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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.
cloudiness in eye. Erosions of the cartilage of the hock joint in a duck with chronic Riemerella anatipestifer infection. Figure 40.Prevention Good husbandry and hygiene. Blindness. through faecal contamination of environment. Vent-pasting. Arizonosis Introduction Caused by the bacterium Arizona hinshawii. Arizona infection. transovarian. renamed Salmonella Arizonae. Diarrhoea. adequate protection. Transmission is vertical. 4 . and is not present in the UK turkey population. Nervous signs. feed etc. from long-term intestinal carriers. reptiles. Autogenous bacterins sometimes used. Mortality is 10-50% in young birds. Inactivated and attenuated vaccines available in some countries. sulphonamides in feed. 'hardening off'. Cheesy plugs in intestine or caecum. Paralysis. Foci in lungs. Congestion of duodenum. mainly in North America. Inappetance. Signs Dejection. Huddling near heat. and also horizontal. rodents. Post-mortem lesions Enlarged mottled liver. older birds are asymptomatic carriers. rigid depopulation and disinfection. correct house relative humidity. It affects turkeys. Unabsorbed yolk sac.
Signs Sudden deaths in rapidly developing birds. spectinomycin. mortality 1-2% but can be 30% at high altitude. Possibly cyanosis. poor ventilation and physiology (oxygen demand. Post-mortem lesions Thickening of right-side myocardium. and respiratory disease. Poor development. monitor sensitivity. Dyspnoea. high altitude. Salpingitis. or gentamycin at the hatchery is used in some countries. Severe muscle congestion. fumigation of hatching eggs. Ascites is a disease of broiler chickens occurring worldwide but especially at high altitude. Dilation of the ventricle. General venous congestion. Lungs and intestines congested. Ophthalmitis. The disease has a complex aetiology and is predisposed by reduced ventilation. 5 . Pulmonary arterial vasoconstriction appears to be the main mechanism of the condition. Perihepatitis. Prevention Eradicate from breeder population. Morbidity is usually 1-5%. Recumbency. methods as per Salmonella spp. good nest and hatchery hygiene. salmonellosis. Formerly in-feed medication with nitrofurans was also used. inject eggs or poults with antibiotics. Thickening of atrioventricular valve. Differentiate from Treatment Injection of streptomycin. Progressive weakness and abdominal distension. may be related to type of stock and strain). Ascites Introduction Associated with inadequate supplies of oxygen. coli-septicaemia. Diagnosis Isolation and identification. Pericarditis.
but may be as high as 12%. Drowsiness. Ascites. Thirst. It affects chickens. Treatment Improve ventilation. in which the typical sign is gasping for breath. A cardiac specific protein (Troponin T) may be measured in the blood. Signs Acute form: Inappetance. 6 . Silent gasping. etc. avoid any genetic tendency. This may offer the ability to identify genetic predisposition.cartilage nodules increased in lung. Occasionally similar lesions are produced by other species ofAspergillus or even other fungi such as Penicillium. The fungus can infect plant material and many species of animals including birds and man. Liver enlargement. caused by Aspergillus fumigatus. control respiratory disease. Morbidity is usually low. Diagnosis Gross pathology is characteristic. worldwide. especially in young chicks. Aspergillosis Introduction A fungal infectious disease. Transmission is by inhalation exposure to an environment with a high spore count. game birds. Prevention Good ventilation (including in incubation and chick transport). Absidia etc. The infection has an incubation period of 2-5 days. Rapid breathing. Weakness. Spores are highly resistant to disinfectants. waterfowl. ducks. Differentiate from broiler Sudden Death Syndrome and bacterial endocarditis. there is usually little bird-to-bird transmission. Vitamin C (500 ppm) has been reported to be of benefit in South America. penguins. turkeys. Microscopic . Mortality among young affected birds is 5-50%. Spleen small. Sometimes the same organism causes eye lesions or chronic lesions in older birds. Nervous signs (rare). Pericardial effusion.
Post-mortem lesions Yellow to grey nodules or plaques in lungs. Differentiate from excessive exposure to formalin or vaccinal reactions in day olds and from heat stress in older birds. mortality none. quail. may have greenish surface. Thiabendazole or Nystatin has been used in feed. It may be confirmed by isolation of the fungus. Brain lesions may be seen in some birds with nervous signs. Growth occurs in 24-48 hours and colonies are powdery green/blue in appearance. The powdery surface is dark green in colour. typically by putting small pieces of affected tissue on Sabouraud agar.Tahir 2 Chronic Forms: Ocular discharge (ocular form only). trachea. pheasants and occurs in most poultry-producing countries. turkeys. Amphotericin B and Nystatin have been used in high-value birds. preferably after digestion in 10% potassium hydroxide. Figure 8. Epidemic tremors for its effect in young birds. Conjunctivitis/keratitis. Treatment Usually none. air sacs. Morbidity 5-60%. Avian Encephalomyelitis Egg Drop Introduction Avian encephalomyelitis virus infection in laying bird causes inapparent infection or drops in egg production. 'Furry' airsacculitis in aspergillosis of an adult duck. See Avian Encephalomyelitis. Diagnosis This is usually based on the signs and lesions and microscopic examination for the fungus. Wasting. good quality litter and feed. Environmental spraying with effective antifungal antiseptic may help reduce challenge. The means of transmission is unknown but 7 . plaques in peritoneal cavity. It affects chickens.M.Abubakar. hygiene. Prevention Dry.
feed. Ataxia and sitting on hocks. Prevention Vaccination of breeders/layers at 9-15 weeks. turkeys. mortality high. Dull expression. Morbidity 5-60% depending on the immune status of the majority of parents.probably by faecal contamination of environment. 8 . transmission occurs over about 1-2 weeks. It has a worldwide distribution. pheasants. Imbalance. rising titre to AE virus. water etc. and quail. Post-mortem lesions None. In breeders there may be a drop in hatchability of about 5%. small (5-10%) and lasting no more than 2 weeks.The embryo protection test has been used in the past. The route of infection is transovarian with an incubation period of 1-7 days. Immunity is usually long lasting. EDS76. lateral transmission is probably by the oral route. subsequent disease in progeny if breeders. Predisposed by immunosuppression. Epidemic Tremors Introduction Avian encephalomyelitis is a viral disease of the central nervous system of chickens. Differentiate from Infectious Bronchitis. attenuated or not. Vertical transmission is very important. lentogenic Newcastle disease. incubation >10 days. Serology . with an oral infection route. Avian Encephalomyelitis. and there is serious disease in the progeny (see next section). Virus in faeces may survive 4 weeks or more. Treatment None. Virus in faeces may survive 4 weeks or more. Paralysis. Diagnosis History. some lateral. now Elisa is used more commonly. Signs Nervous signs. Signs Drop in egg production.
In addition official control measures disrupt trade in poultry products from affected areas. This is a test in which the virus is inoculated into susceptible chickens that are then kept under observation. Tremor may be inapparent but is accentuated if chicks are held inverted in the hand. Mycotic Encephalitis. pigeons. The embryo protection test has been used in the past. Tremor of head. The cause is a virus. toxicities. Prevention Vaccination of breeders at 9-15 weeks. vitamin deficiency (E. Differentiate from Newcastle disease. A few recovered birds may develop cataracts weeks after infection. This viral disease can cause exceptionally high mortality. and lack of significant lesions. ducks. Brain abscess. EE (especially in pheasant in the Americas). Enterococcus hirae infection. The virus infects chickens. and ostriches.nonpurulent diffuse encephalomyelitis with perivascular cuffing. and/or viral isolation may be carried out if required. quail. Avian Influenza-Highly Plague Introduction Pathogenic (HPAI). pheasants. the equivalent of the World Health Organisation for animal diseases. signs.2 . riboflavin). Effectively all 9 . its pathogenicity is variable. Marek's disease. Diagnosis A presumptive diagnosis is based on the history. Fowl One of only two 'Class A' diseases of poultry targeted for emergency disease control measures by OIE. and isolates are designated sero-type/ species/location/reference number/year/subtype designation(H/N). partridges. Orthomyxovirus type A. There may be focal white areas in gizzard muscle (inconstant). 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. The higher the proportion of the chickens dying or showing signs the higher the IVPI. Post-mortem lesions Gross lesions are mild or absent. Immunity is long lasting. Histopathology is usually diagnostic and IFA. neck and wings. attenuated or not. The definitive classification of high pathogenicity is an intravenous pathogenicity test (IVPI) in 6-week-old chickens result of greater than 1. Treatment None. turkeys. especially in turkeys. Microscopic . now Elisa is used more commonly. A.
by acid pH. equipment. Transmission is by direct contact with secretions from infected birds. It is inactivated by a temperature of 56°C in 3 hours and 60°Cin 30 min. It can remain viable for long periods in tissues. More recently outbreaks have occurred in Australia. and the high mortality that 'low-path' AI can cause in turkeys. Pakistan. 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. Swollen face. H5 viruses of low pathogenicity may become highly pathogenic usually after circulating in poultry flocks for a time (Pennsylvania. 10 . even with 'low pathogenicity' strains. from December 1999.g. reduced feed consumption. air sacs and conjunctiva. Avian Influenza is a potential zoonosis.birds are considered to be at risk of infection. Post-mortem lesions Inflammation of sinuses. especially faeces. waterfowl. Nervous signs such as paralysis. Drops in egg production. Pasteurella) may increase mortality. The route of infection is probably oral initially. Morbidity is high but mortality usually relatively low. but possibly by the conjunctival or respiratory route and the incubation period is 3-5 days. in northern Italy. Highly pathogenic avian influenza A (HPAI) viruses of the H5 and H7 HA subtypes have been isolated occasionally from free-living birds. Italy). Depression. Avirulent in one species may be virulent in others. It can result in inapparent infection. by oxidising agent and by formalin and iodine compounds. OIE and other bodies are currently examining ways to improve control of LPAI. over 30 days at 0°C. The virus is moderately resistant. Apathogenic and mildly pathogenic influenza A viruses occur worldwide. Infections with other pathogens (e. Marked loss of appetite. trachea. Coughing. Diarrhoea (often green). in the years 1983-84. Nasal and ocular discharge. clothing. Broken contaminated eggs may infect chicks in the incubator simulating vertical transmission. can survive 4 days in water at 22°C. Ovarian regression or haemorrhage. USA. Signs Sudden death. Cessation of normal flock vocalisation. Outbreaks due to HPAI were recorded in the Pennsylvania area. Because of this. The virus replicates mainly in respiratory tissues of chickens and turkeys but in the intestinal tract of clinically normal waterfowl. drinking water. 550%. Cyanosis of comb/wattles. A serious outbreak occurred in The Netherlands in 2003 with a few linked cases in Belgium and one in Germany. See current OIE records for up to date information on distribution of HPAI. Mexico and.
isolation. It has occured in Europe. Morbidity is low. all-in/all-out production. The agar gel precipitation test is non-group-specific and is used to confirm any positives. Myelocytomatosis Introduction Caused by an avian retrovirus. However. other respiratory infections. lesionless carriers of highly pathogenic virus. vaccinated birds may remain carriers if exposed to the infection. nutrition and antibiotics may reduce losses. disinfection. Eradication by slaughter is usual in chickens and turkeys. fowl cholera. Congenitally infected birds tend to remain 11 . Survivors can be expected to have a high degree of immunity but may harbour virulent virus. though there is high mortality of affected birds. Treatment None. but good husbandry. correct disposal of carcases. This condition has until now been seen only in meat-type chickens. Subcutaneous oedema of head and neck. DID+. with considerable strain-to-strain variation. NDV-. while ducks may be symptomless. Dehydration. In outbreaks a regime of slaughter. Transmission is by congenital infection from antibody-negative females. Haemorrhage in proventricular and gizzard mucosae and lymphoid tissue of intestinal tract. North and South America. bacterial sinusitis in ducks. infectious laryngotracheitis. Vaccines have been used in recent outbreaks in Mexico and Pakistan. The incubation period is 10-20 weeks. 21-day interval to re-stocking should be followed. Turkey lesions tend to be less marked than those of chickens. Avian Leukosis (Serotype J). bleeding and vaccination needles. Diagnosis A presumptive diagnosis may be made on history and postmortem lesions. Minimise contact with wild birds. Differentiate from Newcastle disease. although it may reduce losses initially. Necrosis of skin of comb and wattles. Confirmation is by viral isolation in chick embryo. Vaccination is not normally recommended because. quarantine. 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. lateral transmission by faecal-oral route (this declines as the bird ages). controlled marketing of recovered birds. Muscles congested. HA+. cleaning. etc. Prevention Hygiene. as with many such tests occasional false positive reactions can occur.
Persistent low mortality. Virus survival is poor but sufficient to allow cross contamination in hatcheries and on farm in rear. 'nonshedders' . sacral joint. Differentiate from Marek's disease. Separation in vaccination. Prevent/ reduce cross-infection in hatchery and on farm. There is also evidence that it is slightly more sensitive than conventional testing.an Elisa test is aviailable to identify antibody positive birds. often with tumour foci. Splenomegaly and enlarged kidneys also occur.most but not all. Critical hatchery practices: Separate infected and uninfected lines. particularly of the sternum. Diagnosis History. preferably on separate hatch days and in separate machines. histology. Handle clean lines before infected lines. birds with egg antigen will be antibody negative.80% produce infected chicks.antibody negative. PCR testing of embryonally infected chicks using DNA testing is uniformly positive for blood and faecal samples. Most characteristically are chalky white tumours in the bone marrow. ribs.tumours usually contain well-differentiated myelocytes. lesions. Signs Depression. Prevention Checking of antigen in the albumen is a basis for eradication . shed virus and develop tumours. Treatment None. 'Shedders' . Enlargement of abdomen. Emaciation. Two cell types may be found in the same tumour. Many are asymptomatic. liver. 12 . Minimise stress.only 3% produced infected chicks. Loss of weight. Microscopic . Serology . ultimately identification of virus by isolation and/or PCR. Lymphoid Leukosis. age. Post-mortem lesions Liver enlargement.
Minimise group sizes. Leukosis/Sarkoma Group Introduction Lymphoid Leukosis. fibrosarcomas. then liver. It affects chickens worldwide with susceptibility varying considerably among different strains and types of stock . initially in the bursa. spleen. In lymphoid leukosis the incubation period is about 4-6 months. coligranuloma. other tumours. age. Vertical transmission is most important by infection of the egg white in infected breeders (who are long-term carriers). There may be increased susceptibility to other infectious diseases due to damage to the immune system. Differentiate from Marek's disease.egg layers are generally more susceptible to lymphoid leukosis. lateral transmission is poor but infection may occur by the faecal-oral route. kidney etc. Persistent low mortality. liver or bursa.Farm practices: Brood and rear lines separately and maintain separate for as long as possible. Avoid migration errors (birds unintentionally moving between pens). Many are asymptomatic. Emaciation. Post-mortem lesions Focal grey to white tumours. osteopetrosis. Egg production is somewhat reduced. Mortality tends to be chronically higher than normal for a prolonged period. Delay live vaccine challenges. The causative viruses are rapidly inactivated at ambient temperature and on exposure to most disinfectants. cytology. Avian Leukosis. Signs Depression. lesions. myxosarcomas. Loss of weight. A complex of viral diseases with various manifestations such as lymphoid leukosis. Liver may be very large. Microscopic .cells lymphoplastic Diagnosis History. Enlargement of abdomen. it may be as short as 6 weeks for some of the other manifestations. 13 . erythroblastosis. Morbidity is low but mortality high. myeloblastosis (see Sero-type J). especially in young birds.
morbidity is 10-100% and mortality can be 110%. turkeys (see separate summary). all-in/all-out production. It is caused by a pneumovirus of the Paramyxoviridae family. control arthropods. Signs Decreased appetite. Dyspnoea. Ocular and nasal discharge. Conjunctivitis. vertical transmission is uncertain. eradication . Facial and head swelling (though this can occur in other conditions). As for many infections. Loss of voice.Treatment None. weight gain and feed efficiency.checking of antigen in the albumen is a basis for eradication (see Sero-type J for details). Diffuse lymphoid tumours in an enlarged liver from a mature broiler parent hen. Avian Rhinotracheitis 'Swollen Head Syndrome' Introduction A viral disease of chickens. Figure 9. guinea fowl and possibly pheasants seen in Europe. South America and North America. 14 . Prevention Good hygiene. There is rapid lateral transmission with infection by aerosol through the respiratory route. first isolated from poults in South Africa in 1978. fomites can be important in moving infection between farms. Africa. Snick. The incubation period is 5-7 days. Two subgroups have been identified on the basis of the G-protein sequence: A (original UK isolates) and B (original southern Europe isolates). This was a case of Myelocytoma Avian Leukosis (Sero-type J).
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.
Prevention Thorough cleaning and disinfection after depletion of an affected flock. Elisa tests have been developed experimentally. Treatment No specific treatment known. 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. Pale livers and kidneys in fatty liver and kidney syndrome. in embryos. Biotin Deficiency. Must be confirmed by laboratory tests. Thickened skin under foot pad. Signs Poor growth. Lung congestion Ovarian regression Yolk peritonitis Pale foci and haemorrhages in pancreas. Diagnosis Typical signs and lesions. Reduced feed intake and blood sugar can precipitate fatty liver and kidney syndrome. webbing between toes. 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. A RT-PCR test may be used to detect viral RNA in tissues. Good biosecurity. Allin/all-out production. 18 . Scabs around eyes and beak. Histopathology may also be used but the findings are not specific to this condition. Sudden deaths in fatty liver and kidney syndrome. Post-mortem lesions See signs. It may be helpful to control other conditions which may be occurring at the same time. Drinking water which is well chlorinated should be helpful in reducing challenge by this route. Viral particles may be demonstrated in bile. Leg weakness. Chondrodystrophy.
Diagnosis Identification of the parasites. bedbugs. Treatment Addition of biotin in feed or water. 19 . Menocanthus stramineus is the most pathogenic and is said to be capable of causing anaemia in heavy infestations. Prevention Supplementation of diets with biotin . The parasites are 1-6 mm in size and their life cycle takes about 3 weeks. Differentiate from pantothenic acid deficiency (skin lesions). They are spread by direct contact between birds and by litter etc. Biting Lice Introduction Various species of lice are common external parasites of poultry worldwide. Loss of condition. may be some feather damage and crustiness of skin. Parasites on birds. Crusty clumps of eggs ('nits') may be visible at the base of feathers. Post-mortem lesions Usually none. Check flocks regulary for rapidly moving insects at the base of the feathers on the abdomen or around the vent. especially around vent. Signs Lack of thrift in young birds. Treatment Malathion powders and pyrethroid sprays where approved for bird application. lesions. Irritation. Drop in egg production.Diagnosis Signs. response to treatment/prevention. Away from birds adults survive about 4-5 days. Loss of vent feathers. Scabs around vent. has very low bioavailability. Lice eggs stuck to feathers.naturally present in many raw materials. Differentiate from mites.
Post-mortem lesions Anaemia. Biological control using a strain of Bacillus thuringensis has had some success and is preferable to insecticides. Swarms of flies. season. Examine for lice regularly. 5 mm long and found in North and South America that are external parasites of birds and mammals. Treatment Treatment is difficult. Blackfly Infestation Introduction Grey-black hump-backed flies. The flies transmit leucocytozoonosis and also a filarial parasite in ducks. It is usually necessary to treat twice at a 7-10 day interval to fully control the condition. Signs Anaemia in young birds. Effective removal of all organic material at flock depletion should be practised in all-in/all-out production systems. although these insects can travel up to 15 miles. Diagnosis Anaemia. local history. The condition tends to occur near to rapidly flowing streams. as the larvae within eggs are not killed by most products. 20 . especially in autumn and winter and treat if required. Weekly treatments are required.Prevention Avoid direct contact with wild and backyard poultry. Prevention Similar measures as for mosquito control. Eggs and larvae survive through the winter to cause new infestations in the following year.
Affected broilers tend to settle with eyes closed when not disturbed. selenium. suspect food and stagnant ponds. The toxin and bacterial spores are relatively stable and may survive for some time in the environment. Prevention Preventing access to toxin. supportive treatment if justifiable. turkeys. maggots) is consumed by the birds. because it rests on the litter. The toxin is produced in decaying animal (usually carcases) and plant waste. antibiotics. Diagnosis History. mouse toxicology on serum or extract of intestinal contents. Feathers may be easily pulled (chicken only). The single most important measure is careful pick-up and removal of all dead birds on a daily basis. 21 . This will reduce the risk of botulism both in the poultry and in any grazing animals on land where poultry litter is spread. A soiled beak. Toxin may also be produced by the bacteria in the caecum. Post-mortem lesions Possibly no significant lesions. weakness. and toxin-containing material (pond-mud. Signs Nervous signs. Differentiate from acute Marek's disease ('Floppy Broiler Syndrome') by histology of the brain. especially in hot weather.Botulism Introduction A condition of chickens. progressive flaccid paralysis of legs. is also quite typical. then sudden death. signs. carcases. Mild enteritis if has been affected for some time. Morbidity is usually low but mortality is high. ducks and other waterfowl occurring worldwide and caused by a bacterial toxin produced byClostridium botulinum mainly types A / C. Treatment Remove source of toxin. Maggots or putrid ingesta may be found in the crop. It has also been suggested that poultry carcases lost in litter can be a cause of botulism in cattle grazing land or consuming silage where poultry litter has been spread. wings then neck.
Morbidity is high but it is not associated with mortality. Poor feather cover and caked or wet litter are predisposing factors. Caecal Worm Introduction Heterakis gallinae. up to 1. Morbidity may reach more than 50% but the condition is not fatal.Breast Blister Introduction A complex condition of chickens and turkeys occurring worldwide associated with trauma. and infection withStaphylococcus spp. control of leg problems. Signs None. Post-mortem lesions Inflammation of sternal bursa along the keel bone which may. leg weakness. The meaning of the technical terms relating to parasite life cycle are defined in the glossary.5 cm in length that occur in the caecum. and a four-week prepatent period. Infection is by the oral route. are small whitish worms with a pointed tail. They are found worldwide. bacteria. give way to scar tissue. or paratenic hosts with partially developed (L2) larvae. Earthworms may be transport hosts for eggs. Diagnosis Based on lesions. There is an incubation period of 2 weeks for eggs to embryonate. in chronic cases. Signs Swelling over the keel bone with bruising and discolouration. Heterakis gallinaeeggs and larvae are a transport hosts for Histomonas. 22 . nematode parasites of poultry and game birds. Prevention Good litter management and handling. Treatment Not usually appropriate. the cause of Blackhead.
Prevention Avoiding access to earth and earthworms. or by an earthworm which is in turn ingested by a chicken. Figure 11. Levamisole. are effective. Death from respiratory and cardiac failure. Diagnosis Adults can be seen in caecal contents at post-mortem examination. Treatment Flubendazole. The egg may be ingested directly by a chicken. 23 . The life cycle ofHeterakis showing the location of adults. Predisposing factors include heat stress with reduced feed intake and panting.Post-mortem lesions Inflammation of caecum. possibly with nodule formation. an undeveloped egg as found in fresh faeces. Routine anthelmintic treatment. especially broiler parents. Signs Paralysis. Calcium Tetany Introduction A metabolic disease of chickens. and the embryonated egg.
Congested lungs. principally in the caecae. Campylobacters are a significant cause of enteritis in man. Active ovary with egg in oviduct. Campylobacter Infection Introduction Campylobacter spp. Campylobacter jejuni is the commonest species found in poultry. 24 . Prevention Keep pullet flocks on low calcium diet until 5% production hen/day. 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'. lesions. The reason for this is unclear. It may be that management that favours dry litter reduces the risk of infection and/or transmission within the flock. and response to treatment. other acute infections and other causes of sudden death. Infected poultry are a potential reservoir of this zoonosis. In poultry they tend to multiply in large numbers in the hindgut. There is an annual cycle with increased risk of infection in the summer months in some countries. are bacteria that commonly infect a broad range of livestock species. All campylobacters are delicate organisms that survive for relatively short periods outside the host unless protected by organic material. pets and wild animals. Differentiate from IB 793b. managing birds for maximum uniformity. Treatment Provide 5 gm of oyster shell per hen on 3 successive days along with vitamin D in drinking water. Diagnosis This is made on signs. There are indications that plantar pododermatitis. carcase quality and litter quality are better on farms which tend to have Campylobacter-negative stock. lack of other significant lesions. biofilm or engulfed by protozoa.Post-mortem lesions Cyanosis.
Prevention In principle. sourcing of water from high quality supplies. For this reason it may be difficult to stop the spread of infection between houses once it becomes established in one house. Key aspects of this include effective sanitation of drinking water. Diagnosis Isolation of the organism from caecal contents. Many infections are introduced during thinning or other forms of partial depopulation. avoidance of contact with pets and other farmed species. The organism is sensitive to air so swabs should be collected into transport medium and other samples placed in airtight containers with minimal airspace. good hand hygiene by stockmen.Signs None. 25 . Samples should be tested as quickly as possible after collection. Treatment Not required on clinical grounds. Research is ongoing on the development of vaccines. and changing of overalls and boots on entering bird areas. Post-mortem lesions None. Insects and rodents may act as a means of transfer of the infection from the general environment into the poultry buildings. housed poultry can be maintained free of Campylobacter infection by consistent application of excellent biosecurity. In practice the success of this will also depend upon the degree of environmental contamination by the organism. as well as processing plant technologies to reduce carcase contamination. cloacal swabs or composite faeces. phage treatments and competitive exclusion approaches.
turkeys. Poor appetite. especially in the crop but sometimes in the proventriculus. Diagnosis Lesions. Prevention Avoid excessive use of antibiotics and other stressors. and associated with gizzard erosion. smooth and with a yeasty smell. Colonies of this fungus appear as white to ivory colour. Control of Candida through drinking water is sometimes practised with chlorination (e. 26 . Moniliasis. The fungus is resistant to many disinfectants. A finely divided powder of copper sulphate (where approved) at 200gm/tonne continually or to 14-16 weeks in replacement pullets. Morbidity and mortality are usually low. characterised by thickening and white plaques on the mucosa. copper sulphate (1 kg/tonne feed) for 5 days.g. Candida albicans and the condition is seen worldwide. oesophagus. Raised focal lesions may slough into lumen as caseous material. histopathology. and sometimes other birds and mammals. The cause is a fungal yeast. or copper sulphate 1gm/2 litre water for 3 days if approved locally. sodium or calcium proprionate at 1 kg per tonne continually. Signs Dejection. Post-mortem lesions White plaques in mouth. Treatment Nystatin (100 ppm in feed) for 7-10 days. intestine and cloaca. Slow growth. 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. possibly confused or masked by signs of the primary disease. crop. Ensure good hygiene. proprionic acid. microscopic examination of a digested smear (heat in 10% potassium hydroxide) to demonstrate the hyphal forms of the yeast in the tissues. Thrush Introduction A disease of the alimentary tract of chickens.Candidiasis. occasionally proventriculus and intestine. Diarrhoea.
Generalised anaemia.Chlorox. through shafts of light in the house). 27 . Provision of a diet that closely matches the nutritional requirements of the stock concerned. Feather-pulling. Differentiate from bacterial dermatitis. feed form (mash takes longer to consume than pellets). anaemia. Signs Pecking at feet (especially young chicks) and vents (adult layers and turkey poults 812 days old). Post-mortem lesions Skin wounding related to particular signs exhibited. If so it should be carried out carefully by trained operators. boredom. Soluble multivitamins and/ or methionine may be of some benefit in some circumstances. Morbidity is usually low but mortality is high among affected birds. Predisposing factors include overcrowding. Take care to provide fresh clean feed and water. Treatment Correct any husbandry problems. excessive light intensity or variation (e. Diagnosis Age. Prevention Proper density and temperature. and strain of bird. distribution of lesions. tenosynovitis and other diseases affecting mobility. control ectoparasites. This is economical and effective. head. wings. low light level. Beak trimming may be necessary. complying with local regulations and any relevant codes of practice. face. uncontaminated by fungi. It should be repeated periodically. nutritional deficiencies.g. high temperatures. sodium hypochlorite) at 5 ppm. Feather pecking Introduction A complex multifactorial behavioural problem of poultry and game birds seen worldwide. Cannibalism. post-mortem cannibalism.
The worms are 7-18 mm long. Infection is by the oral route. Fenbendazole has been shown to have high efficacy . effective cleaning of houses. prepatent period about 21-25 days according to species. Dejection. Diagnosis This may be by a combination of macroscopic examination. seiving intestinal contents. Prevention Separation of birds from possible transport and intermediate hosts. C. game birds and pigeons ofCapillaria species. Post-mortem lesions Enteritis. Morbidity and mortality are usually low. some are transmitted direct from bird to bird. Signs Diarrhoea. obsignata in the small intestine. or characteristic worm eggs in faeces in patent infections. Treatment Coumphos has been licensed in some markets. small intestine or caecum. Worm eggs take about 20 days to embryonate with an L1 larvae. Levamisole.05 mm wide and hair-like in appearance.other approved benzimidazoles can be expected also to have activity. Some species have earthworms as intermediate hosts. Differentiate from other causes of enteritis. 28 . Worm eggs in the environment are resistant. about 0.Capillariasis . Hairworms in mucosa of crop. C. contorta in the crop and oesophagus. Wasting Poor growth.Hairworm Infection Introduction Nematode parasitic worms of poultry.
Post-mortem lesions Typically it presents as exudate ranging from liquid and pale cream pus to yellowish solid plaques of caseous material under the skin of the abdomen and/or in the leg. though most of the birds showing toe scrapes will not go on to develop cellulitis. Treatment Treatment would not be possible if the problem is identified at a final depletion. coli. particularly broiler chickens. Signs Affected flocks tend to have poorer than average productivity and uniformity. The condition is caused by infection of. It typically occurs between skin and muscles and between muscles and may be an incidental finding in a range of conditions. Many affected birds have no other lesions and are reasonably well grown. skin wounds by particular strains of E. Careful flock management with a view to reducing toe wounds has the greatest impact in controlling cellulitis. Diagnosis Typical lesions.Cellulitis Introduction Cellulitis is literally an inflammation of connective tissues. which can replicate in the tissues. 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. Routine monitoring of skin damage at about 25 days of age may be helpful in fostering good practices. Prevention Toe scrapes at 15-25 days of age when feather cover is poor are the most likely predisposing factors. However its main importance is as a cause of condemnation in meat poultry. 29 . but the affected birds are not readily detectable prior to slaughter. Many meat inspectors become skilled at detecting subtle differences in skin colour in the affected birds. often minor. In the USA it is called 'Inflammatory Process'.
Post-mortem lesions Pale bone marrow. Discoloured liver and kidney. legs wings or neck.Chicken Anaemia Introduction A viral disease of chickens caused by Chicken Anaemia Virus or CAV. virus may be isolated in lymphoblastoid cell line (MDCC-MSB1). and control of other diseases as appropriate.) or poor management (e. Diagnosis Gross lesions. heat (70°C for 1 hour. If gangrenous dermatitis is a problem then periodic medication may be required. Gumboro. No clinical signs or effect on egg production or fertility in parent flock during seroconversion. lateral transmission may result in poor productivity in broilers. may be beneficial. ether. Treatment Good hygiene and management. poor litter quality). Atrophy of thymus and bursa. PCV of 5-15% (normal 27-36%). Inclusion body heptatitis etc. Signs Poor growth. 80°C for 5 minutes) and many disinfectants even for 2 hours at 37°C. Gangrenous dermatitis on feet.g. Sudden rise in mortality (usually at 13-16 days of age). Prior to confirmation that it is in fact a virus it was known as Chicken Anaemia Agent or CAA. Hypochlorite appears most effective in vitro. 30 . Transmission is usually vertical during sero-conversion of a flock in lay. The virus is resistant to pH 2. chloroform. Mortality is typically 5-10% but may be up to 60% if there are predisposing factors present such as intercurrent disease (Aspergillosis. Pale birds. demonstration of ongoing sero-conversion in parent flock. Acute mycotic pneumonia.
Ornithosis Introduction An infection of turkeys. man. Psittacosis. say. Immunity: there is a good response to field challenge (in birds over 4 weeks of age) and to attenuated live vaccines. 15 weeks. Weight loss. Production drops in naive laying flocks Post-mortem lesions Vascular congestion. Serology: antibodies develop 3-6 weeks after infection. and may be detected by SN. a bacterium of highly variable pathogenicity. Morbidity is 50-80%. other infections may be predisposing factors. Elisa. It is transmitted by contact. Their use may be restricted to those flocks that have not sero-converted by. Occasional transient ataxia in pigeons. mortality 5-40%. 31 . caused by Chlamydia psittaci. It is a 'Scheduled Disease' rarely diagnosed in UK. perhaps. Intercurrent salmonellosis and. psittacines. ducks. Weakness. rarely chickens. They should be used at least 6 weeks prior to collecting eggs for incubation. Wasting. phenolics are less so. Conjunctivitis. Nasal discharge. pigeons. Chlamydiosis.Prevention Live vaccines are available for parents. but occurring probably worldwide. their degree of attenuation is variable. or IFA. Fibrinous pericarditis. Egg transmission does not occur. Greenish-yellow diarrhoea. Elementary bodies are highly resistant and can survive in dried faeces for many months. faecal dust and wild bird carriers. Inappetance. Signs Respiratory signs. Iodophores and formaldehyde are effective disinfecting agents. especially pigeons and robins. Depression. Airsacculitis.
Signs Short legs. Slipping of Achilles tendon (or perosis). Necrotic foci in liver. Elisa and gel diffusion. folic acid. Distortion of hock. Prevention Biosecurity. Lameness. Malposition of leg distal to hock. Live and inactivated vaccines are protective although the former result in carriers and the latter require several applications. may rupture in pigeons. 32 . Perihepatitis. niacin may also be involved). Congested lungs and air sacs in the turkey. Treatment Tetracycline (200-800 ppm in feed for 3-4 weeks) and/or quinolone medication and supervised slaughter. In turkeys it may be an inherited deficiency of galactosamine. Differentiate from Duck viral hepatitis. Chondrodystrophy. Diagnosis History. signs. zinc. either singly or in combination (although deficiencies of pyridoxine. biotin. lesions. choline. In embryos parrot beak. This condition is seen in chickens. Duck septicaemia. exclusion of wild birds. Spleen enlarged and congested. Slipped Tendon or Perosis Introduction Caused by deficiency of manganese. Intracytoplasmic inclusions are helpful but confirmation requires demonstration of causal organisms (Giemsa stain. ducks and turkeys. shortened bones. Serology: complement fixation. Fibrinous pneumonia. IFA).
meleagridis affect the lower small intestine rectum and caecae. Watery diarrhoea that may occasionally be blood stained or contain clumps of mucus or shed mucosa. dispersa is found in the small intestine. Differentiate from twisted leg. while E. adenoides affects the caecae and rectum. ruffled feathers. Five species of Eimeria have been identified that cause lesions in turkeys. This disease is not very common in commercially reared turkeys though most turkey growers receive preventative medication for at least part of their lives. E. Tibia and metatarsus bowed. Shallow trochlea. analysis of feed. rickets. Tucked appearance. infectious synovitis.Post-mortem lesions Shortening and thickening of long bones. 33 . Lateral slipping of tendon. Signs Huddling. meleagrimitis affects the upper small intestine. infectious arthritis. The contents may be haemorrhagic or be watery with white material shed from the mucosa. gallopavonis and E. Coccidiosis of Turkeys Introduction Infection of turkeys with Eimeria spp. of which two are associated with significant disease effects. Diagnosis Lesions. vitamins. choline. E. Post-mortem lesions The affected area of intestine shows thickening of the wall and dilation. Prevention Addition of manganese. Weight loss. while E. no value to affected bird. correct mineral balance. Treatment For flock proceed as for prevention. Depression. ruptured ligaments.
The exudate can range from semi-liquid to solid white cores. Figure 37. typically to 12 weeks of age. Dosage levels of ionophores may be critical to efficacy and safety. Avoid use of tiamulin in ionophore treated birds. Turkey caecal coccidiosis caused by E. Diclazuril is also used for this purpose. Sulphaquinoxaline). Prevention The ionophore coccidiostats lasalocid and monensin are routinely used in turkey growers. gamonts). show some spotty congestion and have abnormal contents due to the sloughed epithelium. Turkey coccidiosis of the upper small intestine caused by E. 34 . meleagrimitis. Figure 38. Differentiate from necrotic enteritis. Amprolium. adenoides. Sulphonamides (e. The intestines are dilated. microscopic exam of scrapings (oocysts. lesions. Exposure of previously unmedicated birds to these compounds can cause toxicity.g. Salinomycin is toxic for turkeys even at very low doses.Diagnosis Signs. Treatment Toltrazuril.
ecchymoses. Differentiate from ulcerative enteritis. It is caused by Eimeria tenella and results in lesions in the caecum of chickens worldwide. 35 . E. E tenella Introduction This was at one time the commonest type of coccidiosis and is certainly the most easily diagnosed. Production less affected than in some of the other forms of coccidiosis. Post-mortem lesions Petechiae. Sulphonamides.Coccidiosis. Caecal. Signs Depression. Thickening. Inappetance. Vaccines are used mainly in breeders but increasingly in broilers. Accumulation of varying quantities of blood and caseous necrotic material in the caecum. Diarrhoea. microscopic examination of scrapings. Morbidity is 10-40% and mortality up to 50%. Closed eyes. Prevention Coccidiostats in feed. of caecal mucosa. blood in faeces. Recovered birds have good immunity to the same parasite. Treatment Toltrazuril. mitis (see above). Ruffled feathers. Transmission as for E. tenella is more common when 'straight' ionophore programmes are used. lesions. histomonosis. Amprolium. hygiene. vaccination by controlled exposure. Diagnosis Signs. Vitamins A and K in feed or water. Shuttle programmes with chemicals in the starter diet usually improve control. In some markets the organic arsenical compound 3-Nitro is used as an aid in the control of caecal coccidiosis.
Post-mortem lesions The lesions are minimal and located in the lower small intestine (ileum) which tends to be pale and flaccid with scattered petechiae. Moderate Eimeria tenella infection in the caecae of a chicken (Score 3). Predisposing factors include exposure to faeces and litter conditions that favour development of the parasite (temperature. which colonises the small intestine. Signs Reduced feed conversion efficiency and weight gain.Figure 15. 36 . Treatment Not usually treated but susceptible to the products used for other forms of intestinal coccidiosis. E mitis Introduction This condition of chickens. is caused by the protozoan parasite Eimeria mitis. humidity). Coccidiosis. secondary bacterial enteritis. The parasite is moderately resistant in the environment and highly resistant to conventional disinfectants. The caecal walls are thickened and haemorrhagic and there is a mass of blood in the caecal lumen. The disease occurring is proportional to the amount of infective agent ingested. The infective agent is found in litter. May predispose to wet litter. Diagnosis Mild lesions. seen worldwide. identification of typical small round oocysts and other stages in fresh scrapings from the small intestine. faeces and on fomites and birds are infected by the oral route with an incubation period of 2-5 days.
it is found in the terminal ileum. This species is not usually included in vaccines for broilers. Ruffled feathers. Prevention Coccidiostats in feed. hygiene. Vitamins A and K in feed or water. Signs Depression. 37 . Closed eyes. Coccidiosis. microscopic examination of scrapings. Diarrhoea. lesions. caecal coccidiosis. Post-mortem lesions Petechiae and thickening of the distal third or more of intestine. Ileorectal.Prevention Normally controlled by anticoccidials in feed. Differentiate from ulcerative enteritis. Of moderate to high pathogenicity. Sulphonamides. Severe necrotising enteritis. extending into caecal tonsils. There is good immunity to the same parasite in recovered birds. May be included in vaccines. E brunetti Introduction A relatively rare form of coccidiosis affecting chickens worldwide caused by Eimeria brunetti. caecum and rectum. Amprolium. Inappetance. vaccination by controlled exposure. blood in faeces. Oocysts in caecum and rectum. Morbidity and mortality are variable. Diagnosis Signs. Treatment Toltrazuril. Poor production.
Vitamins A and K in feed or water. Blood-stained vent. Coccidiosis. Tucked appearance. 3 days on. compared to four per oocyst forEimeria. microscopic examination of scrapings (usually few or no oocysts.g. Post-mortem lesions Massive haemorrhage in upper small intestine. Diagnosis Signs. 38 . Moderate Eimeria brunettiinfection in the terminal ileum and rectum of a chicken. Differentiate from Duck viral hepatitis. There is thickening of the intestinal mucosa and there are lines of haemorrhagic spots in the mucosa. Coccidiosis occurs only very rarely in commercially reared ducks in the UK. anseris is the most important. 2 days off. In the goose E. lesions. of Ducks and Geese Introduction Young ducks and geese may suffer from Eimeria spp infection. Duck viral enteritis. Depression. Tyzerria has eight sporocysts in each oocyst.Figure 16. large number of merozoites). Signs Sudden death. anatipestifer. while in ducksTyzzeria perniciosa is most pathogenic. Intestinal. Treatment Sulphonamides (e. Sulphadimidine 30-600gm/100 birds/day. 3 days on). Amprolium.
presence of coccidial stages in fresh scrapings of kidney lesions. Treatment Controlled trials of treatments have not been published. Coccidiosis. 39 . it can also infect Barbary ducks and swans. Kidneys light grey to greyish pink.Prevention If required coccidiostats could be used in feed. Signs Depression. Weakness. Hygiene. Prevention Good Hygiene.faeces tend to be whitish. Tiny white foci and petechiae in the kidneys. Diagnosis Lesions. Post-mortem lesions Enlarged kidneys. Reduced feed intake. Diarrhoea . Kidney Introduction A disease of geese caused by Eimeria truncata that can cause high mortality in geese of 312 weeks of age. however this is not routinely practised.
Post-mortem lesions Petechiae and thickening of middle third of intestine. Amprolium. Differentiate from necrotic enteritis. of moderate to high pathogenicity it is seen worldwide. Blood or pigment in the faeces. Poor absorption of nutrients/pigments. Caused by Eimeria maxima. Signs Depression. Vitamins A and K in feed or water. Poor production. 40 . Mild to severe enteritis. Ruffled feathers. This is one of the less immunogenic species. Because of the area of intestine affected it tends to have a significant effect on productivity and susceptibility to necrotic enteritis. maxima. hygiene. Depigmentation of skin and plasma is especially evident in this form of cocccidiosis and this is commercially important in some markets. Morbidity and mortality are variable.Coccidiosis. This infection is often associated with E. non-specific enteritis. mucosa tends to be pinker than normal. lesions. Inappetance. microscopic examination of scrapings. Closed eyes. vaccination. contents often orange in colour. Prevention Coccidiostats in feed. acervulina coccidiosis and there may be large numbers of characteristic oocysts in smears. Treatment Sulphonamides. E maxima Introduction One of the more common forms of coccidiosis in commercial broilers. Mid-intestinal. commercial vaccines commonly contain more than one strain of E. Diagnosis Signs.
It occurs in chickens worldwide and has variable morbidity but mortality is high in severely affected birds. Signs Reduced feed consumption. in which the parasite is present in the small intestine and in the caecum. Severe necrotising enteritis. Oocyts in caecal scrapings. Closed eyes. Post-mortem lesions Petechiae and thickening. The lesions are subtle compared to other forms of coccidiosis. Mid-intestinal. caused by Eimeria necatrix. Depression. Poor production. of middle to posterior third or more of small intestine. 41 . microscopic examination of scrapings Differentiate from necrotic enteritis. Diarrhoea. Inappetance. Deep scrapings necessary to show large schizonts. 'Sausage-like' intestine.Figure 13. blood in faeces. Moderate Eimeria maxima infection in the jejunum of a chicken (Score 2). E necatrix Introduction A highly pathogenic form of coccidiosis. Coccidiosis. Ruffled feathers. Diagnosis Signs. The intestine is slightly thickened and there are scattered haemorrhages in the mucosa when seen from the inside. Schizonts seen as white spots through the serosa interspersed with petechiae. lesions. other types of coccidiosis.
It is seen in layers and in broilers. hygiene. Signs Depression. Poor production. Depigmentation. Ruffled feathers. Morbidity is variable and mortality low or absent. Vitamins A and K in feed or water. In this case the intestine is thickened and can become ballooned and sausage-like. Inappetance. Coccidiosis. both alone and in association with other species of coccidia and is caused by Eimeria acervulina. Figure 14. Upper Intestinal. Amprolium. which is moderately pathogenic. Haemorrhages and white spots are visible from the outside of the intestine.Treatment Toltrazuril. E acervulina Introduction This is probably the commonest cause of coccidiosis in chickens and occurs worldwide. Moderate Eimeria necatrix infection in the jejunum of a chicken (Score 3). Sulphonamides. Closed eyes. commercial vaccines commonly contain more than one strain of E. acervulina. maxima. Eimeria mivatiis currently considered not to be a valid species distinct from E. Diarrhoea. vaccination. This is one of the less immunogenic species. Prevention Coccidiostats in feed. Post-mortem lesions 42 .
White spots or bands in the mucosa. and other lesions. In general terms a score of 0 indicates no lesions and a score of 4 indicates maximal severity of lesion or death. in feed or water. Immunity is quite short lived (about 30 days) in the absence of continued challenge. Thickening. Figure 12. Sulphonamides. In milder infections there may be scattered white spots. 43 . Poor absorption of nutrients/pigments. lesions. A detailed description is beyond the scope of this book. Petechiae. vaccination by controlled exposure. restricted to upper third of small intestine . hygiene. A system of assessing the severity of coccidial challenge by attributing a 'score' is often used. In severe infections they become confluent and cause sloughing of the mucosa. Various publications provide a photographic key to severity of lesion. microscopic exam of scrapings. Diagnosis Signs.the duodenum and part of the ileum. Amprolium. Prevention Coccidiostats in feed. Differentiate from necrotic and non-specific enteritis. Treatment Toltrazuril. Moderate Eimeria acervulinainfection (score 2) in chicken duodenum. in severe the entire surface is pale or denuded of epithelium.
Perihepatitis. and via shell membranes/yolk/navel. mortality is 5-20%. Omphalitis. Infection is by the oral or inhalation routes. Diagnosis Isolation. sero-typing. with an incubation period of 3-5 days. Omphalitis. Pericarditis.Colibacillosis. Granulomata in liver and spleen. Poor growth. It is frequently associated with immunosuppressive diseases such as Infectious Bursal Disease Virus (Gumboro Disease) in chickens or Haemorrhagic Enteritis in turkeys. Colisepticemia Introduction Coli-septicaemia is the commonest infectious disease of farmed poultry. Poor navel healing. fomites. etc. or in young birds that are immunologically immature. Aerobic culture yields colonies of 2-5mm on both blood and McConkey agar after 18 hours . Snick. The infectious agent is moderately resistant in the environment. Enteritis. Synovitis. Morbidity varies. turkeys. Cellulitis over the abdomen or in the leg. Reduced appetite. coughing. Swollen liver and spleen. water. It is caused by the bacteriumEscherichia coli and is seen worldwide in chickens. mucosal damage due to viral infections and immunosuppression are predisposing factors. Salpingitis. pathology. It is most commonly seen following upper respiratory disease (such as Infectious Bronchitis) or Mycoplasmosis.most strains are rapidly lactose-fermenting producing 44 . Lesions vary from acute to chronic in the various forms of the disease. Dejection. sneezing. Peritonitis. Post-mortem lesions Airsacculitis. but is susceptible to disinfectants and to temperatures of 80°C. Signs Respiratory signs. Arthritis.
Staphylococcus spp. Hock Burn. whereas others progress to deep ulcers so the size. when severe. Figure 17. feed and water. tetracyclines. Some lesions are superficial. Severe perihepatitis in colibacillosis in a broiler parent chicken. good sanitation of house. Immunity is not well documented though both autogenous and commercial vaccines have been used. flouroquinolones. Control of predisposing factors and infections (usually by vaccination). etc. Prevention Good hygiene in handling of hatching eggs. The liver is almost entirely covered by a substantial layer of fibrin and pus. Well-nourished embryo and optimal incubation to maximise day-old viability. Contact dermatitis is commonly monitored at processing as a means of measuring 'welfare status'. Treatment Amoxycillin. stage of resolution and severity of lesion is likely to affect the degree of discomfort or pain suffered. Contact Dermatitis. the foot pad. It is seen in growing broiler chickens and turkeys. Differentiate from acute and chronic infections with Salmonella spp.brick-red colonies on McConkey agar. Pododermatitis Introduction Contact dermatitis affects skin surfaces which have prolonged contact with litter. gentamycin or ceftiofur (where hatchery borne). neomycin (intestinal activity only). rear surface of the hock and. potentiated sulphonamide. hatchery hygiene. and in broiler parents. other enterobacteria such as Proteus. the breast area. 45 . as well as Pseudomonas.
and sometimes in the breast area. drinker management. level of soya bean meal in feed (according to some authors. at the back of the hocks. and adequate ventilation to remove moisture are all important. litter moisture. Figure 18. and. It can be reproduced by adding water to the litter. Choice of drinker type (nipple as opposed to bell).Pododermatitis is often related to high droppings pH. Treatment Not applicable. Post-mortem lesions As described under signs. proper insulation in cold climates. Prevention This condition is closely linked to intestinal function as this is the prime determinent of faecal consistency and stickiness. Diagnosis Signs and lesions. Signs Blackened skin progressing to erosions and fibrosis on the lower surface of the foot pad. See the discussion in the section on Dysbacteriosis. most importantly. If severe the foot and hock lesions may contribute to lameness or serve as a portal of entry for secondary infections. 46 . stickiness of droppings). Moderate pododermatitis on a foot pad.
Prevention Effective cleaning of housing. White convoluted tracks in the mucosa. and vice versa. Avoidance of access to intermediate hosts. Post-mortem lesions Inflammation and thickening of mucosa of crop and oesophagus. The oocysts are excreted ready sporulated in the faeces and infection occurs by inhalation and ingestion. Cryptosporidiosis Introduction Cryptosporidia are related to the coccidia. acervulinaoocyst). turkeys.C. Cryptosporidium baileyi can cause respiratory disease in chickens and turkeys. Diagnosis Microscopic examination of mucosal scraping. A further species causes respiratory disease in quail. They also differ from coccidia in being poorly host specific. and ducks. Emaciation. Some have beetle or earthworms as intermediate hosts. Signs Anaemia. They replicate in the brush border on the surface of epithelial cells. 47 .Cropworms Introduction The nematode worms Capillaria spp and Gongylonema ingluvicolainfect the mucosa of the crop and oesophagous of poultry and game birds. Routine worming. The same species causes infections of the hindgut and cloacal bursa in chickens. although bird strains do not infect mammals very well. Treatment Levamisole. meleagridis also infects both species. but much smaller (typically oocysts are less than ¼ of the size of an E. Coumaphos.
It is becoming increasingly common for water companies to screen water supplies for cryptosporidia because of the human health implications of mammalian strains. There are no effective preventative medicines or feed additives. Airsacculitis. Pneumonia. Cough. Tremors. Treatment Unfortunately there is currently no known effective treatment in poultry. Swollen sinuses. Diagnosis Identification of the parasites attached to the epithelium by microscopic examination (smears histopathology acid-fast staining). If other disease processes are complicating the situation (e. Post-mortem lesions Sinusitis. Circling. Low weight gain. 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. Signs Incoordination. coli-septicaemia) there may be benefit in medicating for these. Torticollis. Prevention The oocysts of cryptosporidia are extremely resistant to chemical disinfection. 48 . recumbency.Signs Snick.g.
Treatment 49 . Microscopically there is necrosis and there may be fissures of articular cartilage and associated osteochondritis. Signs Lameness. Diagnosis Lesions. but it may result from physical damage. Post-mortem lesions Damaged epiphyseal articular cartilage. air sacs etc. especially of femoral anti-trochanter but also other leg joints. Morbidity and mortality are low but affected birds are more likely to be 'picked upon' and may end up suffering damage and needing to be culled. The cause remains to be confirmed. or developmental defects. Degenerative Joint Disease Introduction A condition of chickens and turkeys seen worldwide. Treatment None. Reduced breeding performance. resulting in erosions. isolation of the fungus.Post-mortem lesions Necrotic lesions with associated congestion in cerebrum. Mycotic lesions in lungs. Diagnosis Gross and microscopic lesions. and cartilage flaps. Rapid growth is a possible predisposing factor. Prevention Use fresh dry litter (avoid old sawdust).
Depluming and Scaly Leg Mites Introduction External parasites of adult chickens. Raised thickened scales. There may be a place for growth-control programmes. Signs Cause irritation and the bird pulls feathers. Post-mortem lesions As described under signs. pheasants. especially during period of rapid growth. up to 0.5mm in diameter. The adult females are short legged. For small flocks dipping the affected parts in a solution of acaricide may be beneficial. Treatment Not usually required in commercial poultry.Knemidocoptes spp. Appropriate management of a segregation pen and early marketing of mildly affected birds may limit losses and improve flock welfare.None available. Mange lesions on legs and unfeathered parts. Application of mineral or vegetable oil is also beneficial. Prevention Avoidance of physical sources of injury to bones and joints. Diagnosis Signs. Exclusion of wild birds from chicken areas is advised as far as possible. It may be best to cull affected birds from small flocks. microscopic examination for mites in scrapings. Unthriftiness. Prevention Careful cleaning of buildings during down-time will help reduce the risk of these infections. 50 . round. pigeons etc.
Duck Viral Hepatitis Introduction A viral disease of ducks occurring worldwide and previously a scheduled disease in UK.Dissecting Aneurysm. Prevention Limit feed in birds of 16+ weeks. a picornavirus may also 51 . Morbidity is around 100% and mortality 0-95%. birds found on breast or side. It has been suggested that degenerative changes in the wall of the artery and copper deficiency may be factors. Possibly blood in the mouth. a tranquilizer. Rupture of major blood vessel at base of heart or by the kidneys. A sudden noise or other cause of excitement can lead to an 'outbreak'. Aspirin at 250 ppm in feed or water may be of benefit. recovered birds carrying the virus for 8 weeks. Reserpine. presumably due to a sudden increase in blood pressure. Post-mortem lesions Carcase anaemic. pericardial sac. Skin pale. Abdominal cavity full of blood. Treatment None currently licensed. was included in feed at 1 ppm for 3-5 days to reduce blood pressure. Diagnosis History and lesions. Signs Sudden death with no warning signs. A longtitudinal split of the abdominal aorta is the most common lesion. The infective agent. genetic condition of turkeys linked to male sex and high growth rate. Haemorrhages in lungs. Reserpine in diet of birds of 4+ weeks (no longer licensed in the UK). Aortic Rupture Introduction A complex. leg muscles. The disease is transmitted by infected ducks and other waterfowl and spreads rapidly. kidneys.
often in opisthotonus. Transmission is by infected birds. Fall on side. All waterfowl are susceptible and the Barbary duck is more susceptible than the Pekin.5 ml serum of recovered birds given intramuscularly. Microscopically . Duck Virus Enteritis. Depression. Recovered birds may carry the virus for a year. 0. in USA since 1967. lesions.survive for ten weeks in brooders and five weeks in faeces. Signs Sudden death. fomites and arthropods. paddling of legs. Punctate/diffuse haemorrhages. Newcastle disease. only slightly attenuated vaccine is applied at day old by foot web stab and may be repeated in breeding birds to provide maternal immunity. Duck Plague Introduction A herpesvirus infection of ducks and geese diagnosed in the UK in 1972. Treatment Antiserum. Differentiate from Duck plague (viral enteritis). A different picornavirus causes a similar condition in North America. coccidiosis. also the Netherlands and other countries. Influenza and a 'Type II Variant' hepatitis caused by Astrovirus. 52 . The disease follows a very acute course with a morbidity of 5-100% and mortality of 5-100%. mostly in ornamental collections. bile duct proliferation and inflammation. breeder vaccination. isolation in CE (causes stunting of 9 day embryo). rapid deterioration and death. Prevention Vaccination and/or antiserum. Diagnosis History. Kidneys and spleen swollen. Post-mortem lesions Liver swollen. Live.focal necrosis. Death in good condition. Duck septicaemia (anatipestifer). arching of back. SN serology.
spleen. intranuclear inclusions Differentiate from Duck hepatitis. oesophagitis (birds on restricted feed).Signs Sudden deaths. Prevention Isolation from waterfowl. Haemorrhage in intestine. body cavities. Photophobia. Young ducks may show thymic and bursal lesions. vaccination if approved by authorities (CE adapted live virus). Dehydration. Severe diarrhoea. Treatment None. Crusty plaques from oesophagus to bursa (covered by yellowish plaques in later stages). but vaccination in face of outbreak is of value. is common in countries with restrictions on the use of antimicrobial growth promoters and pressure to reduce therapeutic antimicrobial usage. Non-specific Bacterial Enteritis Introduction Inflammation of the small intestine associated with wet litter. pasteurellosis. Rapidly spreading disease. probably through interference. Tremor. vent gleet. liver. coccidiosis. heart. 53 . Dysbacteriosis. Closed eyes. excess caecal volume and fermentation. Ataxia. Thirst. Paresis. Occasionally cyanosis of the bill in the young. Diagnosis Isolation: Duck CAMs 12 day embryos die in 4 days. Post-mortem lesions Severe enteritis. Drop egg production. pericardium. Occasionally penile prolapse in the penis in drakes. HA-. sometimes dysentery. The condition is seen mainly in rapidly growing broiler chickens with good food intake.
especially where treatment is initiated early. Diagnosis Signs. Holland. first isolated in Northern Ireland in 1976. In the autumn of 1976 a distinct egg drop syndrome was first identified in Northern Ireland. Treatment Amoxycillin and tylosin treatment appear to be beneficial. Circumstantial evidence suggests that the main route of transmission is through the eggs (vertical transmission) 54 . 127. feed interruptions and subclinical coccidiosis may be contributory factors. Spain. Uruguay. Feed acidification may be helpful in some circumstances. often with gas bubbles. The cause has been identified as Adenovirus BC14. Prophylactic antimicrobial medication may be necessary in some circumstances. It affects chickens and has occurred in Ireland. England. Germany. microscopic examination of scrapings from the wall of the small intestine (to exclude coccidiosis and perhaps to assess the bacterial flora). lesions. Good control of coccidiosis. Treatment should coincide with good relittering and it is important to provide fresh sanitary drinking water. Signs Diarrhoea.Dietary changes. Prevention Competitive exclusion ('normal adult flora') use in day-old chicks reduces the risk of this condition. Voluminous caecae. rather we are dealing with a disruption in the normal flora of the gut. Apparently a similar disease had been seen over a 4-year period in broiler parents in Holland. 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. Post-mortem lesions Excessive fluid content throughout the small intestine. France. Wet faeces in the rectum. Peru. Argentina. Careful choice of any feed enzymes and their matching with local raw materials can have an impact on substrates made available to intestinal bacteria. Mortality is usually negligible. Water intake may be increased or irregular. No single bacterium appears to be responsible. Brazil.
Drops may be of 5 to 50% and last for 3-4 weeks. as may wildfowl and biting insects. Loss of shell pigment. Poor internal quality. which can be caused by a large number of factors acting individually or in combination. intoxication by sulphonamides. inadequate lighting programme. Post-mortem lesions No specific lesion . Serology: HI. extremes of temperature. Spread from house to house may take 5-10 weeks. Parasites. Management problems may be involved: inadequate water supply. Diphtheritic Fowl Pox). Contamination of egg trays at packing stations may play a part in transmission. signs/lesions (mainly lack of).followed by latent infection during rear with viral excretion starting shortly before sexual maturity. Coryza. Isolation of haemagglutinatin agent in duck eggs or cell culture. and D as well as calcium. Clinical disease occurs during sexual maturity.it may be possible to demonstrate degenerative changes in the epithelial cells of the magnum of the oviduct. Cholera. phosporus. Histopathology . Diseases in which egg drop occurs. group antigen distinct from classical adenoviruses (white cells. oviduct). may be infectious or metabolic. The infection is commonly present in ducks and geese but does not cause disease. Signs Egg drop at peak or failure to peak. SN. thin or soft-shelled eggs and shell-less eggs. Diagnosis History. Newcastle disease. DID. 55 . Marek's disease/Leukosis or any infectious disease causing a significant systemic disturbance (CRD. Infectious diseases include Infectious Bronchitis. Lack of signs in the birds themselves. Elisa. Avian Encephalomyelitis. selenium. sudden changes of feed. throat swabs. It is important to rule out other possible reasons for egg drop. Infectious Laryngotracheitis. Unvaccinated flocks with antibodies before lay do not peak normally. Rough. Lateral transmission from bird to bird is slow and may be prevented or slowed for weeks by netting divisions.only a slight atrophy of ovary and oviduct. Nutritional deficiency should be considered. B 12. specifically vitamins E. Metabolic diseases include Fatty Liver Syndrome. insecticides or nicarbazin.
If successive flocks are affected on the same site prophylactic medication ahead of the anticipated problem may be of benefit. Signs Fluid-distended abdomen. Prevention Vaccination with inactivated vaccine prior to lay. growth plate disease. Vegetative lesions usually on the right atrioventricular valve. bacterial infection. The choice should depend on sensitivity testing of an isolate. Post-mortem lesions Right ventricular failure and ascites. Erysipelothrixetc. 56 . Peripheral vessels congested.Treatment None. Epiphysiolysis Introduction A complex condition of chickens that may be associated with trauma. Prevention Good hygiene at turn-around. and /or trauma. Endocarditis Introduction A condition of chickens associated with several bacterial infections such as staphylococci. rickets. Diagnosis Differentiate from broiler ascites syndrome by examination of the interior of the heart. Culture of lesions to confirm the bacterium involved. osteomyelitis. Soluble multivitamins may be recommended as a nonspecific measure. Treatment Medication is only likely to be of value in reducing deterioration in birds that are starting to develop lesions. streptococci.
The natural hosts are wild birds and rodents. Circling. 57 . histology may be helpful in identifying underlying problems such as rickets or 'FHN'. wild birds. Prevention Control of predisposing factors. Horses are also seriously affected. Signs Nervous symptoms. turkeys. partridges. sometimes seen in vivo. Microscopic lesions not pathognomonic. Tremors. Post-mortem lesions No gross lesions. Paralysis. ducks and pigeons having a high morbidity and high mortality. Flaccid neck. Post-mortem lesions Separation of epiphyses at the growth plate. chickens. Diagnosis Gross inspection. VEE) Introduction A viral disease of pheasants. It is transmitted between birds by pecking and by mosquitoes. often occurs or is identified in the processed carcase. These conditions currently only occur from northern South America to North America. Treatment Not applicable. Ataxia. Paresis.Signs Apparent dislocation at extremities of long bones. WEE. Equine Encephalitis (EEE. May also be asymptomatic.
Chronic scabby skin. pheasants. Vaccinate at 5-6 week. Prevention Protection from mosquitoes. rarely in geese. Erysipelas Introduction A sudden onset infection with the bacterium Erysipelothrix insidiosa (E. Signs Inappetance. There is likely to be an increased risk if housing or land has been previously used by pigs or sheep. fishmeal and semen and by cannibalism. Haemorrhages in fat. Endocarditis.Diagnosis Isolation in mice. The bacterium is fairly resistant to environmental effects or disinfectants and may persist in alkaline soil for years. Treatment None. TC. 58 . Liver. ducks. Marked catarrhal enteritis. Joint lesions. May be diarrhoea and respiratory signs. Perineal congestion. Sudden death. It may be transmitted by faecal carriers for 41 days. in soil. COFAL. epicardium. It is also seen in some mammals. kidney. Post-mortem lesions Carcase congestion. especially snood. Swollen snood. control cannibalism. ID by VN. muscle. and CE. Depression. rhusiopathiae) seen in turkeys and increasingly in free-range chickens. spleen swollen. Sleepiness. water.
salmonellosis. and identification. Vaccination or natural infection may cause false positive reactions in the Mycoplasma gallisepticum and M. the demonstration of the organism in stained impression smears from tissues. Diagnosis Lesions. especially caged layers and with a complex set of causes including excessive calories. Treatment Penicillin . Death by internal exsanguination after rupture of haematocyst. 59 . Tetracyclines in feed may also be helpful. Sudden drop in egg production.a combination of the procaine and benzathine salts may be injected. Sudden death. synoviae plate tests for a few weeks. Some birds with pale comb and wattles. history. vaccine at 16-20 weeks if the condition is enzootic. Liver yellow. deficiency and stress. colibacillosis. Differentiate from pasteurellosis. Fatty Liver Haemorrhagic Syndrome Introduction A condition occurring worldwide in chickens. Post-mortem lesions Obesity. greasy and soft with numerous haemorrhages. Headparts pale. and acute Newcastle disease. Signs Overweight typically by 25%. mycotoxins.Diagnosis Isolation on blood agar. Prevention Good biosecurity to prevent spread from other susceptible species. often along with bacterin.
Post-mortem lesions See signs (above). Prevention Feed to avoid obesity. Diagnosis Lesions. avoid mycotoxins and stress. It is very rare in commercial poultry production. Favus Introduction A fungal infection. of chickens and turkeys. 'Honeycomb' skin. isolation. vitamin E. 60 . Thick crusty skin. supplement with choline. culling affected birds. powdery spots and wrinkled crusts and scab on comb and wattles. Loss of condition. Prevention Good hygiene of facilities. Treatment Formalin in petroleum jelly.Treatment Reduce energy intake. Trichophyton gallinae. B 12 and inositol. Signs White. Feather loss.
Use of a wing for support during walking and hip flexion. Predisposing factors include immunosuppresive viruses such as Infectious Bursal Disease Virus and Chicken Anaemia Virus and non-infectious bone pathologies such as hypophosphaetamic rickets. indicated that 0.g. It is seen worldwide and was one of the first infectious 61 . highly contagious disease caused by the bacterium Pasteurella multocida in a range of avian species including chickens. (increasing order of susceptibility). Pasteurellosis Introduction Fowl Cholera is a serious. especially hypophosphataemic.FHN Introduction A condition of chickens and turkeys that may be associated with several different bacterial infections e.Femoral Head Necrosis . Post-mortem studies of birds culled due to lameness and of birds found dead. staphylococci. Post-mortem lesions Degeneration of the epiphyses of long bones with thinning of the cortex and tendency to break when force is applied.75% of all male broilers placed had lesions in the hip bone. Signs Lameness. Careful attention to mineral and Vitamin D nutrition to avoid subclinical. rickets. Diagnosis Base on post-mortem lesions and isolation of a causative organism. spondylolisthesis. FHN is the commonest infectious cause of lameness in broilers in the UK. E. Differentiate from synovitis. 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. and water fowl. coli. Fowl Cholera. Prevention Exclusion of floor eggs and dirty eggs from the hatchery. streptococci. turkeys. arthritis.
streptomycin. and people. isolation (aerobic culture on trypticase soy or blood agar yields colonies up to 3mm in 24 hours . and possibly pigs. but may persist for prolonged periods in soil. Lungs with a consolidated pink 'cooked' appearance in turkeys. Diarrhoea. Purulent pneumonia (especially turkeys). Swollen and cyanotic wattles and face. Post-mortem lesions Sometimes none. The incubation period is usually 5-8 days. Yolk peritonitis. ocular and oral discharge. septicaemic viral and other bacterial diseases. The disease can range from acute septicaemia to chronic and localised infections and the morbidity and mortality may be up to 100%. cats. Coughing. Lameness. by Louis Pasteur in 1880. The route of infection is oral or nasal with transmission via nasal exudate. Sudden death. faeces. 62 . Predisposing factors include high density and concurrent infections such as respiratory viruses. Ruffled feathers. tetracyclines. The bacterium is easily destroyed by environmental factors and disinfectants. Purulent arthritis. equipment. or limited to haemorrhages at few sites. Signs Dejection. Cellulitis of face and wattles. erythromycin.diseases to be recognised. Focal hepatitis. Treatment Sulphonamides. Swollen joints.no growth on McConkey). penicillin. confirmed with biochemical tests. Loss of appetite. The disease often recurs after medication is stopped. Reservoirs of infection may be present in other species such as rodents. Diagnosis Impression smears. Enteritis. Differentiate from Erysipelas. necessitating long-term or periodic medication. contaminated soil. Nasal.
Fowl Pox. It is transmitted by birds. throat and sometimes trachea. and mosquitoes (infected for 6 weeks). Depression.Prevention Biosecurity. The swelling is made up of oedema and purulent exudates (pus). Signs Warty. Morbidity is 1095% and mortality usually low to moderate. good rodent control. spreading eruptions and scabs on comb and wattles. Inappetance. Avian Pox Introduction A relatively slow-spreading viral disease characterised by skin lesions and/or plaques in the pharynx and affecting chickens. The duration of the disease is about 14 days on an individual bird basis. Severe localised Pasteurella infection in the swollen wattle of a 30-week-old male broiler parent chicken. 63 . fomites. hygiene. Figure 19. bacterins at 8 and 12 weeks. Pox. Caseous deposits in mouth. turkeys. pigeons and canaries worldwide. 0-50%. and where there are biting insects. Infection occurs through skin abrasions and bites. It is more common in males because of their tendency to fight and cause skin damage. The virus persists in the environment for months. live oral vaccine at 6 weeks. or by the respiratory route. Poor growth. Poor egg production.
in the diptheritic form. be caseous plaques in mouth. reproduction in susceptible birds. Flocks and individuals still unaffected may be vaccinated. Less commonly there may. check take at 7-10 days post vaccination. signs and post-mortem lesions. Diagnosis A presumptive diagnosis may be made on history.intra-cytoplasmic inclusions (Bollinger bodies) with elementary bodies (Borrel bodies). pharynx. Microscopically . 64 . Differentiate from Trichomoniasis or physical damage to skin. Figure 20. There is good cross-immunity among the different viral strains. If there is evidence of secondary bacterial infection broad-spectrum antibiotics may be of some benefit.Post-mortem lesions Papules progressing to vesicles then pustules and scabs with distribution described above. usually with chicken strain by wing web puncture. Chickens well before production. Turkeys by thigh-stick at 2-3 months. Fowl pox lesions on the wattle of an adult broiler parent chicken. Prevention By vaccination (except canary). trachea and/or nasal cavities. DNA probes. Treatment None. isolation (pocks on CE CAM) with IC inclusions. It is confirmed by IC inclusions in sections/ scrapings.
Immunosuppression is therefore a predisposing factor. Recovery of an abundant growth of causative organism in recently dead birds. sometimes thighs and other parts. Necrotic Dermatitis Introduction A bacterial condition seen in chickens and usually caused byClostridium septicum. Foci in liver. Sudden mortality. especially following congenital Chick Anaemia Virus infection or early Infectious Bursal Disease Virus infection (Gumboro Disease). Swelling and infarction of the liver. rarely Clostridium noyvi / oedematiens.Gangrenous Dermatitis. Gangrenous skin. wings. Treatment Sulphaquinoxaline. usually over wings and breast. The spores of Clostridial bacteria are highly resistant in the environment. Avoid skin trauma and immunosuppression (congenital CAV infection. Prevention Good hygiene and management. early Infectious Bursal Disease Virus infection). It occurs due to invasion of 'normal' wounds by 'normal' bacteria in immunosuppressed birds. wattles. Severe cellulitis especially of thighs. spleen. penicillin or amoxycillin. 65 . Morbidity may be up to 50% and mortality is high. Signs Occasionally dejection. Post-mortem lesions Patches of gangrenous skin with underlying emphysematous and/or sanguinous cellulitis. Diagnosis Clinical signs and/or lesions. occasionally Staphylococcus aureus. Loss of appetite.
Severe gangrenous dermatitis on the upper surface of the wing of a broiler chicken. There is an 18-20 day prepatent period.Figure 21. Signs Gasping.g. a nematode worm parasite of chickens. Post-mortem lesions Tracheitis. levamisole. confirmation of presence of the parasite. Head shaking. Gape Introduction Syngamus trachea. The condition is seen more commonly in poultry on free range where ground may be contaminated by wild birds e. Loss of appetite and condition. Diagnosis Signs and lesions. Treatment Flubendazole in feed. paired parasites up to 2 cm long. slugs and snails acting as transfer hosts but the life cycle may also be direct. and other game and ornamental birds occurring worldwide. Prevention Flubendazole. Dyspnoea. Infection is by the oral route with earthworms. 66 . turkeys. pheasants. by ingestion of embryonated egg or L3. from rookeries. Presence of worms.
Loss in condition and weight. Loss in condition and weight. Worms develop to L3 in eggs and infection is by the oral route direct from environment. routine worming. Treatment Levamisole. Amidostomum anseris. Gizzard worms .Chickens Introduction Cheilospirura. Post-mortem lesions Ulceration. They are more common in free-range birds because of their increased access to intermediate hosts. and Histiocephalus are nematode worm parasites of chickens. weevils. Signs Depression. necrosis and partial sloughing of gizzard lining. affecting geese and ducks. 67 . Cheilospirura and Streptocara are seen worldwide but Histiocephalus is restricted to Europe. Signs Depression. benzimidazoles such as flubendazole. Slow growth. confirmation of presence of the worms.Gizzard worms . Streptocara. Diagnosis Lesions. Adults are 2-4 cm long and usually bright red. beetles etc act as intermediate hosts.Geese Introduction A nematode worm parasite. muscular wall may be sacculated or ruptured. Slow growth. Grasshoppers. Prevention Prevention of access to intermediate hosts.
benzimidazoles. Vertical transmission resulting in congenital infection may occur. The amount of maternal antibody passed from the breeding birds will affect the severity and timing and severity of the condition in the young birds. Swelling and congestion of liver. Post-mortem lesions Pale myocardium. Loss of down. muscular wall may be sacculated or ruptured. Goose Parvovirus (Derzsy's Disease) Introduction Goose Parvovirus is a highly contagious condition of geese and young Muscovy ducks. Losses are negligible in birds over 5 weeks of age. Excessive water intake. Adults are 2-4 cm long and usually bright red.Post-mortem lesions Ulceration. Prevention Rotation of ground on annual basis. Swollen eyelids and eye and nasal discharge. necrosis and partial sloughing of gizzard lining. Derzsy's Disease is caused by a parvovirus distinct from chicken and mammalian parvoviruses. The younger the bird affected the more acute the condition and the higher the mortality. Reduced feed intake. Diagnosis Lesions. Treatment Levamisole. Profuse white diarrhoea. visualisation of worms. 68 . Membrane covering tongue. Reddening of skin. spleen and pancreas. Signs Prostration and death in acutely affected goslings.
liver. Carcase anaemia. Haemorrhagic Anaemia Introduction A complex condition of chickens associated with drug toxicities. heart. muscles. The preferred approach is to immunise breeding birds with an attenuated live vaccine. Loss of appetite. mortality is 5-50%. Blood in droppings. Treatment No specific treatment. Antimicrobials may be of value in reducing the effects of secondary bacterial infections. Pale comb and wattles. Poor growth. Haemorrhagic Disease. Ascites. Post-mortem lesions Haemorrhages in one or more sites: skin. 69 . Administration of immune serum has been shown to be effective but may require two doses (day old and around 3 weeks). Morbidity varies. serosa and mucosae. mycotoxins and viral infections and usually following a course of approximately 3 weeks. Signs Dejection. Aplastic Anaemia. Ideally flocks that have suffered the disease should not be used for breeding as they may become persistent excreters of the infection. Prevention Hatching and brooding geese from different parent flocks together should be avoided. Bone marrow pale with fatty change. Fibrinous pericarditis. Diagnosis Signs and lesions in birds of the appropriate age and species. Fibrinous perihepatitis. Liver yellow.
double-immuno-diffusion of splenic extract. signs. add liver solubles to feed. Elisa . 70 . reticulo-endothelial hyperplasia and intranuclear inclusions. Prevention Avoid causative factors. Diarrhoea. Course 10-21 days. lesions. Diagnosis Typical lesions. The virulence of the virus varies but morbidity may be 100% and mortality 10-60%. The source of virus is unknown but there is easy lateral spread within flocks. Haemorrhagic Enteritis Introduction A viral disease of turkeys. Signs Sudden deaths. Post-mortem lesions Petechiae in various tissues. Blood from vent of moribund birds. reproduction with filtered contents. and weeks in litter. the virus surviving in frozen faeces for months. similar to pheasant Marble Spleen disease. remove sulphonamides. Spleen mottled and enlarged. Drop in feed and water consumption.sero-conversion frequently occurs in absence of clinical disease. Treatment Vitamin K. The route of infection is usually oral.Diagnosis History. Serology: DID. caused by Type II Adenovirus distinct from classical fowl adenovirus and occurring in most turkey-producing areas. May induce immunosupression and precipitate respiratory disease or coccidiosis.spleen shows lymphoid hyperplasia. Intestine distended with blood. Microscopic .
71 . good hygiene and biosecurity. Some are produced in live turkeys. Ducks are relatively resistant to heat stress. Maternal antibody may interfere with vaccination. good management. Disinfect and 3-4 weeks house rest. acclimation. high stocking density. Reduced feed consumption. nicarbazin in feed. In this case a loop of intestine has been opened to show the blood. Prevention All-in/all-out production. oral tetraycline.Treatment Warmth and good management. Heat Stress Introduction A condition seen in chickens. Live vaccines are commonly used in many countries at 4-5 weeks of age. Increased thirst. some in turkey B-lymphoblastoid cell lines. Turkeys dying with haemorrhagic enteritis commonly have the small intestine distended with blood. and turkeys caused by high environmental temperature. Pathogenic strains can depress both B.and T-line lymphocytes for up to 5 weeks following exposure. drinking water temperature and availability. especially associated with high relative humidity and low air speed. Immunity: there is an early age resistance irrespective of maternal antibody status. Predisposing factors include genetics. feather cover. Figure 39. Immunity to the disease is long lasting. Signs Panting. convalescent serum.
Inter-species transmission may occur. Prevention Houses of optimal height and insulation. contains excessive mucus and gas. Diagnosis Temperature records. fomites. Reduced egg production. maximise airflow. Treatment Cool water. Intestine flabby with some bulbous dilation. Inappetance. lesions. Frothy. Hexamitiasis Introduction Hexamita meleagridis (pigeons H. Loss in weight. columbae) is a protozoan parasite of turkeys. Mucoid exudate in nostrils and mouth. chirping. Feeding during cooler hours may be beneficial. In commercial ducks a related parasiteTetratrichomonas can cause poor growth and drops in egg production. feed with a reduced protein:energy ratio. pheasants. Later depression. evaporative coolers. and some game birds. Post-mortem lesions Carcases congested. Reductions in stocking density of meat poultry may be quickly achieved by partial depletion ('thinning'). pattern of losses. Signs Initially birds nervous. if relative humidity is low then wet the roof and fog. carriers. pigeons. signs. It is transmitted by faeces. watery diarrhoea. Legs and wings outstretched. 72 . painted white to reflect heat. Prostration. Terminal coma and convulsions. exclusion of other conditions. Post-mortem lesions Dehydration.
Histamonosis. The effect of antibiotic may be related to the control of secondary bacterial enteritis. Although chickens are relatively resistant to the condition. 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. This condition has high morbidity and mortality in turkeys. if possible. Progressive depression and emaciation. gallinae the parasite is easily destroyed. dimetridazole and ipronidazole have been used in the past. Sulphur-yellow diarrhoea. Diagnosis Lesions. dimetridazole. Inappetance. Prevention Depopulation. Furazolidone. Cyanosis of head. Treatment Tetracycline. presumably introduced with worm eggs. Poor growth. The problem is seen in high-biosecurity facilities. Outwith earth worms orH. 73 . all-in/all-out production. pheasants and game birds that acts together with facultative bacteria to produce the condition of Blackhead. Differentiate from transmissible enteritis. and also. First half of intestine inflamed. histomonosis. paratyphoid. significant disease has been seen in breeding chickens and free-range layers. Caecal tonsils congested. Histomoniasis. It has recently been demonstrated that infection occurs readily via the cloaca when birds are on contaminated litter. increase ambient temperature. Blackhead Introduction Histomonas melagridis is a protozoan parasite of turkeys. and occasionally chickens. and mixing groups of different ages. hygiene. Blood in faeces (chickens). trichomoniasis. Signs Depression. scrapings from fresh material. Within a turkey shed transmission is rapid in spite of the fact that it is difficult to infect birds orally with unprotected parasites. avoid interspecies mixing.
especially in chickens. nifursol) and arsenicals (e. grey or green areas. The disease is readily reproduced by inoculating birds with a bacteria-free filtrate of a liver extract from an affected bird. nitrofurans (e.M. Ulcers. Use of an anti-histomonas product in feed where such products are approved but due care with respect to residue avoidance would be required. Intensive relittering may help reduce the level of infection. Arsenicals are less effective in treatment than they are in prevention. given recent new knowledge on the mechanism of transmission. Liver may have irregular-round depressed lesions.g. 74 . Mortality may reach 60% but more typically 10-30%. It is a condition caused by an adenovirus. Angara Disease Introduction This condition was first identified in broilers in Pakistan in 1987. and only nitarsone is approved in the USA.nitarsone) have been used to treat this important disease of poultry. possibly in combination with an RNA virus and immunosuppression caused by Chick Anaemia Virus or Infectious Bursal Disease. dimetridazole). Diagnosis Lesions.g. Some herbal products based on the essential oils (e. avoid mixing species. however they may not be present in the early stages. Having both chickens and turkeys on the same property is likely to increase the risk of this disease in turkeys.g. Treatment Historically nitro-imidazoles (e. scrapings from fresh material. usually grey in colour. At the time of writing no products of these groups are approved for use in the European Union.Abubakar. Regular worming to help control the intermediate hosts. furazolidone. It affects mainly broilers and broiler parents in rear and has also been seen in pigeons. caseous cores with yellow. Hydropericardium-Hepatitis Syndrome. Prevention Good sanitation.g. concrete floors.Tahir Post-mortem lesions Enlargement of caeca. 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. 'Herban)' have been used with some apparent success though controlled trials and formal approval for this purpose are not recorded.
Signs Sudden increase in mortality. The normal function of the gizzard is to aid in the physical grinding of food materials. Treatment None.5% iodophor solution) appears to be beneficial. Most young commercial poultry consume feeds that have a small particle size. Good water sanitation (e. string etc.g. virology. Impacted gizzards are then found in 'non-starter' type chicks or poults. however if young chicks to do not begin to eat feed properly they often consume litter instead. histopathology. grass. to reduce their particle size to aid digestion. Prevention The condition typically occurs in areas of high poultry density where multi-age operation is traditional. Lethargy. Control of predisposing immunosuppressive diseases may help limit losses. Yellow mucoid droppings. Gizzard activity also acts as a pacemaker of intestinal activity and controls the speed at which food is passed to the small intestine. Impaction and Foreign Bodies of Gizzard Introduction The gizzard or crop may become impacted with litter. Huddling with ruffled feathers. however sometimes free-range poultry consume large stones. Post-mortem lesions Excessive straw-coloured fluid distending the pericardium (up to 10 mls). Grit would not be classed as a foreign body. This condition usually affects only a small number of birds. Older birds ingest grit to facilitate the grinding activity in the gizzard. treatment of drinking water with 0. Formalin-inactivated oil adjuvant vaccines are reported to be highly effective and are used in areas where the condition is endemic. Enlarged. Diagnosis Lesions. and birds of any age can 75 . pale friable liver and kidney.1% of a 2. Congestion of the carcase. Lungs oedematous.
Prevention Good brooding management to encourage early adaptation to the diet and adequate consumption of feed and water. and on opening is found to contain a mass of fibrous material. Reduced weight gain. Sweep floors after maintenance activities to remove nails and other potentially dangerous foreign bodies. This may extend into the proventriculus and on into the duodeunum. Infected birds remain carriers for a few weeks. Nails commonly penetrate the lining of the gizzard. A foreign body may be found in the interior of the gizzard. A number of different sero-types have been isolated from disease outbreaks but they may also be isolated from healthy chickens. This usually happens after maintenance activities have been carred out in the housing. Daily monitoring of the crop-fill is a useful procedure. caused by an adenovirus. often with severe anaemia. Australia. the UK. Obvious non-starters should be culled in this situation.consume nails. Italy. It allows us to confirm the proportion of chicks consuming feed and can give inexperienced poultry keepers feedback on the effectiveness of their brooding management. Signs Reduced feed intake. It has a course of 9. 76 . staples etc. France and Ireland. Diagnosis Lesions. Treatment None effective in young birds. and may penetrate the body wall. Inclusion Body Hepatitis Introduction A disease of chickens characterised by acute mortality. The disease was first described in the USA in 1963 and has also been reported in Canada. Post-mortem lesions The gizzard is more firm than normal and.15 days with a morbidity of 1-10% and a mortality of 1-10%.
for instance due to early IBD challenge or congenital CAV infection. SN for individual sero-types. but on the other hand many field cases show eosinophilic inclusions that do not appear to have adenovirus particles. fatty liver syndrome. chloroform. pH).basophilic intranuclear inclusions. mottled with petechiae and ecchymoses. The virus is generally resistant to disinfectants (ether. Diagnosis A presumptive diagnosis may be made on history and lesions. Signs Depression. vibrionic hepatitis. perhaps because they have lower levels of maternal antibody. Inappetance. Immunosuppression. Treatment None. Blood thin. Differentiate from Chick anaemia syndrome. Curiously. yellow. Microscopically . Formaldehyde and iodides work better. Progeny of high health status breeding flocks appear to be at greater risk. Serology: DID for group antigen. Ruffled feathers. Soluble multivitamins may help with the recovery process. Pallor of comb and wattles. isolation alone does not confirm that they are the cause of a particular problem.Transmission may be vertical or lateral and may involve fomites. Post-mortem lesions Liver swollen. The virus grows well in tissue culture (CEK. CEL). Infectious Bursal Disease. may be important. 77 . Kidneys and bone marrow pale. and high temperatures. Confirmation is made on finding inclusions in the liver. and deficiency of vitamin B12. many different sero-types have been isolated from different cases. sulphonamide intoxication. Since adenoviruses are commonly found in healthy poultry. A form of the disease affecting birds under 3 weeks of age in Australia has been reproduced with serotype 8 adenovirus. Bursa and spleen small.
Diarrhoea. The virus. Tracheal oedema. The cause is a Coronavirus that is antigenically highly variable.Prevention Quarantine and good sanitary precautions. which may survive 4 weeks in premises. gasping. Huddling. Poor ventilation and high density are predisposing factors. E. prior vaccination. Diuresis. Typing by haemagglutination-inhibition is also used. Morbidity may vary 50-100% and mortality 0-25%. 78 . Newcastle disease). IB Introduction This infection. depending on secondary infections. Tracheitis. maternal immunity (young birds). Infection is via the conjunctiva or upper respiratory tract with an incubation period of 18-36 hours. prevention of immunosuppression. heat (56°C for 15 mins). new sero-types continue to emerge. Post-mortem lesions Mild to moderate respiratory tract inflammation. dyspnoea. Airsacculitis. The infection is highly contagious and spreads rapidly by contact. These differences are due to structural differences in the spike proteins (S1 fraction). Wet litter. is sensitive to solvents. coli. Coughing. Dakota. probably the commonest respiratory disease of chickens. 1931). Signs Depression. disinfectants (Formal 1% for 3 mins). Kidneys and bronchi may be swollen and they and the ureters may have urates. was first described in the USA (N. Infectious Bronchitis. About eight sero-groups are recognised by sero-neutralization. fomites or aerosol. the age of the bird. Loss of appetite. Some birds/viral strains can be carriers to 1 year. alkalis. Caseous plugs in bronchi. and complicating infections (Mycoplasma. Its affects vary with: the virulence of the virus.
Signs Sudden death. which may survive 4 weeks in premises. flourescent antibody positive and ciliostasis in tracheal organ culture. Serology: HI. alkalis. Avian Influenza and Laryngotracheitis. fomites or aerosol. heat (56°C for 15 mins). depending on secondary infections. Muscular shivering. vaccinal reactions. Prevention Live vaccines of appropriate sero-type and attenuation. Local immunity is first line of defence. The infection spreads rapidly by contact. Poor ventilation and high density are predisposing factors. 79 . Otherwise as for standard IB. Differentiate from Newcastle disease (lentogenic and mesogenic forms). mycoplasmosis. Treatment Sodium salicylate 1gm/litre (acute phase) where permitted . short duration.v. lesions and serology. The virus. IB . SN (type specific). HA negative.antibiotics to control secondary colibacillosis (q. Some birds/viral strains can be carriers for up to 1 year. Elisa (both group specific). group specific). with typical lesions. Infectious Bronchitis.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%. Humoral immunity appears 10-14 days post vaccination. is sensitive to solvents. Cellmediated immunity may also be important.). DID (poor sensitivity. disinfectants (Formal 1% for 3 mins). possible reactions depending on virulence and particle size.Diagnosis Tentative diagnosis is based on clinical sgns. Maternal immunity provides protection for 2-3 weeks. Infection is via the conjunctiva or upper respiratory tract with an incubation period of 18-36 hours. Definitive diagnosis is based on viral isolation after 3-5 passages in chick embryo.
FA. The virus is moderately resistant and may survive 4 weeks in premises. Elisa (both group specific). typical lesions. Infection is via the conjunctiva or upper respiratory tract. Loss of internal egg quality. sneezing.). SN (type specific). Coughing. group specific). A few birds are carriers up to 49 days post infection. short duration. cell culture (Vero. DID (poor sensitivity. with much antigenic variation. Other lesions of 'classical' IB may be encountered. ciliostatic in tracheal organ culture. fomites or aerosol. Prevention Live vaccines of appropriate sero-type and attenuation. Rales may or may not be present. Poor ventilation and high density are predisposing factors. Signs Drop in egg production (20-50%). CK) only after adaptation Serology: HI. lesions progress to necrosis and scarring of deep pectorals in convalescence.antibiotics to control secondary colibacillosis (q. HA-.Post-mortem lesions Oedema of pectoral muscles and subcutaneously on abdomen. IB Egg-layers Introduction A Coronavirus infection of chickens. 80 . There is rapid spread by contact. Rough shells. possible reactions depending on virulence and particle size. Diagnosis 3-5 passages in CE allantoic cavity. Infectious Bronchitis.v. In layers the ovules may be intensely congested. The condition has a morbidity of 10-100% and mortality of 0-1%. Soft-shelled eggs. Treatment Sodium salicylate 1gm/litre (acute phase) where permitted .
DID. virulence. Maternal immunity provides protection for 2-3 weeks. HA-.v. Diagnosis 3-5 passages in CE. FA. Humoral immunity appears 10-14 days post vaccination. although reactions can occur depending on prior immunity.). Treatment Sodium salicylate 1gm/litre (acute phase) where permitted .Post-mortem lesions Follicles flaccid. Prevention Live vaccines of appropriate sero-type and attenuation. Figure 22. Yolk in peritoneal cavity (non-specific). Serology: HI. particle size (if sprayed) and general health status. Differentiate from Egg Drop Syndrome. Local immunity is the first line of defence. Elisa. EDS76.antibiotics to control secondary colibacillosis (q. Flaccid ovarian follicles in a broiler parent chicken undergoing challenge with Infectious Bronchitis virus. Cell-mediated immunity may also be important. 81 . typical lesions. SN.
The virus is moderately resistant and may survive 4 weeks in premises. Yolk in peritoneal cavity (non-specific). FA. EDS76. Rales may or may not be present. A few birds are carriers up to 49 days post infection. The condition has a morbidity of 10-100% and mortality of 0-1%. Loss of internal egg quality. Poor ventilation and high density are predisposing factors. Infection is via the conjunctiva or upper respiratory tract. Serology: HI. Cell-mediated immunity may also be important. 82 . Signs Drop in egg production (20-50%). Elisa. HA-. DID.Infectious Bronchitis. Post-mortem lesions Follicles flaccid. Prevention Live vaccines of appropriate sero-type and attenuation. typical lesions. Humoral immunity appears 10-14 days post vaccination. IB Egg-layers Introduction A Coronavirus infection of chickens. Rough shells. Diagnosis 3-5 passages in CE. Soft-shelled eggs. particle size (if sprayed) and general health status.v.antibiotics to control secondary colibacillosis (q. virulence. with much antigenic variation. although reactions can occur depending on prior immunity. Coughing. Treatment Sodium salicylate 1gm/litre (acute phase) where permitted . Local immunity is the first line of defence.). There is rapid spread by contact. Differentiate from Egg Drop Syndrome. Maternal immunity provides protection for 2-3 weeks. fomites or aerosol. sneezing. SN.
Gumboro Introduction A viral disease. IBD. Sero-type 1 only.20% but sometimes up to 60%. Morbidity is high with a mortality usually 0. The route of infection is usually oral. There is no vertical transmission. first identified in the USA in 1962. susceptibility to Inclusion Body Hepatitis and gangrenous dermatitis and increased susceptibility to CRD. 83 . The infective agent is a Birnavirus (Birnaviridae). but may be via the conjunctiva or respiratory tract. the damage caused to the immune system interacts with other pathogens to cause significant effects. Signs are most pronounced in birds of 4-6 weeks and White Leghorns are more susceptible than broilers and brown-egg layers. and affected birds excrete large amounts of virus for about 2 weeks post infection. The virus is very resistant. In addition to the direct economic effects of the clinical disease. Generally speaking the earlier the damage occurs the more severe the effects. seen worldwide. (Turkeys and ducks show infection only. especially with sero-type 2). Subclinical infection in young chicks results in: deficient immunological response to Newcastle disease. with an incubation period of 2-3 days. faeces etc. which targets the bursal component of the immune system of chickens. 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. Infectious Bursal Disease. The disease is highly contagious.Figure 22. The age up to which infection can cause serious immunosuppression varies between 14 and 28 days according to the antigen in question. Mealworms and litter mites may harbour the virus for 8 weeks.
5.1% are highly suggestive. 84 . Vent pecking. lesions. (previously SN and DID). subsequent diagnosis of 'immunosuppression diseases' (especially inclusion body hepatitis and gangrenous dermatitis) is highly suggestive. rapidly proceeds to atrophy. Coccidiosis. normal size or reduced in size depending on the stage). Swollen kidneys with urates. Haemorrhagic syndrome. Variants: There have been serious problems with early Gumboro disease in chicks with maternal immunity. weights below 0. Unsteady gait. Subclinical disease . Differentiate clinical disease from: Infectious bronchitis (renal). Other possible causes of early immunosuppression are severe mycotoxicosis and managment problems leading to severe stress. especially in the Delmarva Peninsula in the USA. They are all serotype 1. Tests used are mainly Elisa.4 days. Inappetance. Diarrhoea with urates in mucus. Treatment No specific treatment is available. IBD viruses have been isolated and shown to have significant but not complete cross-protection. especially if present prior to 20 days of age.History. 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. Half-life of maternally derived antibodies is 3. histopathology.3% of bodyweight. Serology: antibodies can be detected as early as 4-7 days after infection and these last for life. Antibiotic medication may be indicated if secondary bacterial infection occurs. Elisa vaccination date prediction < 7 days). Huddling under equipment.A history of chicks with very low levels of maternal antibody (Fewer than 80% positive in the immunodifusion test at day old. Diagnosis Clinical disease . Cryptosporidiosis of the bursa (rare). The normal weight of the bursa in broilers is about 0. Use of a multivitamin supplement and facilitating access to water may help. may have haemorrhages. Post-mortem lesions Oedematous bursa (may be slightly enlarged. Haemorrhages in skeletal muscle (especially on thighs). Dehydration. This may be confirmed by demonstrating severe atrophy of the bursa.Signs Depression.
Immunity after a live vaccine can be poor if maternal antibody was still high at the time of vaccination. especially nasal and sinus mucosae. occasionally pheasants and guinea-fowl. characterised by catarrhal inflammation of the upper respiratory tract. biosecurity measures may be helpful in limiting the spread between sites. Infectious Coryza is caused by the bacterium Haemophilus paragallinarum and is seen in many countries especially in multi-age farms that are never depopulated. resulting in increased culling. and tracing of contacts may indicate sites on which a more rebust vaccination programme is indicated. When outbreaks do occur. sometimes chronic. This bursa is from an acutely affected broiler. the rectum and the vent. vaccination of progeny depending on virulence and age of challenge. 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. including passive protection via breeders. A strong immunity follows field challenge. It is enlarged. It is not egg transmitted. Carriers are important with transmission via exudates and by direct contact.Prevention Vaccination. 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. This shows the anatomical relationship between the bursa. turgid and oedematous. Morbidity is high but mortality low if uncomplicated although it may be up to 20%. Infectious Coryza Introduction A usually acute. 85 . highly infectious disease of chickens. Figure 23.
Purulent ocular and nasal discharge. sulphonamides. drying and disinfectants. Diagnosis A presumptive diagnosis may be made on signs. at least two doses are required. Dyspnoea. Dihydrostreptomycin. Intercurrent respiratory viral and bacterial infections are predisposing factors. Vaccines are used in areas of high incidence. respiratory viruses. while bacterins only protect against homologous strains. Caseous material in conjunctiva/sinus. Live attenutated strains have been used but are more risky. Post-mortem lesions Catarrhal inflammation of nasal passages and sinuses. Signs Facial swelling. Treatment Streptomycin. Eye-lid adherence. tylosin. Differentiate from Mycoplasmosis. lesions. 86 .requires X (Haematin) and V (NAD) factors. identification of the bacteria in a Gram-stained smear from sinus. Prevention Stock coryza-free birds on an all-in/all-out production policy.The bacterium survives 2-3 days outside the bird but is easily killed by heat. Controlled exposure has also been practised. preferably in raised CO 2 such as a candle jar. Drop in egg production of 10-40%. chronic or localised pasteurellosis and vitamin A deficiency. Commercial bacterins may not fully protect against all field strains but reduce the severity of reactions. DID. Sneezing. Birds recovered from challenge of one serotype are resistant to others. Bacterin at intervals if history justifies or if multi-age. Serology: HI. Inappetance. Flouroquinolones are bactericidal and might prevent carriers. erythromycin. Loss in condition. Conjunctivitis. Confirmation is by isolation and identification . Tracheitis. agglutination and IF have all been used but are not routine. Swollen wattles.
87 . IFA. Keep susceptible stock separate from vaccinated or recovered birds. Movement and mixing of stock and reaching point of lay are predisposing factors. All-in/allout operation. Microscopically . Differentiate from Newcastle disease. Prevention Quarantine. 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. pheasants. ILT Introduction A herpesvirus (pathogenicity can vary) infection of chickens. PCR. Diagnosis Signs. Isolation in CE CAMs. Nasal discharge (low pathogenicity strains).Infectious Laryngotracheitis. Post-mortem lesions Severe laryngotracheitis. Transmission between farms can occur by airborne particles or fomites. Apply strict biosecurity in moving equipment or materials between these these categories of stock. Gasping.intranuclear inclusions in tracheal epithelium. peafowl and turkeys with a morbidity of 50-100% and a mortality usually 10-20% but sometimes up to 70%. Recovered and vaccinated birds are long-term carriers. Signs Dyspnoea. Sinusitis. Fairly slow lateral spread occurs in houses. Ocular discharge. vaccination. antibiotics to control secondary bacterial infection if this is marked. severe bronchitis. often with blood in lumen. in severe form may be enough. Drop in egg production. The virus is highly resistant outside host but is susceptible to disinfectants. Treatment None. Coughing of mucus and blood. after 4 weeks of age. lesions. if enzootic or epizootic in an area. histology. caseous plugs may be present. Sera may be examined by VN or Elisa.
worms and other forms of enteritis are predisposing factors. Asia and Africa. it may actually protrude at the vent and be cannibalised. Signs Mainly sudden deaths. 88 . Coccidiosis. Thirst. ducks. The disease has a short course and morbidity and mortality are high. Signs Sudden onset of depression. Rapid breathing. Loss of equilibrium. Anorexia. Survivors may carry infection. Prevention Control of coccidiosis and other causes of intestinal inflammation.Intussusception Introduction A condition of chickens associated with increased intestinal motility. protozoan parasites of turkeys. Simulid flies or culicoid midges are intermediate hosts. usually in the lower small intestine. Different species of this parasite have been reported from North America. Leukocytozoonosis Introduction Caused by Leucocytozoon species. Diagnosis Typical post-mortem lesions Treatment As appropriate for the underlying disease condition. Post-mortem lesions Telescoping of the bowel. guinea fowl. rarely chickens. Careful attention to feeding practices to avoid anticipation of feed arrival if on restricted feeding.
Diagnosis Lesions. Post-mortem lesions Focal tumours. Differentiate from Reticuloendotheliosis. Post-mortem lesions Splenomegaly. Treatment None known. gametes in erythrocytes. schizonts in liver. especially in enlarged spleen. cytology. Signs Depression. Treatment 89 . Microscopically . Loss of weight. Enlargement of abdomen. liver or bursa. disposal of recovered birds. Lymphoproliferative Disease (LPD) Introduction A Type C retrovirus infection of turkeys with low morbidity and high mortality. Persistent low mortality.megaschizonts in brains of birds with nervous signs. Hepatomegaly. Anaemia. age. Anaemia. histology and blood smears. Diagnosis History. Prevention Separation from intermediate hosts. Emaciation. lesions. May be asymptomatic.
(maize-) fed birds (often associated with orange intestinal contents and/or faeces). Pancreatic atrophy/fibrosis and pancreatic atrophy (rather variable). rotavirus etc. 90 . Diarrhoea. Eating faeces. It is suspected that these viruses can be vertically transmitted and the most severe signs in young birds are associated with this. Stunting (temporary). temperature control) may lead to a similar picture in the absence of specific infection. The condition has been seen in Europe. Malabsorption Syndrome.M. Sometimes osteomyelitis and/or rickets. Diarrhoea in older birds may be an effect of on-farm infection. in future eradication. Poor feathering. North and South America and Australia. Post-mortem lesions Enteritis. enterovirus-like particles. Poor management may contribute to the problem. Runting/Stunting Introduction A condition of chickens and turkeys that may be associated with several different viruses. Abnormal feathers ('helicopter wings' 'yellow-heads'). Runting (permanent). for example enteroviruses.Abubakar. Pale shanks in corn. reoviruses. Diagnosis Pathology. control arthropods. Poor early management (feed and water supply. Signs Uneven growth.Tahir None. direct electron microscope examination of intestinal contents. all-in/all-out production. Pot-bellied appearance. Prevention Good hygiene. Treatment Daily cull of affected birds between 14 and 28 days.
fomites. etc. Vertical transmission is not considered to be important.Tumours of feather follicles.poorly digested food enclosed in mucus.Acute infiltration of the CNS and nerves resulting in 'floppy broiler syndrome' and transient paralysis. The route of infection is usually respiratory and the disease is highly contagious being spread by infective feather-follicle dander. good parent nutrition and egg selection and santitation. The virus survives at ambient temperature for a long time (65 weeks) when cell associated 91 . The disease has various manifestations: a) Neurological . Infected birds remain viraemic for life. ovary. muscles. both parasitic and bacterial. and rarely turkeys in close association with chickens. b) Visceral . Mortality in an affected flock typically continues at a moderate or high rate for quite a few weeks. Marek's disease Introduction Marek's disease is a Herpes virus infection of chickens. seen worldwide. Affected birds are more susceptible to other diseases. A sample of the faeces produced is shown at the bottom of the picture . Intestines of a young broiler chick suffering from malabsorption syndrome. avoidance of intercurrent disease and management problems (such as chilling).Tumours in heart. as well as more longstanding paralysis of legs or wings and eye lesions. lungs. From the 1980s and 1990s highly virulent strains have become a problem in North America and Europe. They are distended with poorly digested feed. Figure 24. c) Cutaneous . Morbidity is 10-50% and mortality up to 100%. In 'late' Marek's the mortality can extend to 40 weeks of age.Prevention Good broiler farm hygiene. tests.
deficiency of Ca/Phosphorus/Vitamin D..Chicken Introduction Infection with Mycoplasma gallisepticum is associated with slow onset. kidney. Differentiate from Lymphoid leukosis. Chronic Respiratory Disease . Vision impairment. histopathology. M. vaccination generally with 1500 PFU of HVT at day old (but increasingly by in-ovo application at transfer). Genetics can help by increasing the frequency of the B21 gene that confers increased resistance to Marek's disease challenge. turkeys. Post-mortem lesions Grey-white foci of neoplastic tissue in liver. Prevention Hygiene. Loss of weight. Ducks and geese can 92 . spleen. gonads. Thickening of nerve trunks and loss of striation.lymphoid infiltration is polymorphic. especially at the start of lay. pigeons and other wild birds. Skin around feather follicles raised and roughened. all-in/all-out production. heart. botulism. Mycoplasma gallisepticum infection. Signs Paralysis of legs. chronic respiratory disease in chickens. Grey iris or irregular pupil.and is resistant to some disinfectants (quaternary ammonium and phenol). association with other strains (SB1 Sero-type 2) and Rispen's. age affected. clinical signs. Treatment None. distribution of lesions. and skeletal muscle. Diagnosis History. game birds. Microscopically . resistant strains. It is common practice to use combinations of the different vaccine types in an effort to broaden the protection achieved. deficiency of thiamine. It is inactivated rapidly when frozen and thawed. wings and neck. lung.g.
Spread is slow between houses and pens suggesting that aerosols are not normally a major route of transmission. Reduced hatchability and chick viability. tenosynovitis and salpingitis in chickens. Occasional encephalopathy and abnormal feathers. or by direct contact with birds. though in some countries this infection is now rare in commercial poultry. Signs Coughing. In others it is actually increasing because of more birds in extensive production systems that expose them more to wild birds. Leg problems. In adult birds. and in lyophilised material. Intercurrent infection with respiratory viruses (IB. and inadequate environmental conditions are predisposing factors for clinical disease. In turkeys it is most associated with severe sinusitis (see separate description in the turkey section). coli infection). Inappetance.become infected when held with infected chickens. and to a lesser extent fomites. Diagnosis Lesions. Fomites appear to a significant factor in transmission between farms. exudates. aerosols. Pasteurella spp. Recovered birds remain infected for life. Pericarditis. The infectious agent survives for only a matter of days outwith birds although prolonged survival has been reported in egg yolk and allantoic fluid. airborne dust and feathers. coli. Catarrhal inflammation of nasal passages. Post-mortem lesions Airsacculitis. serology. Survival seems to be improved on hair and feathers. isolation and identification of organism. Occasionally arthritis. ART). trachea and bronchi. virulent E. Stunting. Culture requires inoculation in mycoplasma-free embryos or. though infection rates are high. sinuses. Transmission may be transovarian. The condition occurs worldwide. Suspect colonies may be identified by immuno-flourescence. Poor productivity. Slow growth. morbidity may be minimal and mortality varies. Nasal and ocular discharge. ND. Haemophilus. The route of infection is via the conjunctiva or upper respiratory tract with an incubation period of 6-10 days. subsequent stress may cause recurrence of disease. demonstration of specific DNA (commercial PCR kit available). Perihepatitis (especially with secondary E. more commonly in Mycoplasma Broth followed by plating out on Mycoplasma Agar. 93 .
. therefore M. Recovered birds remain infected for life. Aspergillosis. 94 . generally as a confirmatory test. biosecurity. hatchingeggs and chicks. viral respiratory diseases.Turkeys Introduction A slow onset chronic respiratory disease of turkeys often with severe sinusitis and associated with Mycoplasma gallisepticuminfection. Infectious Sinusitis . Elisa is accepted as the primary screening test in some countries.g.Serology: serum agglutination is the standard screening test. Some inactivated vaccines for other diseases induce 'false positives' in serological testing for 3-8 weeks. M. tetracyclines. Suspect flocks should be re-sampled after 2-3 weeks. Prevention Eradication of this infection has been the central objective of official poultry health programmes in most countries. Transmission may be transovarian. exudates. aerosols. Morbidity is low to moderate and mortality low. and routine serological monitoring. synoviae and M. and fomites.g. tylosin. or by direct contact with birds. suspect reactions are examined further by heat inactivation and/or dilution. The route of infection is via the conjunctiva or upper respiratory tract with an incubation period of 6-10 days. Productivity in challenged and vaccinated birds is not as good as in M. other Mycoplasma infections such as M. Mycoplasma gallisepticum infection. HI may be used. though in many countries this infection is now rare in commercial poultry. subsequent stress may cause recurrence of disease. infection status is important for trade in birds. fluoroquinolones. Treatment Tilmicosin. Differentiate from Infectious Coryza. spiramycin. Effort should be made to reduce dust and secondary infections. meleagridis(turkeys).-free stock. vitamin A deficiency. It is seen worldwide.g. all-in/all-out production. Live attenuated or naturally mild strains are used in some countries and may be helpful in gradually displacing field strains on multi-age sites. These programmes are based on purchase of uninfected chicks. PCR is possible if it is urgent to determine the flock status. In some circumstances preventative medication of known infected flocks may be of benefit.
Post-mortem lesions Swollen infraorbital sinuses. especially Turkey Rhinotracheitis. Slow growth. Leg problems. Stunting. Some inactivated vaccines induce 'false positives' in serological testing. intercurrent viral disease such as Newcastle disease (even lentogenic) and Turkey Rhinotracheitis are predisposing factors. all-in/allout production. Survival seems to be improved on hair and feathers. fluoroquinolones. often with inspissated pus. Stress. Treatment Tilmicosin. HI may also be used. requires inoculation in mycoplasma-free embryos or. of swabs taken from the trachea or lesions. These are based on purchase of uninfected poults. Effort should be made to reduce dust and secondary infections. PCR is possible if it is urgent to determine the flock status. tylosin. tetracyclines. although prolonged survival has been reported in egg yolk and allantoic fluid. Nasal and ocular discharge. In some circumstances preventative medication of known infected flocks may be of benefit. Signs Coughing. Serology: serum agglutination is the standard screening test. spiramycin. and in lyophilised material. Suspect flocks should be re-sampled after 2-3 weeks. Culture. Suspect colonies may be identified by immunofluorescence. more commonly in Mycoplasma Broth followed by plating out on Mycoplasma Agar. Perihepatitis. Inappetance. Pericarditis. Prevention Eradication of this infection has been the central objective of official poultry health programmes in most countries. serology. Swollen sinuses. isolation and identification of organism. demonstration of specific DNA (commercial kit available). Airsacculitis. Differentiate from viral respiratory disease. malnutrition. Diagnosis Lesions. and biosecurity.The infectious agent survives for only a matter of days outwith birds. 95 . suspect reactions are examined further by heat inactivation and/or dilution.
M.i. Infection occurs via the conjunctiva or upper respiratory tract and transmission among poults may be vertical. Mycoplasma iowae infection. Leg lesions can be shown in inoculated birds but do not seem to occur naturally. Treatment As for M.Mycoplasma immitans infection Introduction Infection with Mycoplasma immitans is seen in geese. perhaps because all affected embryos fail to hatch. ducks (France). Introduction Infection with Mycoplasma iowae is seen in turkeys.g.g.g. and partridges (UK). Prevention As for M. and can occur in other poultry and wild bird species. Signs Swollen sinuses. 96 . Reduced hatchability. venereal or horizontal. although DNA homology is only 40%. Signs Embryonic mortality. Diagnosis Shows cross reaction in IFA to M. Post-mortem lesions Sinusitis. some with down abnormality. Post-mortem lesions Stunted embryos with hepatitis and enlarged spleens.
Diagnosis Isolation and identification of the causative organism from dead-in-shell embryos.m. Transmission is venereal in breeders. This can increase hatchability by 510% in this situation. morbidity may be minimal. Crooked necks. In adult birds though infection rates are high. Mortality is low. maintenance of this status by good biosecurity. 97 . though up to 25% of infected birds show lesions at slaughter. M. Mycoplasma meleagridis infection. Pathogenicity is quite variable. Predisposing factors include stress and viral respiratory infections. Infection is via the conjunctiva or upper respiratory tract with an incubation period of 6-10 days.-free stock. Treatment Pressure differential dipping has been used where breeder flocks are infected. Leg problems. Specialised dip tanks are subjected to negative pressure which partially collapses the air cell of the submerged eggs. Antibiotics that have been used are tylosin and enrofloxacin. The infective agent does not survive well outside the bird. When the vacuum is released the eggs draw in antibiotic solution which is subsequently absorbed through the shell membranes. Prevention Eradication of the infection from breeding stock. The organism has also been isolated from raptors. Introduction A disease of turkeys characterised by respiratory and skeletal problems caused by Mycoplasma meleagridis. Infected parents may be asymptomatic.i. Mild respiratory problems. purchase of M. Infected eggs result in widespread distribution of infection and increased risk of further vertical transmission. it occurs in most turkey-producing countries but is now much rarer in commercial stock. For eradication purposes egg injection provides more consistent dosing per egg than does egg dipping. Slow growth. Stunting. Signs Reduced hatchability. with transovarian and then lateral spread in meat animals.
Suspect colonies may be identified by immuno-fluorescence. Survival of the infectious agent outwith the bird is poor but fomite transmission between farms is important. Infected birds do develop some immunity. Vaccines are not normally used. fluoroquinolones. 11-21 days following contact exposure. more commonly in Mycoplasma Broth followed by plating out on Mycoplasma Agar. or lateral via respiratory aerosols and direct contact. Infection rates may be very high. Transmission may be transovarian. Mycoplasma synoviae infection. Spread is generally rapid within and between houses on a farm. These are based on purchase of uninfected poults. Birds infected from their parents seem to be immuno-tolerant and particularly prone themselves to transmit. Infected males are particularly prone to transmit infection and may warrant special attention. M. tetracyclines. serology. Differentiate from Mycoplasma gallisepticum. and biosecurity. Predisposing factors include stress and viral respiratory infections.culture used to confirm. demonstration of specific DNA (commercial kit available). Effort should be made to reduce dust and secondary infections. Mycoplasma synoviae. Treatment Tylosin. Diagnosis Lesions. Prevention Eradication of this infection is also possible using similar techniques as for Mycoplasma gallisepticum. other respiratory viruses. isolation and identification of organism. 98 . Culture requires inoculation in mycoplasma-free embryos or. Serology: SAG used routinely . In some circumstances preventative medication of known infected flocks may be of benefit. Airsacculitis (rarely) seen in adult birds.s. Infection is via the conjunctiva or upper respiratory tract with a long incubation period. spiramycin. It occurs in most poultry-producing countries.Post-mortem lesions Airsacculitis in infected pipped embryos and poults. whilst illness is variable and mortality less than 10%. all-in/all-out production. especially in commercial layer flocks. Infectious Synovitis Introduction Infection with Mycoplasma synoviae may be seen in chickens and turkeys in association with synovitis and/or airsacculitis.
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.
Ruffled feathers. high viscosity diets (often associated with high rye and wheat inclusions in the diet). Intestinal contents may be dark brown with necrotic material.g. Post-mortem lesions Small intestine (usually middle to distal) thickened and distended.Abubakar. Predisposing factors include coccidiosis/coccidiasis. Spores of the causative organism are highly resistant. Probiotics may limit multiplication of bacteria and toxin 102 . turkeys and ducks worldwide. Water medication for 3-5 days and in-feed medication for 5-7 days depending on the severity. usually of the mid. Sudden death in good condition (ducks). high levels of most growth promotors and normal levels of ionophore anticoccidials also help. Infection occurs by faecal-oral transmission.small intestine. 100 ppm). Dark coloured diarrhoea. Reflux of bile-stained liquid in the crop if upper small intestine affected. diet (high protein). phenoxymethyl penicillin. Inappetance. Affected birds tend to be dehydrated and to undergo rapid putrefaction. Intestinal mucosa with diptheritic membrane. caused by Clostridium perfringens and characterised by a fibrino-necrotic enteritis. 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. or Bacitracin in feed (e. usually around 10%. in ducks possibly heavy strains. Prevention Penicillin in feed is preventive. neomycin and erythromycin are used in the USA. amoxycillin). other debilitating diseases. Mortality may be 5-50%. Closed eyes. Treatment Penicillins (e. usually in less than 48 hours.g. contaminated feed and/or water. in drinking water.Tahir Necrotic Enteritis Introduction An acute or chronic enterotoxemia seen in chickens. Signs Depression. Treatment of ducks is not very successful. Immobility.M.
Transmission is via aerosols. fomites. Four manifestations have been identified: ND . Morbidity is usually high and mortality varies 0-100%. 103 . The sample at the bottom of the picture is still focal. birds. visitors and imported psittacines (often asymptomatic). Severe lesions of necrotic enteritis affecting the small intestine of broilers.production. Other species can be infected including mammals occasionally (e.g. It is not usually vertical (but chicks may become infected in hatcheries from contaminated shells). Figure 25. respiratory or reproductive systems. conjunctivitis in man). Signs are typically of disease of the nervous. It is highly virulent for chickens. ND . ND .Mesogenic . Intestinal lesions are absent. Strains can be developed as vaccines. the upper has formed a thick crust of necrotic material. These viruses have sometimes been used as vaccines in previously immunised birds. The virus involved is Paramyxovirus PMV-1. which is of variable pathogenicity. In many countries local regulations or market conditions prevent the routine use of many of these options. less for turkeys and relatively apathogenic in psittacines.sometimes called 'asiatic' or exotic. Higher mortality is seen in velogenic disease in unvaccinated stock.Lentogenic .Mild disease. The condition is rarely diagnosed in ducks but is a possible cause of production drops/fertility problems. pigeons and ducks. Can affect any age. sometimes subclinical.Acute and fatal in chickens of any age causing neurological and some respiratory signs. Affected species include chickens. Newcastle Disease (Paramyxovirus 1) Introduction Paramyxovirus 1 or Newcastle Disease is a highly contagious viral disease affecting poultry of all ages.Mortality and nervous signs in adult. ND .Neurotropic Velogenic .Velogenic Viscerotropic (VVND) . turkeys.
infectious coryza. Differentiate from Infectious bronchitis. EDS-76. formalin and phenol. Nervous signs. intestine. Diarrhoea. Cross-reactions have mainly been with PMV-3. Sudden Death Depression. the infective dose and the degree of immunity from previous exposure or vaccination. Necrotic plaques in proventriculus. Post-mortem lesions Airsacculitis. pneumovirus infection. especially in faeces and can persist in houses (in faeces. avian influenza. haemorrhagic disease.The virus survives for long periods at ambient temperature. Haemorrhage in proventriculus. intoxications. Samples . Inappetance. Paralysis. intracerebral or IV pathogenicity in chicks. However it is quite sensitive to disinfectants. 104 . Severe drop in egg production. Intestinal lesions primarily occur in the viscerotropic form. IFA. middle ear infection/skull osteitis. Treatment None. fumigants and sunlight. encephalomyelitis. post-mortem lesions. acid pH. antibiotics to control secondary bacteria. Dyspnoea. It is confirmed by isolation in CE. Signs Signs are highly variable and will depend on the nature of the infecting virus (see above). Coughing. It is inactivated by temperatures of 56°C for 3 hours or 60°C for 30 min. Diagnosis A presumptive diagnosis may be made on signs. laryngotracheitis. HI with ND serum or DID (less cross reactions). for up to 12 months. dust etc). encephalomalacia.tracheal or cloacal. Moult. Tracheitis. rising titre in serology. caecal tonsil. Twisted neck. HA+. Pathogenicity evaluated by Mean Death Time in embryos. and is ether sensitive.
Prevention Quarantine. Mortality peaks at 3-5 days for birds that fail to eat at all. 105 . however. Morbidity is up to 10% and mortality close to 100%. 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). It is commonest in progeny of young parent flocks (relatively small yolks) or where managers are inexperienced. Use of spray application is recommended but it needs to be applied with care to achieve good protection with minimal reaction. It is common to monitor response to vaccination. Acute viral infections or heavily contaminated drinking water may have a similar effect to bad management in reducing feed intake. and is associated with difficulty maintaining brooding temperature and poor management of feeders and drinkers. Figure 28. Use of Mycoplasma gallisepticum free stock under good management reduces the risk of vaccinal reactions. 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. snicking. which are adequately stored and take into account the local conditions. Elisa is now also used. In some countries it has been customary to provide antibiotics prophylactically during periods of anticipated vaccinal reaction. Vaccination programmes should use vaccines of high potency. biosecurity. Vaccinal reactions may present as conjunctivitis. A typical programme may involve Hitchner B1 vaccine at day old followed by LaSota-type vaccine at 14 days. HI has been used extensively. especially in breeding birds by the use of routine serological monitoring. These tests do not directly evaluate mucosal immunity. Inactivated vaccines have largely replaced the use of live vaccines in lay but they do not prevent local infections. vaccination. all-in/all-out production. 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. and occasionally gasping due to a plug of pus in the lower trachea. The LaSota-type vaccine may even repeated at 35-40 days of age if risk is high.
bile staining of adjacent tissues. Diagnosis Based on post-mortem lesions. Treatment Correction of management problems. Gizzard may be impacted with litter. 106 . or suffer necrosis. any swelling of the muscle tends to cut off the blood supply. soluble multivitamin supplementation may help. Without adequate blood supply the tissue of the muscle begins to die. 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. Prevention Review brooding management. nutrition of young parents. The condition can be reproduced by causing intense exercise of this muscle. Gall bladder distended. good hygiene and biosecurity in brooding areas to minimise early disease challenges. Because it is enclosed in a relatively unyielding membrane.Signs Failure to grow. aspergillosis. Post-mortem lesions Crop empty. 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. Poor development. age of collection and weight of hatching eggs. It has since been seen in turkeys. in broiler parent chickens and also in large broiler chickens in various places. good drinking water hygiene. Most organs normal. Differentiate from omphalitis/ yolk sac infection. It is caused by a reduction in the blood supply to the deep pectoral muscles.
with oedema within it and on its surface. A typical case of the chronic stages deep pectoral myopathy in a broiler chicken. greenish yellow. 107 . It is very difficult to detect affected carcases in standard meat inspection. artificial insemination in breeding turkeys. it may become a healed scar. Treatment Not applicable. Transillumination of the breast may help identify affected carcases and may be worthwhile if the incidence is high. This will normally be due to excessive flapping in association with management activities (e. Prevention Avoidance of physical damage of this muscle. thinning operations in meat birds. Diagnosis Lesions. If inactivated vaccines are administered into the breast muscle it is preferable that they go into the superficial muscle which is better able to cope with swelling. If recent. weighing birds etc). the muscle may be swollen and pale.g. Figure 26. Post-mortem lesions Acute or chronic necrosis of the deep pectoral muscle on one or both sides.Signs None. in particular excessive exercise. and. If the condition is of over 7 days duration the muscle is dry and often shows greenish tinges. and flaking. If of very long duration. The tissue in the centre is dry. It may also start to be enclosed in a fibrous capsule.
ventilation problems. age at infection etc. The organism grows slowly producing tiny colonies on blood agar. Cultures from the trachea of birds showing typical signs are preferred. and E. This was first identified as a new disease syndrome of turkeys in Germany in the early 1990s. tracheitis. Some uncertainty exists about mechanisms of transmission. Bordetella aviuminfection. Post-mortem lesions Airsacculitis. 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. Signs Coughing. Infectious Bronchitis). It had been previously isolated in a number of other countries. A range of sero-types have been identified. preferably as a flock test comparing results before and after the challenge. The severity of its effects depends on the pathogenicity of the particular strain and other risk factors such as viral infections. Within the poultry house it is likely to be by aerosols. It is a Gram-negative pleomorphic organism. severe bronchopneumonia. Diagnosis Clinical signs and lesions. perhaps through survival of the organism on shell surfaces or shell membranes.Ornithobacterium Infection. field challenge with respiratory viruses. Reduced weight gain. Reduced egg production. coli overgrowth may occur. The slow-growing bacterium was named in 1994. ORT Introduction Ornithobacterium Infection is an infection of chickens and turkeys with the bacterium Ornithobacterium rhinotracheale(ORT). There is some evidence that hatcheries may play a role in the epidemiology. The infection is common in chickens and turkeys. Growth is more rapid and consistent in an anaerobic jar. E. Most isolates are oxidase positive and galactosidase positive Serology using Elisa tests has been used. Confirmation is by isolation of the organism. This can cause significant losses through condemnations. Important cofactors may include respiratory viral vaccines (Newcastle disease. coli infections. It commonly exacerbates respiratory disease caused by pneumovirus infections in turkeys. In broiler chickens its main importance seems to be as a cause of airsacculitis in apparently healthy flocks that is only identified at slaughter. sneezing. The range occurring in turkeys is wider than that seen in chickens. 108 . direct contact and drinkers.
Preventative medication with the products listed in the previous section may be beneficial in some circumstances. Hygiene .amoxycillin at 250 ppm in water for 3-7 days or chlortetracycline at 500 ppm for 4-5 days. Initially in Germany most strains were sensitive to amoxycillin. Tilmicosin is also effective at 10-20mg/kg and should be used in the early stages of the disease. this is unlikely to work in turkeys. Routine treatment . Satisfactory disease control depends on good management and biosecurity. Vaccination of breeder flocks to protect progeny has shown benefits in chickens but. Amoxycillin sensitivity remains good. In France and Belgium most strains were sensitive to enrofloxacin.it is very sensitive in vitro to a range of chemicals.Treatment The sensitivity of ORT to antibiotic is highly variable. regulation. Some work has been done on live vaccine in the USA. neomycin and enrofloxacin. ORT is a major problem on multi-age sites. because of the age of slaughter. Some vaccines seem to have difficulty in producing a longlasting serological response to ORT. An inactivated vaccine is licensed for broiler parents in Europe. Severely consolidated lung from an acute ORT infection in 14-week-old turkey growers. though 54% were sensitive to tetracycline. also most are sensitive to tiamulin.there are issues relating to availability. 109 . Similar lesions may be found in Pasteurellosis. chlortetracycline but not to enrofloxacin. cost etc. it requires two doses. Figure 27. The lung is solid and covered by pus/ purulent exudate. In the USA in 1998 all strains were sensitive to penicillins and many other microbials. Prevention This is based on good hygiene. Vaccination . therapy and vaccination.
Birds rest squatting. Signs None. Signs Lameness. Treatment Not applicable .only identified at slaughter. The green discolouration is used to identify carcases that require closer inspection of the other tissues. Gram-variable pleomorphic bacteria have been isolated from affected livers and bones. Birds go off legs. Post-mortem lesions Green discolouration of the liver at slaughter. Predisposing factors include small body size. Drop in production. 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. Osteoporosis. Cage Fatigue Introduction A condition of chickens. Diagnosis Lesions. 110 . high production. Prevention Unknown. Soft-shelled eggs.Osteomyelitis Complex. Enlarged hocks. turkeys and ducks seen worldwide and due to Vitamin D or calcium deficiency. Soft bones and beak.
Drop in egg production. whereas turkeys are more severely affected. Transmission is by wild birds and fomites.Yucaipa Disease Introduction An infection of chickens.Abubakar. depending on the species affected and whether infection is complicated by other factors and diseases. Differentiate from Marek's disease. Beak soft. Paramyxovirus 2 . Treatment Over-correct ration vitamin D. 111 . Diagnosis History. Post-mortem lesions Not characteristic. As birds progressively mobilise skeletal calcium for egg production through lay. skeletal size and mineral content at point of lay are critical. bone ash. Coughing. antioxidants. Wild birds are believed to be especially important. spondylitis. Vertical transmission does not usually occur.Tahir Post-mortem lesions Bones soft and rubbery. signs. turkeys and passerine cage birds with Paramyxovirus PMV-2 results in disease with variable mortality. place on litter. Epiphyses of long bones enlarged.M. Signs Depression. Prevention Supplementation of vitamin D. lesions. Parathyroids enlarged. In chickens it is usually mild. calcium carbonate capsules. proper Ca and P levels and ratio. Beading and fracture of ribs. Inappetance.
including wild bird contact and fomites. biosecurity. Inappetance. Treatment No specific treatment. HI with ND serum or DID (less cross reactions). Signs Depression. antibiotics to control secondary bacteria. Treatment No specific treatment. all-in/all-out production. Vertical transmission does not usually occur. IFA. The infection is transmitted by birds. 112 . haemorrhagic disease. EDS-76. High mortality (cage birds). HA+. occasionally chickens and psittacine cage birds. Drop in egg production (turkeys). laryngotracheitis. antibiotics to control secondary bacteria. Mortality is usually low in poultry. Prevention Quarantine. Differentiate from Infectious bronchitis. Coughing. Diagnosis Isolation in CE. IFA. Paramyxovirus-3 Introduction Paramyxovirus PMV-3 infects turkeys. HI with ND serum or DID (less cross reactions). Post-mortem lesions No specific lesions. Loss of shell pigment Nervous symptoms (psittacines). HA+.Diagnosis Isolation in CE.
Vaccination has been used in turkeys but may not be cost-effective. biosecurity. all-in/all-out production. including wild bird contact and fomites. Mild respiratory signs. Signs Reduction in egg production. A range of 113 .Prevention Quarantine. HI with ND serum or DID (less cross reactions). Vertical transmission does not usually occur. HA+. Post-mortem lesions No specific lesions. Treatment No specific treatment. 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. It is an infectious and transmissible cause of sudden increases in mortality in turkeys between 7 and 28 days of age. A less acute form of the disease appears to produce more of a lingering mortality. antibiotics to control secondary bacteria. Diagnosis Isolation in CE. Paramyxovirus-6 Introduction Paramyxovirus PMV-6 infection of turkeys. In both cases mortality can be high and can be associated with a marked depression in growth. The infection is transmitted by birds. The infection is inapparent in ducks and geese. Prevention Quarantine. Mortality is 0-5%. all-in/all-out production. biosecurity. IFA.
multivitamins and milk replacer products are helpful for nutritional support in the acute phase. Prevention Biosecurity to reduce the introduction of new infections into brooding facilities. Emaciation. Effective terminal disinfection. Wet litter. Good quality diets of a suitable form . Droppings watery. Post-mortem lesions Dehydration. This syndrome is clearly distinguished from typical viral enteritis in young turkeys because of the high mortality and severe growth depression. huddling. Reduced feed consumption and growth. Increasing weakness. Muscle atrophy.mash and poor quality crumbles increase risk. A highly digestible diet with fat at 7. Picking at feed. Pendulous Crop Introduction A complex condition of turkeys and chickens associated with coarse fibrous feed. pale brown. All-in/all-out production. 114 .5-8% will encourage feed intake and recovery. eating litter. Overdistension of crop in young birds because of an interruption in feed supply may predispose. lesions. Treatment A range of antibiotics and arsenicals have been used to control the bacterial component of this condition.viruses have been isolated from affected flocks. Liquid intestinal contents. Diagnosis Signs. Weight loss. Signs Initial hyperactivity and increased vocalisation. Fluoroquinolone antimicrobials appear to be especially effective. Increased water consumption. Caseous cores in bursae (late in the process). To replicate the condition in full it appears to be necessary to include bacteria in the inoculum. seeking heat.
Tetrameres and Cyrnea are nematodes. Lack of muscle tone. Infection is by the oral route on exposure to the intermediate hosts. Prevention Remove predisposing factors. Emaciation in heavily infected young chicks (Tetrameres). Diagnosis Macroscopic examination of lesions. They are found in the mucosa of crop and proventriculus causing mainly inapparent infections. Signs Anaemia. Proventricular Worms Introduction Dispharynx. and thickening of mucosa of proventriculus. identification of worms. lesions. grasshoppers and cockroaches. Diarrhoea. ulceration. Crop contents semi-liquid and foul smelling. if these can be identified. have ulcerations and sometimes mycosis. haemorrhage. including crustaceans. Post-mortem lesions Crop distended with feed. 115 .Signs Enlargement of crop. may be impacted. Diagnosis Signs. spiruroid worm parasites of poultry and game birds. necrosis. Treatment None. Post-mortem lesions Inflammation.
Diarrhoea. Post-mortem lesions Miliary lesions in a variety of organs but especially in the liver.Treatment Not usually required. other poultry. tuberculosis. Ruffled feathers. Prevention Prevention of access to intermediate hosts. adequate protection. colibacillosis. isolation. Signs Weakness. sulphonamides in feed. Diagnosis Lesions. 116 . The disease has a mortality of 5-75%. Sometimes sudden death. duck viral hepatitis. coccidiosis. rodents and man with the bacterium Yersinia pseudotuberculosis. Treatment Tetracyclines. 'hardening off'. Pseudotuberculosis Introduction An infection of ducks. Differentiate from Duck viral enteritis. wild birds. In peracute disease the only lesion may be enteritis. Prevention Good husbandry and hygiene.
Diagnosis History. Treatment Adequate water supply. Kidneys swollen. Differentiate from fowl cholera. vibriosis. It was commonly reported prior to 1960 but is now rare. diet and water supply. Post-mortem lesions Dehydration. hygiene.Abubakar. multivitamins in water. Drop in egg production. 117 . Catarrhal enteritis. elimination of other causes. molasses.M. It is associated with hot weather. IBD and typhoid. mucoid casts in intestine. Avian Monocytosis Introduction A sudden onset condition of chickens early in lay with high morbidity and a mortality of 050%. Pancreas chalky. Signs Depression. Loss of appetite. lesions. toxin and possibly a virus infection. Watery diarrhoea. capillariasis. Bluecomb. Prevention Good management. Skeletal muscle necrosis. coccidiosis. Crop distended. Liver swollen with foci. water deprivation. Crop distension. antibiotics. Affected birds have an increase in circulating monocytes in their blood. Skin cyanosis of head.Tahir Pullet disease. Dehydration. Dark comb and wattles.
organophosphates. Spots on eggs. cracks. Filling of cracks and crevices. vegetable oil and mineralbased products (both liquid sand dusts) have been used to control red mites in the environment. For northern fowl mite it is essential to apply approved insecticides to the affected birds. Treatment Pyrethroids. May cause anaemia and death in young birds. mainly at night and may transmit fowl cholera and other diseases. Post-mortem lesions Anaemia. 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. Prevention Thorough cleaning. in nest boxes. Signs Presence of grey to red mites up to 0. fumigation and insecticide treatment at turnaround. Drop in egg production. the Northern Fowl Mite spends its entire life cycle on the bird and can multiply more rapidly as a result. Ornithonyssus bursae. Diagnosis Number and type of mites identified. and good design of new equipment to limit harbourages for red mites. Staff complaints . Birds restless.itching. which are external parasites of chickens and turkeys. Effective monitoring of mite numbers and implementation of control measures before birds are heavily infested improves control. Dermanyssus gallinae. Pale comb and wattles. Loss of condition.7 mm. feeds by sucking blood. citrus extracts. carbamates. 118 . the Common Red Mite.Red Mite and Northern Fowl Mite Introduction Arachnid mites. crevices etc.
A number of respiratory viruses (Infectious Bronchitis.Abubakar. Avian pneumovirus. 'Mild Respiratory Disease' Introduction An adenovirus infection of chickens with a morbidity of 1-10% and a mortality of 1-10%. chloroform. The virus grows well in tissue culture (CE kidney. The virus is generally resistant to disinfectants (ether. lesions. and by fomites. Post-mortem lesions Mild catarrhal tracheitis.M. and other factors associated with poor ventilation. CE liver).Tahir Respiratory Adenovirus Infection. Treatment None. Respiratory Disease Complex Introduction Respiratory infections in chicken and turkeys are seen worldwide but especially in temperate poultry-producing areas in winter months. coli) may be involved. Transmission may be vertical and lateral. vaccinal and field strains) and bacteria (Ornithobacterium rhinotracheale. E. It may occur as an exacerbating factor in other types of respiratory disease. at least 12 sero-types have been described and these may be isolated from healthy chickens. Infected birds may remain carriers for a few weeks. pH). Prevention Quarantine and good sanitary precautions. Dust. ammonia and other gases. formaldehyde and iodides work better. Diagnosis History. temperature. prevention of immunosuppression. Signs Mild snick and cough without mortality. Opinions vary as to whether adenovirus can be characterised as a primary respiratory pathogen. intranuclear inclusions in liver. may act as 119 . Lentogenic Newcastle disease virus.
and have been cut into to reveal a cheesy (caseous) mass of pus. The air sacs are thickened and congested. Pericarditis. Prevention Effective ventilation. carefully applied appropriate viral vaccines. Rattling noises. Head swelling. sanitation of drinking water. Sneezing. Nasal exudate.10%. mortality 5. Airsacculitis. Figure 29. response to environmental changes. of course. Conjunctivitis. be challenged by some of these pathogens). There is also percarditis evident (at top right). 120 . serology. Severe airsacculitis of thoracic air sacs in a broiler close to slaughter. Diagnosis Lesions. Signs Snick. If condemned birds are included mortality may be more than 10%.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.catarrhal to purulent. Morbidity is typically 10-20%. Differentiate from Chronic Respiratory Disease (Mycoplasmosis). Treatment Antimicrobial treatment of specific bacterial infections. Post-mortem lesions Severe tracheitis with variable exudate .
usually higher in females than males. Treatment None. spleen and kidney. and quail with morbidity up to 25%. Reticuloendotheliosis. 121 . Diarrhoea. Transmission is lateral and possibly transovarian. There is an incubation period of 5-15 days. geese. ducks. A gradual increase in mortality and poor growth in broilers may be the main signs. Leg weakness. Signs There may be no obvious signs. chick inoculation. and the infection can be spread by mosquitoes or in contaminated Marek's disease vaccines. Lympoid Tumour Disease Introduction A retrovirus infection of chickens. Sometimes enteritis and proventriculitis (especially in broilers infected with contaminated Marek's disease vaccine).Figure 30. Post-mortem lesions Neoplastic lesions in liver. Severe tracheitis is broilers with respiratory disease complex. Both tracheas were congested and the upper sample had mucopurulent material in the lumen. turkeys. Diagnosis Pathology. Marked stunting when Marek's disease vaccine is contaminated. Sometimes nodules in intestine and caecae.
lesions. Treatment Over-correct ration with three times vitamin D for 2 weeks. Post-mortem lesions Bones soft and rubbery. Birds rest squatting. Poor growth. Signs Lameness. antioxidants. Birds go off legs. or Vitamin D or 25-hydroxy vitamin D in drinking water. Beading and fracture of ribs. Avoidance of contamination of live vaccines is the main control measure practised. turkeys and ducks worldwide. Hock swelling. Parathyroids enlarged. Growth plates widened and disorganised. Epiphyses of long bones enlarged. Differentiate from Encephalomalacia. Rickets (hypocalcaemic) Introduction Vitamin D deficiency or phosphorus/calcium imbalance is seen in chickens. Diagnosis History. Beak soft.Prevention Formal control programmes have not been documented as the condition is sporadic and relatively self-limiting. proper calcium and phosphorus levels and ratio. 122 . Reduction in bodyweight. Prevention Supplementation of vitamin D. Soft bones and beak. Femoral Head Necrosis. signs.
signs. Prevention Supplementation of Vitamin D. Parathyroids enlarged. Beading and fracture of ribs. lesions (analyse Vitamin A or manganese as a guide to premix inclusion). Poor growth. Post-mortem lesions Bones soft and rubbery. This has led feed manufacturers to try various approaches to reduce added phosphorus in diets.Tahir Rickets (hypophosphataemic) Introduction Phosphorus deficiency in chickens. Signs Lameness. Reduction in bodyweight.Abubakar. Enlarged hocks.M. proper calcium and phosphorus levels and ratio. 123 . Epiphyses of long bones enlarged. Intestinal diseases may reduce absorption. Soft bones and beak. Hock swelling. Birds rest squatting. Some countries have regulations governing the use of phosphorus in fertiliser with a view to reducing water pollution. Growth plates widened and disorganised. Birds go off legs. or vitamin D in drinking water. Beak soft. Even subclinical levels of this condition can predispose to Femoral Head Necrosis. Diagnosis History. antioxidants. Treatment Over-correct ration with 3 times vitamin D for 2 weeks. turkeys and duck is seen worldwide.
electron microscopy or Elisa on intestinal contents .5 g faeces).submit 6 x . columbae in pigeons. Post-mortem lesions Viruses replicate mainly in the mature villous epithelial cells. seen worldwide. large . A. The route of infection is oral usually by direct ingestion of the embryonated egg and there is a 5-10-week prepatent period. and A. The parasite species vary: A. guinea fowl. The route of infection is oral and maximum viral excretion occurs 2-5 days post infection. Roundworm. The life cycle is similar to that illustrated in the section on the caecal worm Heterakis. Prevention Good hygiene in brooding areas. Adult birds can tolerate burdens asymptomatically.Tahir Rotavirus Infection Introduction Rotavirus infection is seen in chickens. Virus may be found in asymptomatic birds. The 124 . stout white worms up to 12 cms in length. except that the adults reside in the small intestine and earthworms are not significant paratenic or transport hosts. It is not known if vertical transmission occurs though virus has been occasionally isolated from embryonated eggs. Treatment No specific treatment for this infection. partridges and pigeons. Use of a good electrolyte solution is beneficial in the acute stage of infection.M. dissimilis in turkeys. pheasants. turkeys. Control of secondary bacterial enteritis may require antimicrobial medication. Diagnosis Demonstration of virus (PAGE. shorter in young birds.Ascaridia Introduction Ascaridia sp.Abubakar. Signs Diarrhoea. are nematode worm parasites. galli in fowl.
especially for young birds. Listlessness. piperazine as locally approved. Signs Loss of condition. pasture rotation and regular treatment. Poor growth. mainly in young birds. oval smooth-shelled nonembryonated eggs in faeces. Diagnosis Macroscopic examination with identification of worms. Treatment Flubendazole. Post-mortem lesions Enteritis.parasites may be transported by grasshoppers and earthworms and are resistant to environmental effects. A collection of mature roundworms (Ascaridia galli) recovered from the small intestine of a layer chicken in rear. Worms up to 12 cm in length in duodenum and ileum. Wasting. In the bottom left quadrant there are also some immature worms. Prevention Prevention of contamination of feeders and drinkers with faeces. levamisole. 125 . Diarrhoea. Figure 31.
sparrows. Broiler chickens have an avascular area of tendon just above the hock that is the usual site of rupture.M. This can cause mortality in birds of any age. parrots. Diagnosis Signs and lesions are obvious. canaries and bullfinches. Salmonella Gallinarum. Histology may be helpful in determining if there is an underlying inflammatory process. Avoidance of physical stresses on the musculoskeletal system through careful handling as well as careful design and layout of equipment. game birds. Ruptures of ligaments and joints are also occasionally seen. The bird may have the hock dropped to the floor. If there is a greenish tinge to the area of swelling it occurred a few days previously.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. Signs Severe lameness. 126 . Salmonella Gallinarum. Chickens are most commonly affected but it also infects turkeys.Abubakar. Infections still occur worldwide in non-commercial poultry but are rare in most commercial systems now. Reoviral or staphylococcal arthritis or tenosynovitis may predispose but many cases have no evidence of an inflammatory response. Broiler parents and brown-shell egg layers are especially susceptible. Prevention Establishment of a steady growth profile. Affected birds should be culled humanely as soon as they are identified. guinea fowls. Treatment None. Fowl Typhoid Introduction Disease caused by one of the two poultry-adapted strains ofSalmonella bacteria.
Tube and rapid plate agglutination tests have been the standard serological tests for many years but have only been validated for chickens. As with other salmonellae. tetracylines. recovered birds are resistant to the effects of infection but may remain carriers. Anaemia. fluoroquinolones. but is susceptible to normal disinfectants. Thirst. Signs Dejection. Reluctance to move. mortality is increased in stressed or immunocompromised flocks and may be up to 100%. clean chicks. Post-mortem lesions Bronzed enlarged liver with small necrotic foci. Enteritis of anterior small intestine. In clinical cases direct plating on Brilliant Green. Differentiate from Pasteurellosis. The route of infection is oral or via the navel/yolk. McConkey and non-selective agar is advisable. LPS-based Elisa assays have been developed but not widely applied commercially. even in adults. Transmission may be transovarian or horizontal by faecal-oral contamination. Engorgement of kidneys and spleen. egg eating etc. and/or congestion. Ruffled feathers. surviving months. potentiated sulponamide. Diagnosis Isolation and identification.Morbidity is 10-100%. Treatment Amoxycillin. Enrichment procedures usually rely on selenite broth followed by plating on selective media. Vaccines for fowl typhoid have been used in some areas. Prevention Biosecurity. Inappetance. 127 . pullorum disease and coli-septicaemia. Yellow diarrhoea. both live (usually based on the Houghton 9R strain) and bacterins. The bacterium is fairly resistant to normal climate.
Occasionally it can cause losses in adult birds. in young broiler chickens. The bacterium is fairly resistant to normal climate. 'Bacillary White Diarrhoea' Introduction Disease caused by one of the two poultry-adapted strains ofSalmonella bacteria. Depression.Figure 32. Similar lesions can be seen in Pullorum Disease and with other causes of septicaemia in young chicks. The liver on the left is normal. the one on the right is slightly enlarged. Salmonella Pullorum. Loud chirping. Vent pasting. Pullorum Disease. Gasping. Morbidity is 10-80%. Lameness. The route of infection is oral or via the navel/yolk. 128 . Transmission may be transovarian or horizontal mainly in young birds and may sometimes be associated with cannibalism. Signs Inappetance. pale and shows focal necrosis. mortality is increased in stressed or immunocompromised flocks and may be up to 100%. ring doves. Salmonella Pullorum. ostriches and peafowl. It affects chickens most commonly. game birds. guinea fowls. but also infects turkeys. usually brown-shell egg layers. Ruffled feathers. sparrows. parrots. this usually only causes mortality in birds up to 3 weeks of age. Bacterial septicaemia caused by Salmonella Gallinarum. surviving months but is susceptible to normal disinfectants. It still occurs worldwide in noncommercial poultry but is now rare in most commercial systems. Closed eyes. White diarrhoea.
Derby. S. Paratyphoid Infections Introduction Salmonellae bacteria other than the species specific sero-typesS. fomites and feed (especially protein supplements but also poorly stored grain). poteniated sulponamide. fluoroquinolones. McConkey and non-selective agar is advisable. Sero-types vary. paracolon. Montevideo. S. Diagnosis Isolation and identification.Post-mortem lesions Grey nodules in lungs. Vaccines are not normally used as they interfere with serological testing and elimination of carriers. Splenomegaly. Anatum. S. Even if these infections do not cause clinical disease. but S. Regardless of the initial source of the infection. S. their presence may be significant with respect to carcase contamination as a potential source of human food poisoning. gizzard wall and heart. Morbidity is 0-90% and mortality is usually low. Enrichment procedures usually rely on selenite broth followed by plating on selective media. Gallinarum. Differentiate from Typhoid. S. They infect chickens. recovered birds are resistant to the effects of infection but may remain carriers. Intestinal or caecal inflammation. Many species are intestinal carriers and infection is spread by faeces. Prevention Eradication from breeder flocks. it may become established on certain farms. As with other salmonellae. Caecal cores. Urate crystals in ureters. are capable of causing enteritis and septicaemia in young birds. in the environment or in rodent populations. chilling and omphalitis Treatment Amoxycillin. other enterobacteria. Newport. liver. tetracylines. Typhimurium (which are considered separately). Certain sero- 129 . Pullorum. Salmonellosis. In clinical cases direct plating on Brilliant Green. The route of infection is oral and transmission may be vertical as a result of shell contamination. Enteritidis andS. Paratyphoid. and also other than S. turkeys and ducks worldwide. Bredeney are among the more common isolates.
Dejection. Cheesy cores in caecae. Temperatures of around 80°C are effective in eliminating low to moderate infection if applied for 1-2 minutes. Dehydration. Signs Signs are generally mild compared to host-specific salmonellae. Senftenberg in hatcheries). but are susceptible to disinfectants that are suitable for the particular contaminated surfaces and conditions. chilling. neomycin. This approach is often used in the heat treatment of feed.g. Closed eyes. Good management. Chemotherapy can prolong carrier status in some circumstances. Focal necrotic intestinal lesions. Vent pasting. S. Treatment Sulphonamides. Rappaport-Vassiliadis) followed by plating on two selective media will greatly increase sensitivity. Enteritis. other bacterial infections and ornithosis (in ducks). fluoroquinolones. or absent. Loss of appetite and thirst. Predisposing factors include nutritional deficiencies.types are prone to remain resident in particular installations (e. Unabsorbed yolk.g. tetracyclines. Pericarditis. Post-mortem lesions In acute disease there may be few lesions. other enterobacteria. especially in dry dusty areas. Diagnosis Isolation and identification. In clinical cases direct plating on Brilliant Green and McConkey agar may be adequate. 130 . The bacteria are often persistent in the environment. applied at sufficient concentrations. Differentiate from Pullorum/Typhoid. Ruffled feathers. Foci in liver. Enrichment media such as buffered peptone followed by selective broth or semi-solid media (e. amoxycillin. Diarrhoea. inadequate water. However this has the potential to reveal the presence of salmonellae that are irrelevant to the clinical problem under investigation.
The prevalence of S. fomites and on eggshells. all-in/all-out production. these bacteria are often specifically cited in zoonosis control legislation. Feed and feed raw material contamination is less common than for other sero-types. especially in dry dusty areas. good feed. 131 . care in avoiding damage to natural flora. chilling. Vertical transmission may be either by shell contamination or internal transovarian contamination of yolk. This approach is often used in the heat treatment of feed.Prevention Uninfected breeders. Salmonella Enteritidis. clean nests. Many infected birds are culled and others are rejected at slaughter. Vaccines are not generally used for this group of infections. because there are differences in the epidemiology as compared to other salmonellae. on the one hand. The bacteria are often persistent in the environment. has become much more common in both poultry and humans since the early 80s. many species are intestinal carriers and infection may be carried by faeces. mills. and. The route of infection is oral. Routine monitoring of breeding flocks. Enteritidis and S. secondly. competitive exclusion. turkeys and ducks cause problems worldwide with morbidity of 0-90% and a low to moderate mortality. elimination of resident infections in hatcheries. hatcheries and feed mills is required for effective control. Typhimurium infections Introduction Salmonella Enteritidis and S. Temperatures of around 80°C are effective in eliminating low to moderate infection if applied for 1-2 minutes. S.Typhimurium has remained relatively stable though the spread of the highly antibiotic-resistant strain DT104 in various farmed species gives some reason for concern. Infections in chickens. breeding and grow-out farms. Predisposing factors include nutritional deficiencies. especially phage type 4. Infection results in a strong immune response manifest by progressive reduction in excretion of the organism and reduced disease and excretion on subsequent challenge. fumigate eggs. but are susceptible to disinfectants that are suitable for the particular contaminated surfaces and conditions.Typhimurium are presented separately from other sero-types of Salmonella because. Salmonellosis. inadequate water and other bacterial infections. These are the predominant sero-types associated with human disease in most countries. applied at sufficient concentrations.
Unabsorbed yolk. Prevention Uninfected breeders. In clinical cases direct plating on Brilliant Green and McConkey agar may be adequate. infection Diagnosis Isolation and identification. Post-mortem lesions In acute disease there may be few lesions. breeding and grow-out farms. Good management. Misshapen ovules in the ovaries in S. Ruffled feathers. Early depletion of infected breeding stock is required in some countries such as those of the European Union. tetracyclines.g. Focal necrotic intestinal lesions. care in avoiding damage to natural flora. mills. Rappaport-Vassiliadis) followed by plating on two selective media will greatly increase sensitivity. Foci in liver. hatcheries and feed mills is required for effective control.Signs Dejection. Lost of appetite and thirst. Differentiate from Pullorum/Typhoid. competitive exclusion. clean nests. Dehydration. other enterobacteria such as E. neomycin. Diarrhoea. all-in/all-out production. Enteritis.Pullorum serum agglutination tests. Stunting in older birds. S. It is possible to detect reactions with specific antigens in agglutination tests but competitive and direct Elisa tests are more commonly used today. Vent pasting. Chemotherapy can prolong carrier status in some circumstances. good feed. Infection 132 . fumigate eggs. Cheesy cores in caecae. Closed eyes. Treatment Sulphonamides. Pericarditis. elimination of resident infections in hatcheries. fluoroquinolones in accordance with the sensitivity. amoxycillin. Perihepatitis.Enteritidiscauses cross-reactions which may be detected with S. Enrichment media such as buffered peptone followed by selective broth or semi-solid media (e. However this has the potential to reveal the presence of salmonellae that are irrelevant to the clinical problem under investigation. Routine monitoring of breeding flocks.E. coli.
Lesions. Some birds may 'lay' a caseous mass of pus (which may be found in a nest or on the egg belt).results in a strong immune response manifest by progressive reduction in excretion of the organism and reduced disease and excretion on subsequent challenge. which normally has many millions of potentially pathogenic bacteria. Death. coliand occasionally Salmonella spp. 133 . Diagnosis Use the signs to select birds for culling and post-mortem investigation. The oviduct is a hollow tube joining the normally sterile environment of the body cavity with the cloaca.). Signs Sporadic loss of lay. or may proceed upwards from the cloaca. Vaccines are increasingly being used for S. Anything that damages the epithelium or disturbs normal oviduct motility is likely to increase the likelihood of salpingitis. Post-mortem lesions Slight to marked distension of oviduct with exudate. leaking urates. Infection may spread downwards from an infected left abdominal air sac. are especially prone to increasing salpingitis. Distended abdomen. Systemic viral infections that cause ovarian regression or damage to the oviduct or cloaca. Peritonitis. Damaged vents. Bacteriology of oviduct. Salpingitis Introduction Salpingitis is an inflammation of the oviduct. both inactivated (bacterins) and attenuated live organisms. May form a multi-layered caseous cast in oviduct or be amorphous. Enteritidis and S. It is a complex condition of chickens and ducks associated with various infections including Mycoplasma and bacteria (especially E. The control of infection in this area is probably achieved by ciliated epithelium that mostly wafts a carpet of mucus towards the cloaca. Typhimurium infection.
Morbidity is 10-20%. immunise effectively against respiratory viral pathogens common in the area. exclusion of other problems. Post-mortem lesions None. Prevention Control any septicaemia earlier in life. possibly associated with tendon injury. 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. Prevention Care in transport of brooded poults. Diagnosis Clinical examination. Shaky Leg Syndrome Introduction A condition of turkeys with a course of often 3-4 weeks. Treatment Multivitamins. 134 . use healthy parent flocks. releasing poults into larger areas and in handling heavier birds. Signs Stand on toes shaking. Shaking or quivering of legs after rising.Treatment Birds with well-developed lesions are unlikely to respond to medication.
typically 7-14day-old. 135 . probably because they are growing faster. Feed intake. and/or carbohydrate absorption are disturbed resulting in a hypoglycaemia. Filtered intestinal contents from affected flocks appear to be capable of reproducing the condition. Avoidance of interruptions in feed supply. This appears to be a multifactorial condition. Diagnosis Pattern of mortality. Prevention Good sanitation of the brooding house. Birds in good condition die after showing neurological signs. 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. suggesting a viral component. Excess fluid in lower small intestine and caecae.Spiking Mortality of Chickens Introduction This is a condition characterised by a sudden increase in mortality in young. Avoidance of physical stress. electrolytes and glucose solution to flock. Males are more susceptible than females. Signs and lesions. Provide multivitamins. Post-mortem lesions Mild enteritis. Orange mucoid droppings. Treatment Leave affected chicks undisturbed. Mortality drops off as sharply as it started. Paralysis. Dehydration. Minimise stress. Death. rapidly growing broiler chickens. Coma. Signs Tremor.
turkey. The bacterium is poorly resistant outside host but may be carried by Argas persicus for 430 days. e. reduced egg production. diarrhoea. Liver enlarged with small haemorrhages. Argas persicus. Prevention Control vectors. grouse and canaries with morbidity and mortality up to 100%. is an intestinal spirochaete that can be associated with inflammation of the large intestine in a broad range of mammals and birds. previously known as Serpulina pilosicoli. Thirst. pheasants. 136 . Mucoid enteritis. isolate in chicken eggs or chicks or poults. and occasionally by infected faeces. and egg soiling in chickens. It has been associated with typhilitis. Spleen mottled with ecchymotic haemorrhages. Necrotic foci. Cyanosis. Diagnosis Haematology. Weakness and progressive paralysis. ducks. Signs Depression. Treatment Various antibiotics including penicillin. Brachyspira pilosicoli. Drops in egg production may be seen in both systemic and intestinal forms Post-mortem lesions Marked splenomegaly.g. geese.Spirochaetosis Introduction The bacterium Borrelia anserina infects chickens. Often diarrhoea with excessive urates. It is transmitted by arthropods. vaccines in some countries.
Abubakar. Treatment None. Figure 33. The sample on the right is normal. legs extended forward. Prevention Selection for satisfactory conformation in primary breeding. with rotation of the body of the vertebra and the pinching of the spinal column that causes paralysis. May walk backwards. 137 . Signs Sitting on hock or rumps.Tahir Spondylolisthesis. Kinky-back Introduction A complex condition of broiler chickens with a morbidity of 1-5% and low mortality associated with rapid growth and possibly having a genetic component. These are cross-sections of the spinal column of 4-5-weekold broilers. Diagnosis Symptoms. That on the left shows the typical lesion of spondylolisthesis. lesions.M. Post-mortem lesions Anterior-posterior rotation of the bodies of the last or penultimate thoracic vertebrae resulting in scoliosis just anterior to the kidney. Use of wings to help in walking.
Staphylococcosis. aureus and seen in chickens and turkeys worldwide. These include good breeder nutrition. Infection is usually by the respiratory route with an incubation period of 2-3 days seen after artificial infection.M. avoidance of excessive hatching egg storage. Morbidity is usually low and mortality 0-15% though affected birds will often be culled on humane grounds. either accidental or induced by interventions such as beak trimming. 138 . Signs Legs splay and chick is unable to stand.Tahir Spraddle Legs or Splay Leg Introduction Occurs in all species in the recent hatchling. Wounds. Prevention All measures that improve chick vitality at hatching are beneficial in reducing this problem.Abubakar. mainly S. Post-mortem lesions Gross lesions are not usually evident. Diagnosis Clinical signs. Staphylococcal Arthritis. Treatment None. The type of chick box liners and the feeding papers used in the brooding house can also influence the occurrence of the condition. Damaged skin due to nutritional deficiencies (such as of biotin) may also be a point of entry. and careful monitoring of incubation conditions. and toe trimming may be a portal of entry with subsequent spread via the bloodstream to the typical sites of lesions. Bumble Foot Introduction Caused by Staphylococcus bacteria.
Signs Ruffled feathers. Prevention Good hygiene in the nest. Treatment Antibiotics. isolation and identification of pathogen. the hatchery and in any intervention or surgery (processing. Streptococcus bovis Septicaemia Introduction An infection of ducks with the bacterium Streptococcus bovis. chronic stress. Post-mortem lesions Tenosynovitis. Salmonella spp. Possibly vaccination against reovirus infection. This condition is a cause of sudden deaths in ducklings of 2-3 weeks of age. Competitive exclusion with a non-pathogenic Staphylococcushas been shown to be effective (no commercial products yet available based on this technology). toe clipping). Swollen above the hock and around the hocks and feet. Predisposing factors include reovirus infection. e. Low mobility. Mycoplasma spp.Transmission occurs in the hatchery and in the general farm environment. and imunosuppression. Some sudden deaths from acute septicaemia if very heavy challenge. This may progress to abscess formation in these areas. low stress and prevention of immunosuppression from any cause will all tend to help. Lameness. Recovered birds may have some immunity but vaccination with staphylococci has not been found to be helpful in preventing the disease to date. synoviae. Differentiate from septicaemia or tenosynovitis due to Colibacillosis. trauma. most commonly in the plantar area of the foot or just above the hock joint. 139 ... Good management. particularly of parent birds. Infected joints may have clear exudate with fibrin clots. and by fomites. especially M. in accordance with sensitivity.g. Diagnosis Lesions.
'Flipover' Introduction A condition of broiler chickens of unknown cause. Post-mortem lesions Intestine filled with feed. isolation. possibly metabolic. Treatment Amoxycillin. extra care in the immediate post-brooding period. Haemorrhages in muscles and kidneys.affected birds respond well to saline injection and will actively seek out salt scattered in the litter. Liver congestion. 140 .). Lung congestion and oedema.Signs Sudden deaths. Sudden Death Syndrome. the ventricles are empty. Splenic hyperplasia. most are found lying on their back. Affected well-grown birds may appear to have died from smothering. Diagnosis History. Livers heavier than those of pen-mates (as a percentage of bodyweight. Leg weakness or incoordination in a few birds. Serum accumulation in lung (may be little if examined shortly after death). Signs Sudden death in convulsion. Post-mortem lesions Beak cyanosis. It can be induced by lactic acidosis and about 70% of birds affected are males. lesions. Prevention Good husbandry and hygiene. The atria of the heart have blood. Sodium deficiency can appear very similar at about the same age .
Diagnosis Identification of the presence of the worms at post-mortem examination. they may not be host specific. 141 . Most have intermediate invertebrate hosts such as beetles or earthworms. Check your local regulations. Signs It is doubtful if any signs are produced under most circumstances. Tapeworms. use of dawn to dusk simulation and avoidance of disturbance. Prevention Lowering carbohydrate intake (change to mash). Treatment Flubendazole is effective at a 60 ppm in diet. Post-mortem lesions Occupy space in intestine and create small lesions at point of attachment. Treatment None possible. feed restriction. low intensity light.Diagnosis Birds found on back with lack of other pathology. lighting programmes. Prevention Control the intermediate hosts. or birds' access to them. however it may not have a zero withdrawal in commercial egg layers. Cestodes Introduction Cestodes are tapeworms that are seen in many species.
It may be associated with rapid growth and have a nutritional factor. Lameness. Prevention Genetic selection using the Lixiscope to identify bone phenotype. chloride levels and acid/base balance. Treatment None. mild lesions may require histology to distinguish from other problems. turkeys and ducks. Mature tapeworms with their heads (scolices) embedded in the intestine. Differentiate from rickets. modifications of calcium and phosphorus ratios. Post-mortem lesions Plug of cartilage in proximal end of tibia. small ovoid lacunae and more matrix than normal.Figure 34. and proximal metatarsus. Lixiscope may identify in vivo as early as 2 weeks of age. in decreasing order of frequency. distal tibia. Vitamin D3 supplementation. Tibial Dyschondroplasia. 142 . TD Introduction A complex condition seen in chickens.a mass of avascular cartilage with transitional chondrocytes. Signs There are usually no signs unless the condition is severe. Microscopically . Swelling and bowing in the region of the knee joints. Diagnosis Gross pathology.
Treatment Elimination of cracks and crevices in the poultry housing. Bluecomb Introduction Some coronaviruses involved in this condition are considered to be bovine coronaviruses (or closely related thereto). with 143 . Post-mortem lesions Anaemia. 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.M. Skin blemishes. and is also found on mammals. Signs Anaemia. spends little time on host. Morbidity is close to 100% and mortality is 5-100%. The infection is seen in turkeys and sometimes pheasants. These parasites are more likely to be a problem of small scale poultry production in the tropics. than in commercial poultry in temperate climates. Prevention As for red mite control. Transmission is lateral with birds and faeces. Transmissible Enteritis. Weakness. Reduced productivity.Abubakar. Diagnosis Identification of the presence of the parasites.Tahir Ticks Introduction Argas persicus is an external parasite of poultry and wild birds. and may also transmit spirochaetosis and Pasteurella infection. Occasionally paralysis from toxins in the tick saliva. Emaciation.
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.
possibly involving fomites. Eggs depigmented and thin-shelled. isolation of ciliostatic agent. Turkey Rhinotracheitis (Adult) Introduction A disease of turkeys caused by the viruses of the Pneumovirus genus. Signs Decreased appetite. Loss of voice. Sudden drop in production that lasts 2-3 weeks. 147 . maternal antibody may protect.live primer followed by inactivated. chlorinate drinking water. Treatment Antibiotics are not very effective. Ocular and nasal discharge. Prevention All-in/all-out production. chlorination of drinking water.30%. Diagnosis Signs. control respiratory stressors.Antibiotics are not very effective. Paramyxoviridae. Serology. vaccination . Prevention All-in/all-out production. Good drinking water hygiene. Rapid transmission occurs laterally. control respiratory stressors. Post-mortem lesions Serous rhinitis and tracheitis. vertical transmission is uncertain. Morbidity is 10-100% and mortality 1.
Turkey Viral Hepatitis Introduction An infection of turkeys caused by an unidentified virus. Signs Decreased appetite. Treatment Antibiotics are not very effective. Morbidity is 10-100% and mortality 1. Sinusitis. Paramyxoviridae. Prevention All-in/all-out production. Dyspnoea. Ocular and nasal discharge. chlorinate drinking water.30%. If there is secondary E. isolation and identification of the ciliostatic virus. vertical transmission is uncertain.M. Post-mortem lesions Serous rhinitis and tracheitis. serology (using an Elisa test to demonstrate rising titre). maternal antibody may protect.Abubakar. Loss of voice. sometimes pus in bronchi. Vaccination at day-old seems to be most effective. Birds remain carriers for up to 16 days. Rapid transmission occurs laterally.Tahir Turkey Rhinotracheitis (in rear) Introduction A disease of turkeys caused by the viruses of the Pneumovirus genus. mortality is 1-25%. Morbidity varies. control respiratory stressors. coli infection then pneumonia. weight gain and feed efficiency. 148 . Transmission may be by direct or indirect contact and possibly vertical. Conjunctivitis. possibly involving fomites. airsacculitis and perihepatitis. Diagnosis Clinical signs. Snick.
Congestion. Gastrocnemius tendon may slip. Focal haemorrhage. Depression and sporadic deaths in birds in good condition. Factors involved may include genetics. lesions pathognomonic. Post-mortem lesions Grey foci (c. with good management many birds recover. Bile staining. Microscopically . Morbidity is 1-20% and mortality is low. 1 mm) coalescing. Grey to pink foci in the pancreas. Post-mortem lesions Linear twisting of growth of long bones. environment and high growth rate. Differentiate from histomonosis. 149 . Prevention Good sanitation and management. Distortion at hock. Signs Lameness. Treatment None.Signs Signs are usually subclinical.no inclusion bodies. nutrition. Valgus/varus. Various angulations of leg. Diagnosis Isolation in CE. Twisted leg Introduction A complex condition seen in chickens and turkeys. bacterial and fungal infections.
Signs Listlessness. Post-mortem lesions Deep ulcers throughout intestine. but mainly ileum and caecae. Drooping wings. lesions. Differentiate from perosis. Treatment None. Watery white faeces (quail). Diagnosis Symptoms. tenella. Ruffled feathers. The condition occurs worldwide. E. greater than 20% is abnormal. Prevention Selection for good conformation in primary breeding. which may coalesce and may be round or lenticular. 150 . highly contagious disease of chickens and quail caused by the bacterium Clostridium colinumand characterised by ulcers of the intestines and caecae. Predisposing factors include Coccidiosis (especially E. Diarrhoea. intertarsal angulation up to 10% is physiological. IBDV and overcrowding. necatrix. Anaemia. The route of infection is oral and transmission is from faeces of sick or carrier birds or via flies. Quail disease Introduction Ulcerative Enteritis is an acute. Peritonitis (if ulcers penetrate). Pale yellow membranes. arthritis and synovitis. Adoption of optimal nutrition and growth patterns for the economic objectives of the production system. Blood in intestine. brunetti). Retracted neck. Changed angulation of tibial condyles. It can start suddenly and cause high mortality: 100% in quail and 10% in chickens. Partially closed eyes. The bacterium resists boiling for 3 minutes. game birds and pigeons may also be affected. Ulcerative Enteritis. Turkeys. and E..
salmonellosis. Diarrhoea. penicillin (50-100 ppm in feed). and disease is precipitated by stress. low level antibiotics as per treatment. Prevention Infection-free birds. Morbidity is low. trichomoniasis. amoxycillin. Response to treatment should occur in 48 to 96 hours. necrotic enteritis. Loss of condition. coccidiosis. Transmission is by faecal contamination. Inappetance. colinum in anaerobic conditions (the agent is often present in pure culture in liver). Tetracyclines. Signs Dejection. possibly probiotics. Confirmation is on absence of other diseases and isolation of Cl. multivitamins. Differentiate from histomonosis ('Blackhead'). Treatment Streptomycin (44 gm/100 litres water). Avian Infectious Hepatitis Introduction An insidious onset disease of chickens caused by Vibrio bacteria. Bacitracin. Treat for coccidiosis if this is a factor. birds remaining carriers for months. all-in/all-out production. Necrotic foci in liver. Figure 35. 151 . Wall of the caecum of a chicken suffering from ulcerative enteritis Vibrionic Hepatitis. Diagnosis A presumptive diagnosis may be made on history and lesions. The infective agent is rather resistant to environment and disinfectants.
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.
Eyelids stuck shut with thick exudate. Differentiate from Infectious coryza. Pale comb and wattles. Microscopically . infectious sinusitis etc. Pustules in mouth and pharynx. Nutritional Roup Introduction Vitamin A deficiency is occasionally seen in chickens and turkeys (insufficient vitamin A during 1-7 weeks of age).squamous metaplasia of epithelia. Poor feathering. feed formulation. Diagnosis Signs. Excessive urates in kidneys and ureters. 155 . Drowsiness.M. antioxidant. Post-mortem lesions Eyelids inflamed and adhered. Prevention Supplementation of diet with vitamin A. As in the case of other nutritional deficiencies. Treatment Vitamin A in drinking water.Tahir Vitamin A Deficiency. good quality raw materials. chronic fowl cholera. Signs Poor growth. Nasal and ocular discharge.Abubakar. classic signs of deficiency are very rare in commercial poultry fed complete diets. lesions.
They act in a broad range of metabolic pathways. including growth in the young animal.M. and egg production in the layer. damage to the intestine or increased demand for some reason may have an effect. The embryo is particularly dependent on having adequate supplies of vitamins deposited in the egg. Diagnosis Signs. exclusion of specific diseases. Most will reduce productivity. because a continuous supply is required. Some deficiencies induce characteristic microscopic effects. However. Vitamin deficiencies are especially prone to cause problems of hatchability. If it is suspected that the vitamin premix may not have been included in the ration (or included at too low a level) it 156 . Signs These may be summarised: Perosis Curled Toe Paralysis Paralysis/'Stargazing' Dermatitis/Scaly Skin Mouth Lesions Conjunctivitis Anaemia Fatty Liver and Kidney Syndrome Poor Feathering Loose feathers Hatchability problems Embryo with clubbed down Thiamine (B1) Riboflavin (B2) Pantothenic acid Pyridoxine (B6) Niacin Folic Acid Cyanocobalmin (B12) Biotin Post-mortem lesions Usually the gross lesions are non-specific.Tahir Vitamin B Deficiencies Introduction The B complex vitamins are water soluble and not stored to any significant extent in the body. response to supplementation. Simple deficiency is now rare as diets are usually well supplemented. See the separate discussion under Chondrodystrophy and Fatty Liver and Kidney Syndrome.Abubakar.
White streaks in muscle. Encephalomalacia and exudative diathesis tends to be seen in young birds of 1-5 weeks of age. Muscular dystrophy is seen more frequently in older and mature birds. Good quality multivitamin solutions are beneficial in the supportive care of a range of problems characterised by reduced feed intake. Encephalomalacia. Haemorrhage. drinking water supplementation with that vitamin is ideal and usually results in a rapid response in birds that are still drinking. Ventral oedema. Staggering. Vitamin E Deficiency. 157 . Green wings. The balance of vitamins present should be similar to the daily nutritional requirement of the stock concerned. occasionally ducklings and other birds. less expensive) to analyse feed for a marker substance such as manganese rather than testing for vitamin levels. seen worldwide. 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. The problem is associated with feed rancidity typically in diets with high fat. Post-mortem lesions Swollen cerebellum with areas of congestion. Treatment If a specific vitamin deficiency is suspected. Uncontrolled movements. characterised by oxidation of various tissues and caused by Vitamin E deficiency. Necrosis. Muscular Dystrophy Introduction A spectrum of diseases of chickens and turkeys. Blood-stained or greenish subcutaneous oedema. Steatitis. Paralysis. Falling over.may be appropriate (faster. Signs Imbalance. Exudative Diathesis.
coli. Omphallitis Introduction A condition seen worldwide in chickens. hatchers or chick boxes. feed rancidity. consistency) that vary according to the bacteria involved. Staphylococci. lesions. Closed eyes. toxicities. Morbidity is 1-10% and mortality is high in affected chicks. and poor hygiene of setters. Differentiate from Encephalomyelitis. antioxidant. Loss of appetite. 'bangers'. Abnormal yolk sac contents (colour. It is seen where there is poor breeder farm nest hygiene. necrotic dermatitis. especially E . use of floor eggs. inadequate hatchery hygiene or poor incubation conditions. Swollen abdomen. 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. 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. Broad-spectrum antibiotics where there are extensive skin lesions. for example poor hygiene of hatching eggs. Post-mortem lesions Enlarged yolk sac with congestion. 158 . Yolk Sac Infection. response to medication. Diarrhoea. Prevention Proper levels of vitamin E. Treatment Vitamin E and/or selenium in feed and/or water. selenium. Pseudomonas.Diagnosis Signs. Disease occurs after an incubation period of 1-3 days.Proteus. Vent pasting. histopathology. good quality raw materials. Signs Dejection. Various bacteria may be involved.
Differentiate from incubation problems resulting in weak chicks. however the prognosis for chicks showing obvious signs is poor.g. There should be routine sanitation monitoring of the hatchery. Multivitamins in the first few days may generally boost ability to fight off mild infections.Diagnosis A presumptive diagnosis is based on the age and typical lesions. most will die before 7 days of age. frequent collection. Confirmation is by isolation and identification of the bacteria involved in the internal lesions. sanitation of eggs. 159 . separate incubation of floor eggs etc. exclusion of severely soiled eggs. clean nests. Treatment Antibiotics in accordance with sensitivity may be beneficial in the acute stages. Prevention Prevention is based on a good programme of hygiene and sanitation from the nest through to the chick box (e.
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