculus and on into the duodeunum. often with severe anaemia. Obvious non-starters should be culled in this situation. Diagnosis Lesions. Reduced weight gain. caused by an adenovirus. staples etc. A number of different sero-types have been isolated from disease outbreaks but they may also be isolated from healthy chickens. and may penetrate the body wall. Inclusion Body Hepatitis Introduction A disease of chickens characterised by acute mortality. It has a course of 9. Infected birds remain carriers for a few weeks. Sweep floors after maintenance activities to remove nails and other potentially dangerous foreign bodies.15 days with a morbidity of 1-10% and a mortality of 1-10%. Nails commonly penetrate the lining of the gizzard.
pH). Microscopically . Differentiate from Chick anaemia syndrome. Signs Depression. Bursa and spleen small. may be important. sulphonamide intoxication. Since adenoviruses are commonly found in healthy poultry. fatty liver syndrome. Confirmation is made on finding inclusions in the liver. Blood thin. vibrionic hepatitis. Kidneys and bone marrow pale. perhaps because they have lower levels of maternal antibody. Inappetance. Progeny of high health status breeding flocks appear to be at greater risk. CEL). SN for individual sero-types. chloroform. Treatment None.Transmission may be vertical or lateral and may involve fomites. Post-mortem lesions Liver swollen. Immunosuppression. Soluble multivitamins may help with the recovery process. for instance due to early IBD challenge or congenital CAV infection. A form of the disease affecting birds under 3 weeks of age in Australia has been reproduced with serotype 8 adenovirus. The virus is generally resistant to disinfectants (ether. but on the other hand many field cases show eosinophilic inclusions that do not appear to have adenovirus particles. Serology: DID for group antigen. Diagnosis A presumptive diagnosis may be made on history and lesions. isolation alone does not confirm that they are the cause of a particular problem. 77 . and deficiency of vitamin B12. The virus grows well in tissue culture (CEK. Pallor of comb and wattles. many different sero-types have been isolated from different cases. Formaldehyde and iodides work better.basophilic intranuclear inclusions. Curiously. yellow. Ruffled feathers. Infectious Bursal Disease. mottled with petechiae and ecchymoses. and high temperatures.
Some birds/viral strains can be carriers to 1 year. About eight sero-groups are recognised by sero-neutralization. depending on secondary infections. E. Diarrhoea. IB Introduction This infection. was first described in the USA (N. dyspnoea. is sensitive to solvents. and complicating infections (Mycoplasma. Tracheitis. The cause is a Coronavirus that is antigenically highly variable. Newcastle disease). The virus. Huddling. Kidneys and bronchi may be swollen and they and the ureters may have urates.Prevention Quarantine and good sanitary precautions. Caseous plugs in bronchi. Typing by haemagglutination-inhibition is also used. Dakota. Loss of appetite. gasping. Post-mortem lesions Mild to moderate respiratory tract inflammation. disinfectants (Formal 1% for 3 mins). Signs Depression. 78 . These differences are due to structural differences in the spike proteins (S1 fraction). alkalis. Poor ventilation and high density are predisposing factors. maternal immunity (young birds). Diuresis. Its affects vary with: the virulence of the virus. prior vaccination. new sero-types continue to emerge. Wet litter. Infection is via the conjunctiva or upper respiratory tract with an incubation period of 18-36 hours. 1931). Airsacculitis. Infectious Bronchitis. which may survive 4 weeks in premises. the age of the bird. The infection is highly contagious and spreads rapidly by contact. probably the commonest respiratory disease of chickens. prevention of immunosuppression. Morbidity may vary 50-100% and mortality 0-25%. heat (56°C for 15 mins). Coughing. fomites or aerosol. Tracheal oedema. coli.
v. Poor ventilation and high density are predisposing factors. fomites or aerosol. The virus. Avian Influenza and Laryngotracheitis. Local immunity is first line of defence. Differentiate from Newcastle disease (lentogenic and mesogenic forms). heat (56°C for 15 mins).).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. The infection spreads rapidly by contact. short duration. Serology: HI. lesions and serology. Treatment Sodium salicylate 1gm/litre (acute phase) where permitted . possible reactions depending on virulence and particle size. HA negative. Otherwise as for standard IB. alkalis. Infection is via the conjunctiva or upper respiratory tract with an incubation period of 18-36 hours. mycoplasmosis. Muscular shivering.Diagnosis Tentative diagnosis is based on clinical sgns. Elisa (both group specific). Infectious Bronchitis. Definitive diagnosis is based on viral isolation after 3-5 passages in chick embryo. disinfectants (Formal 1% for 3 mins). DID (poor sensitivity. depending on secondary infections. SN (type specific). vaccinal reactions. is sensitive to solvents. Cellmediated immunity may also be important. Some birds/viral strains can be carriers for up to 1 year. which may survive 4 weeks in premises. group specific). IB . flourescent antibody positive and ciliostasis in tracheal organ culture. Maternal immunity provides protection for 2-3 weeks. Prevention Live vaccines of appropriate sero-type and attenuation. Humoral immunity appears 10-14 days post vaccination. Signs Sudden death. 79 .antibiotics to control secondary colibacillosis (q.
There is rapid spread by contact. The virus is moderately resistant and may survive 4 weeks in premises. DID (poor sensitivity. Diagnosis 3-5 passages in CE allantoic cavity. Rales may or may not be present. short duration. fomites or aerosol. Other lesions of 'classical' IB may be encountered.Post-mortem lesions Oedema of pectoral muscles and subcutaneously on abdomen.v. sneezing. Loss of internal egg quality. with much antigenic variation. cell culture (Vero. Signs Drop in egg production (20-50%).). 80 . group specific). HA-. Elisa (both group specific). FA. possible reactions depending on virulence and particle size. In layers the ovules may be intensely congested. Prevention Live vaccines of appropriate sero-type and attenuation. typical lesions.antibiotics to control secondary colibacillosis (q. Infection is via the conjunctiva or upper respiratory tract. Treatment Sodium salicylate 1gm/litre (acute phase) where permitted . ciliostatic in tracheal organ culture. The condition has a morbidity of 10-100% and mortality of 0-1%. CK) only after adaptation Serology: HI. Soft-shelled eggs. Infectious Bronchitis. SN (type specific). lesions progress to necrosis and scarring of deep pectorals in convalescence. IB Egg-layers Introduction A Coronavirus infection of chickens. Rough shells. Coughing. A few birds are carriers up to 49 days post infection. Poor ventilation and high density are predisposing factors.
DID. SN. 81 . Cell-mediated immunity may also be important. Yolk in peritoneal cavity (non-specific).antibiotics to control secondary colibacillosis (q. virulence. Humoral immunity appears 10-14 days post vaccination. although reactions can occur depending on prior immunity. Differentiate from Egg Drop Syndrome. Diagnosis 3-5 passages in CE. Serology: HI. Prevention Live vaccines of appropriate sero-type and attenuation. typical lesions. Elisa. FA. Figure 22. Flaccid ovarian follicles in a broiler parent chicken undergoing challenge with Infectious Bronchitis virus. Maternal immunity provides protection for 2-3 weeks. Treatment Sodium salicylate 1gm/litre (acute phase) where permitted .Post-mortem lesions Follicles flaccid. Local immunity is the first line of defence. EDS76. HA-.v.). particle size (if sprayed) and general health status.
Serology: HI. Signs Drop in egg production (20-50%). Prevention Live vaccines of appropriate sero-type and attenuation. particle size (if sprayed) and general health status.antibiotics to control secondary colibacillosis (q. Treatment Sodium salicylate 1gm/litre (acute phase) where permitted . FA. Soft-shelled eggs. SN. Rales may or may not be present. fomites or aerosol. A few birds are carriers up to 49 days post infection. EDS76. DID. Coughing. HA-. There is rapid spread by contact. Infection is via the conjunctiva or upper respiratory tract. Loss of internal egg quality.). Local immunity is the first line of defence. Yolk in peritoneal cavity (non-specific). Diagnosis 3-5 passages in CE. The condition has a morbidity of 10-100% and mortality of 0-1%. Cell-mediated immunity may also be important. although reactions can occur depending on prior immunity. Differentiate from Egg Drop Syndrome. Maternal immunity provides protection for 2-3 weeks. The virus is moderately resistant and may survive 4 weeks in premises. Rough shells. Elisa. IB Egg-layers Introduction A Coronavirus infection of chickens. Poor ventilation and high density are predisposing factors. with much antigenic variation. sneezing.v.Infectious Bronchitis. typical lesions. 82 . virulence. Post-mortem lesions Follicles flaccid. Humoral immunity appears 10-14 days post vaccination.
20% but sometimes up to 60%. Infectious Bursal Disease. The disease is highly contagious. and affected birds excrete large amounts of virus for about 2 weeks post infection. Signs are most pronounced in birds of 4-6 weeks and White Leghorns are more susceptible than broilers and brown-egg layers. faeces etc. with an incubation period of 2-3 days. The age up to which infection can cause serious immunosuppression varies between 14 and 28 days according to the antigen in question. which targets the bursal component of the immune system of chickens. Mealworms and litter mites may harbour the virus for 8 weeks. Gumboro Introduction A viral disease. 83 . Flaccid ovarian follicles in a broiler parent chicken undergoing challenge with Infectious Bronchitis virus. Marek's disease and Infectious Bronchitis. persisting for months in houses. Sero-type 1 only. There is no vertical transmission. the damage caused to the immune system interacts with other pathogens to cause significant effects. The route of infection is usually oral. Morbidity is high with a mortality usually 0. but may be via the conjunctiva or respiratory tract. The virus is very resistant. especially with sero-type 2). susceptibility to Inclusion Body Hepatitis and gangrenous dermatitis and increased susceptibility to CRD. Subclinical infection in young chicks results in: deficient immunological response to Newcastle disease. In addition to the direct economic effects of the clinical disease. (Turkeys and ducks show infection only. Generally speaking the earlier the damage occurs the more severe the effects.Figure 22. The infective agent is a Birnavirus (Birnaviridae). first identified in the USA in 1962. IBD. seen worldwide.
Dehydration. IBD viruses have been isolated and shown to have significant but not complete cross-protection. Vent pecking. 84 . normal size or reduced in size depending on the stage). Elisa vaccination date prediction < 7 days). rapidly proceeds to atrophy.Signs Depression. Post-mortem lesions Oedematous bursa (may be slightly enlarged. Subclinical disease .4 days. 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.5. Antibiotic medication may be indicated if secondary bacterial infection occurs. Diarrhoea with urates in mucus. (previously SN and DID). Haemorrhagic syndrome. especially in the Delmarva Peninsula in the USA. Treatment No specific treatment is available.3% of bodyweight. The normal weight of the bursa in broilers is about 0.A history of chicks with very low levels of maternal antibody (Fewer than 80% positive in the immunodifusion test at day old. may have haemorrhages. histopathology. Use of a multivitamin supplement and facilitating access to water may help. Coccidiosis. Half-life of maternally derived antibodies is 3. Other possible causes of early immunosuppression are severe mycotoxicosis and managment problems leading to severe stress. Serology: antibodies can be detected as early as 4-7 days after infection and these last for life. Differentiate clinical disease from: Infectious bronchitis (renal). especially if present prior to 20 days of age. Diagnosis Clinical disease . lesions. Swollen kidneys with urates.1% are highly suggestive.History. Huddling under equipment. weights below 0. This may be confirmed by demonstrating severe atrophy of the bursa. subsequent diagnosis of 'immunosuppression diseases' (especially inclusion body hepatitis and gangrenous dermatitis) is highly suggestive. Cryptosporidiosis of the bursa (rare). Variants: There have been serious problems with early Gumboro disease in chicks with maternal immunity. Tests used are mainly Elisa. Unsteady gait. Haemorrhages in skeletal muscle (especially on thighs). Inappetance. They are all serotype 1.
This shows the anatomical relationship between the bursa. It is enlarged. including passive protection via breeders. Figure 23. and tracing of contacts may indicate sites on which a more rebust vaccination programme is indicated. When outbreaks do occur. turgid and oedematous. characterised by catarrhal inflammation of the upper respiratory tract. 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. occasionally pheasants and guinea-fowl. the rectum and the vent. Infectious Coryza is caused by the bacterium Haemophilus paragallinarum and is seen in many countries especially in multi-age farms that are never depopulated. Immunity after a live vaccine can be poor if maternal antibody was still high at the time of vaccination. This bursa is from an acutely affected broiler. sometimes chronic. Morbidity is high but mortality low if uncomplicated although it may be up to 20%. especially nasal and sinus mucosae. 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.Prevention Vaccination. Carriers are important with transmission via exudates and by direct contact. It is not egg transmitted. Infectious Coryza Introduction A usually acute. vaccination of progeny depending on virulence and age of challenge. 85 . resulting in increased culling. biosecurity measures may be helpful in limiting the spread between sites. A strong immunity follows field challenge. highly infectious disease of chickens.
requires X (Haematin) and V (NAD) factors. Eye-lid adherence. lesions. Treatment Streptomycin. Bacterin at intervals if history justifies or if multi-age. preferably in raised CO 2 such as a candle jar. Inappetance. Dihydrostreptomycin. Post-mortem lesions Catarrhal inflammation of nasal passages and sinuses. Flouroquinolones are bactericidal and might prevent carriers. drying and disinfectants. sulphonamides. Controlled exposure has also been practised. while bacterins only protect against homologous strains. Tracheitis. chronic or localised pasteurellosis and vitamin A deficiency. Swollen wattles. Loss in condition. identification of the bacteria in a Gram-stained smear from sinus. agglutination and IF have all been used but are not routine. 86 . Prevention Stock coryza-free birds on an all-in/all-out production policy. Commercial bacterins may not fully protect against all field strains but reduce the severity of reactions.The bacterium survives 2-3 days outside the bird but is easily killed by heat. Diagnosis A presumptive diagnosis may be made on signs. Dyspnoea. respiratory viruses. DID. Birds recovered from challenge of one serotype are resistant to others. Sneezing. Serology: HI. Intercurrent respiratory viral and bacterial infections are predisposing factors. Live attenutated strains have been used but are more risky. Purulent ocular and nasal discharge. at least two doses are required. erythromycin. Differentiate from Mycoplasmosis. Signs Facial swelling. Confirmation is by isolation and identification . Vaccines are used in areas of high incidence. Conjunctivitis. tylosin. Caseous material in conjunctiva/sinus. Drop in egg production of 10-40%.
pheasants. The virus is highly resistant outside host but is susceptible to disinfectants. Nasal discharge (low pathogenicity strains). Isolation in CE CAMs. Sera may be examined by VN or Elisa. Signs Dyspnoea. Apply strict biosecurity in moving equipment or materials between these these categories of stock. severe bronchitis. vaccination. 87 . after 4 weeks of age. Differentiate from Newcastle disease. ILT Introduction A herpesvirus (pathogenicity can vary) infection of chickens. Recovered and vaccinated birds are long-term carriers. Post-mortem lesions Severe laryngotracheitis.Infectious Laryngotracheitis. Treatment None. Fairly slow lateral spread occurs in houses. lesions. IFA. Keep susceptible stock separate from vaccinated or recovered birds. antibiotics to control secondary bacterial infection if this is marked. Prevention Quarantine. Coughing of mucus and blood. if enzootic or epizootic in an area. Sinusitis. caseous plugs may be present. histology. Transmission between farms can occur by airborne particles or fomites. All-in/allout operation. in severe form may be enough. Diagnosis Signs. peafowl and turkeys with a morbidity of 50-100% and a mortality usually 10-20% but sometimes up to 70%. Ocular discharge. Gasping. PCR. Movement and mixing of stock and reaching point of lay are predisposing factors. 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. Drop in egg production.intranuclear inclusions in tracheal epithelium. Microscopically . often with blood in lumen.
guinea fowl. Survivors may carry infection. Prevention Control of coccidiosis and other causes of intestinal inflammation. Leukocytozoonosis Introduction Caused by Leucocytozoon species. it may actually protrude at the vent and be cannibalised. Signs Sudden onset of depression. Anorexia. ducks. Careful attention to feeding practices to avoid anticipation of feed arrival if on restricted feeding. Coccidiosis. Loss of equilibrium. Simulid flies or culicoid midges are intermediate hosts. usually in the lower small intestine. protozoan parasites of turkeys. Different species of this parasite have been reported from North America. 88 . Asia and Africa. worms and other forms of enteritis are predisposing factors. Post-mortem lesions Telescoping of the bowel.Intussusception Introduction A condition of chickens associated with increased intestinal motility. rarely chickens. Rapid breathing. Signs Mainly sudden deaths. The disease has a short course and morbidity and mortality are high. Thirst. Diagnosis Typical post-mortem lesions Treatment As appropriate for the underlying disease condition.
lesions. Persistent low mortality.megaschizonts in brains of birds with nervous signs. Lymphoproliferative Disease (LPD) Introduction A Type C retrovirus infection of turkeys with low morbidity and high mortality. disposal of recovered birds. histology and blood smears. Hepatomegaly. age. Treatment None known. especially in enlarged spleen. Signs Depression. May be asymptomatic. Treatment 89 . Post-mortem lesions Focal tumours. Microscopically . Diagnosis History. Enlargement of abdomen. cytology. Emaciation. schizonts in liver. Loss of weight. Prevention Separation from intermediate hosts. Post-mortem lesions Splenomegaly. Differentiate from Reticuloendotheliosis. Anaemia. Anaemia. liver or bursa. gametes in erythrocytes. Diagnosis Lesions.
Poor feathering.M. Pot-bellied appearance. temperature control) may lead to a similar picture in the absence of specific infection. Poor early management (feed and water supply. Stunting (temporary). Signs Uneven growth. Abnormal feathers ('helicopter wings' 'yellow-heads'). Diarrhoea in older birds may be an effect of on-farm infection. Poor management may contribute to the problem. Diagnosis Pathology. North and South America and Australia. all-in/all-out production. Malabsorption Syndrome. direct electron microscope examination of intestinal contents. for example enteroviruses. control arthropods.Tahir None.(maize-) fed birds (often associated with orange intestinal contents and/or faeces). Pale shanks in corn. Prevention Good hygiene. Diarrhoea. Runting/Stunting Introduction A condition of chickens and turkeys that may be associated with several different viruses. Treatment Daily cull of affected birds between 14 and 28 days. in future eradication.Abubakar. Runting (permanent). Eating faeces. rotavirus etc. reoviruses. Sometimes osteomyelitis and/or rickets. The condition has been seen in Europe. Pancreatic atrophy/fibrosis and pancreatic atrophy (rather variable). Post-mortem lesions Enteritis. It is suspected that these viruses can be vertically transmitted and the most severe signs in young birds are associated with this. 90 . enterovirus-like particles.
Tumours of feather follicles. fomites.poorly digested food enclosed in mucus. muscles. good parent nutrition and egg selection and santitation. seen worldwide. The route of infection is usually respiratory and the disease is highly contagious being spread by infective feather-follicle dander. as well as more longstanding paralysis of legs or wings and eye lesions. Morbidity is 10-50% and mortality up to 100%.Acute infiltration of the CNS and nerves resulting in 'floppy broiler syndrome' and transient paralysis. They are distended with poorly digested feed. tests. c) Cutaneous . The disease has various manifestations: a) Neurological . In 'late' Marek's the mortality can extend to 40 weeks of age. From the 1980s and 1990s highly virulent strains have become a problem in North America and Europe. Infected birds remain viraemic for life. Vertical transmission is not considered to be important. 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. Intestines of a young broiler chick suffering from malabsorption syndrome. Figure 24. Marek's disease Introduction Marek's disease is a Herpes virus infection of chickens. lungs.Tumours in heart. A sample of the faeces produced is shown at the bottom of the picture . avoidance of intercurrent disease and management problems (such as chilling). ovary. Affected birds are more susceptible to other diseases. b) Visceral . The virus survives at ambient temperature for a long time (65 weeks) when cell associated 91 .Prevention Good broiler farm hygiene. both parasitic and bacterial. etc.
deficiency of Ca/Phosphorus/Vitamin D. histopathology. age affected.lymphoid infiltration is polymorphic. Vision impairment. M. Chronic Respiratory Disease . deficiency of thiamine. distribution of lesions. Differentiate from Lymphoid leukosis. It is inactivated rapidly when frozen and thawed. Mycoplasma gallisepticum infection. botulism. pigeons and other wild birds. kidney. wings and neck. Post-mortem lesions Grey-white foci of neoplastic tissue in liver. Genetics can help by increasing the frequency of the B21 gene that confers increased resistance to Marek's disease challenge. Grey iris or irregular pupil. Microscopically . turkeys. resistant strains. Skin around feather follicles raised and roughened. game birds. association with other strains (SB1 Sero-type 2) and Rispen's. Signs Paralysis of legs. especially at the start of lay. Loss of weight. and skeletal muscle. It is common practice to use combinations of the different vaccine types in an effort to broaden the protection achieved. Thickening of nerve trunks and loss of striation. gonads. Ducks and geese can 92 . heart.g. spleen. all-in/all-out production. clinical signs. Diagnosis History. chronic respiratory disease in chickens.. lung. vaccination generally with 1500 PFU of HVT at day old (but increasingly by in-ovo application at transfer).Chicken Introduction Infection with Mycoplasma gallisepticum is associated with slow onset. Prevention Hygiene. Treatment None.and is resistant to some disinfectants (quaternary ammonium and phenol).
coli. serology. airborne dust and feathers. Reduced hatchability and chick viability. sinuses. Perihepatitis (especially with secondary E. and in lyophilised material. more commonly in Mycoplasma Broth followed by plating out on Mycoplasma Agar. Spread is slow between houses and pens suggesting that aerosols are not normally a major route of transmission. subsequent stress may cause recurrence of disease. trachea and bronchi. Transmission may be transovarian. Occasional encephalopathy and abnormal feathers. though in some countries this infection is now rare in commercial poultry. Signs Coughing. ART). The infectious agent survives for only a matter of days outwith birds although prolonged survival has been reported in egg yolk and allantoic fluid. morbidity may be minimal and mortality varies. Slow growth. demonstration of specific DNA (commercial PCR kit available). Leg problems. Occasionally arthritis. Diagnosis Lesions. ND. aerosols. Pasteurella spp. and to a lesser extent fomites. Suspect colonies may be identified by immuno-flourescence. or by direct contact with birds. Pericarditis. isolation and identification of organism. Nasal and ocular discharge. 93 . Intercurrent infection with respiratory viruses (IB. Poor productivity. Stunting. virulent E. In turkeys it is most associated with severe sinusitis (see separate description in the turkey section). Recovered birds remain infected for life. and inadequate environmental conditions are predisposing factors for clinical disease. 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. Haemophilus. exudates. Survival seems to be improved on hair and feathers. Post-mortem lesions Airsacculitis. tenosynovitis and salpingitis in chickens. coli infection). though infection rates are high. The condition occurs worldwide. The route of infection is via the conjunctiva or upper respiratory tract with an incubation period of 6-10 days. Fomites appear to a significant factor in transmission between farms. Culture requires inoculation in mycoplasma-free embryos or.become infected when held with infected chickens. In adult birds. Inappetance.
Prevention Eradication of this infection has been the central objective of official poultry health programmes in most countries. tylosin. hatchingeggs and chicks. aerosols. It is seen worldwide. biosecurity. Elisa is accepted as the primary screening test in some countries. synoviae and M.Serology: serum agglutination is the standard screening test. PCR is possible if it is urgent to determine the flock status. HI may be used. Aspergillosis. Differentiate from Infectious Coryza.. other Mycoplasma infections such as M. therefore M. generally as a confirmatory test. tetracyclines. all-in/all-out production. vitamin A deficiency. M.g. infection status is important for trade in birds. suspect reactions are examined further by heat inactivation and/or dilution.Turkeys Introduction A slow onset chronic respiratory disease of turkeys often with severe sinusitis and associated with Mycoplasma gallisepticuminfection. and routine serological monitoring. exudates. These programmes are based on purchase of uninfected chicks. subsequent stress may cause recurrence of disease. Infectious Sinusitis . spiramycin. Some inactivated vaccines for other diseases induce 'false positives' in serological testing for 3-8 weeks.g. and fomites. 94 . Recovered birds remain infected for life. Morbidity is low to moderate and mortality low. Treatment Tilmicosin. Suspect flocks should be re-sampled after 2-3 weeks. or by direct contact with birds. Mycoplasma gallisepticum infection.-free stock. fluoroquinolones. viral respiratory diseases. though in many countries this infection is now rare in commercial poultry. Live attenuated or naturally mild strains are used in some countries and may be helpful in gradually displacing field strains on multi-age sites. Effort should be made to reduce dust and secondary infections.g. Transmission may be transovarian. Productivity in challenged and vaccinated birds is not as good as in M. In some circumstances preventative medication of known infected flocks may be of benefit. meleagridis(turkeys). The route of infection is via the conjunctiva or upper respiratory tract with an incubation period of 6-10 days.
Culture. tylosin. demonstration of specific DNA (commercial kit available). and biosecurity. serology. Airsacculitis. These are based on purchase of uninfected poults. requires inoculation in mycoplasma-free embryos or. PCR is possible if it is urgent to determine the flock status. isolation and identification of organism. intercurrent viral disease such as Newcastle disease (even lentogenic) and Turkey Rhinotracheitis are predisposing factors. Differentiate from viral respiratory disease. Effort should be made to reduce dust and secondary infections. Some inactivated vaccines induce 'false positives' in serological testing. especially Turkey Rhinotracheitis.The infectious agent survives for only a matter of days outwith birds. Stunting. suspect reactions are examined further by heat inactivation and/or dilution. more commonly in Mycoplasma Broth followed by plating out on Mycoplasma Agar. malnutrition. Leg problems. Pericarditis. although prolonged survival has been reported in egg yolk and allantoic fluid. spiramycin. Perihepatitis. often with inspissated pus. of swabs taken from the trachea or lesions. and in lyophilised material. Nasal and ocular discharge. Diagnosis Lesions. fluoroquinolones. Treatment Tilmicosin. Signs Coughing. Prevention Eradication of this infection has been the central objective of official poultry health programmes in most countries. Slow growth. Suspect colonies may be identified by immunofluorescence. Swollen sinuses. Suspect flocks should be re-sampled after 2-3 weeks. tetracyclines. Serology: serum agglutination is the standard screening test. Post-mortem lesions Swollen infraorbital sinuses. In some circumstances preventative medication of known infected flocks may be of benefit. all-in/allout production. Stress. Inappetance. 95 . HI may also be used. Survival seems to be improved on hair and feathers.
Leg lesions can be shown in inoculated birds but do not seem to occur naturally. Post-mortem lesions Sinusitis.g. Post-mortem lesions Stunted embryos with hepatitis and enlarged spleens.g. Introduction Infection with Mycoplasma iowae is seen in turkeys. Prevention As for M.i.g.Mycoplasma immitans infection Introduction Infection with Mycoplasma immitans is seen in geese. M. although DNA homology is only 40%. venereal or horizontal. some with down abnormality. and partridges (UK). Signs Swollen sinuses. ducks (France). 96 . Treatment As for M. Signs Embryonic mortality. Reduced hatchability. Diagnosis Shows cross reaction in IFA to M. and can occur in other poultry and wild bird species. perhaps because all affected embryos fail to hatch. Infection occurs via the conjunctiva or upper respiratory tract and transmission among poults may be vertical. Mycoplasma iowae infection.
Mortality is low. Pathogenicity is quite variable.m.i. Signs Reduced hatchability. Leg problems. Crooked necks. it occurs in most turkey-producing countries but is now much rarer in commercial stock.Diagnosis Isolation and identification of the causative organism from dead-in-shell embryos. In adult birds though infection rates are high. Treatment Pressure differential dipping has been used where breeder flocks are infected. Antibiotics that have been used are tylosin and enrofloxacin.-free stock. M. Prevention Eradication of the infection from breeding stock. The infective agent does not survive well outside the bird. Transmission is venereal in breeders. Predisposing factors include stress and viral respiratory infections. When the vacuum is released the eggs draw in antibiotic solution which is subsequently absorbed through the shell membranes. The organism has also been isolated from raptors. Slow growth. with transovarian and then lateral spread in meat animals. Stunting. Infected eggs result in widespread distribution of infection and increased risk of further vertical transmission. This can increase hatchability by 510% in this situation. Specialised dip tanks are subjected to negative pressure which partially collapses the air cell of the submerged eggs. Infected parents may be asymptomatic. Infection is via the conjunctiva or upper respiratory tract with an incubation period of 6-10 days. Introduction A disease of turkeys characterised by respiratory and skeletal problems caused by Mycoplasma meleagridis. maintenance of this status by good biosecurity. For eradication purposes egg injection provides more consistent dosing per egg than does egg dipping. Mild respiratory problems. 97 . though up to 25% of infected birds show lesions at slaughter. purchase of M. morbidity may be minimal. Mycoplasma meleagridis infection.
Infection is via the conjunctiva or upper respiratory tract with a long incubation period. 98 . fluoroquinolones. whilst illness is variable and mortality less than 10%. demonstration of specific DNA (commercial kit available). tetracyclines. spiramycin. Serology: SAG used routinely . Spread is generally rapid within and between houses on a farm. Mycoplasma synoviae. 11-21 days following contact exposure. Predisposing factors include stress and viral respiratory infections. Infectious Synovitis Introduction Infection with Mycoplasma synoviae may be seen in chickens and turkeys in association with synovitis and/or airsacculitis. Differentiate from Mycoplasma gallisepticum. Survival of the infectious agent outwith the bird is poor but fomite transmission between farms is important. all-in/all-out production. Prevention Eradication of this infection is also possible using similar techniques as for Mycoplasma gallisepticum. serology. In some circumstances preventative medication of known infected flocks may be of benefit.culture used to confirm. Infection rates may be very high. Suspect colonies may be identified by immuno-fluorescence. Vaccines are not normally used. Effort should be made to reduce dust and secondary infections. especially in commercial layer flocks. Culture requires inoculation in mycoplasma-free embryos or. Treatment Tylosin. Infected birds do develop some immunity. Mycoplasma synoviae infection. other respiratory viruses. and biosecurity. more commonly in Mycoplasma Broth followed by plating out on Mycoplasma Agar. or lateral via respiratory aerosols and direct contact. These are based on purchase of uninfected poults. Airsacculitis (rarely) seen in adult birds.Post-mortem lesions Airsacculitis in infected pipped embryos and poults. isolation and identification of organism. Diagnosis Lesions.s. Birds infected from their parents seem to be immuno-tolerant and particularly prone themselves to transmit. M. Infected males are particularly prone to transmit infection and may warrant special attention. It occurs in most poultry-producing countries. Transmission may be transovarian.
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.
high viscosity diets (often associated with high rye and wheat inclusions in the diet). Spores of the causative organism are highly resistant. in drinking water. or Bacitracin in feed (e. Immobility. Prevention Penicillin in feed is preventive. Water medication for 3-5 days and in-feed medication for 5-7 days depending on the severity. contaminated feed and/or water. Treatment Penicillins (e. Closed eyes. Affected birds tend to be dehydrated and to undergo rapid putrefaction. turkeys and ducks worldwide. Treatment of ducks is not very successful. Dark coloured diarrhoea. amoxycillin). Signs Depression.g. neomycin and erythromycin are used in the USA. 100 ppm). Probiotics may limit multiplication of bacteria and toxin 102 .Abubakar. Intestinal mucosa with diptheritic membrane. caused by Clostridium perfringens and characterised by a fibrino-necrotic enteritis. phenoxymethyl penicillin. Inappetance.Tahir Necrotic Enteritis Introduction An acute or chronic enterotoxemia seen in chickens. diet (high protein). Sudden death in good condition (ducks). in ducks possibly heavy strains. Post-mortem lesions Small intestine (usually middle to distal) thickened and distended. Ruffled feathers.g.M. Intestinal contents may be dark brown with necrotic material. Mortality may be 5-50%. other debilitating diseases. usually in less than 48 hours.small intestine. 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. usually around 10%. Reflux of bile-stained liquid in the crop if upper small intestine affected. Predisposing factors include coccidiosis/coccidiasis. usually of the mid. Infection occurs by faecal-oral transmission. high levels of most growth promotors and normal levels of ionophore anticoccidials also help.
production. which is of variable pathogenicity. Can affect any age.Mortality and nervous signs in adult. 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.Velogenic Viscerotropic (VVND) .Lentogenic . Other species can be infected including mammals occasionally (e. Higher mortality is seen in velogenic disease in unvaccinated stock. The virus involved is Paramyxovirus PMV-1. It is not usually vertical (but chicks may become infected in hatcheries from contaminated shells). Figure 25.Neurotropic Velogenic .sometimes called 'asiatic' or exotic. birds. Four manifestations have been identified: ND . sometimes subclinical. Severe lesions of necrotic enteritis affecting the small intestine of broilers. fomites. visitors and imported psittacines (often asymptomatic). 103 .Mild disease. less for turkeys and relatively apathogenic in psittacines. Affected species include chickens. Morbidity is usually high and mortality varies 0-100%. Signs are typically of disease of the nervous. It is highly virulent for chickens. conjunctivitis in man). ND . These viruses have sometimes been used as vaccines in previously immunised birds. The condition is rarely diagnosed in ducks but is a possible cause of production drops/fertility problems.g. respiratory or reproductive systems. pigeons and ducks. turkeys.Mesogenic . Intestinal lesions are absent. Newcastle Disease (Paramyxovirus 1) Introduction Paramyxovirus 1 or Newcastle Disease is a highly contagious viral disease affecting poultry of all ages. The sample at the bottom of the picture is still focal. Transmission is via aerosols.Acute and fatal in chickens of any age causing neurological and some respiratory signs. Strains can be developed as vaccines. ND . ND .
formalin and phenol. Necrotic plaques in proventriculus. avian influenza. intoxications. 104 . haemorrhagic disease. Severe drop in egg production. Haemorrhage in proventriculus. middle ear infection/skull osteitis. dust etc). Dyspnoea. pneumovirus infection. Cross-reactions have mainly been with PMV-3. fumigants and sunlight. intestine.The virus survives for long periods at ambient temperature. Nervous signs. encephalomalacia. post-mortem lesions. Post-mortem lesions Airsacculitis. antibiotics to control secondary bacteria. IFA. Paralysis. HI with ND serum or DID (less cross reactions). Samples . infectious coryza. It is confirmed by isolation in CE. EDS-76. Tracheitis. laryngotracheitis. HA+. Signs Signs are highly variable and will depend on the nature of the infecting virus (see above). the infective dose and the degree of immunity from previous exposure or vaccination. Treatment None. Diagnosis A presumptive diagnosis may be made on signs. However it is quite sensitive to disinfectants. intracerebral or IV pathogenicity in chicks. Sudden Death Depression. It is inactivated by temperatures of 56°C for 3 hours or 60°C for 30 min. and is ether sensitive. Pathogenicity evaluated by Mean Death Time in embryos. rising titre in serology. Moult. encephalomyelitis. Inappetance. for up to 12 months. acid pH. Coughing. caecal tonsil. Twisted neck. Intestinal lesions primarily occur in the viscerotropic form. Diarrhoea. especially in faeces and can persist in houses (in faeces. Differentiate from Infectious bronchitis.tracheal or cloacal.
and occasionally gasping due to a plug of pus in the lower trachea. 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). however. Inactivated vaccines have largely replaced the use of live vaccines in lay but they do not prevent local infections. all-in/all-out production. whereas it tends to peak between 6-10 days for chicks that begin eating but then cease. To prevent or reduce vaccinal reactions in young chicks it is important that day old have uniform titres of maternal immunity. It is common to monitor response to vaccination. Use of Mycoplasma gallisepticum free stock under good management reduces the risk of vaccinal reactions. 105 . 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. HI has been used extensively. vaccination. It is commonest in progeny of young parent flocks (relatively small yolks) or where managers are inexperienced.Prevention Quarantine. snicking. and is associated with difficulty maintaining brooding temperature and poor management of feeders and drinkers. which are adequately stored and take into account the local conditions. Morbidity is up to 10% and mortality close to 100%. Mortality peaks at 3-5 days for birds that fail to eat at all. biosecurity. Vaccination programmes should use vaccines of high potency. The LaSota-type vaccine may even repeated at 35-40 days of age if risk is high. Figure 28. Use of spray application is recommended but it needs to be applied with care to achieve good protection with minimal reaction. Elisa is now also used. Vaccinal reactions may present as conjunctivitis. In some countries it has been customary to provide antibiotics prophylactically during periods of anticipated vaccinal reaction. Acute viral infections or heavily contaminated drinking water may have a similar effect to bad management in reducing feed intake. These tests do not directly evaluate mucosal immunity. A typical programme may involve Hitchner B1 vaccine at day old followed by LaSota-type vaccine at 14 days. especially in breeding birds by the use of routine serological monitoring.
Because it is enclosed in a relatively unyielding membrane. age of collection and weight of hatching eggs. Gizzard may be impacted with litter. Diagnosis Based on post-mortem lesions. The condition can be reproduced by causing intense exercise of this muscle. Poor development. 106 . good hygiene and biosecurity in brooding areas to minimise early disease challenges. Without adequate blood supply the tissue of the muscle begins to die. It is caused by a reduction in the blood supply to the deep pectoral muscles. Prevention Review brooding management. soluble multivitamin supplementation may help. or suffer necrosis.Signs Failure to grow. It does not usually cause any mortality or obvious clinical signs and so it is usually identified after slaughter.Deep Pectoral Myopathy Introduction This condition is so named because it was first identified in adult breeding turkeys in Oregon State. any swelling of the muscle tends to cut off the blood supply. It has since been seen in turkeys. Treatment Correction of management problems. Post-mortem lesions Crop empty. in broiler parent chickens and also in large broiler chickens in various places. Differentiate from omphalitis/ yolk sac infection. Gall bladder distended. Most organs normal. aspergillosis. Oregon Disease . 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. nutrition of young parents. bile staining of adjacent tissues. good drinking water hygiene.
The tissue in the centre is dry. Transillumination of the breast may help identify affected carcases and may be worthwhile if the incidence is high. in particular excessive exercise. Figure 26.Signs None. and flaking. Treatment Not applicable. 107 . with oedema within it and on its surface. the muscle may be swollen and pale. it may become a healed scar. It is very difficult to detect affected carcases in standard meat inspection. and. If the condition is of over 7 days duration the muscle is dry and often shows greenish tinges.g. 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. This will normally be due to excessive flapping in association with management activities (e. It may also start to be enclosed in a fibrous capsule. A typical case of the chronic stages deep pectoral myopathy in a broiler chicken. Post-mortem lesions Acute or chronic necrosis of the deep pectoral muscle on one or both sides. weighing birds etc). Diagnosis Lesions. Prevention Avoidance of physical damage of this muscle. If recent. If of very long duration. artificial insemination in breeding turkeys. greenish yellow. thinning operations in meat birds.
In broiler chickens its main importance seems to be as a cause of airsacculitis in apparently healthy flocks that is only identified at slaughter.Ornithobacterium Infection. The range occurring in turkeys is wider than that seen in chickens. age at infection etc. It is a Gram-negative pleomorphic organism. Bordetella aviuminfection. perhaps through survival of the organism on shell surfaces or shell membranes. Important cofactors may include respiratory viral vaccines (Newcastle disease. The infection is common in chickens and turkeys. Most isolates are oxidase positive and galactosidase positive Serology using Elisa tests has been used. Post-mortem lesions Airsacculitis. There is some evidence that hatcheries may play a role in the epidemiology. The severity of its effects depends on the pathogenicity of the particular strain and other risk factors such as viral infections. A range of sero-types have been identified. ORT Introduction Ornithobacterium Infection is an infection of chickens and turkeys with the bacterium Ornithobacterium rhinotracheale(ORT). Diagnosis Clinical signs and lesions. preferably as a flock test comparing results before and after the challenge. It had been previously isolated in a number of other countries. Reduced weight gain. 108 . Growth is more rapid and consistent in an anaerobic jar. 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. Confirmation is by isolation of the organism. sneezing. This can cause significant losses through condemnations. Signs Coughing. E. The slow-growing bacterium was named in 1994. severe bronchopneumonia. coli infections. The organism grows slowly producing tiny colonies on blood agar. field challenge with respiratory viruses. It commonly exacerbates respiratory disease caused by pneumovirus infections in turkeys. tracheitis. Infectious Bronchitis). Reduced egg production. and E. coli overgrowth may occur. Cultures from the trachea of birds showing typical signs are preferred. ventilation problems. This was first identified as a new disease syndrome of turkeys in Germany in the early 1990s. direct contact and drinkers. Some uncertainty exists about mechanisms of transmission. Within the poultry house it is likely to be by aerosols.
Routine treatment . In France and Belgium most strains were sensitive to enrofloxacin.it is very sensitive in vitro to a range of chemicals.there are issues relating to availability.amoxycillin at 250 ppm in water for 3-7 days or chlortetracycline at 500 ppm for 4-5 days. Preventative medication with the products listed in the previous section may be beneficial in some circumstances. Some vaccines seem to have difficulty in producing a longlasting serological response to ORT. Figure 27. Similar lesions may be found in Pasteurellosis. Prevention This is based on good hygiene. ORT is a major problem on multi-age sites. Satisfactory disease control depends on good management and biosecurity. this is unlikely to work in turkeys. also most are sensitive to tiamulin. Tilmicosin is also effective at 10-20mg/kg and should be used in the early stages of the disease. therapy and vaccination. though 54% were sensitive to tetracycline. Hygiene . Vaccination of breeder flocks to protect progeny has shown benefits in chickens but. neomycin and enrofloxacin.Treatment The sensitivity of ORT to antibiotic is highly variable. Initially in Germany most strains were sensitive to amoxycillin. Severely consolidated lung from an acute ORT infection in 14-week-old turkey growers. because of the age of slaughter. regulation. Vaccination . The lung is solid and covered by pus/ purulent exudate. Amoxycillin sensitivity remains good. 109 . Some work has been done on live vaccine in the USA. In the USA in 1998 all strains were sensitive to penicillins and many other microbials. An inactivated vaccine is licensed for broiler parents in Europe. cost etc. it requires two doses. chlortetracycline but not to enrofloxacin.
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. 110 . The green discolouration is used to identify carcases that require closer inspection of the other tissues. Osteoporosis. Prevention Unknown. Birds go off legs.Osteomyelitis Complex. Soft-shelled eggs. Birds rest squatting. Diagnosis Lesions. turkeys and ducks seen worldwide and due to Vitamin D or calcium deficiency. Soft bones and beak. Enlarged hocks. Drop in production. high production. Signs None. Gram-variable pleomorphic bacteria have been isolated from affected livers and bones. Post-mortem lesions Green discolouration of the liver at slaughter. Cage Fatigue Introduction A condition of chickens. Predisposing factors include small body size. Signs Lameness. Treatment Not applicable .only identified at slaughter.
Wild birds are believed to be especially important. whereas turkeys are more severely affected. skeletal size and mineral content at point of lay are critical. In chickens it is usually mild. Epiphyses of long bones enlarged.Abubakar.Yucaipa Disease Introduction An infection of chickens. Parathyroids enlarged. Transmission is by wild birds and fomites. Post-mortem lesions Not characteristic. bone ash. spondylitis. Diagnosis History. Differentiate from Marek's disease. Beading and fracture of ribs. turkeys and passerine cage birds with Paramyxovirus PMV-2 results in disease with variable mortality. Drop in egg production.M. Signs Depression. signs. Beak soft. proper Ca and P levels and ratio. Paramyxovirus 2 . Vertical transmission does not usually occur. Treatment Over-correct ration vitamin D. place on litter. depending on the species affected and whether infection is complicated by other factors and diseases. lesions. 111 . calcium carbonate capsules.Tahir Post-mortem lesions Bones soft and rubbery. Inappetance. As birds progressively mobilise skeletal calcium for egg production through lay. Prevention Supplementation of vitamin D. antioxidants. Coughing.
Post-mortem lesions No specific lesions. Drop in egg production (turkeys). Prevention Quarantine. occasionally chickens and psittacine cage birds. HA+. HA+. Vertical transmission does not usually occur. Paramyxovirus-3 Introduction Paramyxovirus PMV-3 infects turkeys. biosecurity. Treatment No specific treatment. laryngotracheitis. Diagnosis Isolation in CE. Inappetance. Loss of shell pigment Nervous symptoms (psittacines). haemorrhagic disease. The infection is transmitted by birds. Treatment No specific treatment.Diagnosis Isolation in CE. including wild bird contact and fomites. all-in/all-out production. IFA. Mortality is usually low in poultry. HI with ND serum or DID (less cross reactions). Differentiate from Infectious bronchitis. HI with ND serum or DID (less cross reactions). High mortality (cage birds). Signs Depression. 112 . IFA. EDS-76. antibiotics to control secondary bacteria. Coughing. antibiotics to control secondary bacteria.
biosecurity. all-in/all-out production. IFA. all-in/all-out production. Prevention Quarantine.Prevention Quarantine. Treatment No specific treatment. HA+. PEMS and Spiking Mortality of Turkeys Introduction Poult Enteritis and Mortality Syndrome (PEMS) was first identified in high density turkey producing areas of the South Eastern USA in 1991. Vaccination has been used in turkeys but may not be cost-effective. The infection is inapparent in ducks and geese. including wild bird contact and fomites. HI with ND serum or DID (less cross reactions). Post-mortem lesions No specific lesions. antibiotics to control secondary bacteria. In both cases mortality can be high and can be associated with a marked depression in growth. Diagnosis Isolation in CE. Mortality is 0-5%. A less acute form of the disease appears to produce more of a lingering mortality. Vertical transmission does not usually occur. A range of 113 . The infection is transmitted by birds. Signs Reduction in egg production. Paramyxovirus-6 Introduction Paramyxovirus PMV-6 infection of turkeys. biosecurity. Mild respiratory signs. It is an infectious and transmissible cause of sudden increases in mortality in turkeys between 7 and 28 days of age.
Prevention Biosecurity to reduce the introduction of new infections into brooding facilities.mash and poor quality crumbles increase risk. pale brown. Pendulous Crop Introduction A complex condition of turkeys and chickens associated with coarse fibrous feed. Effective terminal disinfection. To replicate the condition in full it appears to be necessary to include bacteria in the inoculum. Overdistension of crop in young birds because of an interruption in feed supply may predispose. eating litter. A highly digestible diet with fat at 7. Liquid intestinal contents.5-8% will encourage feed intake and recovery. This syndrome is clearly distinguished from typical viral enteritis in young turkeys because of the high mortality and severe growth depression. Weight loss. Droppings watery. Reduced feed consumption and growth. Caseous cores in bursae (late in the process). Increasing weakness. lesions. seeking heat. Diagnosis Signs. Wet litter. Increased water consumption. All-in/all-out production.viruses have been isolated from affected flocks. Muscle atrophy. Fluoroquinolone antimicrobials appear to be especially effective. Post-mortem lesions Dehydration. huddling. Emaciation. Treatment A range of antibiotics and arsenicals have been used to control the bacterial component of this condition. multivitamins and milk replacer products are helpful for nutritional support in the acute phase. Picking at feed. Good quality diets of a suitable form . Signs Initial hyperactivity and increased vocalisation. 114 .
115 . including crustaceans. necrosis. Diagnosis Macroscopic examination of lesions. if these can be identified. and thickening of mucosa of proventriculus. Diarrhoea. Tetrameres and Cyrnea are nematodes. Emaciation in heavily infected young chicks (Tetrameres). Post-mortem lesions Crop distended with feed. Lack of muscle tone. Treatment None. Diagnosis Signs. identification of worms. They are found in the mucosa of crop and proventriculus causing mainly inapparent infections. Signs Anaemia. may be impacted. have ulcerations and sometimes mycosis. Proventricular Worms Introduction Dispharynx. Crop contents semi-liquid and foul smelling.Signs Enlargement of crop. Prevention Remove predisposing factors. grasshoppers and cockroaches. lesions. Post-mortem lesions Inflammation. Infection is by the oral route on exposure to the intermediate hosts. ulceration. haemorrhage. spiruroid worm parasites of poultry and game birds.
coccidiosis. Signs Weakness. Diarrhoea. duck viral hepatitis. Pseudotuberculosis Introduction An infection of ducks. tuberculosis. rodents and man with the bacterium Yersinia pseudotuberculosis. Prevention Good husbandry and hygiene. wild birds.Treatment Not usually required. colibacillosis. Ruffled feathers. other poultry. Differentiate from Duck viral enteritis. sulphonamides in feed. 116 . The disease has a mortality of 5-75%. isolation. Sometimes sudden death. 'hardening off'. In peracute disease the only lesion may be enteritis. Diagnosis Lesions. Prevention Prevention of access to intermediate hosts. Post-mortem lesions Miliary lesions in a variety of organs but especially in the liver. adequate protection. Treatment Tetracyclines.
Post-mortem lesions Dehydration. multivitamins in water. capillariasis. Skin cyanosis of head. antibiotics. IBD and typhoid. Affected birds have an increase in circulating monocytes in their blood. Treatment Adequate water supply. Catarrhal enteritis. molasses. It is associated with hot weather. Crop distension. Avian Monocytosis Introduction A sudden onset condition of chickens early in lay with high morbidity and a mortality of 050%.Abubakar. toxin and possibly a virus infection. hygiene. 117 . Prevention Good management. Differentiate from fowl cholera. Skeletal muscle necrosis. Watery diarrhoea.Tahir Pullet disease. diet and water supply. elimination of other causes. vibriosis. Loss of appetite. Diagnosis History. Kidneys swollen. water deprivation. Crop distended. Bluecomb. Drop in egg production. Pancreas chalky. Signs Depression. It was commonly reported prior to 1960 but is now rare. Dehydration. mucoid casts in intestine. Dark comb and wattles.M. Liver swollen with foci. coccidiosis. lesions.
carbamates. Diagnosis Number and type of mites identified. Pale comb and wattles. May cause anaemia and death in young birds. Drop in egg production. Filling of cracks and crevices. Dermanyssus gallinae. in nest boxes. Staff complaints . vegetable oil and mineralbased products (both liquid sand dusts) have been used to control red mites in the environment. feeds by sucking blood. Post-mortem lesions Anaemia. the Northern Fowl Mite spends its entire life cycle on the bird and can multiply more rapidly as a result. and good design of new equipment to limit harbourages for red mites. citrus extracts. cracks. Ornithonyssus bursae. For northern fowl mite it is essential to apply approved insecticides to the affected birds. which are external parasites of chickens and turkeys. 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. Treatment Pyrethroids. crevices etc. organophosphates. Signs Presence of grey to red mites up to 0. Effective monitoring of mite numbers and implementation of control measures before birds are heavily infested improves control.itching. Spots on eggs. fumigation and insecticide treatment at turnaround. 118 .7 mm. Prevention Thorough cleaning. the Common Red Mite. mainly at night and may transmit fowl cholera and other diseases.Red Mite and Northern Fowl Mite Introduction Arachnid mites. Birds restless. Loss of condition.
Infected birds may remain carriers for a few weeks. Treatment None. pH). It may occur as an exacerbating factor in other types of respiratory disease. chloroform. Diagnosis History. Lentogenic Newcastle disease virus. formaldehyde and iodides work better. Avian pneumovirus. Post-mortem lesions Mild catarrhal tracheitis. and other factors associated with poor ventilation. Respiratory Disease Complex Introduction Respiratory infections in chicken and turkeys are seen worldwide but especially in temperate poultry-producing areas in winter months. E.Abubakar.M. intranuclear inclusions in liver. ammonia and other gases. vaccinal and field strains) and bacteria (Ornithobacterium rhinotracheale. and by fomites. CE liver). temperature. A number of respiratory viruses (Infectious Bronchitis. prevention of immunosuppression. Signs Mild snick and cough without mortality. coli) may be involved. 'Mild Respiratory Disease' Introduction An adenovirus infection of chickens with a morbidity of 1-10% and a mortality of 1-10%. The virus grows well in tissue culture (CE kidney. Transmission may be vertical and lateral. The virus is generally resistant to disinfectants (ether. lesions. may act as 119 . at least 12 sero-types have been described and these may be isolated from healthy chickens.Tahir Respiratory Adenovirus Infection. Opinions vary as to whether adenovirus can be characterised as a primary respiratory pathogen. Prevention Quarantine and good sanitary precautions. Dust.
mortality 5. of course. response to environmental changes. Treatment Antimicrobial treatment of specific bacterial infections. The air sacs are thickened and congested. Pericarditis. and have been cut into to reveal a cheesy (caseous) mass of pus. Conjunctivitis. Airsacculitis. Post-mortem lesions Severe tracheitis with variable exudate . serology. Differentiate from Chronic Respiratory Disease (Mycoplasmosis).predisposing factors. 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. Morbidity is typically 10-20%. If condemned birds are included mortality may be more than 10%. Sneezing.catarrhal to purulent. 120 . Prevention Effective ventilation. Diagnosis Lesions. Figure 29. Nasal exudate. Severe airsacculitis of thoracic air sacs in a broiler close to slaughter. Head swelling. sanitation of drinking water. Signs Snick. There is also percarditis evident (at top right). be challenged by some of these pathogens). carefully applied appropriate viral vaccines. Rattling noises.10%.
Sometimes nodules in intestine and caecae. Lympoid Tumour Disease Introduction A retrovirus infection of chickens. Severe tracheitis is broilers with respiratory disease complex. There is an incubation period of 5-15 days. Reticuloendotheliosis. Transmission is lateral and possibly transovarian. Both tracheas were congested and the upper sample had mucopurulent material in the lumen. geese. Leg weakness. and quail with morbidity up to 25%.Figure 30. Sometimes enteritis and proventriculitis (especially in broilers infected with contaminated Marek's disease vaccine). Treatment None. Marked stunting when Marek's disease vaccine is contaminated. Post-mortem lesions Neoplastic lesions in liver. Signs There may be no obvious signs. chick inoculation. Diarrhoea. Diagnosis Pathology. ducks. 121 . spleen and kidney. A gradual increase in mortality and poor growth in broilers may be the main signs. usually higher in females than males. turkeys. and the infection can be spread by mosquitoes or in contaminated Marek's disease vaccines.
or Vitamin D or 25-hydroxy vitamin D in drinking water. Differentiate from Encephalomalacia. Diagnosis History. Signs Lameness. Parathyroids enlarged. turkeys and ducks worldwide. Growth plates widened and disorganised. signs. antioxidants. Birds rest squatting. Beading and fracture of ribs. Post-mortem lesions Bones soft and rubbery. Reduction in bodyweight. Hock swelling. Prevention Supplementation of vitamin D. lesions. proper calcium and phosphorus levels and ratio. Beak soft. Epiphyses of long bones enlarged. Birds go off legs.Prevention Formal control programmes have not been documented as the condition is sporadic and relatively self-limiting. Treatment Over-correct ration with three times vitamin D for 2 weeks. 122 . Soft bones and beak. Poor growth. Femoral Head Necrosis. Rickets (hypocalcaemic) Introduction Vitamin D deficiency or phosphorus/calcium imbalance is seen in chickens. Avoidance of contamination of live vaccines is the main control measure practised.
Hock swelling. Treatment Over-correct ration with 3 times vitamin D for 2 weeks. Enlarged hocks. Intestinal diseases may reduce absorption. Even subclinical levels of this condition can predispose to Femoral Head Necrosis. or vitamin D in drinking water. Prevention Supplementation of Vitamin D. Birds go off legs. Soft bones and beak. Reduction in bodyweight. signs. Signs Lameness.Abubakar. Poor growth.M. Beading and fracture of ribs.Tahir Rickets (hypophosphataemic) Introduction Phosphorus deficiency in chickens. Some countries have regulations governing the use of phosphorus in fertiliser with a view to reducing water pollution. Epiphyses of long bones enlarged. proper calcium and phosphorus levels and ratio. This has led feed manufacturers to try various approaches to reduce added phosphorus in diets. Birds rest squatting. lesions (analyse Vitamin A or manganese as a guide to premix inclusion). Parathyroids enlarged. turkeys and duck is seen worldwide. Beak soft. Diagnosis History. antioxidants. 123 . Growth plates widened and disorganised. Post-mortem lesions Bones soft and rubbery.
Adult birds can tolerate burdens asymptomatically.Tahir Rotavirus Infection Introduction Rotavirus infection is seen in chickens. partridges and pigeons. Signs Diarrhoea. turkeys. A.5 g faeces). except that the adults reside in the small intestine and earthworms are not significant paratenic or transport hosts. Use of a good electrolyte solution is beneficial in the acute stage of infection. The route of infection is oral usually by direct ingestion of the embryonated egg and there is a 5-10-week prepatent period. electron microscopy or Elisa on intestinal contents . stout white worms up to 12 cms in length. columbae in pigeons. are nematode worm parasites. Diagnosis Demonstration of virus (PAGE. The life cycle is similar to that illustrated in the section on the caecal worm Heterakis. large . seen worldwide. Virus may be found in asymptomatic birds. The 124 . Control of secondary bacterial enteritis may require antimicrobial medication.Ascaridia Introduction Ascaridia sp. pheasants. Roundworm. Prevention Good hygiene in brooding areas. Treatment No specific treatment for this infection.Abubakar. The parasite species vary: A. The route of infection is oral and maximum viral excretion occurs 2-5 days post infection. Post-mortem lesions Viruses replicate mainly in the mature villous epithelial cells. dissimilis in turkeys.M. galli in fowl. and A. guinea fowl.submit 6 x . shorter in young birds. It is not known if vertical transmission occurs though virus has been occasionally isolated from embryonated eggs.
125 . especially for young birds. pasture rotation and regular treatment. Diarrhoea. Prevention Prevention of contamination of feeders and drinkers with faeces. Worms up to 12 cm in length in duodenum and ileum. Figure 31. Diagnosis Macroscopic examination with identification of worms. Wasting. mainly in young birds. Treatment Flubendazole.parasites may be transported by grasshoppers and earthworms and are resistant to environmental effects. Signs Loss of condition. Poor growth. In the bottom left quadrant there are also some immature worms. levamisole. A collection of mature roundworms (Ascaridia galli) recovered from the small intestine of a layer chicken in rear. Listlessness. piperazine as locally approved. oval smooth-shelled nonembryonated eggs in faeces. Post-mortem lesions Enteritis.
Broiler parents and brown-shell egg layers are especially susceptible. Affected birds should be culled humanely as soon as they are identified. Avoidance of physical stresses on the musculoskeletal system through careful handling as well as careful design and layout of equipment. If there is a greenish tinge to the area of swelling it occurred a few days previously. Reoviral or staphylococcal arthritis or tenosynovitis may predispose but many cases have no evidence of an inflammatory response. Salmonella Gallinarum. The bird may have the hock dropped to the floor. Diagnosis Signs and lesions are obvious. This can cause mortality in birds of any age. sparrows. Salmonella Gallinarum. Broiler chickens have an avascular area of tendon just above the hock that is the usual site of rupture. Infections still occur worldwide in non-commercial poultry but are rare in most commercial systems now. Prevention Establishment of a steady growth profile. game birds. parrots. guinea fowls.Abubakar. Signs Severe lameness. 126 . Fowl Typhoid Introduction Disease caused by one of the two poultry-adapted strains ofSalmonella bacteria.M. Histology may be helpful in determining if there is an underlying inflammatory process. Ruptures of ligaments and joints are also occasionally seen. 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. Post-mortem lesions The fresh lesion contains a haematoma with the end of the ruptured tendon within or adjacent to it. Chickens are most commonly affected but it also infects turkeys.
both live (usually based on the Houghton 9R strain) and bacterins. Tube and rapid plate agglutination tests have been the standard serological tests for many years but have only been validated for chickens. clean chicks. and/or congestion. fluoroquinolones. but is susceptible to normal disinfectants. mortality is increased in stressed or immunocompromised flocks and may be up to 100%. tetracylines. pullorum disease and coli-septicaemia. Transmission may be transovarian or horizontal by faecal-oral contamination. egg eating etc. surviving months. As with other salmonellae. Prevention Biosecurity. potentiated sulponamide. Thirst. Enteritis of anterior small intestine. In clinical cases direct plating on Brilliant Green. The bacterium is fairly resistant to normal climate. even in adults. Anaemia. Diagnosis Isolation and identification. Differentiate from Pasteurellosis. Ruffled feathers. Post-mortem lesions Bronzed enlarged liver with small necrotic foci. Enrichment procedures usually rely on selenite broth followed by plating on selective media. Vaccines for fowl typhoid have been used in some areas. Reluctance to move. recovered birds are resistant to the effects of infection but may remain carriers. Signs Dejection. 127 . Treatment Amoxycillin. LPS-based Elisa assays have been developed but not widely applied commercially. Yellow diarrhoea. The route of infection is oral or via the navel/yolk. McConkey and non-selective agar is advisable. Engorgement of kidneys and spleen.Morbidity is 10-100%. Inappetance.
Gasping. Signs Inappetance. The route of infection is oral or via the navel/yolk. surviving months but is susceptible to normal disinfectants. Pullorum Disease. the one on the right is slightly enlarged. Lameness. sparrows. Transmission may be transovarian or horizontal mainly in young birds and may sometimes be associated with cannibalism. Closed eyes. Bacterial septicaemia caused by Salmonella Gallinarum. 'Bacillary White Diarrhoea' Introduction Disease caused by one of the two poultry-adapted strains ofSalmonella bacteria. guinea fowls. this usually only causes mortality in birds up to 3 weeks of age. in young broiler chickens. game birds. Similar lesions can be seen in Pullorum Disease and with other causes of septicaemia in young chicks. ring doves. parrots. 128 . ostriches and peafowl. Salmonella Pullorum. The liver on the left is normal. but also infects turkeys. White diarrhoea. Loud chirping. usually brown-shell egg layers.Figure 32. Morbidity is 10-80%. Occasionally it can cause losses in adult birds. The bacterium is fairly resistant to normal climate. mortality is increased in stressed or immunocompromised flocks and may be up to 100%. pale and shows focal necrosis. It affects chickens most commonly. Depression. Ruffled feathers. Salmonella Pullorum. It still occurs worldwide in noncommercial poultry but is now rare in most commercial systems. Vent pasting.
Anatum. poteniated sulponamide. Intestinal or caecal inflammation. in the environment or in rodent populations. Salmonellosis. Splenomegaly. Derby. Morbidity is 0-90% and mortality is usually low. Differentiate from Typhoid. Montevideo. liver. As with other salmonellae. Certain sero- 129 . The route of infection is oral and transmission may be vertical as a result of shell contamination. paracolon. Newport. Sero-types vary. turkeys and ducks worldwide. gizzard wall and heart. recovered birds are resistant to the effects of infection but may remain carriers. They infect chickens.Post-mortem lesions Grey nodules in lungs. fomites and feed (especially protein supplements but also poorly stored grain). Caecal cores. In clinical cases direct plating on Brilliant Green. S. Even if these infections do not cause clinical disease. Bredeney are among the more common isolates. their presence may be significant with respect to carcase contamination as a potential source of human food poisoning. Many species are intestinal carriers and infection is spread by faeces. are capable of causing enteritis and septicaemia in young birds. and also other than S. fluoroquinolones. Prevention Eradication from breeder flocks. Typhimurium (which are considered separately). S. Vaccines are not normally used as they interfere with serological testing and elimination of carriers. other enterobacteria. Paratyphoid. Urate crystals in ureters. S. Diagnosis Isolation and identification. Enteritidis andS. Paratyphoid Infections Introduction Salmonellae bacteria other than the species specific sero-typesS. Enrichment procedures usually rely on selenite broth followed by plating on selective media. S. Pullorum. it may become established on certain farms. S. tetracylines. chilling and omphalitis Treatment Amoxycillin. Regardless of the initial source of the infection. Gallinarum. McConkey and non-selective agar is advisable. but S.
Focal necrotic intestinal lesions. chilling. Ruffled feathers. Chemotherapy can prolong carrier status in some circumstances. especially in dry dusty areas. other bacterial infections and ornithosis (in ducks). Post-mortem lesions In acute disease there may be few lesions. Temperatures of around 80°C are effective in eliminating low to moderate infection if applied for 1-2 minutes. applied at sufficient concentrations. 130 .g. fluoroquinolones. Treatment Sulphonamides. In clinical cases direct plating on Brilliant Green and McConkey agar may be adequate. Diarrhoea. The bacteria are often persistent in the environment. neomycin. Enteritis. Rappaport-Vassiliadis) followed by plating on two selective media will greatly increase sensitivity. amoxycillin. Vent pasting. Dejection. Closed eyes. Foci in liver.types are prone to remain resident in particular installations (e. Predisposing factors include nutritional deficiencies. Unabsorbed yolk. Pericarditis. Good management. Signs Signs are generally mild compared to host-specific salmonellae. but are susceptible to disinfectants that are suitable for the particular contaminated surfaces and conditions. or absent. tetracyclines. However this has the potential to reveal the presence of salmonellae that are irrelevant to the clinical problem under investigation. S. Senftenberg in hatcheries).g. Dehydration. other enterobacteria. Differentiate from Pullorum/Typhoid. This approach is often used in the heat treatment of feed. Loss of appetite and thirst. inadequate water. Diagnosis Isolation and identification. Cheesy cores in caecae. Enrichment media such as buffered peptone followed by selective broth or semi-solid media (e.
Vertical transmission may be either by shell contamination or internal transovarian contamination of yolk. chilling. Typhimurium infections Introduction Salmonella Enteritidis and S. S. good feed. has become much more common in both poultry and humans since the early 80s. especially phage type 4. Enteritidis and S. secondly. This approach is often used in the heat treatment of feed. Salmonella Enteritidis.Typhimurium are presented separately from other sero-types of Salmonella because.Prevention Uninfected breeders. Feed and feed raw material contamination is less common than for other sero-types. Infections in chickens. Vaccines are not generally used for this group of infections. Predisposing factors include nutritional deficiencies. many species are intestinal carriers and infection may be carried by faeces. Many infected birds are culled and others are rejected at slaughter. turkeys and ducks cause problems worldwide with morbidity of 0-90% and a low to moderate mortality. The route of infection is oral. because there are differences in the epidemiology as compared to other salmonellae. Temperatures of around 80°C are effective in eliminating low to moderate infection if applied for 1-2 minutes. and. inadequate water and other bacterial infections. on the one hand. The prevalence of S. clean nests. elimination of resident infections in hatcheries. breeding and grow-out farms. these bacteria are often specifically cited in zoonosis control legislation. 131 . fumigate eggs. competitive exclusion. but are susceptible to disinfectants that are suitable for the particular contaminated surfaces and conditions. Infection results in a strong immune response manifest by progressive reduction in excretion of the organism and reduced disease and excretion on subsequent challenge. care in avoiding damage to natural flora.Typhimurium has remained relatively stable though the spread of the highly antibiotic-resistant strain DT104 in various farmed species gives some reason for concern. The bacteria are often persistent in the environment. hatcheries and feed mills is required for effective control. mills. Routine monitoring of breeding flocks. especially in dry dusty areas. These are the predominant sero-types associated with human disease in most countries. applied at sufficient concentrations. all-in/all-out production. Salmonellosis. fomites and on eggshells.
Enteritis. In clinical cases direct plating on Brilliant Green and McConkey agar may be adequate. It is possible to detect reactions with specific antigens in agglutination tests but competitive and direct Elisa tests are more commonly used today. clean nests. Infection 132 . breeding and grow-out farms. Routine monitoring of breeding flocks. Misshapen ovules in the ovaries in S.Signs Dejection. Closed eyes. Diarrhoea. Enrichment media such as buffered peptone followed by selective broth or semi-solid media (e. hatcheries and feed mills is required for effective control. elimination of resident infections in hatcheries. Ruffled feathers. infection Diagnosis Isolation and identification. Stunting in older birds. Dehydration. fumigate eggs. competitive exclusion. tetracyclines. Perihepatitis. Treatment Sulphonamides. good feed. Lost of appetite and thirst. mills. Cheesy cores in caecae. Unabsorbed yolk. fluoroquinolones in accordance with the sensitivity. Good management. Early depletion of infected breeding stock is required in some countries such as those of the European Union. care in avoiding damage to natural flora. However this has the potential to reveal the presence of salmonellae that are irrelevant to the clinical problem under investigation. all-in/all-out production.E.Pullorum serum agglutination tests. neomycin. Chemotherapy can prolong carrier status in some circumstances. Differentiate from Pullorum/Typhoid. Post-mortem lesions In acute disease there may be few lesions. Prevention Uninfected breeders.Enteritidiscauses cross-reactions which may be detected with S. other enterobacteria such as E. S. Pericarditis. Vent pasting. Rappaport-Vassiliadis) followed by plating on two selective media will greatly increase sensitivity. Foci in liver. amoxycillin. coli. Focal necrotic intestinal lesions.g.
Damaged vents. It is a complex condition of chickens and ducks associated with various infections including Mycoplasma and bacteria (especially E. both inactivated (bacterins) and attenuated live organisms. Post-mortem lesions Slight to marked distension of oviduct with exudate. Typhimurium infection. Signs Sporadic loss of lay. 133 . Distended abdomen. The control of infection in this area is probably achieved by ciliated epithelium that mostly wafts a carpet of mucus towards the cloaca. Infection may spread downwards from an infected left abdominal air sac. Lesions. Enteritidis and S. Diagnosis Use the signs to select birds for culling and post-mortem investigation. Anything that damages the epithelium or disturbs normal oviduct motility is likely to increase the likelihood of salpingitis. are especially prone to increasing salpingitis. Salpingitis Introduction Salpingitis is an inflammation of the oviduct.results in a strong immune response manifest by progressive reduction in excretion of the organism and reduced disease and excretion on subsequent challenge. May form a multi-layered caseous cast in oviduct or be amorphous. Peritonitis. Some birds may 'lay' a caseous mass of pus (which may be found in a nest or on the egg belt). Bacteriology of oviduct. Vaccines are increasingly being used for S. or may proceed upwards from the cloaca. coliand occasionally Salmonella spp. which normally has many millions of potentially pathogenic bacteria. leaking urates. Death.). Systemic viral infections that cause ovarian regression or damage to the oviduct or cloaca. The oviduct is a hollow tube joining the normally sterile environment of the body cavity with the cloaca.
Diagnosis Clinical examination. possibly associated with tendon injury. Morbidity is 10-20%. Use of a suitable antimicrobial may be beneficial for birds in the early stages and if associated with efforts to minimise risk factors. aspirin may be helpful if locally approved. Signs Stand on toes shaking. Prevention Care in transport of brooded poults. exclusion of other problems. 134 . immunise effectively against respiratory viral pathogens common in the area. releasing poults into larger areas and in handling heavier birds. Prevention Control any septicaemia earlier in life. Shaking or quivering of legs after rising.Treatment Birds with well-developed lesions are unlikely to respond to medication. use healthy parent flocks. Treatment Multivitamins. Post-mortem lesions None. Shaky Leg Syndrome Introduction A condition of turkeys with a course of often 3-4 weeks.
Dehydration. electrolytes and glucose solution to flock. Prevention Good sanitation of the brooding house. Birds in good condition die after showing neurological signs. Feed intake. Coma. Males are more susceptible than females. Diagnosis Pattern of mortality. Treatment Leave affected chicks undisturbed. Post-mortem lesions Mild enteritis. and/or carbohydrate absorption are disturbed resulting in a hypoglycaemia. Avoidance of physical stress. Minimise stress. Avoidance of interruptions in feed supply. rapidly growing broiler chickens. Filtered intestinal contents from affected flocks appear to be capable of reproducing the condition. probably because they are growing faster. This appears to be a multifactorial condition. Signs and lesions. Death.Spiking Mortality of Chickens Introduction This is a condition characterised by a sudden increase in mortality in young. suggesting a viral component. 135 . Orange mucoid droppings. Mortality drops off as sharply as it started. Excess fluid in lower small intestine and caecae. Provide multivitamins. Paralysis. Signs Tremor. typically 7-14day-old. 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.
e. Mucoid enteritis. It has been associated with typhilitis. 136 . Treatment Various antibiotics including penicillin. grouse and canaries with morbidity and mortality up to 100%.g. Thirst. Prevention Control vectors. previously known as Serpulina pilosicoli. Weakness and progressive paralysis. and egg soiling in chickens. pheasants. Drops in egg production may be seen in both systemic and intestinal forms Post-mortem lesions Marked splenomegaly. isolate in chicken eggs or chicks or poults. vaccines in some countries. is an intestinal spirochaete that can be associated with inflammation of the large intestine in a broad range of mammals and birds.Spirochaetosis Introduction The bacterium Borrelia anserina infects chickens. Necrotic foci. Cyanosis. Diagnosis Haematology. Signs Depression. reduced egg production. and occasionally by infected faeces. Spleen mottled with ecchymotic haemorrhages. Argas persicus. Liver enlarged with small haemorrhages. geese. turkey. ducks. diarrhoea. The bacterium is poorly resistant outside host but may be carried by Argas persicus for 430 days. Brachyspira pilosicoli. It is transmitted by arthropods. Often diarrhoea with excessive urates.
Figure 33. legs extended forward. Prevention Selection for satisfactory conformation in primary breeding. May walk backwards. Treatment None. The sample on the right is normal. These are cross-sections of the spinal column of 4-5-weekold broilers.Tahir Spondylolisthesis. Diagnosis Symptoms. lesions.M.Abubakar. Signs Sitting on hock or rumps. Use of wings to help in walking. 137 . with rotation of the body of the vertebra and the pinching of the spinal column that causes paralysis. That on the left shows the typical lesion of spondylolisthesis. 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. Post-mortem lesions Anterior-posterior rotation of the bodies of the last or penultimate thoracic vertebrae resulting in scoliosis just anterior to the kidney.
Abubakar. Damaged skin due to nutritional deficiencies (such as of biotin) may also be a point of entry. Treatment None.M. 138 . Diagnosis Clinical signs. The type of chick box liners and the feeding papers used in the brooding house can also influence the occurrence of the condition. Post-mortem lesions Gross lesions are not usually evident. and careful monitoring of incubation conditions. Morbidity is usually low and mortality 0-15% though affected birds will often be culled on humane grounds. Prevention All measures that improve chick vitality at hatching are beneficial in reducing this problem. aureus and seen in chickens and turkeys worldwide. Infection is usually by the respiratory route with an incubation period of 2-3 days seen after artificial infection. and toe trimming may be a portal of entry with subsequent spread via the bloodstream to the typical sites of lesions. Staphylococcosis. either accidental or induced by interventions such as beak trimming. Bumble Foot Introduction Caused by Staphylococcus bacteria. avoidance of excessive hatching egg storage.Tahir Spraddle Legs or Splay Leg Introduction Occurs in all species in the recent hatchling. Signs Legs splay and chick is unable to stand. Wounds. mainly S. Staphylococcal Arthritis. These include good breeder nutrition.
Treatment Antibiotics. Recovered birds may have some immunity but vaccination with staphylococci has not been found to be helpful in preventing the disease to date. synoviae. This may progress to abscess formation in these areas. Swollen above the hock and around the hocks and feet. e. the hatchery and in any intervention or surgery (processing. especially M. Infected joints may have clear exudate with fibrin clots. Low mobility. toe clipping). trauma. Salmonella spp. Predisposing factors include reovirus infection.Transmission occurs in the hatchery and in the general farm environment. low stress and prevention of immunosuppression from any cause will all tend to help. particularly of parent birds. Mycoplasma spp.g. Streptococcus bovis Septicaemia Introduction An infection of ducks with the bacterium Streptococcus bovis. 139 . Diagnosis Lesions. Differentiate from septicaemia or tenosynovitis due to Colibacillosis... Lameness. Good management. in accordance with sensitivity. and imunosuppression. Prevention Good hygiene in the nest. This condition is a cause of sudden deaths in ducklings of 2-3 weeks of age. isolation and identification of pathogen. Signs Ruffled feathers. Competitive exclusion with a non-pathogenic Staphylococcushas been shown to be effective (no commercial products yet available based on this technology). and by fomites. Some sudden deaths from acute septicaemia if very heavy challenge. most commonly in the plantar area of the foot or just above the hock joint. chronic stress. Possibly vaccination against reovirus infection. Post-mortem lesions Tenosynovitis.
Splenic hyperplasia. most are found lying on their back. Sudden Death Syndrome. Leg weakness or incoordination in a few birds. the ventricles are empty. extra care in the immediate post-brooding period. Serum accumulation in lung (may be little if examined shortly after death). Lung congestion and oedema. possibly metabolic. 140 . It can be induced by lactic acidosis and about 70% of birds affected are males. Sodium deficiency can appear very similar at about the same age . Post-mortem lesions Beak cyanosis. Diagnosis History. Haemorrhages in muscles and kidneys. Post-mortem lesions Intestine filled with feed.).affected birds respond well to saline injection and will actively seek out salt scattered in the litter.Signs Sudden deaths. The atria of the heart have blood. Livers heavier than those of pen-mates (as a percentage of bodyweight. lesions. Treatment Amoxycillin. Signs Sudden death in convulsion. Liver congestion. 'Flipover' Introduction A condition of broiler chickens of unknown cause. Affected well-grown birds may appear to have died from smothering. Prevention Good husbandry and hygiene. isolation.
Check your local regulations. Post-mortem lesions Occupy space in intestine and create small lesions at point of attachment. Most have intermediate invertebrate hosts such as beetles or earthworms. Treatment Flubendazole is effective at a 60 ppm in diet. Prevention Control the intermediate hosts. lighting programmes. Prevention Lowering carbohydrate intake (change to mash). Cestodes Introduction Cestodes are tapeworms that are seen in many species.Diagnosis Birds found on back with lack of other pathology. or birds' access to them. Signs It is doubtful if any signs are produced under most circumstances. they may not be host specific. however it may not have a zero withdrawal in commercial egg layers. Tapeworms. Treatment None possible. low intensity light. 141 . use of dawn to dusk simulation and avoidance of disturbance. feed restriction. Diagnosis Identification of the presence of the worms at post-mortem examination.
a mass of avascular cartilage with transitional chondrocytes. Differentiate from rickets. and proximal metatarsus. chloride levels and acid/base balance. Vitamin D3 supplementation. Prevention Genetic selection using the Lixiscope to identify bone phenotype. Swelling and bowing in the region of the knee joints. modifications of calcium and phosphorus ratios.Figure 34. small ovoid lacunae and more matrix than normal. It may be associated with rapid growth and have a nutritional factor. Signs There are usually no signs unless the condition is severe. in decreasing order of frequency. Lixiscope may identify in vivo as early as 2 weeks of age. Lameness. Mature tapeworms with their heads (scolices) embedded in the intestine. Post-mortem lesions Plug of cartilage in proximal end of tibia. Tibial Dyschondroplasia. Diagnosis Gross pathology. Microscopically . distal tibia. mild lesions may require histology to distinguish from other problems. 142 . TD Introduction A complex condition seen in chickens. Treatment None. turkeys and ducks.
Transmissible Enteritis. with 143 . and may also transmit spirochaetosis and Pasteurella infection. Insecticide sprays in these areas are more likely to be effective than treatment of the birds. others are avian coronaviruses closely related to infectious bronchitis virus. It is more common in warm climates. Skin blemishes. Emaciation. Signs Anaemia. Morbidity is close to 100% and mortality is 5-100%. These parasites are more likely to be a problem of small scale poultry production in the tropics. Prevention As for red mite control.Tahir Ticks Introduction Argas persicus is an external parasite of poultry and wild birds. Weakness. Post-mortem lesions Anaemia. than in commercial poultry in temperate climates.M. Diagnosis Identification of the presence of the parasites. The infection is seen in turkeys and sometimes pheasants. and is also found on mammals. Bluecomb Introduction Some coronaviruses involved in this condition are considered to be bovine coronaviruses (or closely related thereto). Reduced productivity.Abubakar. spends little time on host. Transmission is lateral with birds and faeces. Occasionally paralysis from toxins in the tick saliva. Treatment Elimination of cracks and crevices in the poultry housing.
rapid spread. The course of the disease is about 2 weeks and birds then remain carriers for months. The viruses survive in frozen faeces for months.
Anorexia. Depression. Frothy diarrhoea. Subnormal body temperature. Darkening of the head. Loss of weight. Huddling.
Dehydration. Emaciation. Enteritis with petechial haemorrhages. Froth ingesta. Sometimes casts. Pancreas chalky. Urates in kidneys/ureters.
Reproduction with filtered contents, isolation in turkey eggs, electron microscopy, immunofluorescence, Elisa. Commercial M4I IB Elisa will detect some infections.
Warmth and good management, antibiotics, milk replacer, potassium chloride. Disinfect and rest houses for 3-4 weeks.
All-in/all-out production, good hygiene and biosecurity, good management.
Trichomoniasis, Canker, Frounce
Trichomonas gallinae is a protozoan parasite of pigeons and doves (canker), raptors (frounce), turkeys and chickens. It has variable pathogenicity. Morbidity is high and mortality varies but may be high. Transmission is via oral secretions in feed and water, and crop milk.
Mouth open. Drooling and repeated swallowing movements. Loss of conditon. Watery eyes in some birds. Nervous symptoms (rare).
Yellow plaques and raised cheesy masses in mouth, pharynx, oesophagus, crop and proventriculus. Raptors may have liver lesions.
Lesions, large numbers of protozoa in secretions. Differentiate from Pox and candidiasis.
Previously approved products included dimetridazole, nithiazide, and enheptin. Organic arsenical compounds (where approved) and some herbal products may be of some benefit in managing this problem in food animals.
Eliminate stagnant water, eliminate known carriers, add no new birds.
A bacterial infection, caused by Mycobacterium avium, of poultry, game birds, cage birds etc. Morbidity and mortality are high. Transmission is via faecal excretion, ingestion, inhalation, offal and fomites. The disease has a slow course through a flock. The bacterium resists heat, cold, water, dryness, pH changes and many disinfectants.
Severe loss of weight with no loss of appetite. Pale comb. Diarrhoea. Lameness. Sporadic deaths.
Grey to yellow nodules attached to intestine. Granulomas in liver, spleen and many other tissues, even bone marrow.
Isolation, acid-fast stain in tissues, TB test. Differentiate from Lymphoid leukosis.
Market after one season, hygiene, cages, elimination of faeces etc.
A condition of turkeys possibly associated with Bordetella avium(previously designated Alkaligenes faecalis) infections. This bacterium usually causes mild respiratory disease in only a proportion of the flocks, and low mortality. It can be synergistic with other respiratory pathogens such as Ornithobacterium,Pasteurella spp, Mycoplasma spp. and pneumoviruses.
Decreased appetite, weight gain and feed efficiency. Loss of voice. Ocular and nasal discharge. Conjunctivitis. Snick. Dyspnoea.
Excessive mucus in nasal passages and trachea. If there is secondary E. coli infection then pneumonia, airsacculitis and perihepatitis.
Clinical signs, isolation of agent.
Loss of voice. Sudden drop in production that lasts 2-3 weeks. maternal antibody may protect.live primer followed by inactivated. Morbidity is 10-100% and mortality 1. Serology. chlorination of drinking water.Antibiotics are not very effective. chlorinate drinking water. Prevention All-in/all-out production. 147 . Ocular and nasal discharge. Post-mortem lesions Serous rhinitis and tracheitis. Eggs depigmented and thin-shelled. Good drinking water hygiene. Paramyxoviridae. Signs Decreased appetite. control respiratory stressors. possibly involving fomites. Diagnosis Signs. control respiratory stressors. vaccination . Rapid transmission occurs laterally. vertical transmission is uncertain.30%. Treatment Antibiotics are not very effective. isolation of ciliostatic agent. Prevention All-in/all-out production. Turkey Rhinotracheitis (Adult) Introduction A disease of turkeys caused by the viruses of the Pneumovirus genus.
chlorinate drinking water. Signs Decreased appetite. possibly involving fomites. Morbidity varies.M.30%. Loss of voice. Birds remain carriers for up to 16 days. maternal antibody may protect. control respiratory stressors. vertical transmission is uncertain. mortality is 1-25%. Turkey Viral Hepatitis Introduction An infection of turkeys caused by an unidentified virus.Tahir Turkey Rhinotracheitis (in rear) Introduction A disease of turkeys caused by the viruses of the Pneumovirus genus. Rapid transmission occurs laterally. Transmission may be by direct or indirect contact and possibly vertical. Snick. Conjunctivitis. 148 . Morbidity is 10-100% and mortality 1. coli infection then pneumonia. sometimes pus in bronchi. airsacculitis and perihepatitis. Vaccination at day-old seems to be most effective.Abubakar. Post-mortem lesions Serous rhinitis and tracheitis. Dyspnoea. isolation and identification of the ciliostatic virus. Treatment Antibiotics are not very effective. If there is secondary E. Prevention All-in/all-out production. serology (using an Elisa test to demonstrate rising titre). Sinusitis. Diagnosis Clinical signs. Ocular and nasal discharge. Paramyxoviridae. weight gain and feed efficiency.
environment and high growth rate. Gastrocnemius tendon may slip. Signs Lameness. Depression and sporadic deaths in birds in good condition. lesions pathognomonic.Signs Signs are usually subclinical. Treatment None. Post-mortem lesions Linear twisting of growth of long bones. Focal haemorrhage. Twisted leg Introduction A complex condition seen in chickens and turkeys.no inclusion bodies. nutrition. Factors involved may include genetics. Bile staining. 1 mm) coalescing. Congestion. Distortion at hock. Prevention Good sanitation and management. 149 . bacterial and fungal infections. Microscopically . Morbidity is 1-20% and mortality is low. Various angulations of leg. Grey to pink foci in the pancreas. Differentiate from histomonosis. Diagnosis Isolation in CE. Post-mortem lesions Grey foci (c. with good management many birds recover. Valgus/varus.
Turkeys. greater than 20% is abnormal. Drooping wings. brunetti). Watery white faeces (quail). Changed angulation of tibial condyles. It can start suddenly and cause high mortality: 100% in quail and 10% in chickens. Ruffled feathers. and E. but mainly ileum and caecae. The route of infection is oral and transmission is from faeces of sick or carrier birds or via flies. Treatment None. IBDV and overcrowding. game birds and pigeons may also be affected. tenella. Predisposing factors include Coccidiosis (especially E. Signs Listlessness. which may coalesce and may be round or lenticular. Retracted neck. Blood in intestine. Differentiate from perosis.. The bacterium resists boiling for 3 minutes. Prevention Selection for good conformation in primary breeding. Post-mortem lesions Deep ulcers throughout intestine. Pale yellow membranes. Diagnosis Symptoms. arthritis and synovitis. Anaemia. Quail disease Introduction Ulcerative Enteritis is an acute. Partially closed eyes. lesions. Adoption of optimal nutrition and growth patterns for the economic objectives of the production system. The condition occurs worldwide. necatrix. highly contagious disease of chickens and quail caused by the bacterium Clostridium colinumand characterised by ulcers of the intestines and caecae. Peritonitis (if ulcers penetrate). Ulcerative Enteritis. 150 . intertarsal angulation up to 10% is physiological. Diarrhoea. E.
coccidiosis. Diarrhoea. Treat for coccidiosis if this is a factor. Differentiate from histomonosis ('Blackhead'). Figure 35. penicillin (50-100 ppm in feed). and disease is precipitated by stress. low level antibiotics as per treatment. Tetracyclines. amoxycillin. Treatment Streptomycin (44 gm/100 litres water). Diagnosis A presumptive diagnosis may be made on history and lesions. Necrotic foci in liver. Loss of condition. Avian Infectious Hepatitis Introduction An insidious onset disease of chickens caused by Vibrio bacteria. Transmission is by faecal contamination. salmonellosis. all-in/all-out production. 151 . The infective agent is rather resistant to environment and disinfectants. Confirmation is on absence of other diseases and isolation of Cl. multivitamins. birds remaining carriers for months. Wall of the caecum of a chicken suffering from ulcerative enteritis Vibrionic Hepatitis. possibly probiotics. colinum in anaerobic conditions (the agent is often present in pure culture in liver). necrotic enteritis. trichomoniasis. Inappetance. Response to treatment should occur in 48 to 96 hours. Prevention Infection-free birds. Morbidity is low. Bacitracin. Signs Dejection.
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. Pustules in mouth and pharynx. Poor feathering. classic signs of deficiency are very rare in commercial poultry fed complete diets. Excessive urates in kidneys and ureters.Abubakar. As in the case of other nutritional deficiencies.M. Post-mortem lesions Eyelids inflamed and adhered. Signs Poor growth. Microscopically . lesions. Drowsiness. Diagnosis Signs. Differentiate from Infectious coryza. Treatment Vitamin A in drinking water. good quality raw materials. feed formulation. Prevention Supplementation of diet with vitamin A. Pale comb and wattles. Nasal and ocular discharge. Eyelids stuck shut with thick exudate. infectious sinusitis etc.squamous metaplasia of epithelia. 155 . chronic fowl cholera.Tahir Vitamin A Deficiency. Nutritional Roup Introduction Vitamin A deficiency is occasionally seen in chickens and turkeys (insufficient vitamin A during 1-7 weeks of age).
They act in a broad range of metabolic pathways. because a continuous supply is required. and egg production in the layer. Vitamin deficiencies are especially prone to cause problems of hatchability. damage to the intestine or increased demand for some reason may have an effect. Simple deficiency is now rare as diets are usually well supplemented. The embryo is particularly dependent on having adequate supplies of vitamins deposited in the egg.Tahir Vitamin B Deficiencies Introduction The B complex vitamins are water soluble and not stored to any significant extent in the body. Most will reduce productivity. See the separate discussion under Chondrodystrophy and Fatty Liver and Kidney Syndrome. Some deficiencies induce characteristic microscopic effects. However.Abubakar. including growth in the young animal. 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. 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 . Diagnosis Signs. exclusion of specific diseases.M. response to supplementation.
Falling over. less expensive) to analyse feed for a marker substance such as manganese rather than testing for vitamin levels. occasionally ducklings and other birds.may be appropriate (faster. The problem is associated with feed rancidity typically in diets with high fat. Steatitis. seen worldwide. Ventral oedema. Haemorrhage. Encephalomalacia. Exudative Diathesis. 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. Vitamin E Deficiency. Muscular Dystrophy Introduction A spectrum of diseases of chickens and turkeys. Signs Imbalance. Treatment If a specific vitamin deficiency is suspected. Paralysis. The balance of vitamins present should be similar to the daily nutritional requirement of the stock concerned. drinking water supplementation with that vitamin is ideal and usually results in a rapid response in birds that are still drinking. 157 . Blood-stained or greenish subcutaneous oedema. Necrosis. characterised by oxidation of various tissues and caused by Vitamin E deficiency. Post-mortem lesions Swollen cerebellum with areas of congestion. White streaks in muscle. Good quality multivitamin solutions are beneficial in the supportive care of a range of problems characterised by reduced feed intake. Staggering. Muscular dystrophy is seen more frequently in older and mature birds. Encephalomalacia and exudative diathesis tends to be seen in young birds of 1-5 weeks of age. Green wings. Uncontrolled movements.
Swollen abdomen. Pseudomonas. response to medication. and poor hygiene of setters. good quality raw materials.coli.Proteus. feed rancidity. Prevention Proper levels of vitamin E. Broad-spectrum antibiotics where there are extensive skin lesions. 'bangers'. Treatment Vitamin E and/or selenium in feed and/or water. selenium. use of floor eggs. Yolk Sac Infection. 158 . inadequate hatchery hygiene or poor incubation conditions. especially E . Staphylococci. It is seen where there is poor breeder farm nest hygiene. Abnormal yolk sac contents (colour. Closed eyes. necrotic dermatitis. hatchers or chick boxes. consistency) that vary according to the bacteria involved. 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. for example poor hygiene of hatching eggs. Omphallitis Introduction A condition seen worldwide in chickens. Signs Dejection. lesions. Differentiate from Encephalomyelitis. Diarrhoea. 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. Post-mortem lesions Enlarged yolk sac with congestion. Disease occurs after an incubation period of 1-3 days. antioxidant. toxicities. Various bacteria may be involved. histopathology. Morbidity is 1-10% and mortality is high in affected chicks.Diagnosis Signs. Loss of appetite. Vent pasting.
clean nests. Treatment Antibiotics in accordance with sensitivity may be beneficial in the acute stages. There should be routine sanitation monitoring of the hatchery. separate incubation of floor eggs etc. Confirmation is by isolation and identification of the bacteria involved in the internal lesions. frequent collection. exclusion of severely soiled eggs.Diagnosis A presumptive diagnosis is based on the age and typical lesions. Differentiate from incubation problems resulting in weak chicks. 159 . sanitation of eggs. Prevention Prevention is based on a good programme of hygiene and sanitation from the nest through to the chick box (e.g. however the prognosis for chicks showing obvious signs is poor. Multivitamins in the first few days may generally boost ability to fight off mild infections. most will die before 7 days of age.