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