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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.
and also horizontal. feed etc. Unabsorbed yolk sac. from long-term intestinal carriers. Huddling near heat. Foci in lungs. Inappetance. Arizona infection.Prevention Good husbandry and hygiene. renamed Salmonella Arizonae. Congestion of duodenum. Cheesy plugs in intestine or caecum. Erosions of the cartilage of the hock joint in a duck with chronic Riemerella anatipestifer infection. cloudiness in eye. rigid depopulation and disinfection. Nervous signs. Signs Dejection. Figure 40. older birds are asymptomatic carriers. 'hardening off'. rodents. 4 . correct house relative humidity. reptiles. through faecal contamination of environment. Autogenous bacterins sometimes used. adequate protection. Diarrhoea. Post-mortem lesions Enlarged mottled liver. transovarian. sulphonamides in feed. mainly in North America. Vent-pasting. Arizonosis Introduction Caused by the bacterium Arizona hinshawii. Paralysis. and is not present in the UK turkey population. Blindness. Inactivated and attenuated vaccines available in some countries. It affects turkeys. Mortality is 10-50% in young birds. Transmission is vertical.
good nest and hatchery hygiene. coli-septicaemia. Perihepatitis. Thickening of atrioventricular valve. poor ventilation and physiology (oxygen demand. The disease has a complex aetiology and is predisposed by reduced ventilation. high altitude. Dilation of the ventricle. Possibly cyanosis. Lungs and intestines congested. and respiratory disease. methods as per Salmonella spp. spectinomycin. Morbidity is usually 1-5%. Differentiate from Treatment Injection of streptomycin. may be related to type of stock and strain). Diagnosis Isolation and identification. Progressive weakness and abdominal distension. Dyspnoea. 5 . Severe muscle congestion. General venous congestion. Poor development. inject eggs or poults with antibiotics. mortality 1-2% but can be 30% at high altitude. Prevention Eradicate from breeder population. Recumbency. Post-mortem lesions Thickening of right-side myocardium. Ophthalmitis. Pulmonary arterial vasoconstriction appears to be the main mechanism of the condition. Signs Sudden deaths in rapidly developing birds. Formerly in-feed medication with nitrofurans was also used. Salpingitis. fumigation of hatching eggs. salmonellosis. or gentamycin at the hatchery is used in some countries. Pericarditis. monitor sensitivity. Ascites Introduction Associated with inadequate supplies of oxygen. Ascites is a disease of broiler chickens occurring worldwide but especially at high altitude.
Thirst. avoid any genetic tendency. caused by Aspergillus fumigatus. Signs Acute form: Inappetance. etc. It affects chickens. This may offer the ability to identify genetic predisposition. Transmission is by inhalation exposure to an environment with a high spore count. penguins. Absidia etc. Spores are highly resistant to disinfectants. Ascites. especially in young chicks. Spleen small. Aspergillosis Introduction A fungal infectious disease. Microscopic . Drowsiness. Differentiate from broiler Sudden Death Syndrome and bacterial endocarditis. Sometimes the same organism causes eye lesions or chronic lesions in older birds. in which the typical sign is gasping for breath. Vitamin C (500 ppm) has been reported to be of benefit in South America. control respiratory disease. Liver enlargement. turkeys. worldwide. game birds. but may be as high as 12%. Occasionally similar lesions are produced by other species ofAspergillus or even other fungi such as Penicillium. Weakness. Morbidity is usually low. ducks. Silent gasping. there is usually little bird-to-bird transmission. A cardiac specific protein (Troponin T) may be measured in the blood. Prevention Good ventilation (including in incubation and chick transport). The fungus can infect plant material and many species of animals including birds and man. Pericardial effusion. Nervous signs (rare).cartilage nodules increased in lung. Mortality among young affected birds is 5-50%. Rapid breathing. waterfowl. The infection has an incubation period of 2-5 days. Diagnosis Gross pathology is characteristic. 6 . Treatment Improve ventilation.
good quality litter and feed. quail. hygiene. Environmental spraying with effective antifungal antiseptic may help reduce challenge. 'Furry' airsacculitis in aspergillosis of an adult duck. Conjunctivitis/keratitis. Growth occurs in 24-48 hours and colonies are powdery green/blue in appearance. It affects chickens. trachea.M. Prevention Dry. Morbidity 5-60%.Tahir 2 Chronic Forms: Ocular discharge (ocular form only). Epidemic tremors for its effect in young birds. Figure 8. mortality none. Amphotericin B and Nystatin have been used in high-value birds. plaques in peritoneal cavity. may have greenish surface.Abubakar. preferably after digestion in 10% potassium hydroxide. Diagnosis This is usually based on the signs and lesions and microscopic examination for the fungus. The powdery surface is dark green in colour. Post-mortem lesions Yellow to grey nodules or plaques in lungs. air sacs. Treatment Usually none. typically by putting small pieces of affected tissue on Sabouraud agar. The means of transmission is unknown but 7 . Thiabendazole or Nystatin has been used in feed. See Avian Encephalomyelitis. Wasting. Avian Encephalomyelitis Egg Drop Introduction Avian encephalomyelitis virus infection in laying bird causes inapparent infection or drops in egg production. Differentiate from excessive exposure to formalin or vaccinal reactions in day olds and from heat stress in older birds. pheasants and occurs in most poultry-producing countries. Brain lesions may be seen in some birds with nervous signs. turkeys. It may be confirmed by isolation of the fungus.
Vertical transmission is very important. attenuated or not. Ataxia and sitting on hocks. The route of infection is transovarian with an incubation period of 1-7 days. Dull expression. Signs Drop in egg production.The embryo protection test has been used in the past. Differentiate from Infectious Bronchitis. In breeders there may be a drop in hatchability of about 5%. mortality high. Morbidity 5-60% depending on the immune status of the majority of parents. transmission occurs over about 1-2 weeks. lentogenic Newcastle disease. Virus in faeces may survive 4 weeks or more. with an oral infection route. subsequent disease in progeny if breeders. water etc. some lateral. and quail. incubation >10 days. Signs Nervous signs. Avian Encephalomyelitis. Diagnosis History. turkeys. feed. Treatment None. and there is serious disease in the progeny (see next section). small (5-10%) and lasting no more than 2 weeks. rising titre to AE virus. lateral transmission is probably by the oral route. Imbalance. Paralysis. Post-mortem lesions None. pheasants. now Elisa is used more commonly. Immunity is usually long lasting. It has a worldwide distribution.probably by faecal contamination of environment. Predisposed by immunosuppression. EDS76. Virus in faeces may survive 4 weeks or more. 8 . Epidemic Tremors Introduction Avian encephalomyelitis is a viral disease of the central nervous system of chickens. Prevention Vaccination of breeders/layers at 9-15 weeks. Serology .
Prevention Vaccination of breeders at 9-15 weeks. vitamin deficiency (E. Tremor may be inapparent but is accentuated if chicks are held inverted in the hand. The higher the proportion of the chickens dying or showing signs the higher the IVPI. The virus infects chickens. neck and wings. 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. pigeons. Enterococcus hirae infection. The definitive classification of high pathogenicity is an intravenous pathogenicity test (IVPI) in 6-week-old chickens result of greater than 1. and ostriches. Effectively all 9 . Tremor of head. This viral disease can cause exceptionally high mortality. riboflavin). now Elisa is used more commonly. Differentiate from Newcastle disease. This is a test in which the virus is inoculated into susceptible chickens that are then kept under observation. There may be focal white areas in gizzard muscle (inconstant). Marek's disease. its pathogenicity is variable. partridges. The embryo protection test has been used in the past. signs. The cause is a virus. Histopathology is usually diagnostic and IFA. Diagnosis A presumptive diagnosis is based on the history.2 . pheasants. Avian Influenza-Highly Plague Introduction Pathogenic (HPAI). turkeys. EE (especially in pheasant in the Americas). Fowl One of only two 'Class A' diseases of poultry targeted for emergency disease control measures by OIE. the equivalent of the World Health Organisation for animal diseases. toxicities. Orthomyxovirus type A. Brain abscess. A few recovered birds may develop cataracts weeks after infection. In addition official control measures disrupt trade in poultry products from affected areas. A. and lack of significant lesions.nonpurulent diffuse encephalomyelitis with perivascular cuffing. attenuated or not. and isolates are designated sero-type/ species/location/reference number/year/subtype designation(H/N). and/or viral isolation may be carried out if required. Treatment None. Immunity is long lasting. ducks. Microscopic . Post-mortem lesions Gross lesions are mild or absent. quail. especially in turkeys. Mycotic Encephalitis.
Avirulent in one species may be virulent in others. in the years 1983-84. by oxidising agent and by formalin and iodine compounds. Depression. Pasteurella) may increase mortality. in northern Italy. 550%.birds are considered to be at risk of infection. The virus is moderately resistant. The virus replicates mainly in respiratory tissues of chickens and turkeys but in the intestinal tract of clinically normal waterfowl. reduced feed consumption. even with 'low pathogenicity' strains. over 30 days at 0°C. Mexico and. It can result in inapparent infection. A serious outbreak occurred in The Netherlands in 2003 with a few linked cases in Belgium and one in Germany. clothing. 10 . The small number of human deaths associated with HPAI appear to have resulted from direct exposure to infected birds on farm or in markets. Diarrhoea (often green). waterfowl. drinking water. Highly pathogenic avian influenza A (HPAI) viruses of the H5 and H7 HA subtypes have been isolated occasionally from free-living birds. Cyanosis of comb/wattles. conjunctivitis or severe pneumonia. Apathogenic and mildly pathogenic influenza A viruses occur worldwide. Marked loss of appetite. USA. air sacs and conjunctiva. Broken contaminated eggs may infect chicks in the incubator simulating vertical transmission. Italy). from December 1999. by acid pH. and the high mortality that 'low-path' AI can cause in turkeys. equipment. Swollen face. especially faeces. trachea.g. but possibly by the conjunctival or respiratory route and the incubation period is 3-5 days. Signs Sudden death. Pakistan. Because of this. More recently outbreaks have occurred in Australia. Drops in egg production. Avian Influenza is a potential zoonosis. Morbidity is high but mortality usually relatively low. Outbreaks due to HPAI were recorded in the Pennsylvania area. Post-mortem lesions Inflammation of sinuses. OIE and other bodies are currently examining ways to improve control of LPAI. It is inactivated by a temperature of 56°C in 3 hours and 60°Cin 30 min. Nasal and ocular discharge. H5 viruses of low pathogenicity may become highly pathogenic usually after circulating in poultry flocks for a time (Pennsylvania. Cessation of normal flock vocalisation. It can remain viable for long periods in tissues. can survive 4 days in water at 22°C. See current OIE records for up to date information on distribution of HPAI. Coughing. Transmission is by direct contact with secretions from infected birds. Nervous signs such as paralysis. Ovarian regression or haemorrhage. Infections with other pathogens (e. The route of infection is probably oral initially.
infectious laryngotracheitis. Vaccines have been used in recent outbreaks in Mexico and Pakistan. vaccinated birds may remain carriers if exposed to the infection. Differentiate from Newcastle disease. Haemorrhage in proventricular and gizzard mucosae and lymphoid tissue of intestinal tract. To be effective inactivated vaccines must be the right subtype for the particular situation (H5 will not protect against H7 and vice versa). However. but good husbandry. though there is high mortality of affected birds. Minimise contact with wild birds. Turkey lesions tend to be less marked than those of chickens. Vaccination is not normally recommended because. The incubation period is 10-20 weeks. Necrosis of skin of comb and wattles. other respiratory infections. lateral transmission by faecal-oral route (this declines as the bird ages). HA+. Myelocytomatosis Introduction Caused by an avian retrovirus. Morbidity is low. nutrition and antibiotics may reduce losses. Muscles congested. although it may reduce losses initially. DID+. Dehydration. disinfection. cleaning. The agar gel precipitation test is non-group-specific and is used to confirm any positives. controlled marketing of recovered birds. It has occured in Europe. while ducks may be symptomless. bleeding and vaccination needles. Congenitally infected birds tend to remain 11 . etc. with considerable strain-to-strain variation. Subcutaneous oedema of head and neck. Eradication by slaughter is usual in chickens and turkeys. North and South America. Transmission is by congenital infection from antibody-negative females. Treatment None. as with many such tests occasional false positive reactions can occur. Prevention Hygiene. Avian Leukosis (Serotype J). Survivors can be expected to have a high degree of immunity but may harbour virulent virus. all-in/all-out production. correct disposal of carcases. fowl cholera. This condition has until now been seen only in meat-type chickens. NDV-. lesionless carriers of highly pathogenic virus. Commercial Elisa test kits are now available. quarantine. isolation. bacterial sinusitis in ducks. 21-day interval to re-stocking should be followed. Confirmation is by viral isolation in chick embryo. In outbreaks a regime of slaughter. Diagnosis A presumptive diagnosis may be made on history and postmortem lesions.
shed virus and develop tumours. 'Shedders' . lesions. Prevention Checking of antigen in the albumen is a basis for eradication .tumours usually contain well-differentiated myelocytes. Lymphoid Leukosis. Two cell types may be found in the same tumour. Loss of weight. often with tumour foci. Persistent low mortality. Emaciation. Virus survival is poor but sufficient to allow cross contamination in hatcheries and on farm in rear.an Elisa test is aviailable to identify antibody positive birds. preferably on separate hatch days and in separate machines. Differentiate from Marek's disease. Handle clean lines before infected lines. Minimise stress. age.80% produce infected chicks. 12 . ribs.antibody negative. Most characteristically are chalky white tumours in the bone marrow. Post-mortem lesions Liver enlargement. histology. sacral joint. Microscopic . birds with egg antigen will be antibody negative. 'nonshedders' .most but not all. Critical hatchery practices: Separate infected and uninfected lines. Signs Depression. Many are asymptomatic. Enlargement of abdomen. Splenomegaly and enlarged kidneys also occur. particularly of the sternum.only 3% produced infected chicks. Separation in vaccination. Prevent/ reduce cross-infection in hatchery and on farm. ultimately identification of virus by isolation and/or PCR. There is also evidence that it is slightly more sensitive than conventional testing. liver. Treatment None. PCR testing of embryonally infected chicks using DNA testing is uniformly positive for blood and faecal samples. Serology . Diagnosis History.
It affects chickens worldwide with susceptibility varying considerably among different strains and types of stock . Many are asymptomatic. Liver may be very large. In lymphoid leukosis the incubation period is about 4-6 months. Leukosis/Sarkoma Group Introduction Lymphoid Leukosis. then liver. 13 . it may be as short as 6 weeks for some of the other manifestations. Enlargement of abdomen. coligranuloma. Avian Leukosis. Morbidity is low but mortality high. erythroblastosis. kidney etc. Persistent low mortality. spleen. The causative viruses are rapidly inactivated at ambient temperature and on exposure to most disinfectants. Signs Depression. fibrosarcomas. A complex of viral diseases with various manifestations such as lymphoid leukosis.egg layers are generally more susceptible to lymphoid leukosis. initially in the bursa. osteopetrosis. Emaciation.cells lymphoplastic Diagnosis History.Farm practices: Brood and rear lines separately and maintain separate for as long as possible. age. especially in young birds. Avoid migration errors (birds unintentionally moving between pens). Loss of weight. Egg production is somewhat reduced. other tumours. lateral transmission is poor but infection may occur by the faecal-oral route. myxosarcomas. lesions. There may be increased susceptibility to other infectious diseases due to damage to the immune system. Mortality tends to be chronically higher than normal for a prolonged period. Vertical transmission is most important by infection of the egg white in infected breeders (who are long-term carriers). Delay live vaccine challenges. liver or bursa. myeloblastosis (see Sero-type J). Minimise group sizes. cytology. Post-mortem lesions Focal grey to white tumours. Differentiate from Marek's disease. Microscopic .
vertical transmission is uncertain. eradication . It is caused by a pneumovirus of the Paramyxoviridae family.Treatment None. Dyspnoea. Africa. Diffuse lymphoid tumours in an enlarged liver from a mature broiler parent hen. Conjunctivitis. Snick. Figure 9. 14 . Facial and head swelling (though this can occur in other conditions). The incubation period is 5-7 days. As for many infections. guinea fowl and possibly pheasants seen in Europe. Prevention Good hygiene. South America and North America. Avian Rhinotracheitis 'Swollen Head Syndrome' Introduction A viral disease of chickens.checking of antigen in the albumen is a basis for eradication (see Sero-type J for details). turkeys (see separate summary). Loss of voice. first isolated from poults in South Africa in 1978. There is rapid lateral transmission with infection by aerosol through the respiratory route. morbidity is 10-100% and mortality can be 110%. This was a case of Myelocytoma Avian Leukosis (Sero-type J). Ocular and nasal discharge. Signs Decreased appetite. Two subgroups have been identified on the basis of the G-protein sequence: A (original UK isolates) and B (original southern Europe isolates). fomites can be important in moving infection between farms. all-in/all-out production. control arthropods. weight gain and feed efficiency.
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.
18 . Histopathology may also be used but the findings are not specific to this condition. Biotin Deficiency. Post-mortem lesions See signs. Scabs around eyes and beak. Pale livers and kidneys in fatty liver and kidney syndrome. Diagnosis Typical signs and lesions. Thickened skin under foot pad. Reduced feed intake and blood sugar can precipitate fatty liver and kidney syndrome. Allin/all-out production. Prevention Thorough cleaning and disinfection after depletion of an affected flock. 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. Signs Poor growth. webbing between toes. Sudden deaths in fatty liver and kidney syndrome. Viral particles may be demonstrated in bile. 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. Leg weakness. Must be confirmed by laboratory tests. Drinking water which is well chlorinated should be helpful in reducing challenge by this route. in embryos. Good biosecurity. It may be helpful to control other conditions which may be occurring at the same time. Elisa tests have been developed experimentally. Lung congestion Ovarian regression Yolk peritonitis Pale foci and haemorrhages in pancreas. Chondrodystrophy. Treatment No specific treatment known.
Signs Lack of thrift in young birds. Treatment Addition of biotin in feed or water. Drop in egg production. Away from birds adults survive about 4-5 days. Diagnosis Identification of the parasites. Differentiate from pantothenic acid deficiency (skin lesions). Treatment Malathion powders and pyrethroid sprays where approved for bird application. Biting Lice Introduction Various species of lice are common external parasites of poultry worldwide. may be some feather damage and crustiness of skin. Irritation. Parasites on birds. The parasites are 1-6 mm in size and their life cycle takes about 3 weeks. Check flocks regulary for rapidly moving insects at the base of the feathers on the abdomen or around the vent. Lice eggs stuck to feathers. Loss of vent feathers. Scabs around vent. Prevention Supplementation of diets with biotin . Crusty clumps of eggs ('nits') may be visible at the base of feathers. has very low bioavailability. Loss of condition. especially around vent.Diagnosis Signs. bedbugs. They are spread by direct contact between birds and by litter etc. Post-mortem lesions Usually none. lesions. Menocanthus stramineus is the most pathogenic and is said to be capable of causing anaemia in heavy infestations. response to treatment/prevention. 19 . Differentiate from mites.naturally present in many raw materials.
Signs Anaemia in young birds.Prevention Avoid direct contact with wild and backyard poultry. Treatment Treatment is difficult. 20 . season. 5 mm long and found in North and South America that are external parasites of birds and mammals. Prevention Similar measures as for mosquito control. Swarms of flies. especially in autumn and winter and treat if required. Weekly treatments are required. local history. The condition tends to occur near to rapidly flowing streams. Biological control using a strain of Bacillus thuringensis has had some success and is preferable to insecticides. It is usually necessary to treat twice at a 7-10 day interval to fully control the condition. Diagnosis Anaemia. Blackfly Infestation Introduction Grey-black hump-backed flies. Examine for lice regularly. Eggs and larvae survive through the winter to cause new infestations in the following year. although these insects can travel up to 15 miles. Post-mortem lesions Anaemia. as the larvae within eggs are not killed by most products. The flies transmit leucocytozoonosis and also a filarial parasite in ducks. Effective removal of all organic material at flock depletion should be practised in all-in/all-out production systems.
The toxin and bacterial spores are relatively stable and may survive for some time in the environment.Botulism Introduction A condition of chickens. Signs Nervous signs. Morbidity is usually low but mortality is high. Prevention Preventing access to toxin. antibiotics. signs. especially in hot weather. progressive flaccid paralysis of legs. It has also been suggested that poultry carcases lost in litter can be a cause of botulism in cattle grazing land or consuming silage where poultry litter has been spread. supportive treatment if justifiable. Post-mortem lesions Possibly no significant lesions. weakness. mouse toxicology on serum or extract of intestinal contents. wings then neck. Treatment Remove source of toxin. 21 . selenium. suspect food and stagnant ponds. ducks and other waterfowl occurring worldwide and caused by a bacterial toxin produced byClostridium botulinum mainly types A / C. The single most important measure is careful pick-up and removal of all dead birds on a daily basis. is also quite typical. Maggots or putrid ingesta may be found in the crop. turkeys. Affected broilers tend to settle with eyes closed when not disturbed. Toxin may also be produced by the bacteria in the caecum. and toxin-containing material (pond-mud. Diagnosis History. carcases. A soiled beak. maggots) is consumed by the birds. Feathers may be easily pulled (chicken only). because it rests on the litter. then sudden death. Mild enteritis if has been affected for some time. The toxin is produced in decaying animal (usually carcases) and plant waste. This will reduce the risk of botulism both in the poultry and in any grazing animals on land where poultry litter is spread. Differentiate from acute Marek's disease ('Floppy Broiler Syndrome') by histology of the brain.
The meaning of the technical terms relating to parasite life cycle are defined in the glossary. Signs None. nematode parasites of poultry and game birds. and a four-week prepatent period. in chronic cases. Treatment Not usually appropriate. There is an incubation period of 2 weeks for eggs to embryonate. or paratenic hosts with partially developed (L2) larvae. Caecal Worm Introduction Heterakis gallinae. Morbidity may reach more than 50% but the condition is not fatal. Post-mortem lesions Inflammation of sternal bursa along the keel bone which may. the cause of Blackhead. Diagnosis Based on lesions. Signs Swelling over the keel bone with bruising and discolouration. Morbidity is high but it is not associated with mortality. Infection is by the oral route.Breast Blister Introduction A complex condition of chickens and turkeys occurring worldwide associated with trauma. Heterakis gallinaeeggs and larvae are a transport hosts for Histomonas. 22 . leg weakness. bacteria.5 cm in length that occur in the caecum. give way to scar tissue. are small whitish worms with a pointed tail. Prevention Good litter management and handling. Earthworms may be transport hosts for eggs. They are found worldwide. control of leg problems. and infection withStaphylococcus spp. Poor feather cover and caked or wet litter are predisposing factors. up to 1.
Diagnosis Adults can be seen in caecal contents at post-mortem examination. Signs Paralysis. and the embryonated egg. Calcium Tetany Introduction A metabolic disease of chickens. Treatment Flubendazole. Routine anthelmintic treatment. Levamisole. or by an earthworm which is in turn ingested by a chicken. 23 . Prevention Avoiding access to earth and earthworms. an undeveloped egg as found in fresh faeces.Post-mortem lesions Inflammation of caecum. The life cycle ofHeterakis showing the location of adults. The egg may be ingested directly by a chicken. Death from respiratory and cardiac failure. possibly with nodule formation. are effective. especially broiler parents. Figure 11. Predisposing factors include heat stress with reduced feed intake and panting.
and response to treatment. carcase quality and litter quality are better on farms which tend to have Campylobacter-negative stock. 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'. Differentiate from IB 793b. Campylobacter jejuni is the commonest species found in poultry. Active ovary with egg in oviduct. principally in the caecae. Treatment Provide 5 gm of oyster shell per hen on 3 successive days along with vitamin D in drinking water. It may be that management that favours dry litter reduces the risk of infection and/or transmission within the flock. pets and wild animals. are bacteria that commonly infect a broad range of livestock species. There are indications that plantar pododermatitis. 24 . Diagnosis This is made on signs. other acute infections and other causes of sudden death. All campylobacters are delicate organisms that survive for relatively short periods outside the host unless protected by organic material. Campylobacter Infection Introduction Campylobacter spp. The reason for this is unclear. biofilm or engulfed by protozoa. lack of other significant lesions. Infected poultry are a potential reservoir of this zoonosis. Campylobacters are a significant cause of enteritis in man. lesions. There is an annual cycle with increased risk of infection in the summer months in some countries. Prevention Keep pullet flocks on low calcium diet until 5% production hen/day. Congested lungs.Post-mortem lesions Cyanosis. In poultry they tend to multiply in large numbers in the hindgut. managing birds for maximum uniformity.
Prevention In principle. cloacal swabs or composite faeces. phage treatments and competitive exclusion approaches. 25 . Diagnosis Isolation of the organism from caecal contents. sourcing of water from high quality supplies. Key aspects of this include effective sanitation of drinking water.Signs None. Treatment Not required on clinical grounds. Many infections are introduced during thinning or other forms of partial depopulation. housed poultry can be maintained free of Campylobacter infection by consistent application of excellent biosecurity. Research is ongoing on the development of vaccines. Insects and rodents may act as a means of transfer of the infection from the general environment into the poultry buildings. and changing of overalls and boots on entering bird areas. Samples should be tested as quickly as possible after collection. In practice the success of this will also depend upon the degree of environmental contamination by the organism. as well as processing plant technologies to reduce carcase contamination. The organism is sensitive to air so swabs should be collected into transport medium and other samples placed in airtight containers with minimal airspace. For this reason it may be difficult to stop the spread of infection between houses once it becomes established in one house. avoidance of contact with pets and other farmed species. good hand hygiene by stockmen. Post-mortem lesions None.
g. and sometimes other birds and mammals. Poor appetite. The fungus is resistant to many disinfectants. Morbidity and mortality are usually low. Diagnosis Lesions. especially in the crop but sometimes in the proventriculus. proprionic acid. Treatment Nystatin (100 ppm in feed) for 7-10 days. Thrush Introduction A disease of the alimentary tract of chickens. microscopic examination of a digested smear (heat in 10% potassium hydroxide) to demonstrate the hyphal forms of the yeast in the tissues. occasionally proventriculus and intestine. 26 . 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. Ensure good hygiene. or copper sulphate 1gm/2 litre water for 3 days if approved locally. Raised focal lesions may slough into lumen as caseous material. A finely divided powder of copper sulphate (where approved) at 200gm/tonne continually or to 14-16 weeks in replacement pullets. Post-mortem lesions White plaques in mouth. smooth and with a yeasty smell. Prevention Avoid excessive use of antibiotics and other stressors. Candida albicans and the condition is seen worldwide. and associated with gizzard erosion. copper sulphate (1 kg/tonne feed) for 5 days. Diarrhoea. histopathology. oesophagus. Control of Candida through drinking water is sometimes practised with chlorination (e. intestine and cloaca. turkeys. Colonies of this fungus appear as white to ivory colour. The cause is a fungal yeast.Candidiasis. Signs Dejection. possibly confused or masked by signs of the primary disease. sodium or calcium proprionate at 1 kg per tonne continually. Slow growth. characterised by thickening and white plaques on the mucosa. Moniliasis. crop.
complying with local regulations and any relevant codes of practice. post-mortem cannibalism. boredom. Diagnosis Age. feed form (mash takes longer to consume than pellets). Differentiate from bacterial dermatitis. Post-mortem lesions Skin wounding related to particular signs exhibited.Chlorox. face. control ectoparasites. Cannibalism. Feather-pulling. This is economical and effective. and strain of bird. excessive light intensity or variation (e. Beak trimming may be necessary. head. low light level. Morbidity is usually low but mortality is high among affected birds. Take care to provide fresh clean feed and water. high temperatures. Feather pecking Introduction A complex multifactorial behavioural problem of poultry and game birds seen worldwide. tenosynovitis and other diseases affecting mobility. Generalised anaemia. distribution of lesions. nutritional deficiencies. Predisposing factors include overcrowding. Treatment Correct any husbandry problems. Signs Pecking at feet (especially young chicks) and vents (adult layers and turkey poults 812 days old). sodium hypochlorite) at 5 ppm. If so it should be carried out carefully by trained operators. 27 . uncontaminated by fungi. wings. Prevention Proper density and temperature. through shafts of light in the house). It should be repeated periodically. anaemia. Provision of a diet that closely matches the nutritional requirements of the stock concerned. Soluble multivitamins and/ or methionine may be of some benefit in some circumstances.g.
C.Hairworm Infection Introduction Nematode parasitic worms of poultry. Signs Diarrhoea. Infection is by the oral route. Morbidity and mortality are usually low. contorta in the crop and oesophagus. Dejection. The worms are 7-18 mm long. some are transmitted direct from bird to bird. small intestine or caecum. obsignata in the small intestine. Post-mortem lesions Enteritis. Diagnosis This may be by a combination of macroscopic examination. C. Levamisole. about 0. Worm eggs take about 20 days to embryonate with an L1 larvae. Some species have earthworms as intermediate hosts. Hairworms in mucosa of crop. prepatent period about 21-25 days according to species. seiving intestinal contents. effective cleaning of houses. Differentiate from other causes of enteritis. 28 . or characteristic worm eggs in faeces in patent infections. Treatment Coumphos has been licensed in some markets.Capillariasis .other approved benzimidazoles can be expected also to have activity.05 mm wide and hair-like in appearance. Worm eggs in the environment are resistant. Prevention Separation of birds from possible transport and intermediate hosts. game birds and pigeons ofCapillaria species. Fenbendazole has been shown to have high efficacy . Wasting Poor growth.
Careful flock management with a view to reducing toe wounds has the greatest impact in controlling cellulitis. It typically occurs between skin and muscles and between muscles and may be an incidental finding in a range of conditions. which can replicate in the tissues. Many meat inspectors become skilled at detecting subtle differences in skin colour in the affected birds. Many affected birds have no other lesions and are reasonably well grown. skin wounds by particular strains of E. 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. Post-mortem lesions Typically it presents as exudate ranging from liquid and pale cream pus to yellowish solid plaques of caseous material under the skin of the abdomen and/or in the leg. Treatment Treatment would not be possible if the problem is identified at a final depletion. but the affected birds are not readily detectable prior to slaughter. The condition is caused by infection of. particularly broiler chickens. though most of the birds showing toe scrapes will not go on to develop cellulitis. In the USA it is called 'Inflammatory Process'. Prevention Toe scrapes at 15-25 days of age when feather cover is poor are the most likely predisposing factors. Diagnosis Typical lesions. coli. Routine monitoring of skin damage at about 25 days of age may be helpful in fostering good practices.Cellulitis Introduction Cellulitis is literally an inflammation of connective tissues. Signs Affected flocks tend to have poorer than average productivity and uniformity. 29 . However its main importance is as a cause of condemnation in meat poultry. often minor.
chloroform. Gumboro. Sudden rise in mortality (usually at 13-16 days of age). Hypochlorite appears most effective in vitro. Pale birds. The virus is resistant to pH 2. may be beneficial.) or poor management (e.g. Discoloured liver and kidney. lateral transmission may result in poor productivity in broilers. poor litter quality). 30 . Prior to confirmation that it is in fact a virus it was known as Chicken Anaemia Agent or CAA. heat (70°C for 1 hour. Signs Poor growth. Diagnosis Gross lesions. virus may be isolated in lymphoblastoid cell line (MDCC-MSB1). PCV of 5-15% (normal 27-36%). Inclusion body heptatitis etc. Mortality is typically 5-10% but may be up to 60% if there are predisposing factors present such as intercurrent disease (Aspergillosis. Acute mycotic pneumonia.Chicken Anaemia Introduction A viral disease of chickens caused by Chicken Anaemia Virus or CAV. Gangrenous dermatitis on feet. 80°C for 5 minutes) and many disinfectants even for 2 hours at 37°C. demonstration of ongoing sero-conversion in parent flock. Treatment Good hygiene and management. Atrophy of thymus and bursa. If gangrenous dermatitis is a problem then periodic medication may be required. Transmission is usually vertical during sero-conversion of a flock in lay. No clinical signs or effect on egg production or fertility in parent flock during seroconversion. Post-mortem lesions Pale bone marrow. legs wings or neck. and control of other diseases as appropriate. ether.
other infections may be predisposing factors. mortality 5-40%. pigeons. 15 weeks. Their use may be restricted to those flocks that have not sero-converted by. and may be detected by SN. It is transmitted by contact. Fibrinous pericarditis. man. rarely chickens. their degree of attenuation is variable.Prevention Live vaccines are available for parents. faecal dust and wild bird carriers. Depression. Greenish-yellow diarrhoea. say. 31 . psittacines. Immunity: there is a good response to field challenge (in birds over 4 weeks of age) and to attenuated live vaccines. Signs Respiratory signs. Chlamydiosis. but occurring probably worldwide. Intercurrent salmonellosis and. It is a 'Scheduled Disease' rarely diagnosed in UK. Production drops in naive laying flocks Post-mortem lesions Vascular congestion. especially pigeons and robins. Serology: antibodies develop 3-6 weeks after infection. Conjunctivitis. Iodophores and formaldehyde are effective disinfecting agents. Elisa. Psittacosis. a bacterium of highly variable pathogenicity. They should be used at least 6 weeks prior to collecting eggs for incubation. Elementary bodies are highly resistant and can survive in dried faeces for many months. Egg transmission does not occur. phenolics are less so. Occasional transient ataxia in pigeons. Weight loss. ducks. perhaps. Airsacculitis. Morbidity is 50-80%. Inappetance. caused by Chlamydia psittaci. Nasal discharge. Wasting. or IFA. Weakness. Ornithosis Introduction An infection of turkeys.
32 . either singly or in combination (although deficiencies of pyridoxine. niacin may also be involved). Live and inactivated vaccines are protective although the former result in carriers and the latter require several applications. IFA). Slipped Tendon or Perosis Introduction Caused by deficiency of manganese. Malposition of leg distal to hock. signs. shortened bones. zinc. folic acid. Congested lungs and air sacs in the turkey. Fibrinous pneumonia. Duck septicaemia. Intracytoplasmic inclusions are helpful but confirmation requires demonstration of causal organisms (Giemsa stain. This condition is seen in chickens. In embryos parrot beak. Necrotic foci in liver. Prevention Biosecurity. Spleen enlarged and congested. Perihepatitis. biotin. lesions. Lameness. choline. Signs Short legs. exclusion of wild birds. Slipping of Achilles tendon (or perosis). Elisa and gel diffusion. Serology: complement fixation. may rupture in pigeons. Differentiate from Duck viral hepatitis. Treatment Tetracycline (200-800 ppm in feed for 3-4 weeks) and/or quinolone medication and supervised slaughter. ducks and turkeys. Distortion of hock. In turkeys it may be an inherited deficiency of galactosamine. Diagnosis History. Chondrodystrophy.
Coccidiosis of Turkeys Introduction Infection of turkeys with Eimeria spp. E. Treatment For flock proceed as for prevention. ruptured ligaments. 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. Differentiate from twisted leg. rickets. no value to affected bird. Five species of Eimeria have been identified that cause lesions in turkeys. analysis of feed. choline. Prevention Addition of manganese. gallopavonis and E. of which two are associated with significant disease effects. infectious synovitis. Diagnosis Lesions. E. Tibia and metatarsus bowed. Lateral slipping of tendon. meleagrimitis affects the upper small intestine. while E. correct mineral balance. dispersa is found in the small intestine. This disease is not very common in commercially reared turkeys though most turkey growers receive preventative medication for at least part of their lives. infectious arthritis. Depression. Shallow trochlea. while E. The contents may be haemorrhagic or be watery with white material shed from the mucosa. ruffled feathers. Tucked appearance. Weight loss. adenoides affects the caecae and rectum. Signs Huddling. Post-mortem lesions The affected area of intestine shows thickening of the wall and dilation. vitamins. 33 .Post-mortem lesions Shortening and thickening of long bones.
Prevention The ionophore coccidiostats lasalocid and monensin are routinely used in turkey growers. lesions. Sulphonamides (e. Dosage levels of ionophores may be critical to efficacy and safety. microscopic exam of scrapings (oocysts. Exposure of previously unmedicated birds to these compounds can cause toxicity. Avoid use of tiamulin in ionophore treated birds. show some spotty congestion and have abnormal contents due to the sloughed epithelium. 34 . Treatment Toltrazuril. meleagrimitis. gamonts). Figure 37. adenoides. Salinomycin is toxic for turkeys even at very low doses.Diagnosis Signs. The exudate can range from semi-liquid to solid white cores. Figure 38.g. Turkey caecal coccidiosis caused by E. Amprolium. Diclazuril is also used for this purpose. Turkey coccidiosis of the upper small intestine caused by E. The intestines are dilated. Differentiate from necrotic enteritis. typically to 12 weeks of age. Sulphaquinoxaline).
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. Diagnosis Signs. Morbidity is 10-40% and mortality up to 50%. hygiene. Vitamins A and K in feed or water. 35 . E. lesions. Amprolium. Recovered birds have good immunity to the same parasite. Vaccines are used mainly in breeders but increasingly in broilers. It is caused by Eimeria tenella and results in lesions in the caecum of chickens worldwide. Treatment Toltrazuril. Production less affected than in some of the other forms of coccidiosis. Caecal. ecchymoses. blood in faeces. Differentiate from ulcerative enteritis. of caecal mucosa.Coccidiosis. Diarrhoea. tenella is more common when 'straight' ionophore programmes are used. Signs Depression. Transmission as for E. Post-mortem lesions Petechiae. vaccination by controlled exposure. Prevention Coccidiostats in feed. Ruffled feathers. Accumulation of varying quantities of blood and caseous necrotic material in the caecum. histomonosis. microscopic examination of scrapings. Closed eyes. Inappetance. E tenella Introduction This was at one time the commonest type of coccidiosis and is certainly the most easily diagnosed. Thickening. mitis (see above). Sulphonamides.
is caused by the protozoan parasite Eimeria mitis. Moderate Eimeria tenella infection in the caecae of a chicken (Score 3). Coccidiosis. E mitis Introduction This condition of chickens.Figure 15. The parasite is moderately resistant in the environment and highly resistant to conventional disinfectants. Diagnosis Mild lesions. The infective agent is found in litter. seen worldwide. humidity). which colonises the small intestine. faeces and on fomites and birds are infected by the oral route with an incubation period of 2-5 days. 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. Signs Reduced feed conversion efficiency and weight gain. Treatment Not usually treated but susceptible to the products used for other forms of intestinal coccidiosis. The disease occurring is proportional to the amount of infective agent ingested. The caecal walls are thickened and haemorrhagic and there is a mass of blood in the caecal lumen. May predispose to wet litter. secondary bacterial enteritis. Predisposing factors include exposure to faeces and litter conditions that favour development of the parasite (temperature. identification of typical small round oocysts and other stages in fresh scrapings from the small intestine. 36 .
Ruffled feathers. vaccination by controlled exposure. Coccidiosis. Treatment Toltrazuril. Oocysts in caecum and rectum. Of moderate to high pathogenicity. lesions. Amprolium. Inappetance. Differentiate from ulcerative enteritis. Severe necrotising enteritis. microscopic examination of scrapings. Closed eyes. extending into caecal tonsils.Prevention Normally controlled by anticoccidials in feed. Poor production. caecal coccidiosis. This species is not usually included in vaccines for broilers. Diarrhoea. Prevention Coccidiostats in feed. Ileorectal. Post-mortem lesions Petechiae and thickening of the distal third or more of intestine. blood in faeces. There is good immunity to the same parasite in recovered birds. Signs Depression. hygiene. Sulphonamides. 37 . it is found in the terminal ileum. Morbidity and mortality are variable. Vitamins A and K in feed or water. E brunetti Introduction A relatively rare form of coccidiosis affecting chickens worldwide caused by Eimeria brunetti. Diagnosis Signs. May be included in vaccines. caecum and rectum.
Intestinal. of Ducks and Geese Introduction Young ducks and geese may suffer from Eimeria spp infection. Tyzerria has eight sporocysts in each oocyst.Figure 16. Blood-stained vent. Vitamins A and K in feed or water. lesions. There is thickening of the intestinal mucosa and there are lines of haemorrhagic spots in the mucosa. Moderate Eimeria brunettiinfection in the terminal ileum and rectum of a chicken. Sulphadimidine 30-600gm/100 birds/day. microscopic examination of scrapings (usually few or no oocysts. Depression. In the goose E. compared to four per oocyst forEimeria. anseris is the most important. Coccidiosis occurs only very rarely in commercially reared ducks in the UK. while in ducksTyzzeria perniciosa is most pathogenic.g. 38 . Tucked appearance. Duck viral enteritis. Amprolium. 2 days off. Differentiate from Duck viral hepatitis. 3 days on). Signs Sudden death. Diagnosis Signs. Post-mortem lesions Massive haemorrhage in upper small intestine. large number of merozoites). Coccidiosis. anatipestifer. 3 days on. Treatment Sulphonamides (e.
however this is not routinely practised. Reduced feed intake. Hygiene.Prevention If required coccidiostats could be used in feed. presence of coccidial stages in fresh scrapings of kidney lesions.faeces tend to be whitish. Kidney Introduction A disease of geese caused by Eimeria truncata that can cause high mortality in geese of 312 weeks of age. Prevention Good Hygiene. Weakness. Kidneys light grey to greyish pink. Treatment Controlled trials of treatments have not been published. Tiny white foci and petechiae in the kidneys. Post-mortem lesions Enlarged kidneys. Signs Depression. Diarrhoea . Coccidiosis. 39 . it can also infect Barbary ducks and swans. Diagnosis Lesions.
Inappetance. 40 . mucosa tends to be pinker than normal. Closed eyes. of moderate to high pathogenicity it is seen worldwide. Vitamins A and K in feed or water. vaccination. hygiene. E maxima Introduction One of the more common forms of coccidiosis in commercial broilers.Coccidiosis. Prevention Coccidiostats in feed. maxima. microscopic examination of scrapings. Treatment Sulphonamides. Signs Depression. Amprolium. Poor production. commercial vaccines commonly contain more than one strain of E. lesions. contents often orange in colour. Mild to severe enteritis. Morbidity and mortality are variable. This infection is often associated with E. Depigmentation of skin and plasma is especially evident in this form of cocccidiosis and this is commercially important in some markets. non-specific enteritis. Mid-intestinal. Diagnosis Signs. Ruffled feathers. Blood or pigment in the faeces. acervulina coccidiosis and there may be large numbers of characteristic oocysts in smears. This is one of the less immunogenic species. Caused by Eimeria maxima. Because of the area of intestine affected it tends to have a significant effect on productivity and susceptibility to necrotic enteritis. Poor absorption of nutrients/pigments. Post-mortem lesions Petechiae and thickening of middle third of intestine. Differentiate from necrotic enteritis.
lesions. caused by Eimeria necatrix. Diarrhoea. microscopic examination of scrapings Differentiate from necrotic enteritis. Inappetance. blood in faeces. Coccidiosis. Oocyts in caecal scrapings. Post-mortem lesions Petechiae and thickening. other types of coccidiosis.Figure 13. Moderate Eimeria maxima infection in the jejunum of a chicken (Score 2). in which the parasite is present in the small intestine and in the caecum. Deep scrapings necessary to show large schizonts. Severe necrotising enteritis. It occurs in chickens worldwide and has variable morbidity but mortality is high in severely affected birds. Mid-intestinal. 41 . Closed eyes. Poor production. Signs Reduced feed consumption. Depression. Diagnosis Signs. The lesions are subtle compared to other forms of coccidiosis. Schizonts seen as white spots through the serosa interspersed with petechiae. E necatrix Introduction A highly pathogenic form of coccidiosis. 'Sausage-like' intestine. Ruffled feathers. of middle to posterior third or more of small intestine. The intestine is slightly thickened and there are scattered haemorrhages in the mucosa when seen from the inside.
maxima. Ruffled feathers. This is one of the less immunogenic species. Diarrhoea. Morbidity is variable and mortality low or absent. Upper Intestinal. Poor production. commercial vaccines commonly contain more than one strain of E. Vitamins A and K in feed or water. Signs Depression. both alone and in association with other species of coccidia and is caused by Eimeria acervulina.Treatment Toltrazuril. Closed eyes. Figure 14. Haemorrhages and white spots are visible from the outside of the intestine. hygiene. Depigmentation. which is moderately pathogenic. Eimeria mivatiis currently considered not to be a valid species distinct from E. In this case the intestine is thickened and can become ballooned and sausage-like. E acervulina Introduction This is probably the commonest cause of coccidiosis in chickens and occurs worldwide. Coccidiosis. vaccination. Prevention Coccidiostats in feed. Amprolium. Sulphonamides. Inappetance. It is seen in layers and in broilers. acervulina. Moderate Eimeria necatrix infection in the jejunum of a chicken (Score 3). Post-mortem lesions 42 .
hygiene. Thickening. Petechiae. Figure 12. in severe the entire surface is pale or denuded of epithelium. and other lesions. Differentiate from necrotic and non-specific enteritis. Immunity is quite short lived (about 30 days) in the absence of continued challenge. Amprolium. Treatment Toltrazuril. in feed or water. Sulphonamides. Diagnosis Signs. restricted to upper third of small intestine . 43 . In milder infections there may be scattered white spots. Various publications provide a photographic key to severity of lesion. A detailed description is beyond the scope of this book. White spots or bands in the mucosa. In severe infections they become confluent and cause sloughing of the mucosa. lesions. microscopic exam of scrapings. vaccination by controlled exposure. Moderate Eimeria acervulinainfection (score 2) in chicken duodenum. In general terms a score of 0 indicates no lesions and a score of 4 indicates maximal severity of lesion or death. Prevention Coccidiostats in feed. A system of assessing the severity of coccidial challenge by attributing a 'score' is often used. Poor absorption of nutrients/pigments.the duodenum and part of the ileum.
mucosal damage due to viral infections and immunosuppression are predisposing factors. Diagnosis Isolation. Synovitis. and via shell membranes/yolk/navel. etc. sero-typing. Infection is by the oral or inhalation routes. Omphalitis. Granulomata in liver and spleen.Colibacillosis. but is susceptible to disinfectants and to temperatures of 80°C. Snick. sneezing. It is most commonly seen following upper respiratory disease (such as Infectious Bronchitis) or Mycoplasmosis. Dejection. Aerobic culture yields colonies of 2-5mm on both blood and McConkey agar after 18 hours . Lesions vary from acute to chronic in the various forms of the disease. The infectious agent is moderately resistant in the environment. Post-mortem lesions Airsacculitis. mortality is 5-20%. Swollen liver and spleen. Poor growth. fomites. It is frequently associated with immunosuppressive diseases such as Infectious Bursal Disease Virus (Gumboro Disease) in chickens or Haemorrhagic Enteritis in turkeys. Cellulitis over the abdomen or in the leg. Signs Respiratory signs. coughing. Salpingitis. Peritonitis. Pericarditis. Poor navel healing.most strains are rapidly lactose-fermenting producing 44 . pathology. with an incubation period of 3-5 days. Arthritis. Colisepticemia Introduction Coli-septicaemia is the commonest infectious disease of farmed poultry. Omphalitis. Reduced appetite. water. or in young birds that are immunologically immature. turkeys. Enteritis. Morbidity varies. Perihepatitis. It is caused by the bacteriumEscherichia coli and is seen worldwide in chickens.
Pododermatitis Introduction Contact dermatitis affects skin surfaces which have prolonged contact with litter. Severe perihepatitis in colibacillosis in a broiler parent chicken. other enterobacteria such as Proteus. gentamycin or ceftiofur (where hatchery borne). Control of predisposing factors and infections (usually by vaccination). the breast area. feed and water. Immunity is not well documented though both autogenous and commercial vaccines have been used. whereas others progress to deep ulcers so the size. The liver is almost entirely covered by a substantial layer of fibrin and pus. 45 . neomycin (intestinal activity only). flouroquinolones. rear surface of the hock and. tetracyclines. as well as Pseudomonas. Hock Burn. Differentiate from acute and chronic infections with Salmonella spp. Contact dermatitis is commonly monitored at processing as a means of measuring 'welfare status'. Figure 17. hatchery hygiene. Some lesions are superficial. when severe. good sanitation of house. Prevention Good hygiene in handling of hatching eggs. and in broiler parents. Contact Dermatitis. Well-nourished embryo and optimal incubation to maximise day-old viability.brick-red colonies on McConkey agar. Treatment Amoxycillin. potentiated sulphonamide. Staphylococcus spp. It is seen in growing broiler chickens and turkeys. etc. the foot pad. stage of resolution and severity of lesion is likely to affect the degree of discomfort or pain suffered.
If severe the foot and hock lesions may contribute to lameness or serve as a portal of entry for secondary infections. Prevention This condition is closely linked to intestinal function as this is the prime determinent of faecal consistency and stickiness. level of soya bean meal in feed (according to some authors.Pododermatitis is often related to high droppings pH. Moderate pododermatitis on a foot pad. and sometimes in the breast area. Treatment Not applicable. proper insulation in cold climates. It can be reproduced by adding water to the litter. Post-mortem lesions As described under signs. stickiness of droppings). Choice of drinker type (nipple as opposed to bell). litter moisture. drinker management. See the discussion in the section on Dysbacteriosis. and. and adequate ventilation to remove moisture are all important. 46 . most importantly. Signs Blackened skin progressing to erosions and fibrosis on the lower surface of the foot pad. Diagnosis Signs and lesions. Figure 18. at the back of the hocks.
but much smaller (typically oocysts are less than ¼ of the size of an E. acervulinaoocyst). Treatment Levamisole. Coumaphos. They replicate in the brush border on the surface of epithelial cells. A further species causes respiratory disease in quail. They also differ from coccidia in being poorly host specific. Post-mortem lesions Inflammation and thickening of mucosa of crop and oesophagus. although bird strains do not infect mammals very well.Cropworms Introduction The nematode worms Capillaria spp and Gongylonema ingluvicolainfect the mucosa of the crop and oesophagous of poultry and game birds. Cryptosporidiosis Introduction Cryptosporidia are related to the coccidia. 47 . Avoidance of access to intermediate hosts. Prevention Effective cleaning of housing. Signs Anaemia. The same species causes infections of the hindgut and cloacal bursa in chickens. meleagridis also infects both species. Emaciation. Some have beetle or earthworms as intermediate hosts. Cryptosporidium baileyi can cause respiratory disease in chickens and turkeys.C. The oocysts are excreted ready sporulated in the faeces and infection occurs by inhalation and ingestion. and vice versa. and ducks. White convoluted tracks in the mucosa. Routine worming. turkeys. Diagnosis Microscopic examination of mucosal scraping.
Torticollis. Circling. coli-septicaemia) there may be benefit in medicating for these. Cough. Tremors. Signs Incoordination. Diarrhoea. Prevention The oocysts of cryptosporidia are extremely resistant to chemical disinfection.g. Diagnosis Identification of the parasites attached to the epithelium by microscopic examination (smears histopathology acid-fast staining).Signs Snick. It is becoming increasingly common for water companies to screen water supplies for cryptosporidia because of the human health implications of mammalian strains. recumbency. Post-mortem lesions Sinusitis. Swollen sinuses. 48 . Pneumonia. Airsacculitis. If other disease processes are complicating the situation (e. Low weight gain. There are no effective preventative medicines or feed additives. Treatment Unfortunately there is currently no known effective treatment in poultry. 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 Lameness. Degenerative Joint Disease Introduction A condition of chickens and turkeys seen worldwide. and cartilage flaps. air sacs etc. The cause remains to be confirmed. Post-mortem lesions Damaged epiphyseal articular cartilage. Treatment 49 . Prevention Use fresh dry litter (avoid old sawdust). isolation of the fungus. Reduced breeding performance. especially of femoral anti-trochanter but also other leg joints. but it may result from physical damage. Diagnosis Lesions. Treatment None. Diagnosis Gross and microscopic lesions. Mycotic lesions in lungs. resulting in erosions.Post-mortem lesions Necrotic lesions with associated congestion in cerebrum. or developmental defects. Rapid growth is a possible predisposing factor. Microscopically there is necrosis and there may be fissures of articular cartilage and associated osteochondritis. 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.
Exclusion of wild birds from chicken areas is advised as far as possible. especially during period of rapid growth. 50 . It may be best to cull affected birds from small flocks. Signs Cause irritation and the bird pulls feathers. Depluming and Scaly Leg Mites Introduction External parasites of adult chickens. Prevention Avoidance of physical sources of injury to bones and joints. The adult females are short legged.Knemidocoptes spp. Unthriftiness. There may be a place for growth-control programmes. round. Raised thickened scales.5mm in diameter.None available. Application of mineral or vegetable oil is also beneficial. Prevention Careful cleaning of buildings during down-time will help reduce the risk of these infections. Post-mortem lesions As described under signs. Appropriate management of a segregation pen and early marketing of mildly affected birds may limit losses and improve flock welfare. Treatment Not usually required in commercial poultry. Diagnosis Signs. For small flocks dipping the affected parts in a solution of acaricide may be beneficial. microscopic examination for mites in scrapings. up to 0. pigeons etc. Mange lesions on legs and unfeathered parts. pheasants.
The infective agent. leg muscles. Reserpine in diet of birds of 4+ weeks (no longer licensed in the UK). Abdominal cavity full of blood. presumably due to a sudden increase in blood pressure. a tranquilizer.Dissecting Aneurysm. A sudden noise or other cause of excitement can lead to an 'outbreak'. a picornavirus may also 51 . Skin pale. Rupture of major blood vessel at base of heart or by the kidneys. It has been suggested that degenerative changes in the wall of the artery and copper deficiency may be factors. Haemorrhages in lungs. Duck Viral Hepatitis Introduction A viral disease of ducks occurring worldwide and previously a scheduled disease in UK. pericardial sac. Prevention Limit feed in birds of 16+ weeks. Reserpine. genetic condition of turkeys linked to male sex and high growth rate. Aortic Rupture Introduction A complex. Treatment None currently licensed. The disease is transmitted by infected ducks and other waterfowl and spreads rapidly. A longtitudinal split of the abdominal aorta is the most common lesion. Post-mortem lesions Carcase anaemic. Aspirin at 250 ppm in feed or water may be of benefit. birds found on breast or side. Morbidity is around 100% and mortality 0-95%. recovered birds carrying the virus for 8 weeks. Signs Sudden death with no warning signs. was included in feed at 1 ppm for 3-5 days to reduce blood pressure. kidneys. Diagnosis History and lesions. Possibly blood in the mouth.
Differentiate from Duck plague (viral enteritis). Depression. arching of back. Punctate/diffuse haemorrhages. Newcastle disease. Transmission is by infected birds. rapid deterioration and death.survive for ten weeks in brooders and five weeks in faeces. mostly in ornamental collections. SN serology. Recovered birds may carry the virus for a year. Live. Post-mortem lesions Liver swollen. Microscopically . Duck Virus Enteritis. Signs Sudden death. coccidiosis. 52 . often in opisthotonus. The disease follows a very acute course with a morbidity of 5-100% and mortality of 5-100%. Diagnosis History. Treatment Antiserum. 0. Kidneys and spleen swollen. Influenza and a 'Type II Variant' hepatitis caused by Astrovirus. Duck septicaemia (anatipestifer). lesions. fomites and arthropods. A different picornavirus causes a similar condition in North America. Fall on side. All waterfowl are susceptible and the Barbary duck is more susceptible than the Pekin. paddling of legs. Duck Plague Introduction A herpesvirus infection of ducks and geese diagnosed in the UK in 1972. only slightly attenuated vaccine is applied at day old by foot web stab and may be repeated in breeding birds to provide maternal immunity. Death in good condition.5 ml serum of recovered birds given intramuscularly. bile duct proliferation and inflammation. also the Netherlands and other countries. Prevention Vaccination and/or antiserum. breeder vaccination.focal necrosis. in USA since 1967. isolation in CE (causes stunting of 9 day embryo).
oesophagitis (birds on restricted feed). HA-. Dehydration. Occasionally penile prolapse in the penis in drakes. Thirst. Severe diarrhoea. Treatment None. Prevention Isolation from waterfowl. Young ducks may show thymic and bursal lesions. heart. pasteurellosis. vent gleet. Paresis. Non-specific Bacterial Enteritis Introduction Inflammation of the small intestine associated with wet litter. Ataxia. but vaccination in face of outbreak is of value. coccidiosis. Closed eyes. pericardium. sometimes dysentery. Crusty plaques from oesophagus to bursa (covered by yellowish plaques in later stages).Signs Sudden deaths. Dysbacteriosis. vaccination if approved by authorities (CE adapted live virus). body cavities. Drop egg production. spleen. Rapidly spreading disease. excess caecal volume and fermentation. Haemorrhage in intestine. The condition is seen mainly in rapidly growing broiler chickens with good food intake. Tremor. probably through interference. Photophobia. liver. intranuclear inclusions Differentiate from Duck hepatitis. is common in countries with restrictions on the use of antimicrobial growth promoters and pressure to reduce therapeutic antimicrobial usage. Diagnosis Isolation: Duck CAMs 12 day embryos die in 4 days. 53 . Occasionally cyanosis of the bill in the young. Post-mortem lesions Severe enteritis.
Spain. Treatment should coincide with good relittering and it is important to provide fresh sanitary drinking water. Voluminous caecae. often with gas bubbles. France. Prophylactic antimicrobial medication may be necessary in some circumstances. rather we are dealing with a disruption in the normal flora of the gut. It affects chickens and has occurred in Ireland.Dietary changes. Wet faeces in the rectum. In the autumn of 1976 a distinct egg drop syndrome was first identified in Northern Ireland. Holland. 127. Signs Diarrhoea. Feed acidification may be helpful in some circumstances. Germany. feed interruptions and subclinical coccidiosis may be contributory factors. lesions. Careful choice of any feed enzymes and their matching with local raw materials can have an impact on substrates made available to intestinal bacteria. Uruguay. Peru. 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. Circumstantial evidence suggests that the main route of transmission is through the eggs (vertical transmission) 54 . Treatment Amoxycillin and tylosin treatment appear to be beneficial. The cause has been identified as Adenovirus BC14. Mortality is usually negligible. especially where treatment is initiated early. Good control of coccidiosis. Prevention Competitive exclusion ('normal adult flora') use in day-old chicks reduces the risk of this condition. Argentina. England. Post-mortem lesions Excessive fluid content throughout the small intestine. first isolated in Northern Ireland in 1976. Brazil. microscopic examination of scrapings from the wall of the small intestine (to exclude coccidiosis and perhaps to assess the bacterial flora). Water intake may be increased or irregular. Diagnosis Signs. Apparently a similar disease had been seen over a 4-year period in broiler parents in Holland. No single bacterium appears to be responsible.
Poor internal quality. and D as well as calcium. DID. Lateral transmission from bird to bird is slow and may be prevented or slowed for weeks by netting divisions. Elisa. Signs Egg drop at peak or failure to peak. The infection is commonly present in ducks and geese but does not cause disease. Metabolic diseases include Fatty Liver Syndrome. Cholera. sudden changes of feed. as may wildfowl and biting insects. throat swabs. Diseases in which egg drop occurs.only a slight atrophy of ovary and oviduct. Infectious Laryngotracheitis. Unvaccinated flocks with antibodies before lay do not peak normally. Contamination of egg trays at packing stations may play a part in transmission. intoxication by sulphonamides. Post-mortem lesions No specific lesion .it may be possible to demonstrate degenerative changes in the epithelial cells of the magnum of the oviduct. selenium. Drops may be of 5 to 50% and last for 3-4 weeks. Newcastle disease. Isolation of haemagglutinatin agent in duck eggs or cell culture. Diagnosis History. phosporus. insecticides or nicarbazin. Rough. Nutritional deficiency should be considered. B 12. Management problems may be involved: inadequate water supply.followed by latent infection during rear with viral excretion starting shortly before sexual maturity. group antigen distinct from classical adenoviruses (white cells. Lack of signs in the birds themselves. 55 . Infectious diseases include Infectious Bronchitis. which can be caused by a large number of factors acting individually or in combination. signs/lesions (mainly lack of). oviduct). inadequate lighting programme. SN. Serology: HI. Spread from house to house may take 5-10 weeks. specifically vitamins E. Parasites. Marek's disease/Leukosis or any infectious disease causing a significant systemic disturbance (CRD. It is important to rule out other possible reasons for egg drop. thin or soft-shelled eggs and shell-less eggs. Histopathology . extremes of temperature. Clinical disease occurs during sexual maturity. Loss of shell pigment. Diphtheritic Fowl Pox). Coryza. Avian Encephalomyelitis. may be infectious or metabolic.
If successive flocks are affected on the same site prophylactic medication ahead of the anticipated problem may be of benefit. Soluble multivitamins may be recommended as a nonspecific measure. bacterial infection. Diagnosis Differentiate from broiler ascites syndrome by examination of the interior of the heart. streptococci.Treatment None. Vegetative lesions usually on the right atrioventricular valve. and /or trauma. rickets. The choice should depend on sensitivity testing of an isolate. osteomyelitis. Signs Fluid-distended abdomen. Erysipelothrixetc. 56 . Prevention Vaccination with inactivated vaccine prior to lay. growth plate disease. Treatment Medication is only likely to be of value in reducing deterioration in birds that are starting to develop lesions. Prevention Good hygiene at turn-around. Peripheral vessels congested. Epiphysiolysis Introduction A complex condition of chickens that may be associated with trauma. Culture of lesions to confirm the bacterium involved. Endocarditis Introduction A condition of chickens associated with several bacterial infections such as staphylococci. Post-mortem lesions Right ventricular failure and ascites.
Microscopic lesions not pathognomonic. May also be asymptomatic. chickens. turkeys. Post-mortem lesions No gross lesions. Prevention Control of predisposing factors. Signs Nervous symptoms. often occurs or is identified in the processed carcase. wild birds. Paresis.Signs Apparent dislocation at extremities of long bones. 57 . Horses are also seriously affected. VEE) Introduction A viral disease of pheasants. These conditions currently only occur from northern South America to North America. Equine Encephalitis (EEE. It is transmitted between birds by pecking and by mosquitoes. Circling. Paralysis. histology may be helpful in identifying underlying problems such as rickets or 'FHN'. Flaccid neck. Treatment Not applicable. The natural hosts are wild birds and rodents. Ataxia. Tremors. sometimes seen in vivo. Diagnosis Gross inspection. WEE. ducks and pigeons having a high morbidity and high mortality. partridges. Post-mortem lesions Separation of epiphyses at the growth plate.
Haemorrhages in fat. control cannibalism. There is likely to be an increased risk if housing or land has been previously used by pigs or sheep. kidney. Treatment None. ducks.Diagnosis Isolation in mice. Joint lesions. Depression. Sudden death. Endocarditis. water. Swollen snood. Perineal congestion. fishmeal and semen and by cannibalism. Vaccinate at 5-6 week. It may be transmitted by faecal carriers for 41 days. Post-mortem lesions Carcase congestion. The bacterium is fairly resistant to environmental effects or disinfectants and may persist in alkaline soil for years. rhusiopathiae) seen in turkeys and increasingly in free-range chickens. and CE. TC. Signs Inappetance. especially snood. Liver. in soil. Chronic scabby skin. COFAL. It is also seen in some mammals. epicardium. rarely in geese. Prevention Protection from mosquitoes. spleen swollen. May be diarrhoea and respiratory signs. Marked catarrhal enteritis. Sleepiness. ID by VN. muscle. 58 . Erysipelas Introduction A sudden onset infection with the bacterium Erysipelothrix insidiosa (E. pheasants.
the demonstration of the organism in stained impression smears from tissues. often along with bacterin. Treatment Penicillin . Tetracyclines in feed may also be helpful. Headparts pale. Diagnosis Lesions. especially caged layers and with a complex set of causes including excessive calories. greasy and soft with numerous haemorrhages. Fatty Liver Haemorrhagic Syndrome Introduction A condition occurring worldwide in chickens. Post-mortem lesions Obesity. vaccine at 16-20 weeks if the condition is enzootic. Death by internal exsanguination after rupture of haematocyst. Sudden drop in egg production. salmonellosis. Signs Overweight typically by 25%. history. and identification. synoviae plate tests for a few weeks. Differentiate from pasteurellosis. Sudden death. Vaccination or natural infection may cause false positive reactions in the Mycoplasma gallisepticum and M. 59 . mycotoxins. Some birds with pale comb and wattles. and acute Newcastle disease. Liver yellow.Diagnosis Isolation on blood agar. deficiency and stress. colibacillosis. Prevention Good biosecurity to prevent spread from other susceptible species.a combination of the procaine and benzathine salts may be injected.
Favus Introduction A fungal infection. B 12 and inositol. Signs White. of chickens and turkeys. Post-mortem lesions See signs (above). Prevention Feed to avoid obesity. Loss of condition. 'Honeycomb' skin. culling affected birds. Thick crusty skin. Trichophyton gallinae.Treatment Reduce energy intake. avoid mycotoxins and stress. Prevention Good hygiene of facilities. It is very rare in commercial poultry production. Treatment Formalin in petroleum jelly. isolation. supplement with choline. 60 . vitamin E. powdery spots and wrinkled crusts and scab on comb and wattles. Feather loss. Diagnosis Lesions.
Fowl Cholera. arthritis. Post-mortem studies of birds culled due to lameness and of birds found dead. It is seen worldwide and was one of the first infectious 61 . streptococci. especially hypophosphataemic. Use of a wing for support during walking and hip flexion. Diagnosis Base on post-mortem lesions and isolation of a causative organism. turkeys. staphylococci. and water fowl.Femoral Head Necrosis . Signs Lameness. Careful attention to mineral and Vitamin D nutrition to avoid subclinical. Post-mortem lesions Degeneration of the epiphyses of long bones with thinning of the cortex and tendency to break when force is applied. highly contagious disease caused by the bacterium Pasteurella multocida in a range of avian species including chickens. FHN is the commonest infectious cause of lameness in broilers in the UK. indicated that 0. Prevention Exclusion of floor eggs and dirty eggs from the hatchery. Differentiate from synovitis. (increasing order of susceptibility). coli. Pasteurellosis Introduction Fowl Cholera is a serious. E. spondylolisthesis. rickets. Predisposing factors include immunosuppresive viruses such as Infectious Bursal Disease Virus and Chicken Anaemia Virus and non-infectious bone pathologies such as hypophosphaetamic rickets. 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.FHN Introduction A condition of chickens and turkeys that may be associated with several different bacterial infections e.75% of all male broilers placed had lesions in the hip bone.g.
Nasal. Focal hepatitis. Swollen joints. Diarrhoea. necessitating long-term or periodic medication. ocular and oral discharge. faeces. The disease can range from acute septicaemia to chronic and localised infections and the morbidity and mortality may be up to 100%. streptomycin. contaminated soil. Yolk peritonitis. Post-mortem lesions Sometimes none. and people. Purulent pneumonia (especially turkeys). confirmed with biochemical tests. Loss of appetite. tetracyclines. Signs Dejection. septicaemic viral and other bacterial diseases. erythromycin. The bacterium is easily destroyed by environmental factors and disinfectants. 62 . Differentiate from Erysipelas. Swollen and cyanotic wattles and face. or limited to haemorrhages at few sites. Reservoirs of infection may be present in other species such as rodents. The incubation period is usually 5-8 days. cats. Predisposing factors include high density and concurrent infections such as respiratory viruses. Cellulitis of face and wattles. Ruffled feathers. Purulent arthritis. equipment. by Louis Pasteur in 1880. isolation (aerobic culture on trypticase soy or blood agar yields colonies up to 3mm in 24 hours . Diagnosis Impression smears. Sudden death. Treatment Sulphonamides. Enteritis. but may persist for prolonged periods in soil.diseases to be recognised. Lungs with a consolidated pink 'cooked' appearance in turkeys.no growth on McConkey). Coughing. The disease often recurs after medication is stopped. The route of infection is oral or nasal with transmission via nasal exudate. penicillin. Lameness. and possibly pigs.
turkeys. hygiene. Severe localised Pasteurella infection in the swollen wattle of a 30-week-old male broiler parent chicken.Prevention Biosecurity. Inappetance. Figure 19. Infection occurs through skin abrasions and bites. Fowl Pox. or by the respiratory route. Poor egg production. Depression. The duration of the disease is about 14 days on an individual bird basis. 0-50%. pigeons and canaries worldwide. spreading eruptions and scabs on comb and wattles. Signs Warty. Morbidity is 1095% and mortality usually low to moderate. throat and sometimes trachea. The swelling is made up of oedema and purulent exudates (pus). fomites. It is transmitted by birds. Caseous deposits in mouth. Poor growth. Pox. good rodent control. It is more common in males because of their tendency to fight and cause skin damage. bacterins at 8 and 12 weeks. The virus persists in the environment for months. Avian Pox Introduction A relatively slow-spreading viral disease characterised by skin lesions and/or plaques in the pharynx and affecting chickens. 63 . and where there are biting insects. and mosquitoes (infected for 6 weeks). live oral vaccine at 6 weeks.
64 . Turkeys by thigh-stick at 2-3 months. Treatment None.intra-cytoplasmic inclusions (Bollinger bodies) with elementary bodies (Borrel bodies). There is good cross-immunity among the different viral strains. usually with chicken strain by wing web puncture. signs and post-mortem lesions. reproduction in susceptible birds. Figure 20. check take at 7-10 days post vaccination. Less commonly there may. be caseous plaques in mouth. pharynx. trachea and/or nasal cavities. Chickens well before production. Flocks and individuals still unaffected may be vaccinated. It is confirmed by IC inclusions in sections/ scrapings. If there is evidence of secondary bacterial infection broad-spectrum antibiotics may be of some benefit. in the diptheritic form. Fowl pox lesions on the wattle of an adult broiler parent chicken. Prevention By vaccination (except canary). DNA probes. Microscopically . Differentiate from Trichomoniasis or physical damage to skin.Post-mortem lesions Papules progressing to vesicles then pustules and scabs with distribution described above. Diagnosis A presumptive diagnosis may be made on history. isolation (pocks on CE CAM) with IC inclusions.
wings. rarely Clostridium noyvi / oedematiens. Sudden mortality. Signs Occasionally dejection. Necrotic Dermatitis Introduction A bacterial condition seen in chickens and usually caused byClostridium septicum. Treatment Sulphaquinoxaline. Post-mortem lesions Patches of gangrenous skin with underlying emphysematous and/or sanguinous cellulitis. 65 . Avoid skin trauma and immunosuppression (congenital CAV infection. occasionally Staphylococcus aureus. especially following congenital Chick Anaemia Virus infection or early Infectious Bursal Disease Virus infection (Gumboro Disease). early Infectious Bursal Disease Virus infection). Swelling and infarction of the liver. It occurs due to invasion of 'normal' wounds by 'normal' bacteria in immunosuppressed birds. spleen. penicillin or amoxycillin. The spores of Clostridial bacteria are highly resistant in the environment. sometimes thighs and other parts. Gangrenous skin. Immunosuppression is therefore a predisposing factor. Severe cellulitis especially of thighs. wattles. usually over wings and breast.Gangrenous Dermatitis. Morbidity may be up to 50% and mortality is high. Loss of appetite. Foci in liver. Recovery of an abundant growth of causative organism in recently dead birds. Prevention Good hygiene and management. Diagnosis Clinical signs and/or lesions.
a nematode worm parasite of chickens.Figure 21. pheasants. Diagnosis Signs and lesions. confirmation of presence of the parasite. Treatment Flubendazole in feed. 66 . Presence of worms. The condition is seen more commonly in poultry on free range where ground may be contaminated by wild birds e. Signs Gasping.g. slugs and snails acting as transfer hosts but the life cycle may also be direct. Dyspnoea. Infection is by the oral route with earthworms. Post-mortem lesions Tracheitis. Head shaking. Prevention Flubendazole. Gape Introduction Syngamus trachea. levamisole. There is an 18-20 day prepatent period. by ingestion of embryonated egg or L3. from rookeries. Severe gangrenous dermatitis on the upper surface of the wing of a broiler chicken. Loss of appetite and condition. paired parasites up to 2 cm long. and other game and ornamental birds occurring worldwide. turkeys.
Worms develop to L3 in eggs and infection is by the oral route direct from environment. Post-mortem lesions Ulceration. confirmation of presence of the worms. weevils. They are more common in free-range birds because of their increased access to intermediate hosts. Signs Depression. Loss in condition and weight. 67 . Diagnosis Lesions. routine worming. Slow growth. Prevention Prevention of access to intermediate hosts.Chickens Introduction Cheilospirura. Amidostomum anseris. and Histiocephalus are nematode worm parasites of chickens. Signs Depression. Treatment Levamisole. beetles etc act as intermediate hosts. Adults are 2-4 cm long and usually bright red. Loss in condition and weight.Gizzard worms . muscular wall may be sacculated or ruptured.Geese Introduction A nematode worm parasite. Grasshoppers. Streptocara. Slow growth. Gizzard worms . necrosis and partial sloughing of gizzard lining. Cheilospirura and Streptocara are seen worldwide but Histiocephalus is restricted to Europe. affecting geese and ducks. benzimidazoles such as flubendazole.
Swollen eyelids and eye and nasal discharge. Reddening of skin. visualisation of worms. The younger the bird affected the more acute the condition and the higher the mortality. Vertical transmission resulting in congenital infection may occur. Goose Parvovirus (Derzsy's Disease) Introduction Goose Parvovirus is a highly contagious condition of geese and young Muscovy ducks. muscular wall may be sacculated or ruptured. benzimidazoles. Swelling and congestion of liver. Prevention Rotation of ground on annual basis. 68 . Losses are negligible in birds over 5 weeks of age. Reduced feed intake. Post-mortem lesions Pale myocardium. Membrane covering tongue. spleen and pancreas. Signs Prostration and death in acutely affected goslings. Profuse white diarrhoea. necrosis and partial sloughing of gizzard lining. Excessive water intake. 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. Loss of down.Post-mortem lesions Ulceration. Diagnosis Lesions. Treatment Levamisole. Adults are 2-4 cm long and usually bright red. Derzsy's Disease is caused by a parvovirus distinct from chicken and mammalian parvoviruses.
Antimicrobials may be of value in reducing the effects of secondary bacterial infections. Loss of appetite. muscles. Carcase anaemia. 69 . Aplastic Anaemia. Pale comb and wattles. Haemorrhagic Anaemia Introduction A complex condition of chickens associated with drug toxicities. Liver yellow. liver. mycotoxins and viral infections and usually following a course of approximately 3 weeks. Poor growth. Morbidity varies. mortality is 5-50%. heart. Haemorrhagic Disease. Ascites. Prevention Hatching and brooding geese from different parent flocks together should be avoided. Administration of immune serum has been shown to be effective but may require two doses (day old and around 3 weeks). Post-mortem lesions Haemorrhages in one or more sites: skin. The preferred approach is to immunise breeding birds with an attenuated live vaccine. Blood in droppings. Treatment No specific treatment. Fibrinous perihepatitis. Fibrinous pericarditis. Signs Dejection. serosa and mucosae. Diagnosis Signs and lesions in birds of the appropriate age and species. Bone marrow pale with fatty change. Ideally flocks that have suffered the disease should not be used for breeding as they may become persistent excreters of the infection.
caused by Type II Adenovirus distinct from classical fowl adenovirus and occurring in most turkey-producing areas. Diarrhoea. signs. 70 . Drop in feed and water consumption. Microscopic . Signs Sudden deaths. Haemorrhagic Enteritis Introduction A viral disease of turkeys. Blood from vent of moribund birds. Post-mortem lesions Petechiae in various tissues.Diagnosis History. reproduction with filtered contents.sero-conversion frequently occurs in absence of clinical disease. add liver solubles to feed. The virulence of the virus varies but morbidity may be 100% and mortality 10-60%. remove sulphonamides. Prevention Avoid causative factors. Course 10-21 days. Serology: DID. May induce immunosupression and precipitate respiratory disease or coccidiosis. reticulo-endothelial hyperplasia and intranuclear inclusions. similar to pheasant Marble Spleen disease.spleen shows lymphoid hyperplasia. double-immuno-diffusion of splenic extract. Intestine distended with blood. Diagnosis Typical lesions. The source of virus is unknown but there is easy lateral spread within flocks. and weeks in litter. Elisa . Spleen mottled and enlarged. Treatment Vitamin K. the virus surviving in frozen faeces for months. The route of infection is usually oral. lesions.
convalescent serum. Pathogenic strains can depress both B. drinking water temperature and availability. and turkeys caused by high environmental temperature. Immunity to the disease is long lasting. nicarbazin in feed. high stocking density. acclimation. good hygiene and biosecurity. especially associated with high relative humidity and low air speed. some in turkey B-lymphoblastoid cell lines. Heat Stress Introduction A condition seen in chickens. Live vaccines are commonly used in many countries at 4-5 weeks of age. Prevention All-in/all-out production. Predisposing factors include genetics. In this case a loop of intestine has been opened to show the blood. 71 . feather cover. oral tetraycline. Ducks are relatively resistant to heat stress.Treatment Warmth and good management. Reduced feed consumption. Maternal antibody may interfere with vaccination. Immunity: there is an early age resistance irrespective of maternal antibody status. Turkeys dying with haemorrhagic enteritis commonly have the small intestine distended with blood. Disinfect and 3-4 weeks house rest. Figure 39. Some are produced in live turkeys. Signs Panting.and T-line lymphocytes for up to 5 weeks following exposure. good management. Increased thirst.
pattern of losses. Intestine flabby with some bulbous dilation. fomites. Post-mortem lesions Dehydration. Treatment Cool water. Reduced egg production. Frothy. lesions. exclusion of other conditions. evaporative coolers. chirping. Post-mortem lesions Carcases congested. Mucoid exudate in nostrils and mouth. Inappetance. pigeons. Prostration. Later depression. Inter-species transmission may occur. signs. Diagnosis Temperature records. 72 . maximise airflow. watery diarrhoea. columbae) is a protozoan parasite of turkeys. contains excessive mucus and gas. Legs and wings outstretched. Reductions in stocking density of meat poultry may be quickly achieved by partial depletion ('thinning'). if relative humidity is low then wet the roof and fog. and some game birds. carriers. Loss in weight. Terminal coma and convulsions. painted white to reflect heat. Feeding during cooler hours may be beneficial. Prevention Houses of optimal height and insulation. feed with a reduced protein:energy ratio. It is transmitted by faeces. pheasants. Hexamitiasis Introduction Hexamita meleagridis (pigeons H. In commercial ducks a related parasiteTetratrichomonas can cause poor growth and drops in egg production. Signs Initially birds nervous.
presumably introduced with worm eggs. Differentiate from transmissible enteritis. Furazolidone. This condition has high morbidity and mortality in turkeys. It has recently been demonstrated that infection occurs readily via the cloaca when birds are on contaminated litter. significant disease has been seen in breeding chickens and free-range layers. Treatment Tetracycline. gallinae the parasite is easily destroyed. and also. dimetridazole. scrapings from fresh material. Diagnosis Lesions. paratyphoid. if possible. Signs Depression. dimetridazole and ipronidazole have been used in the past. pheasants and game birds that acts together with facultative bacteria to produce the condition of Blackhead. and mixing groups of different ages. The problem is seen in high-biosecurity facilities. Blood in faeces (chickens). histomonosis. Poor growth. Histamonosis. The effect of antibiotic may be related to the control of secondary bacterial enteritis. Within a turkey shed transmission is rapid in spite of the fact that it is difficult to infect birds orally with unprotected parasites. all-in/all-out production. trichomoniasis. hygiene. increase ambient temperature. Blackhead Introduction Histomonas melagridis is a protozoan parasite of turkeys. Progressive depression and emaciation. Histomoniasis. Inappetance. Caecal tonsils congested. 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. Cyanosis of head. Outwith earth worms orH. 73 . avoid interspecies mixing. Prevention Depopulation. and occasionally chickens. First half of intestine inflamed. Although chickens are relatively resistant to the condition. Sulphur-yellow diarrhoea.
Regular worming to help control the intermediate hosts. scrapings from fresh material. Ulcers. Having both chickens and turkeys on the same property is likely to increase the risk of this disease in turkeys.g. and only nitarsone is approved in the USA. Angara Disease Introduction This condition was first identified in broilers in Pakistan in 1987. usually grey in colour. The disease is readily reproduced by inoculating birds with a bacteria-free filtrate of a liver extract from an affected bird. grey or green areas. however they may not be present in the early stages. Liver may have irregular-round depressed lesions.g. Mortality may reach 60% but more typically 10-30%. Some herbal products based on the essential oils (e. Diagnosis Lesions. Hydropericardium-Hepatitis Syndrome. Prevention Good sanitation. 'Herban)' have been used with some apparent success though controlled trials and formal approval for this purpose are not recorded. nifursol) and arsenicals (e.nitarsone) have been used to treat this important disease of poultry. especially in chickens. nitrofurans (e. concrete floors. furazolidone. It is a condition caused by an adenovirus. It affects mainly broilers and broiler parents in rear and has also been seen in pigeons.M. Treatment Historically nitro-imidazoles (e.Abubakar. caseous cores with yellow.g. given recent new knowledge on the mechanism of transmission. At the time of writing no products of these groups are approved for use in the European Union.g. dimetridazole). avoid mixing species. 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. possibly in combination with an RNA virus and immunosuppression caused by Chick Anaemia Virus or Infectious Bursal Disease. 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. 74 .Tahir Post-mortem lesions Enlargement of caeca. Arsenicals are less effective in treatment than they are in prevention.
however sometimes free-range poultry consume large stones. Older birds ingest grit to facilitate the grinding activity in the gizzard. Most young commercial poultry consume feeds that have a small particle size. Diagnosis Lesions. Impaction and Foreign Bodies of Gizzard Introduction The gizzard or crop may become impacted with litter. Lethargy. grass. Formalin-inactivated oil adjuvant vaccines are reported to be highly effective and are used in areas where the condition is endemic. however if young chicks to do not begin to eat feed properly they often consume litter instead. Control of predisposing immunosuppressive diseases may help limit losses. Enlarged. Congestion of the carcase. Grit would not be classed as a foreign body. The normal function of the gizzard is to aid in the physical grinding of food materials. Good water sanitation (e. to reduce their particle size to aid digestion.1% of a 2.g. string etc. Huddling with ruffled feathers. and birds of any age can 75 . Gizzard activity also acts as a pacemaker of intestinal activity and controls the speed at which food is passed to the small intestine. Post-mortem lesions Excessive straw-coloured fluid distending the pericardium (up to 10 mls). histopathology.Signs Sudden increase in mortality. Yellow mucoid droppings. treatment of drinking water with 0. Treatment None. Lungs oedematous. This condition usually affects only a small number of birds. Impacted gizzards are then found in 'non-starter' type chicks or poults. Prevention The condition typically occurs in areas of high poultry density where multi-age operation is traditional. virology.5% iodophor solution) appears to be beneficial. pale friable liver and kidney.
This usually happens after maintenance activities have been carred out in the housing.consume nails. Reduced weight gain. Nails commonly penetrate the lining of the gizzard. Italy. Diagnosis Lesions. Post-mortem lesions The gizzard is more firm than normal and. and on opening is found to contain a mass of fibrous material. It allows us to confirm the proportion of chicks consuming feed and can give inexperienced poultry keepers feedback on the effectiveness of their brooding management. France and Ireland. Obvious non-starters should be culled in this situation. Treatment None effective in young birds. Signs Reduced feed intake. This may extend into the proventriculus and on into the duodeunum. caused by an adenovirus. Prevention Good brooding management to encourage early adaptation to the diet and adequate consumption of feed and water. It has a course of 9. The disease was first described in the USA in 1963 and has also been reported in Canada. Infected birds remain carriers for a few weeks. the UK. A number of different sero-types have been isolated from disease outbreaks but they may also be isolated from healthy chickens. and may penetrate the body wall. Australia. Daily monitoring of the crop-fill is a useful procedure. 76 . often with severe anaemia. A foreign body may be found in the interior of the gizzard. staples etc. Inclusion Body Hepatitis Introduction A disease of chickens characterised by acute mortality. Sweep floors after maintenance activities to remove nails and other potentially dangerous foreign bodies.15 days with a morbidity of 1-10% and a mortality of 1-10%.
Infectious Bursal Disease. may be important. chloroform. Soluble multivitamins may help with the recovery process. Treatment None. and deficiency of vitamin B12. but on the other hand many field cases show eosinophilic inclusions that do not appear to have adenovirus particles. sulphonamide intoxication. The virus grows well in tissue culture (CEK. The virus is generally resistant to disinfectants (ether. fatty liver syndrome. Bursa and spleen small. pH). Pallor of comb and wattles. Blood thin. mottled with petechiae and ecchymoses. CEL). Signs Depression. Serology: DID for group antigen. Differentiate from Chick anaemia syndrome. Diagnosis A presumptive diagnosis may be made on history and lesions. vibrionic hepatitis. Ruffled feathers. Curiously. isolation alone does not confirm that they are the cause of a particular problem. Immunosuppression. and high temperatures. SN for individual sero-types. yellow. Microscopically . Formaldehyde and iodides work better. 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. Kidneys and bone marrow pale. Confirmation is made on finding inclusions in the liver.Transmission may be vertical or lateral and may involve fomites. Inappetance. 77 .basophilic intranuclear inclusions. Post-mortem lesions Liver swollen. many different sero-types have been isolated from different cases. Progeny of high health status breeding flocks appear to be at greater risk. for instance due to early IBD challenge or congenital CAV infection. perhaps because they have lower levels of maternal antibody.
dyspnoea. Typing by haemagglutination-inhibition is also used. Dakota. alkalis. Signs Depression. Infection is via the conjunctiva or upper respiratory tract with an incubation period of 18-36 hours. coli. prevention of immunosuppression. the age of the bird. Huddling. 1931). Newcastle disease). The virus. was first described in the USA (N. Wet litter. These differences are due to structural differences in the spike proteins (S1 fraction). gasping. heat (56°C for 15 mins). Its affects vary with: the virulence of the virus. maternal immunity (young birds). which may survive 4 weeks in premises. Airsacculitis. Post-mortem lesions Mild to moderate respiratory tract inflammation. Tracheal oedema. Morbidity may vary 50-100% and mortality 0-25%. Some birds/viral strains can be carriers to 1 year. and complicating infections (Mycoplasma. The cause is a Coronavirus that is antigenically highly variable. disinfectants (Formal 1% for 3 mins). Diarrhoea. Kidneys and bronchi may be swollen and they and the ureters may have urates. prior vaccination. The infection is highly contagious and spreads rapidly by contact. fomites or aerosol. About eight sero-groups are recognised by sero-neutralization. IB Introduction This infection. Poor ventilation and high density are predisposing factors. Loss of appetite. Tracheitis. E. depending on secondary infections. probably the commonest respiratory disease of chickens. Diuresis. Caseous plugs in bronchi.Prevention Quarantine and good sanitary precautions. 78 . new sero-types continue to emerge. is sensitive to solvents. Infectious Bronchitis. Coughing.
Infection is via the conjunctiva or upper respiratory tract with an incubation period of 18-36 hours.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%. depending on secondary infections. Elisa (both group specific). possible reactions depending on virulence and particle size. IB . group specific). Avian Influenza and Laryngotracheitis.Diagnosis Tentative diagnosis is based on clinical sgns. vaccinal reactions. Treatment Sodium salicylate 1gm/litre (acute phase) where permitted .antibiotics to control secondary colibacillosis (q. is sensitive to solvents. Prevention Live vaccines of appropriate sero-type and attenuation. Serology: HI. The infection spreads rapidly by contact. heat (56°C for 15 mins). Muscular shivering. Maternal immunity provides protection for 2-3 weeks. SN (type specific). 79 . Definitive diagnosis is based on viral isolation after 3-5 passages in chick embryo. The virus. Cellmediated immunity may also be important. Some birds/viral strains can be carriers for up to 1 year. lesions and serology. short duration. DID (poor sensitivity. Differentiate from Newcastle disease (lentogenic and mesogenic forms). HA negative. disinfectants (Formal 1% for 3 mins). Humoral immunity appears 10-14 days post vaccination. Poor ventilation and high density are predisposing factors. Otherwise as for standard IB. Local immunity is first line of defence.v. mycoplasmosis. with typical lesions. flourescent antibody positive and ciliostasis in tracheal organ culture. Infectious Bronchitis. which may survive 4 weeks in premises.). alkalis. Signs Sudden death. fomites or aerosol.
Soft-shelled eggs. A few birds are carriers up to 49 days post infection. typical lesions. Rough shells. Loss of internal egg quality. Diagnosis 3-5 passages in CE allantoic cavity. Signs Drop in egg production (20-50%). Prevention Live vaccines of appropriate sero-type and attenuation. Poor ventilation and high density are predisposing factors. Infection is via the conjunctiva or upper respiratory tract. Treatment Sodium salicylate 1gm/litre (acute phase) where permitted . DID (poor sensitivity. Rales may or may not be present. fomites or aerosol. with much antigenic variation. possible reactions depending on virulence and particle size. short duration. The virus is moderately resistant and may survive 4 weeks in premises. Infectious Bronchitis. cell culture (Vero. 80 . SN (type specific). sneezing. Elisa (both group specific). lesions progress to necrosis and scarring of deep pectorals in convalescence. Coughing. The condition has a morbidity of 10-100% and mortality of 0-1%. group specific).Post-mortem lesions Oedema of pectoral muscles and subcutaneously on abdomen.v.antibiotics to control secondary colibacillosis (q. FA. HA-. There is rapid spread by contact. ciliostatic in tracheal organ culture.). In layers the ovules may be intensely congested. CK) only after adaptation Serology: HI. Other lesions of 'classical' IB may be encountered. IB Egg-layers Introduction A Coronavirus infection of chickens.
particle size (if sprayed) and general health status. typical lesions. EDS76. Yolk in peritoneal cavity (non-specific).Post-mortem lesions Follicles flaccid. FA. DID. Diagnosis 3-5 passages in CE. Serology: HI. although reactions can occur depending on prior immunity. Prevention Live vaccines of appropriate sero-type and attenuation. Treatment Sodium salicylate 1gm/litre (acute phase) where permitted . Humoral immunity appears 10-14 days post vaccination. SN. Flaccid ovarian follicles in a broiler parent chicken undergoing challenge with Infectious Bronchitis virus.). Cell-mediated immunity may also be important.v. Maternal immunity provides protection for 2-3 weeks. Local immunity is the first line of defence. Figure 22. Differentiate from Egg Drop Syndrome. Elisa. virulence.antibiotics to control secondary colibacillosis (q. 81 . HA-.
Diagnosis 3-5 passages in CE. typical lesions. The virus is moderately resistant and may survive 4 weeks in premises. IB Egg-layers Introduction A Coronavirus infection of chickens. Coughing. virulence. fomites or aerosol. There is rapid spread by contact. although reactions can occur depending on prior immunity. Local immunity is the first line of defence. Soft-shelled eggs. The condition has a morbidity of 10-100% and mortality of 0-1%. Rales may or may not be present. particle size (if sprayed) and general health status. Cell-mediated immunity may also be important. HA-. Serology: HI. 82 . Treatment Sodium salicylate 1gm/litre (acute phase) where permitted . Signs Drop in egg production (20-50%).Infectious Bronchitis. with much antigenic variation. Post-mortem lesions Follicles flaccid. Yolk in peritoneal cavity (non-specific). Rough shells. Maternal immunity provides protection for 2-3 weeks. Prevention Live vaccines of appropriate sero-type and attenuation. A few birds are carriers up to 49 days post infection.antibiotics to control secondary colibacillosis (q. Infection is via the conjunctiva or upper respiratory tract. Loss of internal egg quality. Humoral immunity appears 10-14 days post vaccination.v. SN. FA. Differentiate from Egg Drop Syndrome. sneezing. EDS76.). Poor ventilation and high density are predisposing factors. Elisa. DID.
which targets the bursal component of the immune system of chickens. faeces etc.20% but sometimes up to 60%. The route of infection is usually oral. The age up to which infection can cause serious immunosuppression varies between 14 and 28 days according to the antigen in question. Generally speaking the earlier the damage occurs the more severe the effects. Infectious Bursal Disease. Subclinical infection in young chicks results in: deficient immunological response to Newcastle disease. susceptibility to Inclusion Body Hepatitis and gangrenous dermatitis and increased susceptibility to CRD. with an incubation period of 2-3 days. persisting for months in houses. but may be via the conjunctiva or respiratory tract. (Turkeys and ducks show infection only. the damage caused to the immune system interacts with other pathogens to cause significant effects. Mealworms and litter mites may harbour the virus for 8 weeks. IBD. first identified in the USA in 1962. Morbidity is high with a mortality usually 0. and affected birds excrete large amounts of virus for about 2 weeks post infection.Figure 22. Gumboro Introduction A viral disease. Signs are most pronounced in birds of 4-6 weeks and White Leghorns are more susceptible than broilers and brown-egg layers. The infective agent is a Birnavirus (Birnaviridae). seen worldwide. Sero-type 1 only. The disease is highly contagious. 83 . Marek's disease and Infectious Bronchitis. There is no vertical transmission. Flaccid ovarian follicles in a broiler parent chicken undergoing challenge with Infectious Bronchitis virus. especially with sero-type 2). The virus is very resistant. In addition to the direct economic effects of the clinical disease.
subsequent diagnosis of 'immunosuppression diseases' (especially inclusion body hepatitis and gangrenous dermatitis) is highly suggestive. Variants: There have been serious problems with early Gumboro disease in chicks with maternal immunity. Elisa vaccination date prediction < 7 days). (previously SN and DID). Vent pecking. Swollen kidneys with urates. normal size or reduced in size depending on the stage). Differentiate clinical disease from: Infectious bronchitis (renal). Dehydration. rapidly proceeds to atrophy. 84 . Other possible causes of early immunosuppression are severe mycotoxicosis and managment problems leading to severe stress. Use of a multivitamin supplement and facilitating access to water may help. Post-mortem lesions Oedematous bursa (may be slightly enlarged. Subclinical disease . Tests used are mainly Elisa. Haemorrhagic syndrome. The normal weight of the bursa in broilers is about 0. IBD viruses have been isolated and shown to have significant but not complete cross-protection. They are all serotype 1. Serology: antibodies can be detected as early as 4-7 days after infection and these last for life. Huddling under equipment. Antibiotic medication may be indicated if secondary bacterial infection occurs. Coccidiosis.History.Signs Depression. weights below 0. may have haemorrhages. Cryptosporidiosis of the bursa (rare). especially in the Delmarva Peninsula in the USA. Diagnosis Clinical disease .1% are highly suggestive. Diarrhoea with urates in mucus. This may be confirmed by demonstrating severe atrophy of the bursa. Treatment No specific treatment is available.A history of chicks with very low levels of maternal antibody (Fewer than 80% positive in the immunodifusion test at day old. Haemorrhages in skeletal muscle (especially on thighs). especially if present prior to 20 days of age. Inappetance. 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.4 days. Half-life of maternally derived antibodies is 3.3% of bodyweight. lesions. Unsteady gait. histopathology.5.
turgid and oedematous. It is not egg transmitted. This shows the anatomical relationship between the bursa. It is enlarged. The route of infection is conjunctival or nasal with an incubation period of 1-3 days followed by rapid onset of disease over a 2-3 day period with the whole flock affected within 10 days. occasionally pheasants and guinea-fowl. Carriers are important with transmission via exudates and by direct contact.Prevention Vaccination. vaccination of progeny depending on virulence and age of challenge. and tracing of contacts may indicate sites on which a more rebust vaccination programme is indicated. biosecurity measures may be helpful in limiting the spread between sites. When outbreaks do occur. This bursa is from an acutely affected broiler. Infectious Coryza is caused by the bacterium Haemophilus paragallinarum and is seen in many countries especially in multi-age farms that are never depopulated. Infectious Coryza Introduction A usually acute. In most countries breeders are immunised with a live vaccine at 6-8 weeks of age and then re-vaccinated with an oil-based inactivated vaccine at 18 weeks. especially nasal and sinus mucosae. characterised by catarrhal inflammation of the upper respiratory tract. 85 . including passive protection via breeders. the rectum and the vent. Immunity after a live vaccine can be poor if maternal antibody was still high at the time of vaccination. Morbidity is high but mortality low if uncomplicated although it may be up to 20%. resulting in increased culling. sometimes chronic. Figure 23. highly infectious disease of chickens. A strong immunity follows field challenge.
The bacterium survives 2-3 days outside the bird but is easily killed by heat. Commercial bacterins may not fully protect against all field strains but reduce the severity of reactions.requires X (Haematin) and V (NAD) factors. Purulent ocular and nasal discharge. erythromycin. drying and disinfectants. tylosin. Differentiate from Mycoplasmosis. Caseous material in conjunctiva/sinus. respiratory viruses. Birds recovered from challenge of one serotype are resistant to others. identification of the bacteria in a Gram-stained smear from sinus. at least two doses are required. Intercurrent respiratory viral and bacterial infections are predisposing factors. preferably in raised CO 2 such as a candle jar. sulphonamides. Eye-lid adherence. Drop in egg production of 10-40%. Swollen wattles. Confirmation is by isolation and identification . Post-mortem lesions Catarrhal inflammation of nasal passages and sinuses. Dihydrostreptomycin. 86 . Flouroquinolones are bactericidal and might prevent carriers. Prevention Stock coryza-free birds on an all-in/all-out production policy. Live attenutated strains have been used but are more risky. while bacterins only protect against homologous strains. Controlled exposure has also been practised. Dyspnoea. Bacterin at intervals if history justifies or if multi-age. Vaccines are used in areas of high incidence. Signs Facial swelling. Inappetance. Loss in condition. Diagnosis A presumptive diagnosis may be made on signs. agglutination and IF have all been used but are not routine. Tracheitis. Sneezing. Treatment Streptomycin. Conjunctivitis. DID. Serology: HI. lesions. chronic or localised pasteurellosis and vitamin A deficiency.
histology. antibiotics to control secondary bacterial infection if this is marked. Nasal discharge (low pathogenicity strains). 87 . Prevention Quarantine. Movement and mixing of stock and reaching point of lay are predisposing factors. ILT Introduction A herpesvirus (pathogenicity can vary) infection of chickens. Diagnosis Signs. severe bronchitis. after 4 weeks of age. Treatment None.Infectious Laryngotracheitis. Drop in egg production. Post-mortem lesions Severe laryngotracheitis.intranuclear inclusions in tracheal epithelium. IFA. PCR. Signs Dyspnoea. Recovered and vaccinated birds are long-term carriers. Apply strict biosecurity in moving equipment or materials between these these categories of stock. Sera may be examined by VN or Elisa. if enzootic or epizootic in an area. Sinusitis. Microscopically . Ocular discharge. peafowl and turkeys with a morbidity of 50-100% and a mortality usually 10-20% but sometimes up to 70%. vaccination. in severe form may be enough. The virus is highly resistant outside host but is susceptible to disinfectants. All-in/allout operation. Gasping. often with blood in lumen. Transmission between farms can occur by airborne particles or fomites. Keep susceptible stock separate from vaccinated or recovered birds. pheasants. Differentiate from Newcastle disease. Fairly slow lateral spread occurs in houses. lesions. Coughing of mucus and blood. 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. caseous plugs may be present. Isolation in CE CAMs.
Thirst. Rapid breathing. Post-mortem lesions Telescoping of the bowel. Signs Sudden onset of depression. Leukocytozoonosis Introduction Caused by Leucocytozoon species. Careful attention to feeding practices to avoid anticipation of feed arrival if on restricted feeding. usually in the lower small intestine. worms and other forms of enteritis are predisposing factors. rarely chickens. Prevention Control of coccidiosis and other causes of intestinal inflammation. Diagnosis Typical post-mortem lesions Treatment As appropriate for the underlying disease condition. ducks. Coccidiosis. protozoan parasites of turkeys. Loss of equilibrium. 88 . Signs Mainly sudden deaths. it may actually protrude at the vent and be cannibalised. The disease has a short course and morbidity and mortality are high.Intussusception Introduction A condition of chickens associated with increased intestinal motility. Simulid flies or culicoid midges are intermediate hosts. Different species of this parasite have been reported from North America. Asia and Africa. Anorexia. guinea fowl. Survivors may carry infection.
Loss of weight. Lymphoproliferative Disease (LPD) Introduction A Type C retrovirus infection of turkeys with low morbidity and high mortality. especially in enlarged spleen. age. cytology. Differentiate from Reticuloendotheliosis. Microscopically . Post-mortem lesions Focal tumours. Anaemia. Diagnosis History.megaschizonts in brains of birds with nervous signs. Persistent low mortality. Emaciation. Post-mortem lesions Splenomegaly. gametes in erythrocytes. disposal of recovered birds. Anaemia. Enlargement of abdomen. liver or bursa. Hepatomegaly. histology and blood smears. May be asymptomatic. Diagnosis Lesions. schizonts in liver. lesions. Treatment 89 . Signs Depression. Prevention Separation from intermediate hosts. Treatment None known.
direct electron microscope examination of intestinal contents. Diarrhoea in older birds may be an effect of on-farm infection. It is suspected that these viruses can be vertically transmitted and the most severe signs in young birds are associated with this. Poor feathering. Stunting (temporary). Malabsorption Syndrome. all-in/all-out production. Pale shanks in corn. Sometimes osteomyelitis and/or rickets. in future eradication.Tahir None. for example enteroviruses. North and South America and Australia. Pancreatic atrophy/fibrosis and pancreatic atrophy (rather variable).Abubakar. Treatment Daily cull of affected birds between 14 and 28 days. rotavirus etc. Pot-bellied appearance. Post-mortem lesions Enteritis. Signs Uneven growth. Poor management may contribute to the problem. The condition has been seen in Europe. control arthropods.(maize-) fed birds (often associated with orange intestinal contents and/or faeces). Diarrhoea. enterovirus-like particles. Runting/Stunting Introduction A condition of chickens and turkeys that may be associated with several different viruses. Poor early management (feed and water supply. Abnormal feathers ('helicopter wings' 'yellow-heads'). Diagnosis Pathology. temperature control) may lead to a similar picture in the absence of specific infection. Eating faeces. 90 . reoviruses.M. Prevention Good hygiene. Runting (permanent).
Marek's disease Introduction Marek's disease is a Herpes virus infection of chickens. lungs. fomites. From the 1980s and 1990s highly virulent strains have become a problem in North America and Europe. ovary. as well as more longstanding paralysis of legs or wings and eye lesions. The route of infection is usually respiratory and the disease is highly contagious being spread by infective feather-follicle dander.Prevention Good broiler farm hygiene. Morbidity is 10-50% and mortality up to 100%.Acute infiltration of the CNS and nerves resulting in 'floppy broiler syndrome' and transient paralysis. tests. In 'late' Marek's the mortality can extend to 40 weeks of age.Tumours of feather follicles. c) Cutaneous .poorly digested food enclosed in mucus. The virus survives at ambient temperature for a long time (65 weeks) when cell associated 91 . Affected birds are more susceptible to other diseases. Vertical transmission is not considered to be important. seen worldwide. Intestines of a young broiler chick suffering from malabsorption syndrome. and rarely turkeys in close association with chickens. They are distended with poorly digested feed. Figure 24. The disease has various manifestations: a) Neurological . muscles. Mortality in an affected flock typically continues at a moderate or high rate for quite a few weeks. Infected birds remain viraemic for life. etc. A sample of the faeces produced is shown at the bottom of the picture .Tumours in heart. b) Visceral . avoidance of intercurrent disease and management problems (such as chilling). both parasitic and bacterial. good parent nutrition and egg selection and santitation.
Vision impairment.lymphoid infiltration is polymorphic. deficiency of Ca/Phosphorus/Vitamin D. gonads. Loss of weight. Microscopically . Skin around feather follicles raised and roughened.Chicken Introduction Infection with Mycoplasma gallisepticum is associated with slow onset. distribution of lesions. kidney. pigeons and other wild birds. clinical signs. M. Genetics can help by increasing the frequency of the B21 gene that confers increased resistance to Marek's disease challenge. It is inactivated rapidly when frozen and thawed. turkeys. Differentiate from Lymphoid leukosis. wings and neck. Diagnosis History. Chronic Respiratory Disease . resistant strains. age affected. Prevention Hygiene. Signs Paralysis of legs.g. deficiency of thiamine. especially at the start of lay. Thickening of nerve trunks and loss of striation. histopathology. spleen. heart. all-in/all-out production. vaccination generally with 1500 PFU of HVT at day old (but increasingly by in-ovo application at transfer). game birds. botulism. Treatment None.and is resistant to some disinfectants (quaternary ammonium and phenol). association with other strains (SB1 Sero-type 2) and Rispen's. Grey iris or irregular pupil. Mycoplasma gallisepticum infection. lung. It is common practice to use combinations of the different vaccine types in an effort to broaden the protection achieved. Post-mortem lesions Grey-white foci of neoplastic tissue in liver.. Ducks and geese can 92 . chronic respiratory disease in chickens. and skeletal muscle.
and inadequate environmental conditions are predisposing factors for clinical disease. virulent E. and in lyophilised material. Occasional encephalopathy and abnormal feathers. Occasionally arthritis. In turkeys it is most associated with severe sinusitis (see separate description in the turkey section). aerosols. Inappetance. Intercurrent infection with respiratory viruses (IB. Suspect colonies may be identified by immuno-flourescence. airborne dust and feathers. sinuses. Catarrhal inflammation of nasal passages. In others it is actually increasing because of more birds in extensive production systems that expose them more to wild birds. coli infection). Fomites appear to a significant factor in transmission between farms. though in some countries this infection is now rare in commercial poultry. Haemophilus. Signs Coughing. Culture requires inoculation in mycoplasma-free embryos or. The condition occurs worldwide. exudates. Pasteurella spp.become infected when held with infected chickens. trachea and bronchi. morbidity may be minimal and mortality varies. coli. isolation and identification of organism. Diagnosis Lesions. Pericarditis. tenosynovitis and salpingitis in chickens. Perihepatitis (especially with secondary E. or by direct contact with birds. subsequent stress may cause recurrence of disease. The route of infection is via the conjunctiva or upper respiratory tract with an incubation period of 6-10 days. and to a lesser extent fomites. serology. In adult birds. Stunting. ART). 93 . Reduced hatchability and chick viability. demonstration of specific DNA (commercial PCR kit available). though infection rates are high. ND. Leg problems. more commonly in Mycoplasma Broth followed by plating out on Mycoplasma Agar. Spread is slow between houses and pens suggesting that aerosols are not normally a major route of transmission. Poor productivity. Post-mortem lesions Airsacculitis. Slow growth. Nasal and ocular discharge. Transmission may be transovarian. Survival seems to be improved on hair and feathers. Recovered birds remain infected for life. The infectious agent survives for only a matter of days outwith birds although prolonged survival has been reported in egg yolk and allantoic fluid.
subsequent stress may cause recurrence of disease. The route of infection is via the conjunctiva or upper respiratory tract with an incubation period of 6-10 days. aerosols. Productivity in challenged and vaccinated birds is not as good as in M. vitamin A deficiency. M. other Mycoplasma infections such as M. exudates. Suspect flocks should be re-sampled after 2-3 weeks. suspect reactions are examined further by heat inactivation and/or dilution. infection status is important for trade in birds. Effort should be made to reduce dust and secondary infections. Transmission may be transovarian. In some circumstances preventative medication of known infected flocks may be of benefit. hatchingeggs and chicks. tylosin.g. It is seen worldwide. and routine serological monitoring. These programmes are based on purchase of uninfected chicks. and fomites. synoviae and M. HI may be used. Infectious Sinusitis .-free stock. generally as a confirmatory test.g. therefore M. spiramycin. viral respiratory diseases. Recovered birds remain infected for life. biosecurity. PCR is possible if it is urgent to determine the flock status.Serology: serum agglutination is the standard screening test. all-in/all-out production. Some inactivated vaccines for other diseases induce 'false positives' in serological testing for 3-8 weeks. Differentiate from Infectious Coryza. meleagridis(turkeys). Mycoplasma gallisepticum infection.g. Aspergillosis.. fluoroquinolones. Prevention Eradication of this infection has been the central objective of official poultry health programmes in most countries. or by direct contact with birds. Live attenuated or naturally mild strains are used in some countries and may be helpful in gradually displacing field strains on multi-age sites. tetracyclines. Treatment Tilmicosin. though in many countries this infection is now rare in commercial poultry.Turkeys Introduction A slow onset chronic respiratory disease of turkeys often with severe sinusitis and associated with Mycoplasma gallisepticuminfection. Morbidity is low to moderate and mortality low. Elisa is accepted as the primary screening test in some countries. 94 .
tetracyclines. and in lyophilised material. demonstration of specific DNA (commercial kit available). Signs Coughing. Treatment Tilmicosin. all-in/allout production. malnutrition. serology. Nasal and ocular discharge. often with inspissated pus. tylosin. In some circumstances preventative medication of known infected flocks may be of benefit. Suspect colonies may be identified by immunofluorescence. Leg problems. especially Turkey Rhinotracheitis. intercurrent viral disease such as Newcastle disease (even lentogenic) and Turkey Rhinotracheitis are predisposing factors. Pericarditis. Suspect flocks should be re-sampled after 2-3 weeks. HI may also be used. Slow growth. spiramycin. 95 . requires inoculation in mycoplasma-free embryos or. Effort should be made to reduce dust and secondary infections. fluoroquinolones. although prolonged survival has been reported in egg yolk and allantoic fluid. isolation and identification of organism. Survival seems to be improved on hair and feathers. Culture. Swollen sinuses. of swabs taken from the trachea or lesions. Serology: serum agglutination is the standard screening test. Differentiate from viral respiratory disease. These are based on purchase of uninfected poults. Some inactivated vaccines induce 'false positives' in serological testing. Inappetance. Post-mortem lesions Swollen infraorbital sinuses. and biosecurity. Diagnosis Lesions. PCR is possible if it is urgent to determine the flock status. more commonly in Mycoplasma Broth followed by plating out on Mycoplasma Agar. Perihepatitis.The infectious agent survives for only a matter of days outwith birds. suspect reactions are examined further by heat inactivation and/or dilution. Stress. Prevention Eradication of this infection has been the central objective of official poultry health programmes in most countries. Stunting. Airsacculitis.
Mycoplasma iowae infection. Diagnosis Shows cross reaction in IFA to M. and can occur in other poultry and wild bird species. Infection occurs via the conjunctiva or upper respiratory tract and transmission among poults may be vertical. Treatment As for M. 96 . although DNA homology is only 40%.Mycoplasma immitans infection Introduction Infection with Mycoplasma immitans is seen in geese. some with down abnormality. Reduced hatchability.i.g. Post-mortem lesions Sinusitis. and partridges (UK). ducks (France). Prevention As for M. perhaps because all affected embryos fail to hatch. Signs Embryonic mortality. Post-mortem lesions Stunted embryos with hepatitis and enlarged spleens. venereal or horizontal. M. Leg lesions can be shown in inoculated birds but do not seem to occur naturally. Signs Swollen sinuses.g.g. Introduction Infection with Mycoplasma iowae is seen in turkeys.
This can increase hatchability by 510% in this situation. 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. The organism has also been isolated from raptors. When the vacuum is released the eggs draw in antibiotic solution which is subsequently absorbed through the shell membranes. Mortality is low. Crooked necks. Prevention Eradication of the infection from breeding stock. though up to 25% of infected birds show lesions at slaughter.i. maintenance of this status by good biosecurity. Transmission is venereal in breeders. Specialised dip tanks are subjected to negative pressure which partially collapses the air cell of the submerged eggs.-free stock. Antibiotics that have been used are tylosin and enrofloxacin. Infected parents may be asymptomatic. Treatment Pressure differential dipping has been used where breeder flocks are infected. The infective agent does not survive well outside the bird.Diagnosis Isolation and identification of the causative organism from dead-in-shell embryos. Introduction A disease of turkeys characterised by respiratory and skeletal problems caused by Mycoplasma meleagridis. Mycoplasma meleagridis infection. Slow growth. Infection is via the conjunctiva or upper respiratory tract with an incubation period of 6-10 days. In adult birds though infection rates are high. M. Mild respiratory problems. Predisposing factors include stress and viral respiratory infections. Infected eggs result in widespread distribution of infection and increased risk of further vertical transmission. purchase of M. 97 . Leg problems. Pathogenicity is quite variable. Signs Reduced hatchability. Stunting. with transovarian and then lateral spread in meat animals.m. morbidity may be minimal.
other respiratory viruses. In some circumstances preventative medication of known infected flocks may be of benefit. spiramycin. isolation and identification of organism. Culture requires inoculation in mycoplasma-free embryos or. 98 . M. Airsacculitis (rarely) seen in adult birds. more commonly in Mycoplasma Broth followed by plating out on Mycoplasma Agar. especially in commercial layer flocks. Effort should be made to reduce dust and secondary infections. Diagnosis Lesions. 11-21 days following contact exposure. and biosecurity. Survival of the infectious agent outwith the bird is poor but fomite transmission between farms is important.s. Mycoplasma synoviae infection. Vaccines are not normally used. These are based on purchase of uninfected poults. Mycoplasma synoviae. Spread is generally rapid within and between houses on a farm. whilst illness is variable and mortality less than 10%. Infected birds do develop some immunity. Treatment Tylosin. Prevention Eradication of this infection is also possible using similar techniques as for Mycoplasma gallisepticum. Infection rates may be very high. Suspect colonies may be identified by immuno-fluorescence. demonstration of specific DNA (commercial kit available). Transmission may be transovarian.culture used to confirm. all-in/all-out production. Infection is via the conjunctiva or upper respiratory tract with a long incubation period. serology.Post-mortem lesions Airsacculitis in infected pipped embryos and poults. Infectious Synovitis Introduction Infection with Mycoplasma synoviae may be seen in chickens and turkeys in association with synovitis and/or airsacculitis. It occurs in most poultry-producing countries. Predisposing factors include stress and viral respiratory infections. Differentiate from Mycoplasma gallisepticum. Birds infected from their parents seem to be immuno-tolerant and particularly prone themselves to transmit. Serology: SAG used routinely . or lateral via respiratory aerosols and direct contact. Infected males are particularly prone to transmit infection and may warrant special attention. tetracyclines. fluoroquinolones.
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. in ducks possibly heavy strains. caused by Clostridium perfringens and characterised by a fibrino-necrotic enteritis. Spores of the causative organism are highly resistant. Probiotics may limit multiplication of bacteria and toxin 102 . usually of the mid. Immobility.M. other debilitating diseases. Infection occurs by faecal-oral transmission. or Bacitracin in feed (e. Affected birds tend to be dehydrated and to undergo rapid putrefaction. Treatment of ducks is not very successful. Dark coloured diarrhoea. usually around 10%. amoxycillin). Signs Depression. phenoxymethyl penicillin.Tahir Necrotic Enteritis Introduction An acute or chronic enterotoxemia seen in chickens. neomycin and erythromycin are used in the USA. Intestinal contents may be dark brown with necrotic material. high levels of most growth promotors and normal levels of ionophore anticoccidials also help. Diagnosis A presumptive diagnosis may be made based on flock history and gross lesions Confirmation is on the observation of abundant rods in smears from affected tissues and a good response to specific medication. usually in less than 48 hours. Inappetance. turkeys and ducks worldwide. Water medication for 3-5 days and in-feed medication for 5-7 days depending on the severity. Sudden death in good condition (ducks).small intestine. 100 ppm). diet (high protein). Treatment Penicillins (e.g. Prevention Penicillin in feed is preventive. Closed eyes. Mortality may be 5-50%. Post-mortem lesions Small intestine (usually middle to distal) thickened and distended. high viscosity diets (often associated with high rye and wheat inclusions in the diet).g. in drinking water. Reflux of bile-stained liquid in the crop if upper small intestine affected.Abubakar. Intestinal mucosa with diptheritic membrane. contaminated feed and/or water. Predisposing factors include coccidiosis/coccidiasis.
Four manifestations have been identified: ND . ND .Neurotropic Velogenic . Newcastle Disease (Paramyxovirus 1) Introduction Paramyxovirus 1 or Newcastle Disease is a highly contagious viral disease affecting poultry of all ages.Mild disease. Morbidity is usually high and mortality varies 0-100%. The condition is rarely diagnosed in ducks but is a possible cause of production drops/fertility problems.Mortality and nervous signs in adult. which is of variable pathogenicity. fomites. Affected species include chickens. the upper has formed a thick crust of necrotic material. ND . 103 . Higher mortality is seen in velogenic disease in unvaccinated stock. ND . Signs are typically of disease of the nervous. visitors and imported psittacines (often asymptomatic). Other species can be infected including mammals occasionally (e.Mesogenic . The virus involved is Paramyxovirus PMV-1.Lentogenic . Transmission is via aerosols. conjunctivitis in man). sometimes subclinical.g. These viruses have sometimes been used as vaccines in previously immunised birds. In many countries local regulations or market conditions prevent the routine use of many of these options. Figure 25. Strains can be developed as vaccines. Severe lesions of necrotic enteritis affecting the small intestine of broilers.sometimes called 'asiatic' or exotic. It is not usually vertical (but chicks may become infected in hatcheries from contaminated shells). birds.Acute and fatal in chickens of any age causing neurological and some respiratory signs. It is highly virulent for chickens.production. less for turkeys and relatively apathogenic in psittacines. Intestinal lesions are absent. pigeons and ducks. Can affect any age. respiratory or reproductive systems. turkeys.Velogenic Viscerotropic (VVND) . The sample at the bottom of the picture is still focal.
HA+. haemorrhagic disease. and is ether sensitive. antibiotics to control secondary bacteria. Post-mortem lesions Airsacculitis. EDS-76. infectious coryza. Twisted neck. laryngotracheitis. Nervous signs. Cross-reactions have mainly been with PMV-3. It is confirmed by isolation in CE. avian influenza. intestine. caecal tonsil. Severe drop in egg production. Differentiate from Infectious bronchitis. encephalomyelitis. Samples . acid pH. pneumovirus infection. Coughing.The virus survives for long periods at ambient temperature. Diagnosis A presumptive diagnosis may be made on signs. Diarrhoea. Dyspnoea. However it is quite sensitive to disinfectants. Paralysis. formalin and phenol. Sudden Death Depression. rising titre in serology. IFA. Treatment None. middle ear infection/skull osteitis. HI with ND serum or DID (less cross reactions). Inappetance. for up to 12 months. Moult. Intestinal lesions primarily occur in the viscerotropic form. post-mortem lesions. intoxications. Signs Signs are highly variable and will depend on the nature of the infecting virus (see above). It is inactivated by temperatures of 56°C for 3 hours or 60°C for 30 min. 104 . encephalomalacia. Tracheitis. Pathogenicity evaluated by Mean Death Time in embryos.tracheal or cloacal. especially in faeces and can persist in houses (in faeces. dust etc). Haemorrhage in proventriculus. Necrotic plaques in proventriculus. intracerebral or IV pathogenicity in chicks. fumigants and sunlight. the infective dose and the degree of immunity from previous exposure or vaccination.
and occasionally gasping due to a plug of pus in the lower trachea. Use of Mycoplasma gallisepticum free stock under good management reduces the risk of vaccinal reactions. especially in breeding birds by the use of routine serological monitoring. Inactivated vaccines have largely replaced the use of live vaccines in lay but they do not prevent local infections. It is commonest in progeny of young parent flocks (relatively small yolks) or where managers are inexperienced. Morbidity is up to 10% and mortality close to 100%. Vaccination programmes should use vaccines of high potency. Use of spray application is recommended but it needs to be applied with care to achieve good protection with minimal reaction. snicking. and is associated with difficulty maintaining brooding temperature and poor management of feeders and drinkers. which are adequately stored and take into account the local conditions. Vaccinal reactions may present as conjunctivitis. HI has been used extensively. A typical programme may involve Hitchner B1 vaccine at day old followed by LaSota-type vaccine at 14 days. 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). The LaSota-type vaccine may even repeated at 35-40 days of age if risk is high. In some countries it has been customary to provide antibiotics prophylactically during periods of anticipated vaccinal reaction. Acute viral infections or heavily contaminated drinking water may have a similar effect to bad management in reducing feed intake. These tests do not directly evaluate mucosal immunity. It is common to monitor response to vaccination. 105 . Mortality peaks at 3-5 days for birds that fail to eat at all. vaccination. 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.Prevention Quarantine. however. whereas it tends to peak between 6-10 days for chicks that begin eating but then cease. biosecurity. To prevent or reduce vaccinal reactions in young chicks it is important that day old have uniform titres of maternal immunity. Figure 28. all-in/all-out production. Elisa is now also used.
in broiler parent chickens and also in large broiler chickens in various places. Diagnosis Based on post-mortem lesions.Deep Pectoral Myopathy Introduction This condition is so named because it was first identified in adult breeding turkeys in Oregon State. Post-mortem lesions Crop empty. Most organs normal. Differentiate from omphalitis/ yolk sac infection. 106 . age of collection and weight of hatching eggs. It has since been seen in turkeys.Signs Failure to grow. aspergillosis. good hygiene and biosecurity in brooding areas to minimise early disease challenges. Poor development. Because it is enclosed in a relatively unyielding membrane. It does not usually cause any mortality or obvious clinical signs and so it is usually identified after slaughter. bile staining of adjacent tissues. Prevention Review brooding management. Gizzard may be impacted with litter. Treatment Correction of management problems. any swelling of the muscle tends to cut off the blood supply. soluble multivitamin supplementation may help. good drinking water hygiene. or suffer necrosis. The condition can be reproduced by causing intense exercise of this muscle. Without adequate blood supply the tissue of the muscle begins to die. 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. Oregon Disease . Gall bladder distended. It is caused by a reduction in the blood supply to the deep pectoral muscles. nutrition of young parents.
If of very long duration. weighing birds etc). and. in particular excessive exercise. 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. thinning operations in meat birds. Prevention Avoidance of physical damage of this muscle. It is very difficult to detect affected carcases in standard meat inspection. It may also start to be enclosed in a fibrous capsule. the muscle may be swollen and pale. it may become a healed scar. Figure 26. The tissue in the centre is dry. 107 . This will normally be due to excessive flapping in association with management activities (e. Diagnosis Lesions. A typical case of the chronic stages deep pectoral myopathy in a broiler chicken. Post-mortem lesions Acute or chronic necrosis of the deep pectoral muscle on one or both sides. Transillumination of the breast may help identify affected carcases and may be worthwhile if the incidence is high.Signs None. If the condition is of over 7 days duration the muscle is dry and often shows greenish tinges.g. Treatment Not applicable. and flaking. with oedema within it and on its surface. greenish yellow. If recent. artificial insemination in breeding turkeys.
Growth is more rapid and consistent in an anaerobic jar. Within the poultry house it is likely to be by aerosols. It commonly exacerbates respiratory disease caused by pneumovirus infections in turkeys. severe bronchopneumonia. 108 . Reduced weight gain. ventilation problems. Some uncertainty exists about mechanisms of transmission. This was first identified as a new disease syndrome of turkeys in Germany in the early 1990s. ORT Introduction Ornithobacterium Infection is an infection of chickens and turkeys with the bacterium Ornithobacterium rhinotracheale(ORT). perhaps through survival of the organism on shell surfaces or shell membranes. coli infections. This can cause significant losses through condemnations.Ornithobacterium Infection. Cultures from the trachea of birds showing typical signs are preferred. Signs Coughing. The severity of its effects depends on the pathogenicity of the particular strain and other risk factors such as viral infections. E. preferably as a flock test comparing results before and after the challenge. It had been previously isolated in a number of other countries. Bordetella aviuminfection. Confirmation is by isolation of the organism. It is a Gram-negative pleomorphic organism. The range occurring in turkeys is wider than that seen in chickens. Inoculation of fresh material from a case can reproduce lung lesions similar to those caused by Pasteurella multocida infection in previously uninfected turkeys over 10 weeks of age. Diagnosis Clinical signs and lesions. In broiler chickens its main importance seems to be as a cause of airsacculitis in apparently healthy flocks that is only identified at slaughter. Most isolates are oxidase positive and galactosidase positive Serology using Elisa tests has been used. direct contact and drinkers. Important cofactors may include respiratory viral vaccines (Newcastle disease. field challenge with respiratory viruses. coli overgrowth may occur. Infectious Bronchitis). The infection is common in chickens and turkeys. and E. The slow-growing bacterium was named in 1994. sneezing. Reduced egg production. There is some evidence that hatcheries may play a role in the epidemiology. A range of sero-types have been identified. Post-mortem lesions Airsacculitis. tracheitis. The organism grows slowly producing tiny colonies on blood agar. age at infection etc.
Amoxycillin sensitivity remains good. though 54% were sensitive to tetracycline.there are issues relating to availability. Vaccination . ORT is a major problem on multi-age sites. In the USA in 1998 all strains were sensitive to penicillins and many other microbials. 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. regulation. In France and Belgium most strains were sensitive to enrofloxacin. it requires two doses.Treatment The sensitivity of ORT to antibiotic is highly variable.it is very sensitive in vitro to a range of chemicals. Prevention This is based on good hygiene. Some work has been done on live vaccine in the USA. chlortetracycline but not to enrofloxacin.amoxycillin at 250 ppm in water for 3-7 days or chlortetracycline at 500 ppm for 4-5 days. 109 . Preventative medication with the products listed in the previous section may be beneficial in some circumstances. Severely consolidated lung from an acute ORT infection in 14-week-old turkey growers. Some vaccines seem to have difficulty in producing a longlasting serological response to ORT. cost etc. Hygiene . Satisfactory disease control depends on good management and biosecurity. Figure 27. neomycin and enrofloxacin. Routine treatment . Vaccination of breeder flocks to protect progeny has shown benefits in chickens but. The lung is solid and covered by pus/ purulent exudate. Similar lesions may be found in Pasteurellosis. An inactivated vaccine is licensed for broiler parents in Europe. because of the age of slaughter. therapy and vaccination. also most are sensitive to tiamulin.
high production. Soft bones and beak. The green discolouration is used to identify carcases that require closer inspection of the other tissues. Drop in production. Prevention Unknown. Diagnosis Lesions. Cage Fatigue Introduction A condition of chickens. Treatment Not applicable . Birds rest squatting. Signs None. Birds go off legs. 110 . turkeys and ducks seen worldwide and due to Vitamin D or calcium deficiency. Osteoporosis. Post-mortem lesions Green discolouration of the liver at slaughter. Gram-variable pleomorphic bacteria have been isolated from affected livers and bones. Soft-shelled eggs. Predisposing factors include small body size. Signs Lameness.only identified at slaughter.Osteomyelitis Complex. Enlarged hocks. Turkey Introduction An association has been shown between green discolouration of the livers of turkey growers at slaughter and the occurrence of inflammatory lesions of bones and/or joints.
proper Ca and P levels and ratio.Tahir Post-mortem lesions Bones soft and rubbery. calcium carbonate capsules. Signs Depression. Diagnosis History. Beading and fracture of ribs.Yucaipa Disease Introduction An infection of chickens. signs. Vertical transmission does not usually occur. skeletal size and mineral content at point of lay are critical. lesions. Differentiate from Marek's disease. antioxidants. Epiphyses of long bones enlarged. whereas turkeys are more severely affected.Abubakar. Prevention Supplementation of vitamin D. Inappetance. Wild birds are believed to be especially important. place on litter.M. Paramyxovirus 2 . Beak soft. turkeys and passerine cage birds with Paramyxovirus PMV-2 results in disease with variable mortality. Transmission is by wild birds and fomites. Post-mortem lesions Not characteristic. In chickens it is usually mild. bone ash. 111 . As birds progressively mobilise skeletal calcium for egg production through lay. Coughing. spondylitis. Drop in egg production. Treatment Over-correct ration vitamin D. Parathyroids enlarged. depending on the species affected and whether infection is complicated by other factors and diseases.
Prevention Quarantine. haemorrhagic disease. Drop in egg production (turkeys). Post-mortem lesions No specific lesions. Loss of shell pigment Nervous symptoms (psittacines). Inappetance. 112 . IFA.Diagnosis Isolation in CE. laryngotracheitis. Paramyxovirus-3 Introduction Paramyxovirus PMV-3 infects turkeys. biosecurity. HI with ND serum or DID (less cross reactions). Differentiate from Infectious bronchitis. High mortality (cage birds). Coughing. all-in/all-out production. HI with ND serum or DID (less cross reactions). HA+. The infection is transmitted by birds. HA+. antibiotics to control secondary bacteria. IFA. Vertical transmission does not usually occur. occasionally chickens and psittacine cage birds. Signs Depression. antibiotics to control secondary bacteria. Mortality is usually low in poultry. Treatment No specific treatment. Treatment No specific treatment. Diagnosis Isolation in CE. EDS-76. including wild bird contact and fomites.
HA+. In both cases mortality can be high and can be associated with a marked depression in growth. Diagnosis Isolation in CE. 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.Prevention Quarantine. biosecurity. biosecurity. including wild bird contact and fomites. It is an infectious and transmissible cause of sudden increases in mortality in turkeys between 7 and 28 days of age. Vaccination has been used in turkeys but may not be cost-effective. Post-mortem lesions No specific lesions. Vertical transmission does not usually occur. Signs Reduction in egg production. Mortality is 0-5%. HI with ND serum or DID (less cross reactions). A range of 113 . all-in/all-out production. Prevention Quarantine. antibiotics to control secondary bacteria. IFA. The infection is inapparent in ducks and geese. A less acute form of the disease appears to produce more of a lingering mortality. all-in/all-out production. The infection is transmitted by birds. Mild respiratory signs. Paramyxovirus-6 Introduction Paramyxovirus PMV-6 infection of turkeys.
Picking at feed. pale brown. Reduced feed consumption and growth.mash and poor quality crumbles increase risk. Pendulous Crop Introduction A complex condition of turkeys and chickens associated with coarse fibrous feed. lesions.viruses have been isolated from affected flocks. Increased water consumption. A highly digestible diet with fat at 7. All-in/all-out production. seeking heat. Prevention Biosecurity to reduce the introduction of new infections into brooding facilities. Droppings watery. To replicate the condition in full it appears to be necessary to include bacteria in the inoculum. 114 . Treatment A range of antibiotics and arsenicals have been used to control the bacterial component of this condition. Liquid intestinal contents. eating litter. Post-mortem lesions Dehydration. Diagnosis Signs. huddling. Good quality diets of a suitable form . multivitamins and milk replacer products are helpful for nutritional support in the acute phase. Muscle atrophy. Increasing weakness. Emaciation. Wet litter. Signs Initial hyperactivity and increased vocalisation. This syndrome is clearly distinguished from typical viral enteritis in young turkeys because of the high mortality and severe growth depression. Weight loss. Overdistension of crop in young birds because of an interruption in feed supply may predispose. Effective terminal disinfection. Fluoroquinolone antimicrobials appear to be especially effective. Caseous cores in bursae (late in the process).5-8% will encourage feed intake and recovery.
spiruroid worm parasites of poultry and game birds. Diagnosis Signs. including crustaceans. grasshoppers and cockroaches. haemorrhage. and thickening of mucosa of proventriculus. necrosis. ulceration. Post-mortem lesions Crop distended with feed. may be impacted. have ulcerations and sometimes mycosis. Diagnosis Macroscopic examination of lesions. Tetrameres and Cyrnea are nematodes. Crop contents semi-liquid and foul smelling. Signs Anaemia. Lack of muscle tone. identification of worms. They are found in the mucosa of crop and proventriculus causing mainly inapparent infections. 115 . Proventricular Worms Introduction Dispharynx. lesions. Infection is by the oral route on exposure to the intermediate hosts. Post-mortem lesions Inflammation. Diarrhoea. if these can be identified. Emaciation in heavily infected young chicks (Tetrameres). Prevention Remove predisposing factors.Signs Enlargement of crop. Treatment None.
Treatment Not usually required. colibacillosis. wild birds. Post-mortem lesions Miliary lesions in a variety of organs but especially in the liver. Prevention Prevention of access to intermediate hosts. Diarrhoea. rodents and man with the bacterium Yersinia pseudotuberculosis. Pseudotuberculosis Introduction An infection of ducks. sulphonamides in feed. Prevention Good husbandry and hygiene. Treatment Tetracyclines. Ruffled feathers. duck viral hepatitis. adequate protection. 'hardening off'. tuberculosis. isolation. coccidiosis. Differentiate from Duck viral enteritis. Sometimes sudden death. other poultry. Signs Weakness. In peracute disease the only lesion may be enteritis. 116 . Diagnosis Lesions. The disease has a mortality of 5-75%.
Prevention Good management. capillariasis. Crop distended. Watery diarrhoea. Skin cyanosis of head. antibiotics. elimination of other causes. Differentiate from fowl cholera. toxin and possibly a virus infection.Tahir Pullet disease. vibriosis. diet and water supply.Abubakar. Pancreas chalky. Dark comb and wattles. Loss of appetite. mucoid casts in intestine. IBD and typhoid. It is associated with hot weather. multivitamins in water. Crop distension. molasses. Kidneys swollen. Treatment Adequate water supply. water deprivation. Avian Monocytosis Introduction A sudden onset condition of chickens early in lay with high morbidity and a mortality of 050%. coccidiosis. Drop in egg production. It was commonly reported prior to 1960 but is now rare. Bluecomb.M. Affected birds have an increase in circulating monocytes in their blood. hygiene. Catarrhal enteritis. lesions. Signs Depression. Diagnosis History. 117 . Post-mortem lesions Dehydration. Liver swollen with foci. Skeletal muscle necrosis. Dehydration.
carbamates. in nest boxes. Ornithonyssus bursae.Red Mite and Northern Fowl Mite Introduction Arachnid mites. Treatment Pyrethroids.itching. which are external parasites of chickens and turkeys. and good design of new equipment to limit harbourages for red mites. Pale comb and wattles. the Common Red Mite. feeds by sucking blood. fumigation and insecticide treatment at turnaround. vegetable oil and mineralbased products (both liquid sand dusts) have been used to control red mites in the environment. mainly at night and may transmit fowl cholera and other diseases. Filling of cracks and crevices. Birds restless. Post-mortem lesions Anaemia. Prevention Thorough cleaning. crevices etc. citrus extracts. Signs Presence of grey to red mites up to 0. Drop in egg production. Effective monitoring of mite numbers and implementation of control measures before birds are heavily infested improves control. For northern fowl mite it is essential to apply approved insecticides to the affected birds. Dermanyssus gallinae. organophosphates. cracks.7 mm. Loss of condition. Diagnosis Number and type of mites identified. Spots on eggs. 118 . May cause anaemia and death in young birds. 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. the Northern Fowl Mite spends its entire life cycle on the bird and can multiply more rapidly as a result. Staff complaints .
Avian pneumovirus. chloroform. Treatment None. The virus is generally resistant to disinfectants (ether. Post-mortem lesions Mild catarrhal tracheitis. may act as 119 .Abubakar. Dust. Infected birds may remain carriers for a few weeks. 'Mild Respiratory Disease' Introduction An adenovirus infection of chickens with a morbidity of 1-10% and a mortality of 1-10%. and other factors associated with poor ventilation. Opinions vary as to whether adenovirus can be characterised as a primary respiratory pathogen. prevention of immunosuppression. Diagnosis History. It may occur as an exacerbating factor in other types of respiratory disease. E. Prevention Quarantine and good sanitary precautions.Tahir Respiratory Adenovirus Infection. Signs Mild snick and cough without mortality. and by fomites. formaldehyde and iodides work better. The virus grows well in tissue culture (CE kidney. A number of respiratory viruses (Infectious Bronchitis. vaccinal and field strains) and bacteria (Ornithobacterium rhinotracheale. CE liver). Respiratory Disease Complex Introduction Respiratory infections in chicken and turkeys are seen worldwide but especially in temperate poultry-producing areas in winter months. pH). at least 12 sero-types have been described and these may be isolated from healthy chickens. lesions. Transmission may be vertical and lateral. coli) may be involved.M. Lentogenic Newcastle disease virus. intranuclear inclusions in liver. temperature. ammonia and other gases.
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. If condemned birds are included mortality may be more than 10%. Signs Snick. serology. Severe airsacculitis of thoracic air sacs in a broiler close to slaughter. Treatment Antimicrobial treatment of specific bacterial infections. Diagnosis Lesions. response to environmental changes. mortality 5. There is also percarditis evident (at top right). Rattling noises. Sneezing.predisposing factors. The air sacs are thickened and congested. Pericarditis. of course.catarrhal to purulent. Nasal exudate. Differentiate from Chronic Respiratory Disease (Mycoplasmosis).10%. Conjunctivitis. sanitation of drinking water. Figure 29. Airsacculitis. Morbidity is typically 10-20%. 120 . Head swelling. Prevention Effective ventilation. and have been cut into to reveal a cheesy (caseous) mass of pus. carefully applied appropriate viral vaccines. Post-mortem lesions Severe tracheitis with variable exudate . be challenged by some of these pathogens).
Signs There may be no obvious signs. Sometimes enteritis and proventriculitis (especially in broilers infected with contaminated Marek's disease vaccine). Reticuloendotheliosis. There is an incubation period of 5-15 days. ducks. Transmission is lateral and possibly transovarian. Diagnosis Pathology. A gradual increase in mortality and poor growth in broilers may be the main signs. and quail with morbidity up to 25%. Post-mortem lesions Neoplastic lesions in liver. Lympoid Tumour Disease Introduction A retrovirus infection of chickens. chick inoculation. Diarrhoea. Severe tracheitis is broilers with respiratory disease complex. usually higher in females than males. geese. Treatment None.Figure 30. Sometimes nodules in intestine and caecae. turkeys. 121 . and the infection can be spread by mosquitoes or in contaminated Marek's disease vaccines. spleen and kidney. Leg weakness. Both tracheas were congested and the upper sample had mucopurulent material in the lumen. Marked stunting when Marek's disease vaccine is contaminated.
Soft bones and beak. Treatment Over-correct ration with three times vitamin D for 2 weeks. or Vitamin D or 25-hydroxy vitamin D in drinking water. Prevention Supplementation of vitamin D. Reduction in bodyweight. Differentiate from Encephalomalacia. Post-mortem lesions Bones soft and rubbery. Poor growth. Diagnosis History. proper calcium and phosphorus levels and ratio. Hock swelling. lesions. turkeys and ducks worldwide. Signs Lameness. Rickets (hypocalcaemic) Introduction Vitamin D deficiency or phosphorus/calcium imbalance is seen in chickens. signs. Avoidance of contamination of live vaccines is the main control measure practised. Birds go off legs. antioxidants. 122 . Beak soft. Growth plates widened and disorganised. Femoral Head Necrosis.Prevention Formal control programmes have not been documented as the condition is sporadic and relatively self-limiting. Epiphyses of long bones enlarged. Beading and fracture of ribs. Parathyroids enlarged. Birds rest squatting.
Poor growth. Beading and fracture of ribs. turkeys and duck is seen worldwide. Birds rest squatting. Hock swelling. 123 .Tahir Rickets (hypophosphataemic) Introduction Phosphorus deficiency in chickens. Reduction in bodyweight. Parathyroids enlarged. Enlarged hocks. lesions (analyse Vitamin A or manganese as a guide to premix inclusion). Growth plates widened and disorganised.Abubakar. antioxidants. Soft bones and beak. Beak soft. signs. Some countries have regulations governing the use of phosphorus in fertiliser with a view to reducing water pollution.M. Even subclinical levels of this condition can predispose to Femoral Head Necrosis. proper calcium and phosphorus levels and ratio. Signs Lameness. Treatment Over-correct ration with 3 times vitamin D for 2 weeks. This has led feed manufacturers to try various approaches to reduce added phosphorus in diets. Intestinal diseases may reduce absorption. or vitamin D in drinking water. Birds go off legs. Diagnosis History. Epiphyses of long bones enlarged. Prevention Supplementation of Vitamin D. Post-mortem lesions Bones soft and rubbery.
It is not known if vertical transmission occurs though virus has been occasionally isolated from embryonated eggs.Ascaridia Introduction Ascaridia sp. seen worldwide. Signs Diarrhoea.Abubakar. Treatment No specific treatment for this infection. electron microscopy or Elisa on intestinal contents .5 g faeces). large . are nematode worm parasites. Control of secondary bacterial enteritis may require antimicrobial medication.submit 6 x . Use of a good electrolyte solution is beneficial in the acute stage of infection. A. columbae in pigeons.M. The life cycle is similar to that illustrated in the section on the caecal worm Heterakis. The parasite species vary: A. shorter in young birds. The route of infection is oral usually by direct ingestion of the embryonated egg and there is a 5-10-week prepatent period. pheasants. Diagnosis Demonstration of virus (PAGE. galli in fowl. The route of infection is oral and maximum viral excretion occurs 2-5 days post infection.Tahir Rotavirus Infection Introduction Rotavirus infection is seen in chickens. partridges and pigeons. Post-mortem lesions Viruses replicate mainly in the mature villous epithelial cells. except that the adults reside in the small intestine and earthworms are not significant paratenic or transport hosts. stout white worms up to 12 cms in length. guinea fowl. Prevention Good hygiene in brooding areas. Roundworm. turkeys. and A. dissimilis in turkeys. Adult birds can tolerate burdens asymptomatically. Virus may be found in asymptomatic birds. The 124 .
Post-mortem lesions Enteritis. especially for young birds. Figure 31. piperazine as locally approved. Poor growth. 125 . In the bottom left quadrant there are also some immature worms. Worms up to 12 cm in length in duodenum and ileum. oval smooth-shelled nonembryonated eggs in faeces.parasites may be transported by grasshoppers and earthworms and are resistant to environmental effects. Prevention Prevention of contamination of feeders and drinkers with faeces. A collection of mature roundworms (Ascaridia galli) recovered from the small intestine of a layer chicken in rear. Listlessness. Diarrhoea. pasture rotation and regular treatment. Wasting. Diagnosis Macroscopic examination with identification of worms. levamisole. mainly in young birds. Treatment Flubendazole. Signs Loss of condition.
Chickens are most commonly affected but it also infects turkeys. guinea fowls.Abubakar. Signs Severe lameness. Post-mortem lesions The fresh lesion contains a haematoma with the end of the ruptured tendon within or adjacent to it.Tahir Ruptured Gastrocnemius Tendon Introduction This is a condition causing severe lameness in roaster type meat chickens and more rarely in turkeys. Infections still occur worldwide in non-commercial poultry but are rare in most commercial systems now. Affected birds should be culled humanely as soon as they are identified. Reoviral or staphylococcal arthritis or tenosynovitis may predispose but many cases have no evidence of an inflammatory response. If there is a greenish tinge to the area of swelling it occurred a few days previously. Broiler chickens have an avascular area of tendon just above the hock that is the usual site of rupture. Ruptures of ligaments and joints are also occasionally seen. 126 . game birds. Broiler parents and brown-shell egg layers are especially susceptible. Prevention Establishment of a steady growth profile. Histology may be helpful in determining if there is an underlying inflammatory process. parrots. Salmonella Gallinarum. canaries and bullfinches. Fowl Typhoid Introduction Disease caused by one of the two poultry-adapted strains ofSalmonella bacteria. Avoidance of physical stresses on the musculoskeletal system through careful handling as well as careful design and layout of equipment. Treatment None. Salmonella Gallinarum. sparrows. The bird may have the hock dropped to the floor.M. This can cause mortality in birds of any age. Diagnosis Signs and lesions are obvious.
The bacterium is fairly resistant to normal climate. clean chicks. Inappetance. potentiated sulponamide. The route of infection is oral or via the navel/yolk. Yellow diarrhoea. Treatment Amoxycillin. Vaccines for fowl typhoid have been used in some areas. and/or congestion. recovered birds are resistant to the effects of infection but may remain carriers. Enrichment procedures usually rely on selenite broth followed by plating on selective media. mortality is increased in stressed or immunocompromised flocks and may be up to 100%. fluoroquinolones. even in adults. Diagnosis Isolation and identification. Thirst. pullorum disease and coli-septicaemia. LPS-based Elisa assays have been developed but not widely applied commercially. Transmission may be transovarian or horizontal by faecal-oral contamination. both live (usually based on the Houghton 9R strain) and bacterins. Engorgement of kidneys and spleen. surviving months. 127 . Reluctance to move. Tube and rapid plate agglutination tests have been the standard serological tests for many years but have only been validated for chickens. Differentiate from Pasteurellosis. but is susceptible to normal disinfectants. McConkey and non-selective agar is advisable. Post-mortem lesions Bronzed enlarged liver with small necrotic foci. In clinical cases direct plating on Brilliant Green. Enteritis of anterior small intestine. Signs Dejection. egg eating etc. As with other salmonellae. Prevention Biosecurity. tetracylines. Anaemia.Morbidity is 10-100%. Ruffled feathers.
Figure 32. Occasionally it can cause losses in adult birds. The bacterium is fairly resistant to normal climate. 'Bacillary White Diarrhoea' Introduction Disease caused by one of the two poultry-adapted strains ofSalmonella bacteria. in young broiler chickens. sparrows. The route of infection is oral or via the navel/yolk. Salmonella Pullorum. Salmonella Pullorum. this usually only causes mortality in birds up to 3 weeks of age. game birds. ring doves. Depression. 128 . Gasping. guinea fowls. Morbidity is 10-80%. Pullorum Disease. pale and shows focal necrosis. usually brown-shell egg layers. Signs Inappetance. mortality is increased in stressed or immunocompromised flocks and may be up to 100%. Ruffled feathers. the one on the right is slightly enlarged. White diarrhoea. surviving months but is susceptible to normal disinfectants. ostriches and peafowl. Similar lesions can be seen in Pullorum Disease and with other causes of septicaemia in young chicks. Closed eyes. Vent pasting. It still occurs worldwide in noncommercial poultry but is now rare in most commercial systems. Loud chirping. Bacterial septicaemia caused by Salmonella Gallinarum. The liver on the left is normal. parrots. Lameness. Transmission may be transovarian or horizontal mainly in young birds and may sometimes be associated with cannibalism. It affects chickens most commonly. but also infects turkeys.
S. Pullorum. recovered birds are resistant to the effects of infection but may remain carriers. Sero-types vary. liver. Derby. The route of infection is oral and transmission may be vertical as a result of shell contamination. As with other salmonellae. Salmonellosis. turkeys and ducks worldwide. chilling and omphalitis Treatment Amoxycillin. McConkey and non-selective agar is advisable. Anatum. paracolon. Differentiate from Typhoid. fomites and feed (especially protein supplements but also poorly stored grain). Newport. are capable of causing enteritis and septicaemia in young birds. other enterobacteria. Vaccines are not normally used as they interfere with serological testing and elimination of carriers. Paratyphoid. their presence may be significant with respect to carcase contamination as a potential source of human food poisoning. Gallinarum. it may become established on certain farms. and also other than S. S. fluoroquinolones.Post-mortem lesions Grey nodules in lungs. Enteritidis andS. Certain sero- 129 . but S. Intestinal or caecal inflammation. Splenomegaly. Even if these infections do not cause clinical disease. Many species are intestinal carriers and infection is spread by faeces. S. Diagnosis Isolation and identification. S. They infect chickens. Morbidity is 0-90% and mortality is usually low. Paratyphoid Infections Introduction Salmonellae bacteria other than the species specific sero-typesS. Regardless of the initial source of the infection. In clinical cases direct plating on Brilliant Green. Urate crystals in ureters. S. in the environment or in rodent populations. Prevention Eradication from breeder flocks. Montevideo. tetracylines. Bredeney are among the more common isolates. Typhimurium (which are considered separately). Enrichment procedures usually rely on selenite broth followed by plating on selective media. poteniated sulponamide. gizzard wall and heart. Caecal cores.
Rappaport-Vassiliadis) followed by plating on two selective media will greatly increase sensitivity. However this has the potential to reveal the presence of salmonellae that are irrelevant to the clinical problem under investigation. but are susceptible to disinfectants that are suitable for the particular contaminated surfaces and conditions. Vent pasting.types are prone to remain resident in particular installations (e. Unabsorbed yolk. Predisposing factors include nutritional deficiencies. fluoroquinolones. Temperatures of around 80°C are effective in eliminating low to moderate infection if applied for 1-2 minutes. Foci in liver. other bacterial infections and ornithosis (in ducks). Good management. neomycin. especially in dry dusty areas. Enteritis. Diagnosis Isolation and identification. The bacteria are often persistent in the environment. In clinical cases direct plating on Brilliant Green and McConkey agar may be adequate. Differentiate from Pullorum/Typhoid. other enterobacteria. Focal necrotic intestinal lesions. Ruffled feathers. This approach is often used in the heat treatment of feed. 130 . S. Post-mortem lesions In acute disease there may be few lesions. amoxycillin. Pericarditis. chilling. Dehydration. Senftenberg in hatcheries). Closed eyes. or absent. Diarrhoea.g. Enrichment media such as buffered peptone followed by selective broth or semi-solid media (e. Dejection. applied at sufficient concentrations. Chemotherapy can prolong carrier status in some circumstances. Signs Signs are generally mild compared to host-specific salmonellae.g. Treatment Sulphonamides. tetracyclines. Loss of appetite and thirst. Cheesy cores in caecae. inadequate water.
these bacteria are often specifically cited in zoonosis control legislation. chilling. and. many species are intestinal carriers and infection may be carried by faeces. Temperatures of around 80°C are effective in eliminating low to moderate infection if applied for 1-2 minutes. on the one hand.Typhimurium has remained relatively stable though the spread of the highly antibiotic-resistant strain DT104 in various farmed species gives some reason for concern. especially in dry dusty areas. S. hatcheries and feed mills is required for effective control. especially phage type 4. fumigate eggs. The prevalence of S.Typhimurium are presented separately from other sero-types of Salmonella because. The route of infection is oral. all-in/all-out production. Infection results in a strong immune response manifest by progressive reduction in excretion of the organism and reduced disease and excretion on subsequent challenge. inadequate water and other bacterial infections. Routine monitoring of breeding flocks. Feed and feed raw material contamination is less common than for other sero-types. because there are differences in the epidemiology as compared to other salmonellae. but are susceptible to disinfectants that are suitable for the particular contaminated surfaces and conditions. Typhimurium infections Introduction Salmonella Enteritidis and S. applied at sufficient concentrations. fomites and on eggshells. turkeys and ducks cause problems worldwide with morbidity of 0-90% and a low to moderate mortality. This approach is often used in the heat treatment of feed. Salmonellosis. Enteritidis and S. Vertical transmission may be either by shell contamination or internal transovarian contamination of yolk. 131 . Salmonella Enteritidis. secondly. good feed. clean nests. mills. competitive exclusion. elimination of resident infections in hatcheries. These are the predominant sero-types associated with human disease in most countries. Infections in chickens.Prevention Uninfected breeders. care in avoiding damage to natural flora. Many infected birds are culled and others are rejected at slaughter. has become much more common in both poultry and humans since the early 80s. Predisposing factors include nutritional deficiencies. The bacteria are often persistent in the environment. breeding and grow-out farms. Vaccines are not generally used for this group of infections.
good feed. fluoroquinolones in accordance with the sensitivity. amoxycillin.Signs Dejection. Prevention Uninfected breeders. Routine monitoring of breeding flocks. It is possible to detect reactions with specific antigens in agglutination tests but competitive and direct Elisa tests are more commonly used today. fumigate eggs. S. Rappaport-Vassiliadis) followed by plating on two selective media will greatly increase sensitivity. Early depletion of infected breeding stock is required in some countries such as those of the European Union.Pullorum serum agglutination tests. Lost of appetite and thirst. Stunting in older birds. tetracyclines. Post-mortem lesions In acute disease there may be few lesions. other enterobacteria such as E. elimination of resident infections in hatcheries. infection Diagnosis Isolation and identification. Diarrhoea. Enrichment media such as buffered peptone followed by selective broth or semi-solid media (e. Unabsorbed yolk. Perihepatitis. mills. Pericarditis. Treatment Sulphonamides.Enteritidiscauses cross-reactions which may be detected with S. Focal necrotic intestinal lesions. Good management. In clinical cases direct plating on Brilliant Green and McConkey agar may be adequate. Foci in liver. Misshapen ovules in the ovaries in S. Ruffled feathers. hatcheries and feed mills is required for effective control.E. competitive exclusion. care in avoiding damage to natural flora.g. coli. Dehydration. Infection 132 . Vent pasting. Cheesy cores in caecae. Enteritis. neomycin. Closed eyes. However this has the potential to reveal the presence of salmonellae that are irrelevant to the clinical problem under investigation. Differentiate from Pullorum/Typhoid. all-in/all-out production. breeding and grow-out farms. Chemotherapy can prolong carrier status in some circumstances. clean nests.
are especially prone to increasing salpingitis. Some birds may 'lay' a caseous mass of pus (which may be found in a nest or on the egg belt). The control of infection in this area is probably achieved by ciliated epithelium that mostly wafts a carpet of mucus towards the cloaca. The oviduct is a hollow tube joining the normally sterile environment of the body cavity with the cloaca. Distended abdomen. Signs Sporadic loss of lay. Post-mortem lesions Slight to marked distension of oviduct with exudate. Anything that damages the epithelium or disturbs normal oviduct motility is likely to increase the likelihood of salpingitis. leaking urates.results in a strong immune response manifest by progressive reduction in excretion of the organism and reduced disease and excretion on subsequent challenge. Vaccines are increasingly being used for S. Peritonitis. which normally has many millions of potentially pathogenic bacteria. It is a complex condition of chickens and ducks associated with various infections including Mycoplasma and bacteria (especially E. or may proceed upwards from the cloaca. Infection may spread downwards from an infected left abdominal air sac. Salpingitis Introduction Salpingitis is an inflammation of the oviduct. Lesions. May form a multi-layered caseous cast in oviduct or be amorphous. Systemic viral infections that cause ovarian regression or damage to the oviduct or cloaca. Damaged vents. Death. both inactivated (bacterins) and attenuated live organisms. Diagnosis Use the signs to select birds for culling and post-mortem investigation. Bacteriology of oviduct.). coliand occasionally Salmonella spp. Typhimurium infection. Enteritidis and S. 133 .
Treatment Multivitamins. Signs Stand on toes shaking. Prevention Care in transport of brooded poults. Morbidity is 10-20%. use healthy parent flocks. Shaky Leg Syndrome Introduction A condition of turkeys with a course of often 3-4 weeks. Use of a suitable antimicrobial may be beneficial for birds in the early stages and if associated with efforts to minimise risk factors. releasing poults into larger areas and in handling heavier birds. Diagnosis Clinical examination.Treatment Birds with well-developed lesions are unlikely to respond to medication. possibly associated with tendon injury. aspirin may be helpful if locally approved. 134 . Post-mortem lesions None. Shaking or quivering of legs after rising. Prevention Control any septicaemia earlier in life. immunise effectively against respiratory viral pathogens common in the area. exclusion of other problems.
Dehydration. Filtered intestinal contents from affected flocks appear to be capable of reproducing the condition. and/or carbohydrate absorption are disturbed resulting in a hypoglycaemia. Signs and lesions. Birds in good condition die after showing neurological signs. probably because they are growing faster. Avoidance of interruptions in feed supply. Paralysis. Males are more susceptible than females. Treatment Leave affected chicks undisturbed. Mortality drops off as sharply as it started. Coma. Prevention Good sanitation of the brooding house.Spiking Mortality of Chickens Introduction This is a condition characterised by a sudden increase in mortality in young. Death. This appears to be a multifactorial condition. Avoidance of physical stress. 135 . rapidly growing broiler chickens. 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. Orange mucoid droppings. Signs Tremor. Diagnosis Pattern of mortality. Excess fluid in lower small intestine and caecae. Feed intake. Minimise stress. electrolytes and glucose solution to flock. Provide multivitamins. suggesting a viral component. typically 7-14day-old. Post-mortem lesions Mild enteritis.
is an intestinal spirochaete that can be associated with inflammation of the large intestine in a broad range of mammals and birds. Brachyspira pilosicoli. Thirst. vaccines in some countries. Treatment Various antibiotics including penicillin. Liver enlarged with small haemorrhages. Diagnosis Haematology. and occasionally by infected faeces. grouse and canaries with morbidity and mortality up to 100%. It is transmitted by arthropods. previously known as Serpulina pilosicoli. geese. 136 . Cyanosis.Spirochaetosis Introduction The bacterium Borrelia anserina infects chickens. Weakness and progressive paralysis. The bacterium is poorly resistant outside host but may be carried by Argas persicus for 430 days. ducks. It has been associated with typhilitis. Drops in egg production may be seen in both systemic and intestinal forms Post-mortem lesions Marked splenomegaly. reduced egg production. Signs Depression. diarrhoea. Mucoid enteritis. Necrotic foci. Often diarrhoea with excessive urates. isolate in chicken eggs or chicks or poults.g. Prevention Control vectors. pheasants. Argas persicus. e. Spleen mottled with ecchymotic haemorrhages. turkey. and egg soiling in chickens.
Signs Sitting on hock or rumps. That on the left shows the typical lesion of spondylolisthesis. Post-mortem lesions Anterior-posterior rotation of the bodies of the last or penultimate thoracic vertebrae resulting in scoliosis just anterior to the kidney. Prevention Selection for satisfactory conformation in primary breeding. The sample on the right is normal. Kinky-back Introduction A complex condition of broiler chickens with a morbidity of 1-5% and low mortality associated with rapid growth and possibly having a genetic component.Tahir Spondylolisthesis. 137 . Treatment None. lesions. with rotation of the body of the vertebra and the pinching of the spinal column that causes paralysis. May walk backwards. legs extended forward. Figure 33.M. Diagnosis Symptoms. These are cross-sections of the spinal column of 4-5-weekold broilers.Abubakar. Use of wings to help in walking.
These include good breeder nutrition. Staphylococcosis. Diagnosis Clinical signs. and careful monitoring of incubation conditions. Infection is usually by the respiratory route with an incubation period of 2-3 days seen after artificial infection. Damaged skin due to nutritional deficiencies (such as of biotin) may also be a point of entry. The type of chick box liners and the feeding papers used in the brooding house can also influence the occurrence of the condition. aureus and seen in chickens and turkeys worldwide. avoidance of excessive hatching egg storage.Tahir Spraddle Legs or Splay Leg Introduction Occurs in all species in the recent hatchling. mainly S. either accidental or induced by interventions such as beak trimming.M. and toe trimming may be a portal of entry with subsequent spread via the bloodstream to the typical sites of lesions. Staphylococcal Arthritis. Bumble Foot Introduction Caused by Staphylococcus bacteria.Abubakar. Morbidity is usually low and mortality 0-15% though affected birds will often be culled on humane grounds. Signs Legs splay and chick is unable to stand. Treatment None. Prevention All measures that improve chick vitality at hatching are beneficial in reducing this problem. 138 . Post-mortem lesions Gross lesions are not usually evident. Wounds.
Prevention Good hygiene in the nest.g. particularly of parent birds. Lameness. Competitive exclusion with a non-pathogenic Staphylococcushas been shown to be effective (no commercial products yet available based on this technology). Swollen above the hock and around the hocks and feet. trauma. low stress and prevention of immunosuppression from any cause will all tend to help. most commonly in the plantar area of the foot or just above the hock joint. Mycoplasma spp. the hatchery and in any intervention or surgery (processing.. chronic stress. synoviae. Some sudden deaths from acute septicaemia if very heavy challenge. Predisposing factors include reovirus infection. Differentiate from septicaemia or tenosynovitis due to Colibacillosis. Treatment Antibiotics. isolation and identification of pathogen. in accordance with sensitivity. Possibly vaccination against reovirus infection. Recovered birds may have some immunity but vaccination with staphylococci has not been found to be helpful in preventing the disease to date. This condition is a cause of sudden deaths in ducklings of 2-3 weeks of age. especially M. e. and by fomites.Transmission occurs in the hatchery and in the general farm environment. 139 . Infected joints may have clear exudate with fibrin clots. Good management. and imunosuppression. Streptococcus bovis Septicaemia Introduction An infection of ducks with the bacterium Streptococcus bovis. This may progress to abscess formation in these areas. Salmonella spp. Low mobility. Post-mortem lesions Tenosynovitis.. Diagnosis Lesions. toe clipping). Signs Ruffled feathers.
lesions.Signs Sudden deaths. Sodium deficiency can appear very similar at about the same age . possibly metabolic. The atria of the heart have blood.). Livers heavier than those of pen-mates (as a percentage of bodyweight. Prevention Good husbandry and hygiene. extra care in the immediate post-brooding period. Lung congestion and oedema. Affected well-grown birds may appear to have died from smothering. Diagnosis History. isolation. the ventricles are empty.affected birds respond well to saline injection and will actively seek out salt scattered in the litter. Liver congestion. most are found lying on their back. Serum accumulation in lung (may be little if examined shortly after death). Post-mortem lesions Intestine filled with feed. Splenic hyperplasia. Treatment Amoxycillin. Signs Sudden death in convulsion. 140 . 'Flipover' Introduction A condition of broiler chickens of unknown cause. Leg weakness or incoordination in a few birds. Haemorrhages in muscles and kidneys. It can be induced by lactic acidosis and about 70% of birds affected are males. Sudden Death Syndrome. Post-mortem lesions Beak cyanosis.
Prevention Lowering carbohydrate intake (change to mash). Treatment Flubendazole is effective at a 60 ppm in diet. Most have intermediate invertebrate hosts such as beetles or earthworms. use of dawn to dusk simulation and avoidance of disturbance. Cestodes Introduction Cestodes are tapeworms that are seen in many species. Signs It is doubtful if any signs are produced under most circumstances. Check your local regulations. they may not be host specific. low intensity light. 141 . lighting programmes. however it may not have a zero withdrawal in commercial egg layers. feed restriction.Diagnosis Birds found on back with lack of other pathology. Treatment None possible. or birds' access to them. Post-mortem lesions Occupy space in intestine and create small lesions at point of attachment. Diagnosis Identification of the presence of the worms at post-mortem examination. Tapeworms. Prevention Control the intermediate hosts.
Diagnosis Gross pathology. TD Introduction A complex condition seen in chickens. mild lesions may require histology to distinguish from other problems. Lixiscope may identify in vivo as early as 2 weeks of age. Treatment None. and proximal metatarsus. Post-mortem lesions Plug of cartilage in proximal end of tibia. Prevention Genetic selection using the Lixiscope to identify bone phenotype. Signs There are usually no signs unless the condition is severe. Microscopically . Vitamin D3 supplementation. small ovoid lacunae and more matrix than normal. turkeys and ducks. chloride levels and acid/base balance. Mature tapeworms with their heads (scolices) embedded in the intestine. It may be associated with rapid growth and have a nutritional factor. distal tibia. modifications of calcium and phosphorus ratios. 142 .Figure 34. Lameness. Tibial Dyschondroplasia. in decreasing order of frequency. Differentiate from rickets. Swelling and bowing in the region of the knee joints.a mass of avascular cartilage with transitional chondrocytes.
These parasites are more likely to be a problem of small scale poultry production in the tropics. Morbidity is close to 100% and mortality is 5-100%.Abubakar. and is also found on mammals.Tahir Ticks Introduction Argas persicus is an external parasite of poultry and wild birds. Transmissible Enteritis. and may also transmit spirochaetosis and Pasteurella infection. spends little time on host. Post-mortem lesions Anaemia. Signs Anaemia. others are avian coronaviruses closely related to infectious bronchitis virus. The infection is seen in turkeys and sometimes pheasants. Prevention As for red mite control. with 143 . Diagnosis Identification of the presence of the parasites. Occasionally paralysis from toxins in the tick saliva.M. Weakness. Emaciation. Reduced productivity. Skin blemishes. Insecticide sprays in these areas are more likely to be effective than treatment of the birds. Bluecomb Introduction Some coronaviruses involved in this condition are considered to be bovine coronaviruses (or closely related thereto). Treatment Elimination of cracks and crevices in the poultry housing. It is more common in warm climates. Transmission is lateral with birds and faeces. than in commercial poultry in temperate climates.
rapid spread. The course of the disease is about 2 weeks and birds then remain carriers for months. The viruses survive in frozen faeces for months.
Anorexia. Depression. Frothy diarrhoea. Subnormal body temperature. Darkening of the head. Loss of weight. Huddling.
Dehydration. Emaciation. Enteritis with petechial haemorrhages. Froth ingesta. Sometimes casts. Pancreas chalky. Urates in kidneys/ureters.
Reproduction with filtered contents, isolation in turkey eggs, electron microscopy, immunofluorescence, Elisa. Commercial M4I IB Elisa will detect some infections.
Warmth and good management, antibiotics, milk replacer, potassium chloride. Disinfect and rest houses for 3-4 weeks.
All-in/all-out production, good hygiene and biosecurity, good management.
Trichomoniasis, Canker, Frounce
Trichomonas gallinae is a protozoan parasite of pigeons and doves (canker), raptors (frounce), turkeys and chickens. It has variable pathogenicity. Morbidity is high and mortality varies but may be high. Transmission is via oral secretions in feed and water, and crop milk.
Mouth open. Drooling and repeated swallowing movements. Loss of conditon. Watery eyes in some birds. Nervous symptoms (rare).
Yellow plaques and raised cheesy masses in mouth, pharynx, oesophagus, crop and proventriculus. Raptors may have liver lesions.
Lesions, large numbers of protozoa in secretions. Differentiate from Pox and candidiasis.
Previously approved products included dimetridazole, nithiazide, and enheptin. Organic arsenical compounds (where approved) and some herbal products may be of some benefit in managing this problem in food animals.
Eliminate stagnant water, eliminate known carriers, add no new birds.
A bacterial infection, caused by Mycobacterium avium, of poultry, game birds, cage birds etc. Morbidity and mortality are high. Transmission is via faecal excretion, ingestion, inhalation, offal and fomites. The disease has a slow course through a flock. The bacterium resists heat, cold, water, dryness, pH changes and many disinfectants.
Severe loss of weight with no loss of appetite. Pale comb. Diarrhoea. Lameness. Sporadic deaths.
Grey to yellow nodules attached to intestine. Granulomas in liver, spleen and many other tissues, even bone marrow.
Isolation, acid-fast stain in tissues, TB test. Differentiate from Lymphoid leukosis.
Market after one season, hygiene, cages, elimination of faeces etc.
A condition of turkeys possibly associated with Bordetella avium(previously designated Alkaligenes faecalis) infections. This bacterium usually causes mild respiratory disease in only a proportion of the flocks, and low mortality. It can be synergistic with other respiratory pathogens such as Ornithobacterium,Pasteurella spp, Mycoplasma spp. and pneumoviruses.
Decreased appetite, weight gain and feed efficiency. Loss of voice. Ocular and nasal discharge. Conjunctivitis. Snick. Dyspnoea.
Excessive mucus in nasal passages and trachea. If there is secondary E. coli infection then pneumonia, airsacculitis and perihepatitis.
Clinical signs, isolation of agent.
maternal antibody may protect. Prevention All-in/all-out production. Diagnosis Signs. Serology.Antibiotics are not very effective. chlorinate drinking water. Eggs depigmented and thin-shelled. Prevention All-in/all-out production. Signs Decreased appetite. Treatment Antibiotics are not very effective. vaccination . Rapid transmission occurs laterally. Turkey Rhinotracheitis (Adult) Introduction A disease of turkeys caused by the viruses of the Pneumovirus genus. Morbidity is 10-100% and mortality 1. vertical transmission is uncertain. Paramyxoviridae. Loss of voice. Post-mortem lesions Serous rhinitis and tracheitis. possibly involving fomites. isolation of ciliostatic agent.30%. 147 . chlorination of drinking water.live primer followed by inactivated. Good drinking water hygiene. Sudden drop in production that lasts 2-3 weeks. control respiratory stressors. Ocular and nasal discharge. control respiratory stressors.
Ocular and nasal discharge. maternal antibody may protect. airsacculitis and perihepatitis. sometimes pus in bronchi. Snick. control respiratory stressors. serology (using an Elisa test to demonstrate rising titre). mortality is 1-25%. If there is secondary E. chlorinate drinking water. Morbidity varies.Abubakar. Morbidity is 10-100% and mortality 1. possibly involving fomites.Tahir Turkey Rhinotracheitis (in rear) Introduction A disease of turkeys caused by the viruses of the Pneumovirus genus. Transmission may be by direct or indirect contact and possibly vertical. Prevention All-in/all-out production. Birds remain carriers for up to 16 days. Conjunctivitis. Sinusitis. isolation and identification of the ciliostatic virus. 148 . Dyspnoea. Treatment Antibiotics are not very effective. Rapid transmission occurs laterally. Signs Decreased appetite. Turkey Viral Hepatitis Introduction An infection of turkeys caused by an unidentified virus. weight gain and feed efficiency. coli infection then pneumonia. vertical transmission is uncertain.M.30%. Post-mortem lesions Serous rhinitis and tracheitis. Diagnosis Clinical signs. Loss of voice. Vaccination at day-old seems to be most effective. Paramyxoviridae.
149 . Treatment None. Gastrocnemius tendon may slip. Twisted leg Introduction A complex condition seen in chickens and turkeys. Depression and sporadic deaths in birds in good condition. Bile staining. Congestion. Distortion at hock. Focal haemorrhage. Various angulations of leg. Microscopically . Valgus/varus. Grey to pink foci in the pancreas. Post-mortem lesions Linear twisting of growth of long bones. environment and high growth rate. Morbidity is 1-20% and mortality is low. with good management many birds recover. bacterial and fungal infections. lesions pathognomonic. Factors involved may include genetics.Signs Signs are usually subclinical. Post-mortem lesions Grey foci (c. Differentiate from histomonosis.no inclusion bodies. Prevention Good sanitation and management. 1 mm) coalescing. Signs Lameness. Diagnosis Isolation in CE. nutrition.
Watery white faeces (quail). which may coalesce and may be round or lenticular. The condition occurs worldwide. Anaemia. Ruffled feathers. The bacterium resists boiling for 3 minutes. Signs Listlessness. Pale yellow membranes. Prevention Selection for good conformation in primary breeding. E. Treatment None. intertarsal angulation up to 10% is physiological. The route of infection is oral and transmission is from faeces of sick or carrier birds or via flies. tenella. greater than 20% is abnormal. Turkeys. Ulcerative Enteritis. arthritis and synovitis. Differentiate from perosis. brunetti). but mainly ileum and caecae. and E. game birds and pigeons may also be affected. Drooping wings. Diarrhoea. Post-mortem lesions Deep ulcers throughout intestine. lesions. 150 . Partially closed eyes. Adoption of optimal nutrition and growth patterns for the economic objectives of the production system. Diagnosis Symptoms.. Retracted neck. IBDV and overcrowding. Quail disease Introduction Ulcerative Enteritis is an acute. It can start suddenly and cause high mortality: 100% in quail and 10% in chickens. highly contagious disease of chickens and quail caused by the bacterium Clostridium colinumand characterised by ulcers of the intestines and caecae. Changed angulation of tibial condyles. Blood in intestine. necatrix. Predisposing factors include Coccidiosis (especially E. Peritonitis (if ulcers penetrate).
colinum in anaerobic conditions (the agent is often present in pure culture in liver). Morbidity is low. Necrotic foci in liver. amoxycillin. Signs Dejection. Diarrhoea. Confirmation is on absence of other diseases and isolation of Cl. coccidiosis. The infective agent is rather resistant to environment and disinfectants. Figure 35. Diagnosis A presumptive diagnosis may be made on history and lesions. possibly probiotics. penicillin (50-100 ppm in feed). Response to treatment should occur in 48 to 96 hours. salmonellosis. Differentiate from histomonosis ('Blackhead'). Loss of condition. Tetracyclines. 151 . Prevention Infection-free birds. Inappetance. and disease is precipitated by stress. multivitamins. low level antibiotics as per treatment. Wall of the caecum of a chicken suffering from ulcerative enteritis Vibrionic Hepatitis. Avian Infectious Hepatitis Introduction An insidious onset disease of chickens caused by Vibrio bacteria. necrotic enteritis. all-in/all-out production. trichomoniasis. birds remaining carriers for months. Transmission is by faecal contamination. Bacitracin. Treatment Streptomycin (44 gm/100 litres water). Treat for coccidiosis if this is a factor.
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.
M. Diagnosis Signs. Nasal and ocular discharge. Microscopically . lesions. Prevention Supplementation of diet with vitamin A. Post-mortem lesions Eyelids inflamed and adhered. As in the case of other nutritional deficiencies. 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). Excessive urates in kidneys and ureters. Eyelids stuck shut with thick exudate. 155 .squamous metaplasia of epithelia. good quality raw materials. antioxidant. Differentiate from Infectious coryza. Drowsiness. Poor feathering. feed formulation. infectious sinusitis etc. chronic fowl cholera. Pale comb and wattles. classic signs of deficiency are very rare in commercial poultry fed complete diets. Signs Poor growth.Tahir Vitamin A Deficiency.Abubakar. Treatment Vitamin A in drinking water.
Simple deficiency is now rare as diets are usually well supplemented. They act in a broad range of metabolic pathways. 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. See the separate discussion under Chondrodystrophy and Fatty Liver and Kidney Syndrome. Signs These may be summarised: Perosis Curled Toe Paralysis Paralysis/'Stargazing' Dermatitis/Scaly Skin Mouth Lesions Conjunctivitis Anaemia Fatty Liver and Kidney Syndrome Poor Feathering Loose feathers Hatchability problems Embryo with clubbed down Thiamine (B1) Riboflavin (B2) Pantothenic acid Pyridoxine (B6) Niacin Folic Acid Cyanocobalmin (B12) Biotin Post-mortem lesions Usually the gross lesions are non-specific. including growth in the young animal.Tahir Vitamin B Deficiencies Introduction The B complex vitamins are water soluble and not stored to any significant extent in the body. Some deficiencies induce characteristic microscopic effects. because a continuous supply is required. response to supplementation. Vitamin deficiencies are especially prone to cause problems of hatchability.M. Diagnosis Signs. 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 . However. exclusion of specific diseases. and egg production in the layer. Most will reduce productivity.Abubakar.
seen worldwide. The problem is associated with feed rancidity typically in diets with high fat. Steatitis. Exudative Diathesis. Staggering. Paralysis. Good quality multivitamin solutions are beneficial in the supportive care of a range of problems characterised by reduced feed intake. drinking water supplementation with that vitamin is ideal and usually results in a rapid response in birds that are still drinking.may be appropriate (faster. characterised by oxidation of various tissues and caused by Vitamin E deficiency. Blood-stained or greenish subcutaneous oedema. less expensive) to analyse feed for a marker substance such as manganese rather than testing for vitamin levels. Falling over. White streaks in muscle. The balance of vitamins present should be similar to the daily nutritional requirement of the stock concerned. Muscular Dystrophy Introduction A spectrum of diseases of chickens and turkeys. Treatment If a specific vitamin deficiency is suspected. occasionally ducklings and other birds. Haemorrhage. Encephalomalacia. 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. Necrosis. Uncontrolled movements. Vitamin E Deficiency. Signs Imbalance. Encephalomalacia and exudative diathesis tends to be seen in young birds of 1-5 weeks of age. Green wings. 157 . Muscular dystrophy is seen more frequently in older and mature birds. Post-mortem lesions Swollen cerebellum with areas of congestion. Ventral oedema.
especially E . Treatment Vitamin E and/or selenium in feed and/or water. good quality raw materials. toxicities. Differentiate from Encephalomyelitis. 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. 158 . hatchers or chick boxes. Vent pasting. use of floor eggs. Loss of appetite. Diarrhoea. Signs Dejection.Diagnosis Signs. inadequate hatchery hygiene or poor incubation conditions. selenium. Swollen abdomen. Pseudomonas.Proteus. Omphallitis Introduction A condition seen worldwide in chickens. Post-mortem lesions Enlarged yolk sac with congestion. Staphylococci. It is seen where there is poor breeder farm nest hygiene. antioxidant. histopathology. Morbidity is 1-10% and mortality is high in affected chicks. Broad-spectrum antibiotics where there are extensive skin lesions.coli. 'bangers'. 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. feed rancidity. Abnormal yolk sac contents (colour. Disease occurs after an incubation period of 1-3 days. Yolk Sac Infection. and poor hygiene of setters. Closed eyes. consistency) that vary according to the bacteria involved. necrotic dermatitis. response to medication. Various bacteria may be involved. lesions. for example poor hygiene of hatching eggs. Prevention Proper levels of vitamin E.
159 . Treatment Antibiotics in accordance with sensitivity may be beneficial in the acute stages. There should be routine sanitation monitoring of the hatchery.g. sanitation of eggs. however the prognosis for chicks showing obvious signs is poor. most will die before 7 days of age. Prevention Prevention is based on a good programme of hygiene and sanitation from the nest through to the chick box (e. Differentiate from incubation problems resulting in weak chicks. Confirmation is by isolation and identification of the bacteria involved in the internal lesions. clean nests. Multivitamins in the first few days may generally boost ability to fight off mild infections. exclusion of severely soiled eggs.Diagnosis A presumptive diagnosis is based on the age and typical lesions. separate incubation of floor eggs etc. frequent collection.