Poultry Diseases and Their Treatment

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.

Post-mortem lesions
   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

Post-mortem lesions
        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.


renamed Salmonella Arizonae.Prevention Good husbandry and hygiene. Signs         Dejection. Post-mortem lesions      Enlarged mottled liver. 'hardening off'. Inappetance. mainly in North America. 4 . and also horizontal. It affects turkeys. older birds are asymptomatic carriers. Mortality is 10-50% in young birds. Autogenous bacterins sometimes used. Paralysis. Transmission is vertical. cloudiness in eye. rodents. Inactivated and attenuated vaccines available in some countries. and is not present in the UK turkey population. Huddling near heat. reptiles. Arizona infection. Diarrhoea. feed etc. correct house relative humidity. Nervous signs. Cheesy plugs in intestine or caecum. Erosions of the cartilage of the hock joint in a duck with chronic Riemerella anatipestifer infection. Figure 40. Blindness. Congestion of duodenum. transovarian. through faecal contamination of environment. rigid depopulation and disinfection. Foci in lungs. from long-term intestinal carriers. sulphonamides in feed. Vent-pasting. adequate protection. Unabsorbed yolk sac. Arizonosis Introduction Caused by the bacterium Arizona hinshawii.

Pericarditis. Perihepatitis. spectinomycin. General venous congestion. Diagnosis Isolation and identification. high altitude. mortality 1-2% but can be 30% at high altitude. Ascites Introduction Associated with inadequate supplies of oxygen. Prevention Eradicate from breeder population. Differentiate from Treatment Injection of streptomycin.    Salpingitis. Dyspnoea. and respiratory disease. poor ventilation and physiology (oxygen demand. Severe muscle congestion. good nest and hatchery hygiene. fumigation of hatching eggs. or gentamycin at the hatchery is used in some countries. Formerly in-feed medication with nitrofurans was also used. Ascites is a disease of broiler chickens occurring worldwide but especially at high altitude. Ophthalmitis. Lungs and intestines congested. Dilation of the ventricle. The disease has a complex aetiology and is predisposed by reduced ventilation. 5 . Signs       Sudden deaths in rapidly developing birds. Recumbency. methods as per Salmonella spp. Post-mortem lesions       Thickening of right-side myocardium. Thickening of atrioventricular valve. Progressive weakness and abdominal distension. Poor development. monitor sensitivity. Pulmonary arterial vasoconstriction appears to be the main mechanism of the condition. salmonellosis. inject eggs or poults with antibiotics. coli-septicaemia. may be related to type of stock and strain). Morbidity is usually 1-5%. Possibly cyanosis.

Pericardial effusion. Prevention Good ventilation (including in incubation and chick transport). Spleen small. Vitamin C (500 ppm) has been reported to be of benefit in South America. A cardiac specific protein (Troponin T) may be measured in the blood. avoid any genetic tendency. 6 . Transmission is by inhalation exposure to an environment with a high spore count. ducks. This may offer the ability to identify genetic predisposition. Rapid breathing. turkeys. Ascites. Drowsiness. Microscopic . Absidia etc. etc. The infection has an incubation period of 2-5 days. penguins. The fungus can infect plant material and many species of animals including birds and man. worldwide. Occasionally similar lesions are produced by other species ofAspergillus or even other fungi such as Penicillium. control respiratory disease. Nervous signs (rare). Morbidity is usually low. but may be as high as 12%.cartilage nodules increased in lung. caused by Aspergillus fumigatus. Thirst. Mortality among young affected birds is 5-50%. Aspergillosis Introduction A fungal infectious disease. in which the typical sign is gasping for breath. Differentiate from broiler Sudden Death Syndrome and bacterial endocarditis. especially in young chicks. waterfowl. Signs  Acute        form: Inappetance. Silent gasping. Diagnosis Gross pathology is characteristic. Treatment Improve ventilation. there is usually little bird-to-bird transmission. Weakness. game birds. Spores are highly resistant to disinfectants. It affects chickens.     Liver enlargement. Sometimes the same organism causes eye lesions or chronic lesions in older birds.

Environmental spraying with effective antifungal antiseptic may help reduce challenge. Post-mortem lesions    Yellow to grey nodules or plaques in lungs. The means of transmission is unknown but 7 . mortality none. Epidemic tremors for its effect in young birds. quail. Prevention Dry. trachea. good quality litter and feed. Morbidity 5-60%. Amphotericin B and Nystatin have been used in high-value birds. See Avian Encephalomyelitis. may have greenish surface.  Wasting.Tahir 2  Chronic Forms:  Ocular discharge (ocular form only). Thiabendazole or Nystatin has been used in feed. Figure 8. Diagnosis This is usually based on the signs and lesions and microscopic examination for the fungus.Abubakar. hygiene. Treatment Usually none. turkeys. typically by putting small pieces of affected tissue on Sabouraud agar. preferably after digestion in 10% potassium hydroxide. Brain lesions may be seen in some birds with nervous signs. Avian Encephalomyelitis Egg Drop Introduction Avian encephalomyelitis virus infection in laying bird causes inapparent infection or drops in egg production. pheasants and occurs in most poultry-producing countries. Differentiate from excessive exposure to formalin or vaccinal reactions in day olds and from heat stress in older birds. 'Furry' airsacculitis in aspergillosis of an adult duck. Growth occurs in 24-48 hours and colonies are powdery green/blue in appearance. plaques in peritoneal cavity. It may be confirmed by isolation of the fungus.M. It affects chickens. The powdery surface is dark green in colour. Conjunctivitis/keratitis. air sacs.

Imbalance. Vertical transmission is very important. It has a worldwide distribution.probably by faecal contamination of environment. Immunity is usually long lasting. with an oral infection route. Dull expression. Prevention Vaccination of breeders/layers at 9-15 weeks. Virus in faeces may survive 4 weeks or more. incubation >10 days. water etc. transmission occurs over about 1-2 weeks. some lateral. 8 . small (5-10%) and lasting no more than 2 weeks. Treatment None. Paralysis. Epidemic Tremors Introduction Avian encephalomyelitis is a viral disease of the central nervous system of chickens. Morbidity 5-60% depending on the immune status of the majority of parents. EDS76. Differentiate from Infectious Bronchitis. and there is serious disease in the progeny (see next section). Predisposed by immunosuppression. Post-mortem lesions  None. In breeders there may be a drop in hatchability of about 5%. subsequent disease in progeny if breeders. feed. mortality high. lateral transmission is probably by the oral route. Diagnosis History. Virus in faeces may survive 4 weeks or more. Signs      Nervous signs. pheasants. rising titre to AE virus. now Elisa is used more commonly. turkeys. Ataxia and sitting on hocks.The embryo protection test has been used in the past. Serology . attenuated or not. Signs   Drop in egg production. The route of infection is transovarian with an incubation period of 1-7 days. Avian Encephalomyelitis. and quail. lentogenic Newcastle disease.

Effectively all 9 . The definitive classification of high pathogenicity is an intravenous pathogenicity test (IVPI) in 6-week-old chickens result of greater than 1. Microscopic . Immunity is long lasting. A.nonpurulent diffuse encephalomyelitis with perivascular cuffing. especially in turkeys. partridges.2 . Marek's disease. In addition official control measures disrupt trade in poultry products from affected areas. 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. signs. quail. Enterococcus hirae infection. Avian Influenza-Highly Plague Introduction Pathogenic (HPAI). Differentiate from Newcastle disease. its pathogenicity is variable. 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. Mycotic Encephalitis. turkeys. The higher the proportion of the chickens dying or showing signs the higher the IVPI. Brain abscess. Orthomyxovirus type A. vitamin deficiency (E. and isolates are designated sero-type/ species/location/reference number/year/subtype designation(H/N). The embryo protection test has been used in the past. now Elisa is used more commonly. Histopathology is usually diagnostic and IFA. attenuated or not. Diagnosis A presumptive diagnosis is based on the history. and ostriches. Post-mortem lesions     Gross lesions are mild or absent. and/or viral isolation may be carried out if required. the equivalent of the World Health Organisation for animal diseases. riboflavin). and lack of significant lesions. Tremor of head. toxicities. EE (especially in pheasant in the Americas). Prevention Vaccination of breeders at 9-15 weeks. The cause is a virus. Tremor may be inapparent but is accentuated if chicks are held inverted in the hand. The virus infects chickens. pigeons. This viral disease can cause exceptionally high mortality. pheasants. ducks. This is a test in which the virus is inoculated into susceptible chickens that are then kept under observation. There may be focal white areas in gizzard muscle (inconstant). Treatment None. neck and wings.

It can result in inapparent infection. A serious outbreak occurred in The Netherlands in 2003 with a few linked cases in Belgium and one in Germany. 550%. Depression. Because of this. Cyanosis of comb/wattles. in the years 1983-84. by acid pH. The virus replicates mainly in respiratory tissues of chickens and turkeys but in the intestinal tract of clinically normal waterfowl. clothing. Pakistan. equipment. Highly pathogenic avian influenza A (HPAI) viruses of the H5 and H7 HA subtypes have been isolated occasionally from free-living birds. Mexico and. Apathogenic and mildly pathogenic influenza A viruses occur worldwide. Avian Influenza is a potential zoonosis. Nervous signs such as paralysis. Morbidity is high but mortality usually relatively low. Cessation of normal flock vocalisation. Ovarian regression or haemorrhage.g. air sacs and conjunctiva. conjunctivitis or severe pneumonia.birds are considered to be at risk of infection. Diarrhoea (often green). but possibly by the conjunctival or respiratory route and the incubation period is 3-5 days. Signs            Sudden death. waterfowl. Swollen face. can survive 4 days in water at 22°C. Drops in egg production. OIE and other bodies are currently examining ways to improve control of LPAI. More recently outbreaks have occurred in Australia. and the high mortality that 'low-path' AI can cause in turkeys. especially faeces. Outbreaks due to HPAI were recorded in the Pennsylvania area. The route of infection is probably oral initially. Marked loss of appetite. Italy). in northern Italy. Coughing. Broken contaminated eggs may infect chicks in the incubator simulating vertical transmission. over 30 days at 0°C. reduced feed consumption. H5 viruses of low pathogenicity may become highly pathogenic usually after circulating in poultry flocks for a time (Pennsylvania. It is inactivated by a temperature of 56°C in 3 hours and 60°Cin 30 min. drinking water. Infections with other pathogens (e. 10 . Post-mortem lesions   Inflammation of sinuses. Nasal and ocular discharge. The small number of human deaths associated with HPAI appear to have resulted from direct exposure to infected birds on farm or in markets. by oxidising agent and by formalin and iodine compounds. It can remain viable for long periods in tissues. Avirulent in one species may be virulent in others. See current OIE records for up to date information on distribution of HPAI. trachea. even with 'low pathogenicity' strains. The virus is moderately resistant. from December 1999. Transmission is by direct contact with secretions from infected birds. Pasteurella) may increase mortality. USA.

though there is high mortality of affected birds. Turkey lesions tend to be less marked than those of chickens. Diagnosis A presumptive diagnosis may be made on history and postmortem lesions. with considerable strain-to-strain variation. Treatment None. Morbidity is low. Survivors can be expected to have a high degree of immunity but may harbour virulent virus. HA+. disinfection. while ducks may be symptomless. The incubation period is 10-20 weeks. Commercial Elisa test kits are now available. cleaning. nutrition and antibiotics may reduce losses. but good husbandry. quarantine. The agar gel precipitation test is non-group-specific and is used to confirm any positives. It has occured in Europe. all-in/all-out production. controlled marketing of recovered birds. DID+. Congenitally infected birds tend to remain 11 . NDV-. 21-day interval to re-stocking should be followed. Transmission is by congenital infection from antibody-negative females. bacterial sinusitis in ducks. Subcutaneous oedema of head and neck. Muscles congested. vaccinated birds may remain carriers if exposed to the infection. etc. fowl cholera. lateral transmission by faecal-oral route (this declines as the bird ages). Haemorrhage in proventricular and gizzard mucosae and lymphoid tissue of intestinal tract. However. correct disposal of carcases. Vaccines have been used in recent outbreaks in Mexico and Pakistan. Vaccination is not normally recommended because. bleeding and vaccination needles. Confirmation is by viral isolation in chick embryo. In outbreaks a regime of slaughter. Dehydration. infectious laryngotracheitis. This condition has until now been seen only in meat-type chickens.      Necrosis of skin of comb and wattles. Prevention Hygiene. Minimise contact with wild birds. as with many such tests occasional false positive reactions can occur. isolation. lesionless carriers of highly pathogenic virus. To be effective inactivated vaccines must be the right subtype for the particular situation (H5 will not protect against H7 and vice versa). Eradication by slaughter is usual in chickens and turkeys. although it may reduce losses initially. Differentiate from Newcastle disease. North and South America. Avian Leukosis (Serotype J). Myelocytomatosis Introduction Caused by an avian retrovirus. other respiratory infections.

histology. Most characteristically are chalky white tumours in the bone marrow. Treatment None. 'Shedders' . Differentiate from Marek's disease. Separation in vaccination. Prevent/ reduce cross-infection in hatchery and on farm. Minimise stress. Loss of weight. age.an Elisa test is aviailable to identify antibody positive birds. Prevention Checking of antigen in the albumen is a basis for eradication . 12 .80% produce infected chicks.antibody negative. Two cell types may be found in the same tumour. Microscopic . 'nonshedders' . Lymphoid Leukosis. sacral joint. lesions. Serology . birds with egg antigen will be antibody negative. Splenomegaly and enlarged kidneys also occur. Persistent low mortality. Enlargement of abdomen. Handle clean lines before infected lines. often with tumour foci. Critical hatchery practices:     Separate infected and uninfected lines. liver. Many are asymptomatic. preferably on separate hatch days and in separate machines.most but not all. Signs       Depression. There is also evidence that it is slightly more sensitive than conventional testing.only 3% produced infected chicks. ribs. shed virus and develop tumours. ultimately identification of virus by isolation and/or PCR. Diagnosis History. Post-mortem lesions     Liver enlargement. PCR testing of embryonally infected chicks using DNA testing is uniformly positive for blood and faecal samples.tumours usually contain well-differentiated myelocytes. Emaciation. Virus survival is poor but sufficient to allow cross contamination in hatcheries and on farm in rear. particularly of the sternum.

Farm practices:     Brood and rear lines separately and maintain separate for as long as possible. myxosarcomas. Mortality tends to be chronically higher than normal for a prolonged period. In lymphoid leukosis the incubation period is about 4-6 months. Egg production is somewhat reduced. other tumours. fibrosarcomas. myeloblastosis (see Sero-type J). Persistent low mortality. Differentiate from Marek's disease. Delay live vaccine challenges. cytology. The causative viruses are rapidly inactivated at ambient temperature and on exposure to most disinfectants. erythroblastosis. Microscopic . Morbidity is low but mortality high. coligranuloma. liver or bursa. Minimise group sizes. Vertical transmission is most important by infection of the egg white in infected breeders (who are long-term carriers). Avoid migration errors (birds unintentionally moving between pens).egg layers are generally more susceptible to lymphoid leukosis. It affects chickens worldwide with susceptibility varying considerably among different strains and types of stock . Loss of weight. A complex of viral diseases with various manifestations such as lymphoid leukosis.cells lymphoplastic Diagnosis History. 13 . osteopetrosis. Avian Leukosis. initially in the bursa. There may be increased susceptibility to other infectious diseases due to damage to the immune system. kidney etc. Liver may be very large. lateral transmission is poor but infection may occur by the faecal-oral route. it may be as short as 6 weeks for some of the other manifestations. lesions. then liver. age. Post-mortem lesions   Focal grey to white tumours. Leukosis/Sarkoma Group Introduction Lymphoid Leukosis. spleen. Signs       Depression. Emaciation. Enlargement of abdomen. Many are asymptomatic. especially in young birds.

South America and North America. Figure 9.Treatment None. This was a case of Myelocytoma Avian Leukosis (Sero-type J). first isolated from poults in South Africa in 1978. vertical transmission is uncertain. Loss of voice.checking of antigen in the albumen is a basis for eradication (see Sero-type J for details). Prevention Good hygiene. Ocular and nasal discharge. Conjunctivitis. Two subgroups have been identified on the basis of the G-protein sequence: A (original UK isolates) and B (original southern Europe isolates). Snick. 14 . guinea fowl and possibly pheasants seen in Europe. Dyspnoea. Facial and head swelling (though this can occur in other conditions). Avian Rhinotracheitis 'Swollen Head Syndrome' Introduction A viral disease of chickens. Africa. The incubation period is 5-7 days. morbidity is 10-100% and mortality can be 110%. control arthropods. weight gain and feed efficiency. all-in/all-out production. As for many infections. fomites can be important in moving infection between farms. Diffuse lymphoid tumours in an enlarged liver from a mature broiler parent hen. eradication . turkeys (see separate summary). There is rapid lateral transmission with infection by aerosol through the respiratory route. It is caused by a pneumovirus of the Paramyxoviridae family. Signs        Decreased appetite.


Post-mortem lesions
  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.


Beak Necrosis
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.

Post-mortem lesions
 See signs.

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.

Bedbug Infestation
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.


Post-mortem lesions
 Anaemia.

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.

Post-mortem lesions
  Enlarged spleen (over 1gm/kg bodyweight, often with pale foci). Liver usually enlarged, sometimes with subcapsular Affected birds may also have: haemorrhage.


It may be helpful to control other conditions which may be occurring at the same time. Scabs around eyes and beak. in embryos. Allin/all-out production. Post-mortem lesions   See signs. Elisa tests have been developed experimentally. 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. Histopathology may also be used but the findings are not specific to this condition. Prevention Thorough cleaning and disinfection after depletion of an affected flock. A RT-PCR test may be used to detect viral RNA in tissues. Thickened skin under foot pad. Chondrodystrophy. Reduced feed intake and blood sugar can precipitate fatty liver and kidney syndrome. Including Fatty Liver and Kidney Syndrome Introduction Biotin deficiency has occured in turkeys and chickens in many countries but is now rare in birds consuming properly formulated feeds. Viral particles may be demonstrated in bile.    Lung congestion Ovarian regression Yolk peritonitis Pale foci and haemorrhages in pancreas. Pale livers and kidneys in fatty liver and kidney syndrome. Diagnosis Typical signs and lesions. Must be confirmed by laboratory tests. Good biosecurity. 18 . Drinking water which is well chlorinated should be helpful in reducing challenge by this route. Sudden deaths in fatty liver and kidney syndrome. Leg weakness. webbing between toes. Treatment No specific treatment known. Signs       Poor growth. Biotin Deficiency.

bedbugs. response to treatment/prevention. lesions. Loss of vent feathers. The parasites are 1-6 mm in size and their life cycle takes about 3 weeks. Drop in egg production.naturally present in many raw materials. Scabs around vent. Crusty clumps of eggs ('nits') may be visible at the base of feathers. Biting Lice Introduction Various species of lice are common external parasites of poultry worldwide. Treatment Malathion powders and pyrethroid sprays where approved for bird application. Menocanthus stramineus is the most pathogenic and is said to be capable of causing anaemia in heavy infestations. Lice eggs stuck to feathers. Parasites on birds. They are spread by direct contact between birds and by litter etc. 19 . has very low bioavailability. Differentiate from mites. especially around vent. Differentiate from pantothenic acid deficiency (skin lesions). Check flocks regulary for rapidly moving insects at the base of the feathers on the abdomen or around the vent. Prevention Supplementation of diets with biotin . Loss of condition. Post-mortem lesions  Usually none. Irritation. Signs         Lack of thrift in young birds. Away from birds adults survive about 4-5 days. Treatment Addition of biotin in feed or water. Diagnosis Identification of the parasites.Diagnosis Signs. may be some feather damage and crustiness of skin.

as the larvae within eggs are not killed by most products. The condition tends to occur near to rapidly flowing streams. Eggs and larvae survive through the winter to cause new infestations in the following year. season. Prevention Similar measures as for mosquito control. 20 . although these insects can travel up to 15 miles. Biological control using a strain of Bacillus thuringensis has had some success and is preferable to insecticides. The flies transmit leucocytozoonosis and also a filarial parasite in ducks. Post-mortem lesions  Anaemia. especially in autumn and winter and treat if required. Weekly treatments are required. Diagnosis Anaemia. It is usually necessary to treat twice at a 7-10 day interval to fully control the condition. local history. Treatment Treatment is difficult. 5 mm long and found in North and South America that are external parasites of birds and mammals. Swarms of flies. Effective removal of all organic material at flock depletion should be practised in all-in/all-out production systems. Blackfly Infestation Introduction Grey-black hump-backed flies. Examine for lice regularly. Signs   Anaemia in young birds.Prevention Avoid direct contact with wild and backyard poultry.

suspect food and stagnant ponds. supportive treatment if justifiable. mouse toxicology on serum or extract of intestinal contents. signs. progressive flaccid paralysis of legs. is also quite typical. Treatment Remove source of toxin. Maggots or putrid ingesta may be found in the crop. Differentiate from acute Marek's disease ('Floppy Broiler Syndrome') by histology of the brain. antibiotics. The toxin and bacterial spores are relatively stable and may survive for some time in the environment. maggots) is consumed by the birds. especially in hot weather. wings then neck. turkeys. This will reduce the risk of botulism both in the poultry and in any grazing animals on land where poultry litter is spread. Feathers may be easily pulled (chicken only). A soiled beak. carcases. then sudden death. because it rests on the litter. and toxin-containing material (pond-mud. The toxin is produced in decaying animal (usually carcases) and plant waste. 21 . Mild enteritis if has been affected for some time. Morbidity is usually low but mortality is high. Toxin may also be produced by the bacteria in the caecum. selenium. Diagnosis History. Signs    Nervous signs. 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. The single most important measure is careful pick-up and removal of all dead birds on a daily basis. ducks and other waterfowl occurring worldwide and caused by a bacterial toxin produced byClostridium botulinum mainly types A / C. Prevention Preventing access to toxin. weakness. Affected broilers tend to settle with eyes closed when not disturbed. Post-mortem lesions     Possibly no significant lesions.

bacteria. or paratenic hosts with partially developed (L2) larvae. Poor feather cover and caked or wet litter are predisposing factors. Diagnosis Based on lesions. leg weakness. the cause of Blackhead. They are found worldwide. and infection withStaphylococcus spp. Earthworms may be transport hosts for eggs. Caecal Worm Introduction Heterakis gallinae. up to 1. Signs  None. 22 . There is an incubation period of 2 weeks for eggs to embryonate. Prevention Good litter management and handling. in chronic cases. control of leg problems. Signs  Swelling over the keel bone with bruising and discolouration. nematode parasites of poultry and game birds. Morbidity may reach more than 50% but the condition is not fatal.5 cm in length that occur in the caecum. Treatment Not usually appropriate. Heterakis gallinaeeggs and larvae are a transport hosts for Histomonas. The meaning of the technical terms relating to parasite life cycle are defined in the glossary. and a four-week prepatent period.Breast Blister Introduction A complex condition of chickens and turkeys occurring worldwide associated with trauma. are small whitish worms with a pointed tail. Morbidity is high but it is not associated with mortality. Infection is by the oral route. Post-mortem lesions  Inflammation of sternal bursa along the keel bone which may. give way to scar tissue.

Diagnosis Adults can be seen in caecal contents at post-mortem examination. possibly with nodule formation. Signs   Paralysis. Predisposing factors include heat stress with reduced feed intake and panting. or by an earthworm which is in turn ingested by a chicken. 23 . an undeveloped egg as found in fresh faeces. Death from respiratory and cardiac failure. The egg may be ingested directly by a chicken. are effective. and the embryonated egg. especially broiler parents. Calcium Tetany Introduction A metabolic disease of chickens.Post-mortem lesions  Inflammation of caecum. The life cycle ofHeterakis showing the location of adults. Treatment Flubendazole. Figure 11. Prevention Avoiding access to earth and earthworms. Levamisole. Routine anthelmintic treatment.

There is an annual cycle with increased risk of infection in the summer months in some countries. Campylobacter jejuni is the commonest species found in poultry. lack of other significant lesions. Diagnosis This is made on signs. managing birds for maximum uniformity. It may be that management that favours dry litter reduces the risk of infection and/or transmission within the flock. Congested lungs. are bacteria that commonly infect a broad range of livestock species. principally in the caecae. 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. Treatment Provide 5 gm of oyster shell per hen on 3 successive days along with vitamin D in drinking water. Active ovary with egg in oviduct. Differentiate from IB 793b. In poultry they tend to multiply in large numbers in the hindgut. The reason for this is unclear. There are indications that plantar pododermatitis. Prevention Keep pullet flocks on low calcium diet until 5% production hen/day.Post-mortem lesions    Cyanosis. 24 . pets and wild animals. All campylobacters are delicate organisms that survive for relatively short periods outside the host unless protected by organic material. other acute infections and other causes of sudden death. biofilm or engulfed by protozoa. Campylobacter Infection Introduction Campylobacter spp. lesions. Infected poultry are a potential reservoir of this zoonosis. and response to treatment. 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'.

avoidance of contact with pets and other farmed species. Treatment Not required on clinical grounds. sourcing of water from high quality supplies. Prevention In principle. The organism is sensitive to air so swabs should be collected into transport medium and other samples placed in airtight containers with minimal airspace. For this reason it may be difficult to stop the spread of infection between houses once it becomes established in one house. good hand hygiene by stockmen. as well as processing plant technologies to reduce carcase contamination. 25 . phage treatments and competitive exclusion approaches.Signs  None. Insects and rodents may act as a means of transfer of the infection from the general environment into the poultry buildings. housed poultry can be maintained free of Campylobacter infection by consistent application of excellent biosecurity. Samples should be tested as quickly as possible after collection. In practice the success of this will also depend upon the degree of environmental contamination by the organism. Post-mortem lesions  None. and changing of overalls and boots on entering bird areas. cloacal swabs or composite faeces. Diagnosis Isolation of the organism from caecal contents. Key aspects of this include effective sanitation of drinking water. Research is ongoing on the development of vaccines. Many infections are introduced during thinning or other forms of partial depopulation.

and associated with gizzard erosion. oesophagus. The fungus is resistant to many disinfectants. 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. Prevention Avoid excessive use of antibiotics and other stressors. The cause is a fungal yeast. copper sulphate (1 kg/tonne feed) for 5 days. possibly confused or masked by signs of the primary disease. Raised focal lesions may slough into lumen as caseous material.Candidiasis. Slow growth. Post-mortem lesions   White plaques in mouth. Moniliasis. microscopic examination of a digested smear (heat in 10% potassium hydroxide) to demonstrate the hyphal forms of the yeast in the tissues. A finely divided powder of copper sulphate (where approved) at 200gm/tonne continually or to 14-16 weeks in replacement pullets. and sometimes other birds and mammals. smooth and with a yeasty smell. intestine and cloaca. proprionic acid. characterised by thickening and white plaques on the mucosa. Control of Candida through drinking water is sometimes practised with chlorination (e. histopathology. crop. Treatment Nystatin (100 ppm in feed) for 7-10 days. Morbidity and mortality are usually low. Poor appetite. Diagnosis Lesions. or copper sulphate 1gm/2 litre water for 3 days if approved locally. turkeys. sodium or calcium proprionate at 1 kg per tonne continually. Thrush Introduction A disease of the alimentary tract of chickens. Colonies of this fungus appear as white to ivory colour. occasionally proventriculus and intestine. especially in the crop but sometimes in the proventriculus.g. Signs     Dejection. 26 . Candida albicans and the condition is seen worldwide. Diarrhoea. Ensure good hygiene.

This is economical and effective. tenosynovitis and other diseases affecting mobility. Soluble multivitamins and/ or methionine may be of some benefit in some circumstances. excessive light intensity or variation (e. high temperatures. Predisposing factors include overcrowding.g. low light level. Cannibalism. sodium hypochlorite) at 5 ppm. through shafts of light in the house). If so it should be carried out carefully by trained operators. It should be repeated periodically. Feather-pulling. Take care to provide fresh clean feed and water.Chlorox. Differentiate from bacterial dermatitis. nutritional deficiencies. control ectoparasites. distribution of lesions. face. post-mortem cannibalism. complying with local regulations and any relevant codes of practice. Feather pecking Introduction A complex multifactorial behavioural problem of poultry and game birds seen worldwide. Post-mortem lesions   Skin wounding related to particular signs exhibited. Generalised anaemia. Provision of a diet that closely matches the nutritional requirements of the stock concerned. Diagnosis Age. Morbidity is usually low but mortality is high among affected birds. feed form (mash takes longer to consume than pellets). boredom. head. Treatment Correct any husbandry problems. anaemia. 27 . Beak trimming may be necessary. and strain of bird. Signs   Pecking at feet (especially young chicks) and vents (adult layers and turkey poults 812 days old). uncontaminated by fungi. Prevention Proper density and temperature. wings.

some are transmitted direct from bird to bird. C. Treatment Coumphos has been licensed in some markets. Post-mortem lesions   Enteritis. seiving intestinal contents. prepatent period about 21-25 days according to species. Differentiate from other causes of enteritis. obsignata in the small intestine. Wasting Poor growth. The worms are 7-18 mm long. C. or characteristic worm eggs in faeces in patent infections. Signs     Diarrhoea.05 mm wide and hair-like in appearance. small intestine or caecum. Morbidity and mortality are usually low. game birds and pigeons ofCapillaria species.Hairworm Infection Introduction Nematode parasitic worms of poultry. Some species have earthworms as intermediate hosts.other approved benzimidazoles can be expected also to have activity. effective cleaning of houses. Dejection. Fenbendazole has been shown to have high efficacy . Levamisole. contorta in the crop and oesophagus. Hairworms in mucosa of crop. Infection is by the oral route. Diagnosis This may be by a combination of macroscopic examination. about 0. Prevention Separation of birds from possible transport and intermediate hosts. Worm eggs take about 20 days to embryonate with an L1 larvae. Worm eggs in the environment are resistant.Capillariasis . 28 .

Many meat inspectors become skilled at detecting subtle differences in skin colour in the affected birds. coli. 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. In the USA it is called 'Inflammatory Process'. Diagnosis Typical lesions. but the affected birds are not readily detectable prior to slaughter. skin wounds by particular strains of E. 29 . 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. It typically occurs between skin and muscles and between muscles and may be an incidental finding in a range of conditions. However its main importance is as a cause of condemnation in meat poultry. Careful flock management with a view to reducing toe wounds has the greatest impact in controlling cellulitis. though most of the birds showing toe scrapes will not go on to develop cellulitis. Many affected birds have no other lesions and are reasonably well grown. which can replicate in the tissues. 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. The condition is caused by infection of. particularly broiler chickens.Cellulitis Introduction Cellulitis is literally an inflammation of connective tissues. often minor. Prevention Toe scrapes at 15-25 days of age when feather cover is poor are the most likely predisposing factors.

Hypochlorite appears most effective in vitro. Transmission is usually vertical during sero-conversion of a flock in lay. poor litter quality). Discoloured liver and kidney. Prior to confirmation that it is in fact a virus it was known as Chicken Anaemia Agent or CAA.g. If gangrenous dermatitis is a problem then periodic medication may be required. Signs     Poor growth. 30 . lateral transmission may result in poor productivity in broilers. Gumboro. virus may be isolated in lymphoblastoid cell line (MDCC-MSB1). demonstration of ongoing sero-conversion in parent flock. No clinical signs or effect on egg production or fertility in parent flock during seroconversion. Diagnosis Gross lesions. Sudden rise in mortality (usually at 13-16 days of age). chloroform. 80°C for 5 minutes) and many disinfectants even for 2 hours at 37°C. and control of other diseases as appropriate. heat (70°C for 1 hour.Chicken Anaemia Introduction A viral disease of chickens caused by Chicken Anaemia Virus or CAV. The virus is resistant to pH 2. Mortality is typically 5-10% but may be up to 60% if there are predisposing factors present such as intercurrent disease (Aspergillosis. may be beneficial. Post-mortem lesions       Pale bone marrow. Acute mycotic pneumonia. Pale birds. legs wings or neck. ether. Inclusion body heptatitis etc. Atrophy of thymus and bursa. Gangrenous dermatitis on feet. Treatment Good hygiene and management.) or poor management (e. PCV of 5-15% (normal 27-36%).

man. other infections may be predisposing factors. and may be detected by SN. Psittacosis. caused by Chlamydia psittaci. Wasting. Nasal discharge. They should be used at least 6 weeks prior to collecting eggs for incubation. pigeons.Prevention Live vaccines are available for parents. but occurring probably worldwide. Chlamydiosis. 31 . Weakness. Elisa. phenolics are less so. Production drops in naive laying flocks Post-mortem lesions     Vascular congestion. Immunity: there is a good response to field challenge (in birds over 4 weeks of age) and to attenuated live vaccines. or IFA. ducks. Iodophores and formaldehyde are effective disinfecting agents. say. Inappetance. It is a 'Scheduled Disease' rarely diagnosed in UK. Airsacculitis. a bacterium of highly variable pathogenicity. It is transmitted by contact. Conjunctivitis. Weight loss. rarely chickens. Fibrinous pericarditis. Occasional transient ataxia in pigeons. faecal dust and wild bird carriers. Morbidity is 50-80%. mortality 5-40%. Greenish-yellow diarrhoea. Elementary bodies are highly resistant and can survive in dried faeces for many months. their degree of attenuation is variable. especially pigeons and robins. Their use may be restricted to those flocks that have not sero-converted by. Egg transmission does not occur. 15 weeks. Intercurrent salmonellosis and. perhaps. psittacines. Signs           Respiratory signs. Ornithosis Introduction An infection of turkeys. Serology: antibodies develop 3-6 weeks after infection. Depression.

Slipping of Achilles tendon (or perosis). Elisa and gel diffusion. Fibrinous pneumonia. Signs       Short legs. Treatment Tetracycline (200-800 ppm in feed for 3-4 weeks) and/or quinolone medication and supervised slaughter. Diagnosis History. Live and inactivated vaccines are protective although the former result in carriers and the latter require several applications. This condition is seen in chickens. exclusion of wild birds. Malposition of leg distal to hock. signs. Differentiate from Duck viral hepatitis. Lameness. ducks and turkeys. shortened bones. may rupture in pigeons. niacin may also be involved). biotin. Distortion of hock. Duck septicaemia. zinc. folic acid. Chondrodystrophy. Intracytoplasmic inclusions are helpful but confirmation requires demonstration of causal organisms (Giemsa stain. Necrotic foci in liver.     Perihepatitis. 32 . Prevention Biosecurity. either singly or in combination (although deficiencies of pyridoxine. In turkeys it may be an inherited deficiency of galactosamine. IFA). In embryos parrot beak. Slipped Tendon or Perosis Introduction Caused by deficiency of manganese. Congested lungs and air sacs in the turkey. Spleen enlarged and congested. Serology: complement fixation. choline. lesions.

Depression. 33 . 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. The contents may be haemorrhagic or be watery with white material shed from the mucosa. meleagridis affect the lower small intestine rectum and caecae. infectious arthritis. no value to affected bird. Weight loss. meleagrimitis affects the upper small intestine.Post-mortem lesions     Shortening and thickening of long bones. Signs      Huddling. dispersa is found in the small intestine. while E. choline. while E. rickets. infectious synovitis. Shallow trochlea. adenoides affects the caecae and rectum. of which two are associated with significant disease effects. Post-mortem lesions  The affected area of intestine shows thickening of the wall and dilation. analysis of feed. Lateral slipping of tendon. Diagnosis Lesions. correct mineral balance. gallopavonis and E. ruptured ligaments. Tucked appearance. Watery diarrhoea that may occasionally be blood stained or contain clumps of mucus or shed mucosa. vitamins. E. Prevention Addition of manganese. Differentiate from twisted leg. Five species of Eimeria have been identified that cause lesions in turkeys. Treatment For flock proceed as for prevention. ruffled feathers. E. Tibia and metatarsus bowed.

typically to 12 weeks of age. show some spotty congestion and have abnormal contents due to the sloughed epithelium. adenoides. Prevention The ionophore coccidiostats lasalocid and monensin are routinely used in turkey growers. Treatment Toltrazuril. Amprolium. Avoid use of tiamulin in ionophore treated birds.Diagnosis Signs. Differentiate from necrotic enteritis. microscopic exam of scrapings (oocysts. The intestines are dilated. Figure 38. The exudate can range from semi-liquid to solid white cores. lesions. Exposure of previously unmedicated birds to these compounds can cause toxicity. 34 . Sulphonamides (e. Dosage levels of ionophores may be critical to efficacy and safety. gamonts).g. Turkey coccidiosis of the upper small intestine caused by E. Turkey caecal coccidiosis caused by E. Salinomycin is toxic for turkeys even at very low doses. Diclazuril is also used for this purpose. Figure 37. meleagrimitis. Sulphaquinoxaline).

Post-mortem lesions    Petechiae. Accumulation of varying quantities of blood and caseous necrotic material in the caecum. Shuttle programmes with chemicals in the starter diet usually improve control. In some markets the organic arsenical compound 3-Nitro is used as an aid in the control of caecal coccidiosis. blood in faeces. It is caused by Eimeria tenella and results in lesions in the caecum of chickens worldwide. E. E tenella Introduction This was at one time the commonest type of coccidiosis and is certainly the most easily diagnosed. tenella is more common when 'straight' ionophore programmes are used. hygiene. Transmission as for E. Production less affected than in some of the other forms of coccidiosis. Inappetance. histomonosis. Vaccines are used mainly in breeders but increasingly in broilers. lesions. Vitamins A and K in feed or water. microscopic examination of scrapings. Diagnosis Signs. vaccination by controlled exposure. Diarrhoea. Closed eyes. Prevention Coccidiostats in feed. Caecal.Coccidiosis. of caecal mucosa. Recovered birds have good immunity to the same parasite. Signs       Depression. Differentiate from ulcerative enteritis. Morbidity is 10-40% and mortality up to 50%. 35 . Thickening. mitis (see above). Amprolium. Sulphonamides. ecchymoses. Treatment Toltrazuril. Ruffled feathers.

The disease occurring is proportional to the amount of infective agent ingested. E mitis Introduction This condition of chickens. Treatment Not usually treated but susceptible to the products used for other forms of intestinal coccidiosis. The parasite is moderately resistant in the environment and highly resistant to conventional disinfectants. 36 . is caused by the protozoan parasite Eimeria mitis. Predisposing factors include exposure to faeces and litter conditions that favour development of the parasite (temperature. identification of typical small round oocysts and other stages in fresh scrapings from the small intestine. faeces and on fomites and birds are infected by the oral route with an incubation period of 2-5 days. Coccidiosis. The caecal walls are thickened and haemorrhagic and there is a mass of blood in the caecal lumen. Diagnosis Mild lesions. The infective agent is found in litter. which colonises the small intestine. humidity). May predispose to wet litter. Post-mortem lesions  The lesions are minimal and located in the lower small intestine (ileum) which tends to be pale and flaccid with scattered petechiae. Signs  Reduced feed conversion efficiency and weight gain. seen worldwide. secondary bacterial enteritis.Figure 15. Moderate Eimeria tenella infection in the caecae of a chicken (Score 3).

vaccination by controlled exposure. Morbidity and mortality are variable. blood in faeces. Differentiate from ulcerative enteritis. Sulphonamides. Diarrhoea. Amprolium. Ruffled feathers. There is good immunity to the same parasite in recovered birds.Prevention Normally controlled by anticoccidials in feed. This species is not usually included in vaccines for broilers. Poor production. Oocysts in caecum and rectum. Treatment Toltrazuril. caecal coccidiosis. Inappetance. Severe necrotising enteritis. Post-mortem lesions    Petechiae and thickening of the distal third or more of intestine. Coccidiosis. extending into caecal tonsils. May be included in vaccines. Prevention Coccidiostats in feed. E brunetti Introduction A relatively rare form of coccidiosis affecting chickens worldwide caused by Eimeria brunetti. Of moderate to high pathogenicity. Closed eyes. hygiene. it is found in the terminal ileum. Signs       Depression. caecum and rectum. Ileorectal. microscopic examination of scrapings. Diagnosis Signs. lesions. 37 . Vitamins A and K in feed or water.

Diagnosis Signs.Figure 16. 3 days on. Duck viral enteritis. Blood-stained vent. Tucked appearance. 2 days off. Treatment Sulphonamides (e. Intestinal. Depression. Post-mortem lesions  Massive haemorrhage in upper small intestine.g. anseris is the most important. Vitamins A and K in feed or water. In the goose E. lesions. Moderate Eimeria brunettiinfection in the terminal ileum and rectum of a chicken. microscopic examination of scrapings (usually few or no oocysts. Amprolium. Differentiate from Duck viral hepatitis. There is thickening of the intestinal mucosa and there are lines of haemorrhagic spots in the mucosa. Coccidiosis occurs only very rarely in commercially reared ducks in the UK. of Ducks and Geese Introduction Young ducks and geese may suffer from Eimeria spp infection. 3 days on). Sulphadimidine 30-600gm/100 birds/day. large number of merozoites). 38 . while in ducksTyzzeria perniciosa is most pathogenic. Coccidiosis. anatipestifer. compared to four per oocyst forEimeria. Tyzerria has eight sporocysts in each oocyst. Signs     Sudden death.

Treatment Controlled trials of treatments have not been published. Reduced feed intake. Post-mortem lesions    Enlarged kidneys.Prevention If required coccidiostats could be used in feed. Hygiene. Diagnosis Lesions. 39 . Signs     Depression. presence of coccidial stages in fresh scrapings of kidney lesions. 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. Coccidiosis. Prevention Good Hygiene.faeces tend to be whitish. Diarrhoea . Kidneys light grey to greyish pink. Tiny white foci and petechiae in the kidneys. Weakness. however this is not routinely practised.

Blood or pigment in the faeces. Ruffled feathers. of moderate to high pathogenicity it is seen worldwide. Because of the area of intestine affected it tends to have a significant effect on productivity and susceptibility to necrotic enteritis. Diagnosis Signs. Amprolium. Differentiate from necrotic enteritis. Prevention Coccidiostats in feed. Vitamins A and K in feed or water. Inappetance. Mild to severe enteritis. Signs        Depression. commercial vaccines commonly contain more than one strain of E. Closed eyes. Mid-intestinal. Treatment Sulphonamides. Post-mortem lesions     Petechiae and thickening of middle third of intestine. vaccination. This is one of the less immunogenic species. Morbidity and mortality are variable. microscopic examination of scrapings.Coccidiosis. acervulina coccidiosis and there may be large numbers of characteristic oocysts in smears. lesions. contents often orange in colour. Poor production. Depigmentation of skin and plasma is especially evident in this form of cocccidiosis and this is commercially important in some markets. non-specific enteritis. E maxima Introduction One of the more common forms of coccidiosis in commercial broilers. maxima. This infection is often associated with E. 40 . Poor absorption of nutrients/pigments. Caused by Eimeria maxima. hygiene. mucosa tends to be pinker than normal.

Severe necrotising enteritis. other types of coccidiosis. Oocyts in caecal scrapings. Depression. The lesions are subtle compared to other forms of coccidiosis. Signs        Reduced feed consumption. caused by Eimeria necatrix. Diagnosis Signs. in which the parasite is present in the small intestine and in the caecum. 'Sausage-like' intestine. The intestine is slightly thickened and there are scattered haemorrhages in the mucosa when seen from the inside. blood in faeces. Inappetance. Post-mortem lesions     Petechiae and thickening. Diarrhoea. Poor production. It occurs in chickens worldwide and has variable morbidity but mortality is high in severely affected birds. microscopic examination of scrapings Differentiate from necrotic enteritis. lesions. Ruffled feathers. Moderate Eimeria maxima infection in the jejunum of a chicken (Score 2).Figure 13. E necatrix Introduction A highly pathogenic form of coccidiosis. Coccidiosis. Closed eyes. Schizonts seen as white spots through the serosa interspersed with petechiae. Deep scrapings necessary to show large schizonts. Mid-intestinal. of middle to posterior third or more of small intestine. 41 .

It is seen in layers and in broilers. which is moderately pathogenic. Morbidity is variable and mortality low or absent. vaccination. Haemorrhages and white spots are visible from the outside of the intestine. Diarrhoea. E acervulina Introduction This is probably the commonest cause of coccidiosis in chickens and occurs worldwide. both alone and in association with other species of coccidia and is caused by Eimeria acervulina. Coccidiosis. Amprolium. maxima. Moderate Eimeria necatrix infection in the jejunum of a chicken (Score 3). Poor production. Closed eyes. Depigmentation. Eimeria mivatiis currently considered not to be a valid species distinct from E.Treatment Toltrazuril. This is one of the less immunogenic species. Vitamins A and K in feed or water. Figure 14. Upper Intestinal. hygiene. Inappetance. Sulphonamides. Signs        Depression. In this case the intestine is thickened and can become ballooned and sausage-like. Ruffled feathers. Prevention Coccidiostats in feed. Post-mortem lesions 42 . acervulina. commercial vaccines commonly contain more than one strain of E.

In severe infections they become confluent and cause sloughing of the mucosa. A system of assessing the severity of coccidial challenge by attributing a 'score' is often used. Treatment Toltrazuril. Poor absorption of nutrients/pigments. hygiene. In general terms a score of 0 indicates no lesions and a score of 4 indicates maximal severity of lesion or death. Moderate Eimeria acervulinainfection (score 2) in chicken duodenum. Various publications provide a photographic key to severity of lesion. Petechiae.     Thickening. Differentiate from necrotic and non-specific enteritis.the duodenum and part of the ileum. Amprolium. restricted to upper third of small intestine . Prevention Coccidiostats in feed. Diagnosis Signs. White spots or bands in the mucosa. In milder infections there may be scattered white spots. A detailed description is beyond the scope of this book. Sulphonamides. and other lesions. lesions. 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. in feed or water. microscopic exam of scrapings. Figure 12. vaccination by controlled exposure. 43 .

fomites. Perihepatitis. Granulomata in liver and spleen. etc.Colibacillosis. coughing. Pericarditis. Salpingitis. pathology. Dejection. Swollen liver and spleen. mucosal damage due to viral infections and immunosuppression are predisposing factors. turkeys. Post-mortem lesions              Airsacculitis. sero-typing. Reduced appetite. Lesions vary from acute to chronic in the various forms of the disease. Signs       Respiratory signs. It is most commonly seen following upper respiratory disease (such as Infectious Bronchitis) or Mycoplasmosis. Poor growth. Poor navel healing. Synovitis. Omphalitis. Infection is by the oral or inhalation routes. sneezing. It is caused by the bacteriumEscherichia coli and is seen worldwide in chickens. Enteritis. Peritonitis. with an incubation period of 3-5 days. It is frequently associated with immunosuppressive diseases such as Infectious Bursal Disease Virus (Gumboro Disease) in chickens or Haemorrhagic Enteritis in turkeys. mortality is 5-20%. or in young birds that are immunologically immature. Arthritis. water.most strains are rapidly lactose-fermenting producing 44 . and via shell membranes/yolk/navel. Omphalitis. Cellulitis over the abdomen or in the leg. The infectious agent is moderately resistant in the environment. Aerobic culture yields colonies of 2-5mm on both blood and McConkey agar after 18 hours . but is susceptible to disinfectants and to temperatures of 80°C. Diagnosis Isolation. Colisepticemia Introduction Coli-septicaemia is the commonest infectious disease of farmed poultry. Snick. Morbidity varies.

It is seen in growing broiler chickens and turkeys. the foot pad. Some lesions are superficial. gentamycin or ceftiofur (where hatchery borne). Contact dermatitis is commonly monitored at processing as a means of measuring 'welfare status'. Treatment Amoxycillin. neomycin (intestinal activity only). The liver is almost entirely covered by a substantial layer of fibrin and pus. stage of resolution and severity of lesion is likely to affect the degree of discomfort or pain suffered. Contact Dermatitis. and in broiler parents. Immunity is not well documented though both autogenous and commercial vaccines have been used. Prevention Good hygiene in handling of hatching eggs.brick-red colonies on McConkey agar. whereas others progress to deep ulcers so the size. Figure 17. flouroquinolones. rear surface of the hock and. Pododermatitis Introduction Contact dermatitis affects skin surfaces which have prolonged contact with litter. hatchery hygiene. tetracyclines. other enterobacteria such as Proteus. 45 . Differentiate from acute and chronic infections with Salmonella spp. as well as Pseudomonas. Staphylococcus spp. the breast area. Hock Burn. good sanitation of house. etc. Severe perihepatitis in colibacillosis in a broiler parent chicken. feed and water. Control of predisposing factors and infections (usually by vaccination). Well-nourished embryo and optimal incubation to maximise day-old viability. potentiated sulphonamide. when severe.

and. Post-mortem lesions  As described under signs. Treatment Not applicable. Signs  Blackened skin progressing to erosions and fibrosis on the lower surface of the foot pad. Prevention This condition is closely linked to intestinal function as this is the prime determinent of faecal consistency and stickiness. 46 . stickiness of droppings). Choice of drinker type (nipple as opposed to bell). drinker management. See the discussion in the section on Dysbacteriosis. and sometimes in the breast area. Moderate pododermatitis on a foot pad. Diagnosis Signs and lesions. litter moisture. If severe the foot and hock lesions may contribute to lameness or serve as a portal of entry for secondary infections. level of soya bean meal in feed (according to some authors. at the back of the hocks. It can be reproduced by adding water to the litter. proper insulation in cold climates.Pododermatitis is often related to high droppings pH. Figure 18. and adequate ventilation to remove moisture are all important. most importantly.

They replicate in the brush border on the surface of epithelial cells. Post-mortem lesions   Inflammation and thickening of mucosa of crop and oesophagus. Cryptosporidiosis Introduction Cryptosporidia are related to the coccidia. Some have beetle or earthworms as intermediate hosts. meleagridis also infects both species. Prevention Effective cleaning of housing. They also differ from coccidia in being poorly host specific. and ducks. Coumaphos. although bird strains do not infect mammals very well. and vice versa. The oocysts are excreted ready sporulated in the faeces and infection occurs by inhalation and ingestion. acervulinaoocyst). Routine worming. 47 . Emaciation. Diagnosis Microscopic examination of mucosal scraping. Treatment Levamisole. The same species causes infections of the hindgut and cloacal bursa in chickens. Avoidance of access to intermediate hosts. but much smaller (typically oocysts are less than ¼ of the size of an E.Cropworms Introduction The nematode worms Capillaria spp and Gongylonema ingluvicolainfect the mucosa of the crop and oesophagous of poultry and game birds. Cryptosporidium baileyi can cause respiratory disease in chickens and turkeys.C. turkeys. White convoluted tracks in the mucosa. Signs   Anaemia. A further species causes respiratory disease in quail.

Signs     Incoordination. It is becoming increasingly common for water companies to screen water supplies for cryptosporidia because of the human health implications of mammalian strains.g. coli-septicaemia) there may be benefit in medicating for these. Post-mortem lesions    Sinusitis. Diarrhoea. Cough. Pneumonia. recumbency.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. Diagnosis Identification of the parasites attached to the epithelium by microscopic examination (smears histopathology acid-fast staining). If other disease processes are complicating the situation (e. Prevention The oocysts of cryptosporidia are extremely resistant to chemical disinfection. Swollen sinuses. Torticollis. Airsacculitis. There are no effective preventative medicines or feed additives. 48 . Low weight gain. Treatment Unfortunately there is currently no known effective treatment in poultry. Circling. Tremors.

isolation of the fungus. especially of femoral anti-trochanter but also other leg joints. air sacs etc. and cartilage flaps. Diagnosis Gross and microscopic lesions. Rapid growth is a possible predisposing factor. 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. Diagnosis Lesions. Microscopically there is necrosis and there may be fissures of articular cartilage and associated osteochondritis. Post-mortem lesions   Damaged epiphyseal articular cartilage. The cause remains to be confirmed. but it may result from physical damage. Treatment None. Degenerative Joint Disease Introduction A condition of chickens and turkeys seen worldwide. Prevention Use fresh dry litter (avoid old sawdust). or developmental defects. Mycotic lesions in lungs.Post-mortem lesions   Necrotic lesions with associated congestion in cerebrum. Signs   Lameness. Reduced breeding performance. Treatment 49 .

Prevention Careful cleaning of buildings during down-time will help reduce the risk of these infections. Application of mineral or vegetable oil is also beneficial. It may be best to cull affected birds from small flocks. 50 . pheasants.Knemidocoptes spp. Signs     Cause irritation and the bird pulls feathers. Unthriftiness. Post-mortem lesions  As described under signs. For small flocks dipping the affected parts in a solution of acaricide may be beneficial. Exclusion of wild birds from chicken areas is advised as far as possible. Diagnosis Signs. Depluming and Scaly Leg Mites Introduction External parasites of adult chickens. up to 0. Appropriate management of a segregation pen and early marketing of mildly affected birds may limit losses and improve flock welfare. The adult females are short legged.5mm in diameter. round. Prevention Avoidance of physical sources of injury to bones and joints. pigeons etc. especially during period of rapid growth. Mange lesions on legs and unfeathered parts. Raised thickened scales. microscopic examination for mites in scrapings. Treatment Not usually required in commercial poultry. There may be a place for growth-control programmes.None available.

Dissecting Aneurysm. A sudden noise or other cause of excitement can lead to an 'outbreak'. Prevention Limit feed in birds of 16+ weeks. Signs    Sudden death with no warning signs. kidneys. birds found on breast or side. Abdominal cavity full of blood. Reserpine in diet of birds of 4+ weeks (no longer licensed in the UK). Diagnosis History and lesions. pericardial sac. presumably due to a sudden increase in blood pressure. Post-mortem lesions      Carcase anaemic. It has been suggested that degenerative changes in the wall of the artery and copper deficiency may be factors. a tranquilizer. Treatment None currently licensed. leg muscles. Haemorrhages in lungs. Morbidity is around 100% and mortality 0-95%. recovered birds carrying the virus for 8 weeks. Skin pale. The disease is transmitted by infected ducks and other waterfowl and spreads rapidly. genetic condition of turkeys linked to male sex and high growth rate. a picornavirus may also 51 . The infective agent. Duck Viral Hepatitis Introduction A viral disease of ducks occurring worldwide and previously a scheduled disease in UK. Aortic Rupture Introduction A complex. Possibly blood in the mouth. Rupture of major blood vessel at base of heart or by the kidneys. Reserpine. Aspirin at 250 ppm in feed or water may be of benefit. A longtitudinal split of the abdominal aorta is the most common lesion. was included in feed at 1 ppm for 3-5 days to reduce blood pressure.

Duck Virus Enteritis. Prevention Vaccination and/or antiserum. Signs     Sudden death. Punctate/diffuse haemorrhages. 0. Fall on side. Newcastle disease. Differentiate from Duck plague (viral enteritis). in USA since 1967. All waterfowl are susceptible and the Barbary duck is more susceptible than the Pekin. 52 .focal necrosis. rapid deterioration and death. Transmission is by infected birds. often in opisthotonus. mostly in ornamental collections. Recovered birds may carry the virus for a year. Post-mortem lesions     Liver swollen. SN serology. Live. coccidiosis. 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. fomites and arthropods.survive for ten weeks in brooders and five weeks in faeces. isolation in CE (causes stunting of 9 day embryo). Duck septicaemia (anatipestifer). Duck Plague Introduction A herpesvirus infection of ducks and geese diagnosed in the UK in 1972. Depression. also the Netherlands and other countries. paddling of legs. Kidneys and spleen swollen. Death in good condition. Influenza and a 'Type II Variant' hepatitis caused by Astrovirus. lesions. arching of back. breeder vaccination. A different picornavirus causes a similar condition in North America. Diagnosis History. Microscopically . only slightly attenuated vaccine is applied at day old by foot web stab and may be repeated in breeding birds to provide maternal immunity. Treatment Antiserum. bile duct proliferation and inflammation.

spleen. sometimes dysentery. Young ducks may show thymic and bursal lesions. HA-. heart. coccidiosis. excess caecal volume and fermentation. pasteurellosis. Dysbacteriosis. Severe diarrhoea. vent gleet. Occasionally cyanosis of the bill in the young. Tremor. Prevention Isolation from waterfowl. Drop egg production. intranuclear inclusions Differentiate from Duck hepatitis. Non-specific Bacterial Enteritis Introduction Inflammation of the small intestine associated with wet litter. but vaccination in face of outbreak is of value. Thirst.Signs              Sudden deaths. oesophagitis (birds on restricted feed). Post-mortem lesions     Severe enteritis. Ataxia. Treatment None. liver. The condition is seen mainly in rapidly growing broiler chickens with good food intake. probably through interference. Dehydration. vaccination if approved by authorities (CE adapted live virus). Closed eyes. pericardium. 53 . Crusty plaques from oesophagus to bursa (covered by yellowish plaques in later stages). Rapidly spreading disease. Diagnosis Isolation: Duck CAMs 12 day embryos die in 4 days. Photophobia. body cavities. Haemorrhage in intestine. 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. Paresis.

Good control of coccidiosis. 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. Prevention Competitive exclusion ('normal adult flora') use in day-old chicks reduces the risk of this condition. Voluminous caecae. Holland. microscopic examination of scrapings from the wall of the small intestine (to exclude coccidiosis and perhaps to assess the bacterial flora). Feed acidification may be helpful in some circumstances. Spain. especially where treatment is initiated early. Treatment Amoxycillin and tylosin treatment appear to be beneficial. Water intake may be increased or irregular. Careful choice of any feed enzymes and their matching with local raw materials can have an impact on substrates made available to intestinal bacteria. feed interruptions and subclinical coccidiosis may be contributory factors. Circumstantial evidence suggests that the main route of transmission is through the eggs (vertical transmission) 54 . Treatment should coincide with good relittering and it is important to provide fresh sanitary drinking water. It affects chickens and has occurred in Ireland. Brazil. Signs   Diarrhoea. first isolated in Northern Ireland in 1976. Mortality is usually negligible. France.Dietary changes. rather we are dealing with a disruption in the normal flora of the gut. Post-mortem lesions    Excessive fluid content throughout the small intestine. In the autumn of 1976 a distinct egg drop syndrome was first identified in Northern Ireland. Apparently a similar disease had been seen over a 4-year period in broiler parents in Holland. No single bacterium appears to be responsible. Germany. Peru. often with gas bubbles. Diagnosis Signs. 127. Uruguay. England. Prophylactic antimicrobial medication may be necessary in some circumstances. The cause has been identified as Adenovirus BC14. Wet faeces in the rectum. Argentina. lesions.

specifically vitamins E. Infectious diseases include Infectious Bronchitis. B 12. Post-mortem lesions   No specific lesion . Diagnosis History. Elisa. insecticides or nicarbazin. Drops may be of 5 to 50% and last for 3-4 weeks. selenium. and D as well as calcium. Histopathology . thin or soft-shelled eggs and shell-less eggs. Lateral transmission from bird to bird is slow and may be prevented or slowed for weeks by netting divisions.followed by latent infection during rear with viral excretion starting shortly before sexual maturity.it may be possible to demonstrate degenerative changes in the epithelial cells of the magnum of the oviduct. Infectious Laryngotracheitis. Management problems may be involved: inadequate water supply. intoxication by sulphonamides. which can be caused by a large number of factors acting individually or in combination. Metabolic diseases include Fatty Liver Syndrome. as may wildfowl and biting insects. oviduct). may be infectious or metabolic. Coryza.only a slight atrophy of ovary and oviduct. Loss of shell pigment. group antigen distinct from classical adenoviruses (white cells. Serology: HI. Clinical disease occurs during sexual maturity. Rough. Contamination of egg trays at packing stations may play a part in transmission. signs/lesions (mainly lack of). Diphtheritic Fowl Pox). Parasites. Marek's disease/Leukosis or any infectious disease causing a significant systemic disturbance (CRD. inadequate lighting programme. phosporus. Signs      Egg drop at peak or failure to peak. Avian Encephalomyelitis. Diseases in which egg drop occurs. throat swabs. Nutritional deficiency should be considered. Lack of signs in the birds themselves. 55 . extremes of temperature. DID. The infection is commonly present in ducks and geese but does not cause disease. Isolation of haemagglutinatin agent in duck eggs or cell culture. Newcastle disease. Spread from house to house may take 5-10 weeks. Unvaccinated flocks with antibodies before lay do not peak normally. Cholera. SN. sudden changes of feed. It is important to rule out other possible reasons for egg drop. Poor internal quality.

bacterial infection. Post-mortem lesions   Right ventricular failure and ascites. Soluble multivitamins may be recommended as a nonspecific measure. Vegetative lesions usually on the right atrioventricular valve. Peripheral vessels congested. If successive flocks are affected on the same site prophylactic medication ahead of the anticipated problem may be of benefit. osteomyelitis. Culture of lesions to confirm the bacterium involved. Signs   Fluid-distended abdomen. 56 . Prevention Vaccination with inactivated vaccine prior to lay. Epiphysiolysis Introduction A complex condition of chickens that may be associated with trauma. streptococci. Treatment Medication is only likely to be of value in reducing deterioration in birds that are starting to develop lesions. The choice should depend on sensitivity testing of an isolate. growth plate disease. Erysipelothrixetc. and /or trauma. rickets. Prevention Good hygiene at turn-around.Treatment None. Diagnosis Differentiate from broiler ascites syndrome by examination of the interior of the heart. Endocarditis Introduction A condition of chickens associated with several bacterial infections such as staphylococci.

The natural hosts are wild birds and rodents. sometimes seen in vivo. VEE) Introduction A viral disease of pheasants. Post-mortem lesions  Separation of epiphyses at the growth plate. Circling. often occurs or is identified in the processed carcase. Tremors.Signs  Apparent dislocation at extremities of long bones. 57 . Microscopic lesions not pathognomonic. May also be asymptomatic. Horses are also seriously affected. WEE. Flaccid neck. These conditions currently only occur from northern South America to North America. chickens. Prevention Control of predisposing factors. Post-mortem lesions   No gross lesions. Diagnosis Gross inspection. partridges. Paresis. Paralysis. Equine Encephalitis (EEE. wild birds. Ataxia. It is transmitted between birds by pecking and by mosquitoes. turkeys. Treatment Not applicable. ducks and pigeons having a high morbidity and high mortality. histology may be helpful in identifying underlying problems such as rickets or 'FHN'. Signs         Nervous symptoms.

pheasants. water. epicardium. It is also seen in some mammals. rarely in geese. Perineal congestion. Chronic scabby skin. Erysipelas Introduction A sudden onset infection with the bacterium Erysipelothrix insidiosa (E. ID by VN. Sudden death. and CE. Joint lesions. Post-mortem lesions       Carcase congestion. TC. control cannibalism. It may be transmitted by faecal carriers for 41 days. rhusiopathiae) seen in turkeys and increasingly in free-range chickens. Vaccinate at 5-6 week. Marked catarrhal enteritis. especially snood. The bacterium is fairly resistant to environmental effects or disinfectants and may persist in alkaline soil for years. Signs         Inappetance. 58 . ducks. May be diarrhoea and respiratory signs.Diagnosis Isolation in mice. Depression. muscle. fishmeal and semen and by cannibalism. kidney. spleen swollen. There is likely to be an increased risk if housing or land has been previously used by pigs or sheep. Endocarditis. Haemorrhages in fat. Prevention Protection from mosquitoes. Swollen snood. COFAL. in soil. Sleepiness. Liver. Treatment None.

Tetracyclines in feed may also be helpful. especially caged layers and with a complex set of causes including excessive calories. deficiency and stress. mycotoxins. Some birds with pale comb and wattles. colibacillosis. and identification.a combination of the procaine and benzathine salts may be injected. the demonstration of the organism in stained impression smears from tissues. Sudden death. Headparts pale. Prevention Good biosecurity to prevent spread from other susceptible species. Treatment Penicillin . history. Diagnosis Lesions. Differentiate from pasteurellosis. often along with bacterin. salmonellosis. Vaccination or natural infection may cause false positive reactions in the Mycoplasma gallisepticum and M. synoviae plate tests for a few weeks.Diagnosis Isolation on blood agar. vaccine at 16-20 weeks if the condition is enzootic. greasy and soft with numerous haemorrhages. 59 . Death by internal exsanguination after rupture of haematocyst. Liver yellow. Sudden drop in egg production. and acute Newcastle disease. Signs     Overweight typically by 25%. Fatty Liver Haemorrhagic Syndrome Introduction A condition occurring worldwide in chickens. Post-mortem lesions     Obesity.

Prevention Good hygiene of facilities. isolation. Diagnosis Lesions. 60 . Thick crusty skin. vitamin E. Trichophyton gallinae. avoid mycotoxins and stress. Post-mortem lesions  See signs (above). culling affected birds. Feather loss. Loss of condition. Treatment Formalin in petroleum jelly. Favus Introduction A fungal infection. Signs      White.Treatment Reduce energy intake. It is very rare in commercial poultry production. powdery spots and wrinkled crusts and scab on comb and wattles. supplement with choline. of chickens and turkeys. B 12 and inositol. Prevention Feed to avoid obesity. 'Honeycomb' skin.

It is seen worldwide and was one of the first infectious 61 . streptococci. rickets.Femoral Head Necrosis . E. Use of a wing for support during walking and hip flexion. especially hypophosphataemic. and water fowl. Pasteurellosis Introduction Fowl Cholera is a serious. staphylococci. FHN is the commonest infectious cause of lameness in broilers in the UK. Prevention Exclusion of floor eggs and dirty eggs from the hatchery. 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. Diagnosis Base on post-mortem lesions and isolation of a causative organism. Post-mortem studies of birds culled due to lameness and of birds found dead. Signs   Lameness.FHN Introduction A condition of chickens and turkeys that may be associated with several different bacterial infections e.75% of all male broilers placed had lesions in the hip bone. arthritis. Post-mortem lesions  Degeneration of the epiphyses of long bones with thinning of the cortex and tendency to break when force is applied. highly contagious disease caused by the bacterium Pasteurella multocida in a range of avian species including chickens. (increasing order of susceptibility). Careful attention to mineral and Vitamin D nutrition to avoid subclinical. coli. turkeys. indicated that 0. spondylolisthesis. Fowl Cholera. Differentiate from synovitis. Predisposing factors include immunosuppresive viruses such as Infectious Bursal Disease Virus and Chicken Anaemia Virus and non-infectious bone pathologies such as hypophosphaetamic rickets.g.

faeces. septicaemic viral and other bacterial diseases. The incubation period is usually 5-8 days. penicillin. Sudden death. Treatment Sulphonamides. confirmed with biochemical tests. Nasal. ocular and oral discharge. Reservoirs of infection may be present in other species such as rodents. Predisposing factors include high density and concurrent infections such as respiratory viruses. Cellulitis of face and wattles. necessitating long-term or periodic medication. streptomycin. Post-mortem lesions         Sometimes none. cats. Purulent arthritis. Swollen joints. The bacterium is easily destroyed by environmental factors and disinfectants. and possibly pigs. Lameness. Purulent pneumonia (especially turkeys). or limited to haemorrhages at few sites. Focal hepatitis. but may persist for prolonged periods in soil. Ruffled feathers.diseases to be recognised. Diarrhoea. isolation (aerobic culture on trypticase soy or blood agar yields colonies up to 3mm in 24 hours . and people. Loss of appetite. tetracyclines. Lungs with a consolidated pink 'cooked' appearance in turkeys. 62 . Differentiate from Erysipelas. The disease can range from acute septicaemia to chronic and localised infections and the morbidity and mortality may be up to 100%.no growth on McConkey). The route of infection is oral or nasal with transmission via nasal exudate. Signs           Dejection. Enteritis. erythromycin. Coughing. contaminated soil. Yolk peritonitis. Swollen and cyanotic wattles and face. equipment. by Louis Pasteur in 1880. The disease often recurs after medication is stopped. Diagnosis Impression smears.

good rodent control. It is more common in males because of their tendency to fight and cause skin damage. The virus persists in the environment for months. The swelling is made up of oedema and purulent exudates (pus). Caseous deposits in mouth. 0-50%. Fowl Pox. and where there are biting insects. or by the respiratory route. live oral vaccine at 6 weeks. It is transmitted by birds. Figure 19. Signs       Warty. Severe localised Pasteurella infection in the swollen wattle of a 30-week-old male broiler parent chicken. pigeons and canaries worldwide. 63 . hygiene. throat and sometimes trachea. spreading eruptions and scabs on comb and wattles. The duration of the disease is about 14 days on an individual bird basis. Morbidity is 1095% and mortality usually low to moderate. bacterins at 8 and 12 weeks. fomites. and mosquitoes (infected for 6 weeks). Poor growth. Inappetance. Depression. Poor egg production. Pox. turkeys.Prevention Biosecurity. Infection occurs through skin abrasions and bites. Avian Pox Introduction A relatively slow-spreading viral disease characterised by skin lesions and/or plaques in the pharynx and affecting chickens.

pharynx. Treatment None. If there is evidence of secondary bacterial infection broad-spectrum antibiotics may be of some benefit. There is good cross-immunity among the different viral strains. Turkeys by thigh-stick at 2-3 months. be caseous plaques in mouth. in the diptheritic form. Figure 20. usually with chicken strain by wing web puncture. It is confirmed by IC inclusions in sections/ scrapings. Fowl pox lesions on the wattle of an adult broiler parent chicken. Microscopically .intra-cytoplasmic inclusions (Bollinger bodies) with elementary bodies (Borrel bodies). reproduction in susceptible birds. check take at 7-10 days post vaccination. isolation (pocks on CE CAM) with IC inclusions. signs and post-mortem lesions. 64 . Less commonly there may. Prevention By vaccination (except canary). Diagnosis A presumptive diagnosis may be made on history.Post-mortem lesions    Papules progressing to vesicles then pustules and scabs with distribution described above. trachea and/or nasal cavities. Chickens well before production. DNA probes. Differentiate from Trichomoniasis or physical damage to skin. Flocks and individuals still unaffected may be vaccinated.

Treatment Sulphaquinoxaline. Prevention Good hygiene and management. Morbidity may be up to 50% and mortality is high. wings. Signs      Occasionally dejection. Diagnosis Clinical signs and/or lesions. penicillin or amoxycillin. 65 . wattles. early Infectious Bursal Disease Virus infection). rarely Clostridium noyvi / oedematiens. Immunosuppression is therefore a predisposing factor. Recovery of an abundant growth of causative organism in recently dead birds. Severe cellulitis especially of thighs. Avoid skin trauma and immunosuppression (congenital CAV infection. especially following congenital Chick Anaemia Virus infection or early Infectious Bursal Disease Virus infection (Gumboro Disease). spleen. Sudden mortality. Gangrenous skin.Gangrenous Dermatitis. Swelling and infarction of the liver. sometimes thighs and other parts. 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. usually over wings and breast. 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. Loss of appetite. Foci in liver. occasionally Staphylococcus aureus.

Treatment Flubendazole in feed. Signs     Gasping. levamisole. Presence of worms. Dyspnoea. Post-mortem lesions   Tracheitis. paired parasites up to 2 cm long. Head shaking. confirmation of presence of the parasite. There is an 18-20 day prepatent period. Loss of appetite and condition. The condition is seen more commonly in poultry on free range where ground may be contaminated by wild birds e. turkeys. by ingestion of embryonated egg or L3. 66 . pheasants. Prevention Flubendazole. from rookeries. Gape Introduction Syngamus trachea. slugs and snails acting as transfer hosts but the life cycle may also be direct.g. Infection is by the oral route with earthworms. Severe gangrenous dermatitis on the upper surface of the wing of a broiler chicken. Diagnosis Signs and lesions.Figure 21. and other game and ornamental birds occurring worldwide. a nematode worm parasite of chickens.

affecting geese and ducks. beetles etc act as intermediate hosts. Cheilospirura and Streptocara are seen worldwide but Histiocephalus is restricted to Europe. Grasshoppers.Gizzard worms . Diagnosis Lesions. Loss in condition and weight. Treatment Levamisole. Worms develop to L3 in eggs and infection is by the oral route direct from environment. Slow growth. Slow growth. Signs    Depression. confirmation of presence of the worms. benzimidazoles such as flubendazole. and Histiocephalus are nematode worm parasites of chickens. weevils. Adults are 2-4 cm long and usually bright red. Streptocara. Post-mortem lesions   Ulceration. necrosis and partial sloughing of gizzard lining. Signs    Depression. routine worming.Chickens Introduction Cheilospirura. muscular wall may be sacculated or ruptured.Geese Introduction A nematode worm parasite. Loss in condition and weight. Gizzard worms . Amidostomum anseris. 67 . They are more common in free-range birds because of their increased access to intermediate hosts. Prevention Prevention of access to intermediate hosts.

Post-mortem lesions   Pale myocardium. Prevention Rotation of ground on annual basis. Profuse white diarrhoea. Excessive water intake. muscular wall may be sacculated or ruptured. Signs         Prostration and death in acutely affected goslings. visualisation of worms. spleen and pancreas. Membrane covering tongue. Diagnosis Lesions. Loss of down. Adults are 2-4 cm long and usually bright red.Post-mortem lesions   Ulceration. Reduced feed intake. 68 . necrosis and partial sloughing of gizzard lining. Goose Parvovirus (Derzsy's Disease) Introduction Goose Parvovirus is a highly contagious condition of geese and young Muscovy ducks. The amount of maternal antibody passed from the breeding birds will affect the severity and timing and severity of the condition in the young birds. The younger the bird affected the more acute the condition and the higher the mortality. Reddening of skin. benzimidazoles. Treatment Levamisole. Derzsy's Disease is caused by a parvovirus distinct from chicken and mammalian parvoviruses. Losses are negligible in birds over 5 weeks of age. Swelling and congestion of liver. Vertical transmission resulting in congenital infection may occur. Swollen eyelids and eye and nasal discharge.

mycotoxins and viral infections and usually following a course of approximately 3 weeks. Loss of appetite. liver. Morbidity varies. Treatment No specific treatment. serosa and mucosae. Antimicrobials may be of value in reducing the effects of secondary bacterial infections. Liver yellow. heart. Ideally flocks that have suffered the disease should not be used for breeding as they may become persistent excreters of the infection. Bone marrow pale with fatty change.   Fibrinous pericarditis. Diagnosis Signs and lesions in birds of the appropriate age and species. The preferred approach is to immunise breeding birds with an attenuated live vaccine. Carcase anaemia. Pale comb and wattles. Fibrinous perihepatitis. Administration of immune serum has been shown to be effective but may require two doses (day old and around 3 weeks). Blood in droppings. 69 . Prevention Hatching and brooding geese from different parent flocks together should be avoided. Haemorrhagic Anaemia Introduction A complex condition of chickens associated with drug toxicities. mortality is 5-50%. muscles. Aplastic Anaemia. Haemorrhagic Disease. Poor growth. Ascites. Signs      Dejection. Post-mortem lesions     Haemorrhages in one or more sites: skin.

reproduction with filtered contents.Diagnosis History. Post-mortem lesions     Petechiae in various tissues. Signs       Sudden deaths. signs. the virus surviving in frozen faeces for months. double-immuno-diffusion of splenic extract. Serology: DID. May induce immunosupression and precipitate respiratory disease or coccidiosis. Drop in feed and water consumption. The source of virus is unknown but there is easy lateral spread within flocks. Diagnosis Typical lesions. caused by Type II Adenovirus distinct from classical fowl adenovirus and occurring in most turkey-producing areas. Intestine distended with blood. reticulo-endothelial hyperplasia and intranuclear inclusions. Blood from vent of moribund birds. and weeks in litter. Course 10-21 days. The route of infection is usually oral.sero-conversion frequently occurs in absence of clinical disease.spleen shows lymphoid hyperplasia. lesions. Haemorrhagic Enteritis Introduction A viral disease of turkeys. 70 . Treatment Vitamin K. similar to pheasant Marble Spleen disease. The virulence of the virus varies but morbidity may be 100% and mortality 10-60%. Diarrhoea. Prevention Avoid causative factors. add liver solubles to feed. remove sulphonamides. Microscopic . Spleen mottled and enlarged. Elisa .

especially associated with high relative humidity and low air speed. drinking water temperature and availability. acclimation. Maternal antibody may interfere with vaccination. Disinfect and 3-4 weeks house rest. 71 . feather cover. Reduced feed consumption. Immunity to the disease is long lasting. In this case a loop of intestine has been opened to show the blood.and T-line lymphocytes for up to 5 weeks following exposure. some in turkey B-lymphoblastoid cell lines.Treatment Warmth and good management. Predisposing factors include genetics. Increased thirst. and turkeys caused by high environmental temperature. Live vaccines are commonly used in many countries at 4-5 weeks of age. Heat Stress Introduction A condition seen in chickens. Pathogenic strains can depress both B. Signs    Panting. Some are produced in live turkeys. Turkeys dying with haemorrhagic enteritis commonly have the small intestine distended with blood. high stocking density. oral tetraycline. nicarbazin in feed. Immunity: there is an early age resistance irrespective of maternal antibody status. Prevention All-in/all-out production. convalescent serum. Figure 39. good hygiene and biosecurity. Ducks are relatively resistant to heat stress. good management.

Signs       Initially birds nervous. Later depression. fomites. and some game birds. signs. Intestine flabby with some bulbous dilation. Post-mortem lesions   Dehydration. chirping. 72 . pigeons. Prevention Houses of optimal height and insulation. Inappetance. Treatment Cool water. exclusion of other conditions. pattern of losses. In commercial ducks a related parasiteTetratrichomonas can cause poor growth and drops in egg production. Diagnosis Temperature records. watery diarrhoea. carriers.   Reduced egg production. columbae) is a protozoan parasite of turkeys. Frothy. Mucoid exudate in nostrils and mouth. Legs and wings outstretched. Prostration. lesions. Inter-species transmission may occur. evaporative coolers. painted white to reflect heat. Post-mortem lesions   Carcases congested. Loss in weight. Hexamitiasis Introduction Hexamita meleagridis (pigeons H. contains excessive mucus and gas. feed with a reduced protein:energy ratio. Terminal coma and convulsions. if relative humidity is low then wet the roof and fog. pheasants. Feeding during cooler hours may be beneficial. maximise airflow. Reductions in stocking density of meat poultry may be quickly achieved by partial depletion ('thinning'). It is transmitted by faeces.

Furazolidone. 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. Sulphur-yellow diarrhoea. increase ambient temperature. The effect of antibiotic may be related to the control of secondary bacterial enteritis. paratyphoid. Blood in faeces (chickens). and occasionally chickens. dimetridazole and ipronidazole have been used in the past. and also. Signs        Depression. The problem is seen in high-biosecurity facilities. histomonosis.  First half of intestine inflamed. Cyanosis of head. Differentiate from transmissible enteritis. Outwith earth worms orH. trichomoniasis. Histamonosis. Blackhead Introduction Histomonas melagridis is a protozoan parasite of turkeys. Caecal tonsils congested. presumably introduced with worm eggs. scrapings from fresh material. gallinae the parasite is easily destroyed. hygiene. and mixing groups of different ages. pheasants and game birds that acts together with facultative bacteria to produce the condition of Blackhead. Inappetance. Diagnosis Lesions. Prevention Depopulation. Although chickens are relatively resistant to the condition. Histomoniasis. dimetridazole. This condition has high morbidity and mortality in turkeys. significant disease has been seen in breeding chickens and free-range layers. Progressive depression and emaciation. if possible. all-in/all-out production. Treatment Tetracycline. 73 . Within a turkey shed transmission is rapid in spite of the fact that it is difficult to infect birds orally with unprotected parasites. avoid interspecies mixing. It has recently been demonstrated that infection occurs readily via the cloaca when birds are on contaminated litter. Poor growth.

Arsenicals are less effective in treatment than they are in prevention. nifursol) and arsenicals (e. It spread rapidly in broiler producing areas in that country and the same or a very similar condition has been seen in North and South America.Abubakar. It affects mainly broilers and broiler parents in rear and has also been seen in pigeons. At the time of writing no products of these groups are approved for use in the European Union. Mortality may reach 60% but more typically 10-30%. Diagnosis Lesions. Some herbal products based on the essential oils (e. grey or green areas.nitarsone) have been used to treat this important disease of poultry. possibly in combination with an RNA virus and immunosuppression caused by Chick Anaemia Virus or Infectious Bursal Disease. Liver may have irregular-round depressed lesions. especially in chickens. The disease is readily reproduced by inoculating birds with a bacteria-free filtrate of a liver extract from an affected bird.g. given recent new knowledge on the mechanism of transmission. caseous cores with yellow. Treatment Historically nitro-imidazoles (e. Regular worming to help control the intermediate hosts. furazolidone.g. Having both chickens and turkeys on the same property is likely to increase the risk of this disease in turkeys. usually grey in colour. Prevention Good sanitation. avoid mixing species. It is a condition caused by an adenovirus. Intensive relittering may help reduce the level of infection.g. scrapings from fresh material.M. Hydropericardium-Hepatitis Syndrome. concrete floors. Use of an anti-histomonas product in feed where such products are approved but due care with respect to residue avoidance would be required.Tahir Post-mortem lesions    Enlargement of caeca. dimetridazole). 74 . and only nitarsone is approved in the USA. Angara Disease Introduction This condition was first identified in broilers in Pakistan in 1987.g. nitrofurans (e. 'Herban)' have been used with some apparent success though controlled trials and formal approval for this purpose are not recorded. Ulcers. however they may not be present in the early stages.

Gizzard activity also acts as a pacemaker of intestinal activity and controls the speed at which food is passed to the small intestine. Control of predisposing immunosuppressive diseases may help limit losses. Prevention The condition typically occurs in areas of high poultry density where multi-age operation is traditional. Grit would not be classed as a foreign body. Formalin-inactivated oil adjuvant vaccines are reported to be highly effective and are used in areas where the condition is endemic. Most young commercial poultry consume feeds that have a small particle size. Congestion of the carcase. however sometimes free-range poultry consume large stones. This condition usually affects only a small number of birds. Lethargy. The normal function of the gizzard is to aid in the physical grinding of food materials. treatment of drinking water with 0.Signs     Sudden increase in mortality.5% iodophor solution) appears to be beneficial. Impacted gizzards are then found in 'non-starter' type chicks or poults.g. pale friable liver and kidney. Yellow mucoid droppings. Post-mortem lesions     Excessive straw-coloured fluid distending the pericardium (up to 10 mls). Good water sanitation (e. Lungs oedematous. histopathology. Impaction and Foreign Bodies of Gizzard Introduction The gizzard or crop may become impacted with litter. Enlarged. Older birds ingest grit to facilitate the grinding activity in the gizzard. Treatment None. string etc. Diagnosis Lesions. Huddling with ruffled feathers. grass. and birds of any age can 75 . virology.1% of a 2. however if young chicks to do not begin to eat feed properly they often consume litter instead. to reduce their particle size to aid digestion.

Inclusion Body Hepatitis Introduction A disease of chickens characterised by acute mortality. A foreign body may be found in the interior of the gizzard. Post-mortem lesions    The gizzard is more firm than normal and. This usually happens after maintenance activities have been carred out in the housing. Nails commonly penetrate the lining of the gizzard. Reduced weight gain. Infected birds remain carriers for a few weeks. staples etc. The disease was first described in the USA in 1963 and has also been reported in Canada. and on opening is found to contain a mass of fibrous material. Treatment None effective in young birds. often with severe anaemia. Sweep floors after maintenance activities to remove nails and other potentially dangerous foreign bodies. 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.consume nails.15 days with a morbidity of 1-10% and a mortality of 1-10%. Obvious non-starters should be culled in this situation. Australia. the UK. France and Ireland. This may extend into the proventriculus and on into the duodeunum. and may penetrate the body wall. Italy. 76 . A number of different sero-types have been isolated from disease outbreaks but they may also be isolated from healthy chickens. Prevention Good brooding management to encourage early adaptation to the diet and adequate consumption of feed and water. Signs   Reduced feed intake. It has a course of 9. Daily monitoring of the crop-fill is a useful procedure. caused by an adenovirus. Diagnosis Lesions.

A form of the disease affecting birds under 3 weeks of age in Australia has been reproduced with serotype 8 adenovirus. many different sero-types have been isolated from different cases. Differentiate from Chick anaemia syndrome. Since adenoviruses are commonly found in healthy poultry. chloroform.Transmission may be vertical or lateral and may involve fomites. for instance due to early IBD challenge or congenital CAV infection. Serology: DID for group antigen. Blood thin. isolation alone does not confirm that they are the cause of a particular problem. yellow. Kidneys and bone marrow pale. Pallor of comb and wattles. Diagnosis A presumptive diagnosis may be made on history and lesions. perhaps because they have lower levels of maternal antibody.basophilic intranuclear inclusions. Post-mortem lesions      Liver swollen. The virus grows well in tissue culture (CEK. Bursa and spleen small. SN for individual sero-types. pH). Microscopically . CEL). Inappetance. Ruffled feathers. Progeny of high health status breeding flocks appear to be at greater risk. Soluble multivitamins may help with the recovery process. 77 . and deficiency of vitamin B12. Treatment None. mottled with petechiae and ecchymoses. but on the other hand many field cases show eosinophilic inclusions that do not appear to have adenovirus particles. Curiously. Infectious Bursal Disease. Signs     Depression. The virus is generally resistant to disinfectants (ether. Immunosuppression. Confirmation is made on finding inclusions in the liver. vibrionic hepatitis. and high temperatures. may be important. fatty liver syndrome. Formaldehyde and iodides work better. sulphonamide intoxication.

Its affects vary with: the virulence of the virus. The cause is a Coronavirus that is antigenically highly variable. IB Introduction This infection. new sero-types continue to emerge. coli. Diuresis. Kidneys and bronchi may be swollen and they and the ureters may have urates. Caseous plugs in bronchi.Prevention Quarantine and good sanitary precautions. gasping. Poor ventilation and high density are predisposing factors. heat (56°C for 15 mins). These differences are due to structural differences in the spike proteins (S1 fraction). prevention of immunosuppression. the age of the bird. 78 . Dakota. Some birds/viral strains can be carriers to 1 year. Typing by haemagglutination-inhibition is also used. Airsacculitis. Post-mortem lesions       Mild to moderate respiratory tract inflammation. Diarrhoea. Coughing. The virus. About eight sero-groups are recognised by sero-neutralization. Tracheal oedema. Infectious Bronchitis. Tracheitis. Infection is via the conjunctiva or upper respiratory tract with an incubation period of 18-36 hours. depending on secondary infections. maternal immunity (young birds). disinfectants (Formal 1% for 3 mins). prior vaccination. Huddling. E. dyspnoea. fomites or aerosol. probably the commonest respiratory disease of chickens. Signs        Depression. Wet litter. alkalis. The infection is highly contagious and spreads rapidly by contact. Morbidity may vary 50-100% and mortality 0-25%. and complicating infections (Mycoplasma. 1931). Loss of appetite. was first described in the USA (N. which may survive 4 weeks in premises. Newcastle disease). is sensitive to solvents.

mycoplasmosis. SN (type specific).Diagnosis Tentative diagnosis is based on clinical sgns. Cellmediated immunity may also be important. fomites or aerosol. Humoral immunity appears 10-14 days post vaccination. Infection is via the conjunctiva or upper respiratory tract with an incubation period of 18-36 hours. short duration. Infectious Bronchitis. vaccinal reactions. IB . possible reactions depending on virulence and particle size. Local immunity is first line of defence. Serology: HI. which may survive 4 weeks in premises. Muscular shivering. Treatment Sodium salicylate 1gm/litre (acute phase) where permitted . is sensitive to solvents. DID (poor sensitivity. disinfectants (Formal 1% for 3 mins). group specific).v. Differentiate from Newcastle disease (lentogenic and mesogenic forms). Some birds/viral strains can be carriers for up to 1 year. The infection spreads rapidly by contact.).antibiotics to control secondary colibacillosis (q. Maternal immunity provides protection for 2-3 weeks. Definitive diagnosis is based on viral isolation after 3-5 passages in chick embryo. Signs    Sudden death. depending on secondary infections. flourescent antibody positive and ciliostasis in tracheal organ culture. Prevention Live vaccines of appropriate sero-type and attenuation. Otherwise as for standard IB. heat (56°C for 15 mins). HA negative. lesions and serology. The virus. Poor ventilation and high density are predisposing factors. alkalis. with typical lesions. Avian Influenza and Laryngotracheitis.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%. Elisa (both group specific). 79 .

Loss of internal egg quality. Rales may or may not be present. possible reactions depending on virulence and particle size. Rough shells. sneezing. Soft-shelled eggs. ciliostatic in tracheal organ culture. Diagnosis 3-5 passages in CE allantoic cavity. Coughing. There is rapid spread by contact. FA. CK) only after adaptation Serology: HI. lesions progress to necrosis and scarring of deep pectorals in convalescence.). SN (type specific). The virus is moderately resistant and may survive 4 weeks in premises. In layers the ovules may be intensely congested. The condition has a morbidity of 10-100% and mortality of 0-1%. Treatment Sodium salicylate 1gm/litre (acute phase) where permitted . 80 . with much antigenic variation. Elisa (both group specific). fomites or aerosol. Signs       Drop in egg production (20-50%). cell culture (Vero. Infection is via the conjunctiva or upper respiratory tract. A few birds are carriers up to 49 days post infection. typical lesions. Poor ventilation and high density are predisposing factors. group specific).antibiotics to control secondary colibacillosis (q. Infectious Bronchitis. DID (poor sensitivity. IB Egg-layers Introduction A Coronavirus infection of chickens.v. Prevention Live vaccines of appropriate sero-type and attenuation. HA-. short duration. Other lesions of 'classical' IB may be encountered.Post-mortem lesions    Oedema of pectoral muscles and subcutaneously on abdomen.

SN. Maternal immunity provides protection for 2-3 weeks.antibiotics to control secondary colibacillosis (q. Humoral immunity appears 10-14 days post vaccination.v.Post-mortem lesions   Follicles flaccid. particle size (if sprayed) and general health status. Elisa. EDS76. although reactions can occur depending on prior immunity. FA. Serology: HI. Diagnosis 3-5 passages in CE. Cell-mediated immunity may also be important. HA-. Treatment Sodium salicylate 1gm/litre (acute phase) where permitted . Yolk in peritoneal cavity (non-specific). virulence. Flaccid ovarian follicles in a broiler parent chicken undergoing challenge with Infectious Bronchitis virus. 81 .). Local immunity is the first line of defence. Figure 22. Prevention Live vaccines of appropriate sero-type and attenuation. typical lesions. Differentiate from Egg Drop Syndrome. DID.

The virus is moderately resistant and may survive 4 weeks in premises. Differentiate from Egg Drop Syndrome. Poor ventilation and high density are predisposing factors. Signs       Drop in egg production (20-50%). Prevention Live vaccines of appropriate sero-type and attenuation. Coughing. Soft-shelled eggs. Cell-mediated immunity may also be important. Maternal immunity provides protection for 2-3 weeks. Elisa. EDS76. Humoral immunity appears 10-14 days post vaccination. IB Egg-layers Introduction A Coronavirus infection of chickens. Infection is via the conjunctiva or upper respiratory tract. Local immunity is the first line of defence. with much antigenic variation. Rough shells. A few birds are carriers up to 49 days post infection. The condition has a morbidity of 10-100% and mortality of 0-1%. There is rapid spread by contact. SN. HA-.Infectious Bronchitis. FA. Loss of internal egg quality. Rales may or may not be present.v. sneezing. Diagnosis 3-5 passages in CE. typical lesions. Serology: HI. virulence. particle size (if sprayed) and general health status. Post-mortem lesions   Follicles flaccid. although reactions can occur depending on prior immunity. fomites or aerosol.).antibiotics to control secondary colibacillosis (q. Treatment Sodium salicylate 1gm/litre (acute phase) where permitted . 82 . Yolk in peritoneal cavity (non-specific). DID.

and affected birds excrete large amounts of virus for about 2 weeks post infection. faeces etc. susceptibility to Inclusion Body Hepatitis and gangrenous dermatitis and increased susceptibility to CRD. In addition to the direct economic effects of the clinical disease. IBD. but may be via the conjunctiva or respiratory tract. Flaccid ovarian follicles in a broiler parent chicken undergoing challenge with Infectious Bronchitis virus. The infective agent is a Birnavirus (Birnaviridae). Generally speaking the earlier the damage occurs the more severe the effects. Subclinical infection in young chicks results in: deficient immunological response to Newcastle disease. seen worldwide. The route of infection is usually oral. There is no vertical transmission. the damage caused to the immune system interacts with other pathogens to cause significant effects. (Turkeys and ducks show infection only. with an incubation period of 2-3 days.20% but sometimes up to 60%. 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. The disease is highly contagious. persisting for months in houses. Morbidity is high with a mortality usually 0. Signs are most pronounced in birds of 4-6 weeks and White Leghorns are more susceptible than broilers and brown-egg layers. 83 . Mealworms and litter mites may harbour the virus for 8 weeks. Sero-type 1 only. Marek's disease and Infectious Bronchitis. which targets the bursal component of the immune system of chickens.Figure 22. first identified in the USA in 1962. Infectious Bursal Disease. The virus is very resistant. especially with sero-type 2).

Half-life of maternally derived antibodies is 3. Elisa vaccination date prediction < 7 days). Variants: There have been serious problems with early Gumboro disease in chicks with maternal immunity. may have haemorrhages. 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. 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). Haemorrhagic syndrome. Use of a multivitamin supplement and facilitating access to water may help. normal size or reduced in size depending on the stage).History. Swollen kidneys with urates. Inappetance. Treatment No specific treatment is available. subsequent diagnosis of 'immunosuppression diseases' (especially inclusion body hepatitis and gangrenous dermatitis) is highly suggestive.4 days. Other possible causes of early immunosuppression are severe mycotoxicosis and managment problems leading to severe stress.Signs       Depression. rapidly proceeds to atrophy. (previously SN and DID). Vent pecking. lesions. Haemorrhages in skeletal muscle (especially on thighs). Antibiotic medication may be indicated if secondary bacterial infection occurs. Diarrhoea with urates in mucus. Differentiate clinical disease from: Infectious bronchitis (renal). Unsteady gait. This may be confirmed by demonstrating severe atrophy of the bursa. Coccidiosis. 84 . Tests used are mainly Elisa.A history of chicks with very low levels of maternal antibody (Fewer than 80% positive in the immunodifusion test at day old.1% are highly suggestive.3% of bodyweight. weights below 0. Dehydration. especially if present prior to 20 days of age. Huddling under equipment.5. IBD viruses have been isolated and shown to have significant but not complete cross-protection. Diagnosis Clinical disease . The normal weight of the bursa in broilers is about 0. histopathology. Subclinical disease . They are all serotype 1. especially in the Delmarva Peninsula in the USA.

85 . biosecurity measures may be helpful in limiting the spread between sites. When outbreaks do occur. It is enlarged.Prevention Vaccination. Immunity after a live vaccine can be poor if maternal antibody was still high at the time of vaccination. Morbidity is high but mortality low if uncomplicated although it may be up to 20%. Infectious Coryza is caused by the bacterium Haemophilus paragallinarum and is seen in many countries especially in multi-age farms that are never depopulated. characterised by catarrhal inflammation of the upper respiratory tract. Infectious Coryza Introduction A usually acute. highly infectious disease of chickens. vaccination of progeny depending on virulence and age of challenge. turgid and oedematous. This shows the anatomical relationship between the bursa. Carriers are important with transmission via exudates and by direct contact. Figure 23. and tracing of contacts may indicate sites on which a more rebust vaccination programme is indicated. 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. A strong immunity follows field challenge. the rectum and the vent. especially nasal and sinus mucosae. including passive protection via breeders. occasionally pheasants and guinea-fowl. It is not egg transmitted. resulting in increased culling. sometimes chronic. The route of infection is conjunctival or nasal with an incubation period of 1-3 days followed by rapid onset of disease over a 2-3 day period with the whole flock affected within 10 days. This bursa is from an acutely affected broiler.

Controlled exposure has also been practised. preferably in raised CO 2 such as a candle jar. Flouroquinolones are bactericidal and might prevent carriers. Vaccines are used in areas of high incidence. 86 . tylosin. Serology: HI. identification of the bacteria in a Gram-stained smear from sinus. Treatment Streptomycin. Sneezing. Loss in condition. Inappetance. Birds recovered from challenge of one serotype are resistant to others. respiratory viruses. at least two doses are required. Dyspnoea. Diagnosis A presumptive diagnosis may be made on signs. Live attenutated strains have been used but are more risky. Bacterin at intervals if history justifies or if multi-age. Differentiate from Mycoplasmosis. agglutination and IF have all been used but are not routine. Commercial bacterins may not fully protect against all field strains but reduce the severity of reactions.requires X (Haematin) and V (NAD) factors. Signs         Facial swelling. chronic or localised pasteurellosis and vitamin A deficiency. Purulent ocular and nasal discharge. Swollen wattles. Drop in egg production of 10-40%. Tracheitis. Caseous material in conjunctiva/sinus. erythromycin. lesions. Intercurrent respiratory viral and bacterial infections are predisposing factors. while bacterins only protect against homologous strains.The bacterium survives 2-3 days outside the bird but is easily killed by heat. Prevention Stock coryza-free birds on an all-in/all-out production policy. Dihydrostreptomycin. Eye-lid adherence. drying and disinfectants. Confirmation is by isolation and identification . Post-mortem lesions      Catarrhal inflammation of nasal passages and sinuses. sulphonamides. Conjunctivitis. DID.

Microscopically . Transmission between farms can occur by airborne particles or fomites. All-in/allout operation. Gasping. pheasants. Apply strict biosecurity in moving equipment or materials between these these categories of stock. histology. vaccination. Movement and mixing of stock and reaching point of lay are predisposing factors. lesions. Coughing of mucus and blood. often with blood in lumen. caseous plugs may be present. antibiotics to control secondary bacterial infection if this is marked. Drop in egg production. Isolation in CE CAMs. PCR. if enzootic or epizootic in an area.Infectious Laryngotracheitis. Prevention Quarantine.intranuclear inclusions in tracheal epithelium. 87 . Fairly slow lateral spread occurs in houses. Keep susceptible stock separate from vaccinated or recovered birds. after 4 weeks of age. IFA. Differentiate from Newcastle disease. Diagnosis Signs. Signs        Dyspnoea. The virus is highly resistant outside host but is susceptible to disinfectants. ILT Introduction A herpesvirus (pathogenicity can vary) infection of chickens. peafowl and turkeys with a morbidity of 50-100% and a mortality usually 10-20% but sometimes up to 70%. Recovered and vaccinated birds are long-term carriers. Post-mortem lesions   Severe laryngotracheitis. Sera may be examined by VN or Elisa. Sinusitis. The route of infection is via upper respiratory tract and conjunctiva or possibly oral and the course of the disease is up to 6 weeks. Treatment None. in severe form may be enough. severe bronchitis. Ocular discharge. Nasal discharge (low pathogenicity strains).

usually in the lower small intestine. Simulid flies or culicoid midges are intermediate hosts.Intussusception Introduction A condition of chickens associated with increased intestinal motility. worms and other forms of enteritis are predisposing factors. Careful attention to feeding practices to avoid anticipation of feed arrival if on restricted feeding. Leukocytozoonosis Introduction Caused by Leucocytozoon species. Prevention Control of coccidiosis and other causes of intestinal inflammation. protozoan parasites of turkeys. Post-mortem lesions  Telescoping of the bowel. The disease has a short course and morbidity and mortality are high. guinea fowl. Survivors may carry infection. Coccidiosis. Different species of this parasite have been reported from North America. Asia and Africa. it may actually protrude at the vent and be cannibalised. ducks. Anorexia. Signs      Sudden onset of depression. Signs  Mainly sudden deaths. rarely chickens. 88 . Thirst. Rapid breathing. Diagnosis Typical post-mortem lesions Treatment As appropriate for the underlying disease condition. Loss of equilibrium.

May be asymptomatic. age. Diagnosis Lesions. liver or bursa. Loss of weight. Emaciation. Enlargement of abdomen. cytology. Treatment 89 . Signs       Depression. histology and blood smears. gametes in erythrocytes. Treatment None known. Anaemia.megaschizonts in brains of birds with nervous signs. schizonts in liver. Lymphoproliferative Disease (LPD) Introduction A Type C retrovirus infection of turkeys with low morbidity and high mortality. especially in enlarged spleen. Post-mortem lesions  Focal tumours. Anaemia. Post-mortem lesions     Splenomegaly. disposal of recovered birds. Diagnosis History. Hepatomegaly. lesions. Prevention Separation from intermediate hosts. Persistent low mortality. Differentiate from Reticuloendotheliosis. Microscopically .

Eating faeces. Poor management may contribute to the problem. temperature control) may lead to a similar picture in the absence of specific infection. Runting/Stunting Introduction A condition of chickens and turkeys that may be associated with several different viruses. North and South America and Australia. Pot-bellied appearance. in future eradication. Prevention Good hygiene. Poor early management (feed and water supply. Sometimes osteomyelitis and/or rickets. enterovirus-like particles. Stunting (temporary). Abnormal feathers ('helicopter wings' 'yellow-heads').Tahir None. all-in/all-out production. Signs         Uneven growth. control arthropods.(maize-) fed birds (often associated with orange intestinal contents and/or faeces). Poor feathering. reoviruses. Diarrhoea in older birds may be an effect of on-farm infection. direct electron microscope examination of intestinal contents. Runting (permanent). It is suspected that these viruses can be vertically transmitted and the most severe signs in young birds are associated with this. Treatment Daily cull of affected birds between 14 and 28 days. Diarrhoea.M. Diagnosis Pathology. 90 . Pale shanks in corn. Malabsorption Syndrome. rotavirus etc. Post-mortem lesions     Enteritis. The condition has been seen in Europe. Pancreatic atrophy/fibrosis and pancreatic atrophy (rather variable). for example enteroviruses.Abubakar.

Prevention Good broiler farm hygiene. lungs.poorly digested food enclosed in mucus. and rarely turkeys in close association with chickens. avoidance of intercurrent disease and management problems (such as chilling). ovary. both parasitic and bacterial. muscles. seen worldwide. A sample of the faeces produced is shown at the bottom of the picture . Intestines of a young broiler chick suffering from malabsorption syndrome. From the 1980s and 1990s highly virulent strains have become a problem in North America and Europe. Figure 24. The virus survives at ambient temperature for a long time (65 weeks) when cell associated 91 . fomites. as well as more longstanding paralysis of legs or wings and eye lesions. Marek's disease Introduction Marek's disease is a Herpes virus infection of chickens. Infected birds remain viraemic for life. The disease has various manifestations: a) Neurological . Mortality in an affected flock typically continues at a moderate or high rate for quite a few weeks. Affected birds are more susceptible to other diseases. tests.Tumours in heart. good parent nutrition and egg selection and santitation. c) Cutaneous . They are distended with poorly digested feed. Vertical transmission is not considered to be important. In 'late' Marek's the mortality can extend to 40 weeks of age. b) Visceral . etc.Tumours of feather follicles. Morbidity is 10-50% and mortality up to 100%. The route of infection is usually respiratory and the disease is highly contagious being spread by infective feather-follicle dander.Acute infiltration of the CNS and nerves resulting in 'floppy broiler syndrome' and transient paralysis.

It is inactivated rapidly when frozen and thawed. all-in/all-out production. deficiency of thiamine. It is common practice to use combinations of the different vaccine types in an effort to broaden the protection achieved. Microscopically . chronic respiratory disease in chickens. pigeons and other wild birds. Prevention Hygiene.Chicken Introduction Infection with Mycoplasma gallisepticum is associated with slow onset.. Thickening of nerve trunks and loss of striation. game birds. heart.g. spleen. age affected. botulism. Grey iris or irregular pupil. Mycoplasma gallisepticum infection. Genetics can help by increasing the frequency of the B21 gene that confers increased resistance to Marek's disease challenge. gonads. Post-mortem lesions    Grey-white foci of neoplastic tissue in liver. turkeys. Differentiate from Lymphoid leukosis. wings and neck. Ducks and geese can 92 .lymphoid infiltration is polymorphic. clinical signs. Diagnosis History. Chronic Respiratory Disease . M. Loss of weight. especially at the start of lay. distribution of lesions. histopathology. vaccination generally with 1500 PFU of HVT at day old (but increasingly by in-ovo application at transfer). lung. Treatment None.and is resistant to some disinfectants (quaternary ammonium and phenol). association with other strains (SB1 Sero-type 2) and Rispen's. and skeletal muscle. deficiency of Ca/Phosphorus/Vitamin D. Vision impairment. kidney. Signs      Paralysis of legs. Skin around feather follicles raised and roughened. resistant strains.

Catarrhal inflammation of nasal passages. 93 . Transmission may be transovarian. Pericarditis. subsequent stress may cause recurrence of disease. Survival seems to be improved on hair and feathers. though in some countries this infection is now rare in commercial poultry. serology. In others it is actually increasing because of more birds in extensive production systems that expose them more to wild birds. Signs          Coughing. ND. and in lyophilised material. more commonly in Mycoplasma Broth followed by plating out on Mycoplasma Agar. Inappetance. The infectious agent survives for only a matter of days outwith birds although prolonged survival has been reported in egg yolk and allantoic fluid. tenosynovitis and salpingitis in chickens. airborne dust and feathers. Spread is slow between houses and pens suggesting that aerosols are not normally a major route of transmission. Occasionally arthritis. though infection rates are high. exudates. coli. aerosols. Occasional encephalopathy and abnormal feathers. Diagnosis Lesions. Reduced hatchability and chick viability. Recovered birds remain infected for life. Perihepatitis (especially with secondary E. The route of infection is via the conjunctiva or upper respiratory tract with an incubation period of 6-10 days. ART). morbidity may be minimal and mortality varies. Poor productivity. Culture requires inoculation in mycoplasma-free embryos or. and inadequate environmental conditions are predisposing factors for clinical disease. Post-mortem lesions      Airsacculitis. or by direct contact with birds. virulent E. In turkeys it is most associated with severe sinusitis (see separate description in the turkey section). Pasteurella spp. and to a lesser extent fomites. sinuses. The condition occurs worldwide. Haemophilus. Fomites appear to a significant factor in transmission between farms. isolation and identification of organism. Leg problems.become infected when held with infected chickens. In adult birds. Intercurrent infection with respiratory viruses (IB. Stunting. demonstration of specific DNA (commercial PCR kit available). Slow growth. trachea and bronchi. Suspect colonies may be identified by immuno-flourescence. coli infection). Nasal and ocular discharge.

or by direct contact with birds. Productivity in challenged and vaccinated birds is not as good as in M. infection status is important for trade in birds.. suspect reactions are examined further by heat inactivation and/or dilution. synoviae and M. biosecurity.g. and fomites. 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.-free stock. vitamin A deficiency. generally as a confirmatory test.Serology: serum agglutination is the standard screening test. and routine serological monitoring. though in many countries this infection is now rare in commercial poultry. These programmes are based on purchase of uninfected chicks. meleagridis(turkeys). HI may be used.g. In some circumstances preventative medication of known infected flocks may be of benefit. viral respiratory diseases. It is seen worldwide. Infectious Sinusitis . tetracyclines. PCR is possible if it is urgent to determine the flock status. Some inactivated vaccines for other diseases induce 'false positives' in serological testing for 3-8 weeks. aerosols. tylosin. Treatment Tilmicosin. other Mycoplasma infections such as M. Transmission may be transovarian. fluoroquinolones.Turkeys Introduction A slow onset chronic respiratory disease of turkeys often with severe sinusitis and associated with Mycoplasma gallisepticuminfection. Elisa is accepted as the primary screening test in some countries.g. Recovered birds remain infected for life. Prevention Eradication of this infection has been the central objective of official poultry health programmes in most countries. Suspect flocks should be re-sampled after 2-3 weeks. therefore M. exudates. Effort should be made to reduce dust and secondary infections. Aspergillosis. spiramycin. The route of infection is via the conjunctiva or upper respiratory tract with an incubation period of 6-10 days. 94 . subsequent stress may cause recurrence of disease. Morbidity is low to moderate and mortality low. Differentiate from Infectious Coryza. Mycoplasma gallisepticum infection. hatchingeggs and chicks. M.

more commonly in Mycoplasma Broth followed by plating out on Mycoplasma Agar. Slow growth. Treatment Tilmicosin. Airsacculitis. and biosecurity. Suspect colonies may be identified by immunofluorescence. malnutrition. fluoroquinolones. Leg problems. HI may also be used. Culture. often with inspissated pus. and in lyophilised material. isolation and identification of organism. suspect reactions are examined further by heat inactivation and/or dilution. PCR is possible if it is urgent to determine the flock status. Pericarditis. all-in/allout production. Differentiate from viral respiratory disease. serology. of swabs taken from the trachea or lesions. Stunting. Stress. tetracyclines. intercurrent viral disease such as Newcastle disease (even lentogenic) and Turkey Rhinotracheitis are predisposing factors. spiramycin. Some inactivated vaccines induce 'false positives' in serological testing. Signs        Coughing. Survival seems to be improved on hair and feathers. requires inoculation in mycoplasma-free embryos or.The infectious agent survives for only a matter of days outwith birds. especially Turkey Rhinotracheitis. tylosin. Serology: serum agglutination is the standard screening test. Nasal and ocular discharge. Perihepatitis. Inappetance. In some circumstances preventative medication of known infected flocks may be of benefit. Effort should be made to reduce dust and secondary infections. Diagnosis Lesions. demonstration of specific DNA (commercial kit available). Post-mortem lesions     Swollen infraorbital sinuses. although prolonged survival has been reported in egg yolk and allantoic fluid. These are based on purchase of uninfected poults. Swollen sinuses. Suspect flocks should be re-sampled after 2-3 weeks. Prevention Eradication of this infection has been the central objective of official poultry health programmes in most countries. 95 .

Post-mortem lesions  Sinusitis. Post-mortem lesions  Stunted embryos with hepatitis and enlarged spleens.g.Mycoplasma immitans infection Introduction Infection with Mycoplasma immitans is seen in geese. Diagnosis Shows cross reaction in IFA to M. Leg lesions can be shown in inoculated birds but do not seem to occur naturally.g. Treatment As for M. and can occur in other poultry and wild bird species. Infection occurs via the conjunctiva or upper respiratory tract and transmission among poults may be vertical. M. some with down abnormality. and partridges (UK). Reduced hatchability. Mycoplasma iowae infection. venereal or horizontal. Prevention As for M. Signs  Swollen sinuses. perhaps because all affected embryos fail to hatch.g. 96 . ducks (France). Introduction Infection with Mycoplasma iowae is seen in turkeys.i. Signs   Embryonic mortality. although DNA homology is only 40%.

Crooked necks. maintenance of this status by good biosecurity. Signs        Reduced hatchability. it occurs in most turkey-producing countries but is now much rarer in commercial stock. 97 . Transmission is venereal in breeders. Stunting. Mycoplasma meleagridis infection. though up to 25% of infected birds show lesions at slaughter. The infective agent does not survive well outside the bird. Pathogenicity is quite variable. Prevention Eradication of the infection from breeding stock. Antibiotics that have been used are tylosin and enrofloxacin. purchase of M. Treatment Pressure differential dipping has been used where breeder flocks are infected. Infected eggs result in widespread distribution of infection and increased risk of further vertical transmission. Slow growth. morbidity may be minimal. When the vacuum is released the eggs draw in antibiotic solution which is subsequently absorbed through the shell membranes. with transovarian and then lateral spread in meat animals. The organism has also been isolated from raptors. Leg problems. Infection is via the conjunctiva or upper respiratory tract with an incubation period of 6-10 days. Mild respiratory problems. Mortality is low. In adult birds though infection rates are high. M. For eradication purposes egg injection provides more consistent dosing per egg than does egg dipping. Specialised dip tanks are subjected to negative pressure which partially collapses the air cell of the submerged eggs. Infected parents may be asymptomatic. Predisposing factors include stress and viral respiratory infections. Introduction A disease of turkeys characterised by respiratory and skeletal problems caused by Mycoplasma meleagridis. This can increase hatchability by 510% in this situation.Diagnosis Isolation and identification of the causative organism from dead-in-shell embryos.i.-free stock.m.

especially in commercial layer flocks. serology. demonstration of specific DNA (commercial kit available). Spread is generally rapid within and between houses on a farm. Effort should be made to reduce dust and secondary infections. Survival of the infectious agent outwith the bird is poor but fomite transmission between farms is important. Differentiate from Mycoplasma gallisepticum. Predisposing factors include stress and viral respiratory infections. spiramycin. M. fluoroquinolones. Airsacculitis (rarely) seen in adult birds. Serology: SAG used routinely . Vaccines are not normally used. Mycoplasma synoviae. isolation and identification of organism. In some circumstances preventative medication of known infected flocks may be of benefit. It occurs in most poultry-producing countries. Infection is via the conjunctiva or upper respiratory tract with a long incubation period. whilst illness is variable and mortality less than 10%. tetracyclines. Birds infected from their parents seem to be immuno-tolerant and particularly prone themselves to transmit. Diagnosis Lesions.s. and biosecurity. These are based on purchase of uninfected poults. Suspect colonies may be identified by immuno-fluorescence. Mycoplasma synoviae infection.culture used to confirm. more commonly in Mycoplasma Broth followed by plating out on Mycoplasma Agar. Culture requires inoculation in mycoplasma-free embryos or. Transmission may be transovarian. Infection rates may be very high. or lateral via respiratory aerosols and direct contact. 11-21 days following contact exposure. Infectious Synovitis Introduction Infection with Mycoplasma synoviae may be seen in chickens and turkeys in association with synovitis and/or airsacculitis. 98 . other respiratory viruses. all-in/all-out production.Post-mortem lesions   Airsacculitis in infected pipped embryos and poults. Infected birds do develop some immunity. Treatment Tylosin. Prevention Eradication of this infection is also possible using similar techniques as for Mycoplasma gallisepticum. Infected males are particularly prone to transmit infection and may warrant special attention.

        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.

Post-mortem lesions
       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.

Post-mortem lesions
  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.


in drinking water. Sudden death in good condition (ducks). usually in less than 48 hours. Inappetance. Water medication for 3-5 days and in-feed medication for 5-7 days depending on the severity. amoxycillin). high levels of most growth promotors and normal levels of ionophore anticoccidials also help. usually around 10%. Intestinal contents may be dark brown with necrotic material. high viscosity diets (often associated with high rye and wheat inclusions in the diet). Ruffled feathers. contaminated feed and/or water. Intestinal mucosa with diptheritic membrane. Signs        Depression. Immobility. Affected birds tend to be dehydrated and to undergo rapid putrefaction.M. 100 ppm). caused by Clostridium perfringens and characterised by a fibrino-necrotic enteritis. diet (high protein). 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. other debilitating diseases.Abubakar.Tahir Necrotic Enteritis Introduction An acute or chronic enterotoxemia seen in chickens. Prevention Penicillin in feed is preventive. Treatment of ducks is not very successful. or Bacitracin in feed (e. Dark coloured diarrhoea. Mortality may be 5-50%. Treatment Penicillins (e. Post-mortem lesions      Small intestine (usually middle to distal) thickened and distended. Infection occurs by faecal-oral transmission. Closed eyes. Predisposing factors include coccidiosis/coccidiasis. Spores of the causative organism are highly resistant. Probiotics may limit multiplication of bacteria and toxin 102 .g. usually of the mid. in ducks possibly heavy strains. phenoxymethyl penicillin.g. turkeys and ducks worldwide. Reflux of bile-stained liquid in the crop if upper small intestine affected. neomycin and erythromycin are used in the USA.small intestine.

g. Signs are typically of disease of the nervous.Mild disease. In many countries local regulations or market conditions prevent the routine use of many of these options. conjunctivitis in man).Acute and fatal in chickens of any age causing neurological and some respiratory signs. Morbidity is usually high and mortality varies 0-100%. the upper has formed a thick crust of necrotic material. Newcastle Disease (Paramyxovirus 1) Introduction Paramyxovirus 1 or Newcastle Disease is a highly contagious viral disease affecting poultry of all ages.sometimes called 'asiatic' or exotic. birds. Transmission is via aerosols. 103 . Higher mortality is seen in velogenic disease in unvaccinated stock. fomites. The condition is rarely diagnosed in ducks but is a possible cause of production drops/fertility problems.production. It is not usually vertical (but chicks may become infected in hatcheries from contaminated shells). turkeys.Mortality and nervous signs in adult.Neurotropic Velogenic . visitors and imported psittacines (often asymptomatic). Affected species include chickens. sometimes subclinical.Mesogenic . ND . It is highly virulent for chickens. Severe lesions of necrotic enteritis affecting the small intestine of broilers. less for turkeys and relatively apathogenic in psittacines. These viruses have sometimes been used as vaccines in previously immunised birds.Lentogenic . respiratory or reproductive systems. Intestinal lesions are absent. ND . The sample at the bottom of the picture is still focal. ND .Velogenic Viscerotropic (VVND) . The virus involved is Paramyxovirus PMV-1. pigeons and ducks. Figure 25. Other species can be infected including mammals occasionally (e. Four manifestations have been identified:     ND . Strains can be developed as vaccines. which is of variable pathogenicity. Can affect any age.

The virus survives for long periods at ambient temperature. antibiotics to control secondary bacteria. Treatment None. Tracheitis. for up to 12 months. Pathogenicity evaluated by Mean Death Time in embryos. pneumovirus infection. Paralysis. and is ether sensitive. Nervous signs. caecal tonsil. However it is quite sensitive to disinfectants. intoxications. intracerebral or IV pathogenicity in chicks. formalin and phenol. Signs Signs are highly variable and will depend on the nature of the infecting virus (see above). laryngotracheitis. It is confirmed by isolation in CE. Coughing. Severe drop in egg production. Diarrhoea. HA+. Intestinal lesions primarily occur in the viscerotropic form.            Sudden Death Depression. Dyspnoea. encephalomalacia. HI with ND serum or DID (less cross reactions). Samples . haemorrhagic disease. middle ear infection/skull osteitis. Haemorrhage in proventriculus. rising titre in serology. encephalomyelitis. Diagnosis A presumptive diagnosis may be made on signs. especially in faeces and can persist in houses (in faeces. Differentiate from Infectious bronchitis. fumigants and sunlight. dust etc). IFA. Twisted neck. 104 . Post-mortem lesions      Airsacculitis. infectious coryza. post-mortem lesions. Inappetance. the infective dose and the degree of immunity from previous exposure or vaccination. EDS-76. Necrotic plaques in proventriculus. acid pH. It is inactivated by temperatures of 56°C for 3 hours or 60°C for 30 min.tracheal or cloacal. avian influenza. intestine. Moult. Cross-reactions have mainly been with PMV-3.

especially in breeding birds by the use of routine serological monitoring. biosecurity. Figure 28. Vaccinal reactions may present as conjunctivitis.Prevention Quarantine. Vaccination programmes should use vaccines of high potency. It is common to monitor response to vaccination. A typical programme may involve Hitchner B1 vaccine at day old followed by LaSota-type vaccine at 14 days. It is commonest in progeny of young parent flocks (relatively small yolks) or where managers are inexperienced. 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). These tests do not directly evaluate mucosal immunity. and occasionally gasping due to a plug of pus in the lower trachea. 105 . Morbidity is up to 10% and mortality close to 100%. whereas it tends to peak between 6-10 days for chicks that begin eating but then cease. all-in/all-out production. Use of spray application is recommended but it needs to be applied with care to achieve good protection with minimal reaction. vaccination. which are adequately stored and take into account the local conditions. Inactivated vaccines have largely replaced the use of live vaccines in lay but they do not prevent local infections. Use of Mycoplasma gallisepticum free stock under good management reduces the risk of vaccinal reactions. Mortality peaks at 3-5 days for birds that fail to eat at all. Acute viral infections or heavily contaminated drinking water may have a similar effect to bad management in reducing feed intake. In some countries it has been customary to provide antibiotics prophylactically during periods of anticipated vaccinal reaction. snicking. HI has been used extensively. and is associated with difficulty maintaining brooding temperature and poor management of feeders and drinkers. however. 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. Elisa is now also used.

bile staining of adjacent tissues. Oregon Disease . Post-mortem lesions      Crop empty. It has since been seen in turkeys. good hygiene and biosecurity in brooding areas to minimise early disease challenges. Because it is enclosed in a relatively unyielding membrane. any swelling of the muscle tends to cut off the blood supply. or suffer necrosis. Poor development. Treatment Correction of management problems. Diagnosis Based on post-mortem lesions. nutrition of young parents. It does not usually cause any mortality or obvious clinical signs and so it is usually identified after slaughter.Signs  Failure to grow. aspergillosis. Differentiate from omphalitis/ yolk sac infection. Most organs normal. good drinking water hygiene. It is caused by a reduction in the blood supply to the deep pectoral muscles. 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. Gall bladder distended. Prevention Review brooding management. 106 .Deep Pectoral Myopathy Introduction This condition is so named because it was first identified in adult breeding turkeys in Oregon State. soluble multivitamin supplementation may help. The condition can be reproduced by causing intense exercise of this muscle. age of collection and weight of hatching eggs. Without adequate blood supply the tissue of the muscle begins to die. in broiler parent chickens and also in large broiler chickens in various places. Gizzard may be impacted with litter.

Treatment Not applicable. Figure 26. and. If of very long duration.Signs  None. 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.g. If recent. A typical case of the chronic stages deep pectoral myopathy in a broiler chicken. Post-mortem lesions   Acute or chronic necrosis of the deep pectoral muscle on one or both sides. The tissue in the centre is dry. with oedema within it and on its surface. it may become a healed scar. This will normally be due to excessive flapping in association with management activities (e. Prevention Avoidance of physical damage of this muscle. 107 . greenish yellow. and flaking. It may also start to be enclosed in a fibrous capsule. Transillumination of the breast may help identify affected carcases and may be worthwhile if the incidence is high. It is very difficult to detect affected carcases in standard meat inspection. Diagnosis Lesions. the muscle may be swollen and pale. artificial insemination in breeding turkeys. in particular excessive exercise. If the condition is of over 7 days duration the muscle is dry and often shows greenish tinges. weighing birds etc). thinning operations in meat birds.

coli overgrowth may occur. In broiler chickens its main importance seems to be as a cause of airsacculitis in apparently healthy flocks that is only identified at slaughter. Bordetella aviuminfection. Diagnosis Clinical signs and lesions. age at infection etc. Post-mortem lesions  Airsacculitis. This can cause significant losses through condemnations. A range of sero-types have been identified. Confirmation is by isolation of the organism. ORT Introduction Ornithobacterium Infection is an infection of chickens and turkeys with the bacterium Ornithobacterium rhinotracheale(ORT). ventilation problems. Reduced weight gain. It commonly exacerbates respiratory disease caused by pneumovirus infections in turkeys. The severity of its effects depends on the pathogenicity of the particular strain and other risk factors such as viral infections. This was first identified as a new disease syndrome of turkeys in Germany in the early 1990s. Reduced egg production. The infection is common in chickens and turkeys. Infectious Bronchitis). E. There is some evidence that hatcheries may play a role in the epidemiology. Growth is more rapid and consistent in an anaerobic jar. perhaps through survival of the organism on shell surfaces or shell membranes. 108 . It is a Gram-negative pleomorphic organism. The slow-growing bacterium was named in 1994.Ornithobacterium Infection. direct contact and drinkers. sneezing. Most isolates are oxidase positive and galactosidase positive Serology using Elisa tests has been used. The range occurring in turkeys is wider than that seen in chickens. preferably as a flock test comparing results before and after the challenge. field challenge with respiratory viruses. and E. It had been previously isolated in a number of other countries. tracheitis. The organism grows slowly producing tiny colonies on blood agar. coli infections. Important cofactors may include respiratory viral vaccines (Newcastle disease. Some uncertainty exists about mechanisms of transmission. Cultures from the trachea of birds showing typical signs are preferred. 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. severe bronchopneumonia. Within the poultry house it is likely to be by aerosols. Signs    Coughing.

Satisfactory disease control depends on good management and biosecurity. cost etc.Treatment The sensitivity of ORT to antibiotic is highly variable. Prevention This is based on good hygiene. Vaccination . therapy and vaccination. ORT is a major problem on multi-age sites.there are issues relating to availability. Routine treatment . Hygiene . regulation. neomycin and enrofloxacin.it is very sensitive in vitro to a range of chemicals. because of the age of slaughter. Initially in Germany most strains were sensitive to amoxycillin. also most are sensitive to tiamulin. Some work has been done on live vaccine in the USA. Vaccination of breeder flocks to protect progeny has shown benefits in chickens but. An inactivated vaccine is licensed for broiler parents in Europe. Preventative medication with the products listed in the previous section may be beneficial in some circumstances. 109 . Figure 27. though 54% were sensitive to tetracycline. In the USA in 1998 all strains were sensitive to penicillins and many other microbials. this is unlikely to work in turkeys. Severely consolidated lung from an acute ORT infection in 14-week-old turkey growers. Similar lesions may be found in Pasteurellosis. Some vaccines seem to have difficulty in producing a longlasting serological response to ORT. Amoxycillin sensitivity remains good. Tilmicosin is also effective at 10-20mg/kg and should be used in the early stages of the disease.amoxycillin at 250 ppm in water for 3-7 days or chlortetracycline at 500 ppm for 4-5 days. chlortetracycline but not to enrofloxacin. The lung is solid and covered by pus/ purulent exudate. In France and Belgium most strains were sensitive to enrofloxacin. it requires two doses.

Prevention Unknown. Treatment Not applicable . Osteoporosis. Soft bones and beak. Gram-variable pleomorphic bacteria have been isolated from affected livers and bones. Diagnosis Lesions.only identified at slaughter. Post-mortem lesions  Green discolouration of the liver at slaughter. high production. turkeys and ducks seen worldwide and due to Vitamin D or calcium deficiency. 110 . Signs  None. Drop in production. Birds go off legs. Soft-shelled eggs. Turkey Introduction An association has been shown between green discolouration of the livers of turkey growers at slaughter and the occurrence of inflammatory lesions of bones and/or joints. Birds rest squatting. Cage Fatigue Introduction A condition of chickens. Signs        Lameness. Enlarged hocks. The green discolouration is used to identify carcases that require closer inspection of the other tissues. Predisposing factors include small body size.Osteomyelitis Complex.

Prevention Supplementation of vitamin D. Beading and fracture of ribs. Diagnosis History. Signs     Depression. place on litter. bone ash. skeletal size and mineral content at point of lay are critical. Parathyroids enlarged.Abubakar. Coughing. spondylitis. signs. Treatment Over-correct ration vitamin D. lesions. 111 .M. Inappetance. proper Ca and P levels and ratio. antioxidants. In chickens it is usually mild. depending on the species affected and whether infection is complicated by other factors and diseases. whereas turkeys are more severely affected. Differentiate from Marek's disease. Drop in egg production. Wild birds are believed to be especially important.Yucaipa Disease Introduction An infection of chickens. turkeys and passerine cage birds with Paramyxovirus PMV-2 results in disease with variable mortality. Post-mortem lesions  Not characteristic.Tahir Post-mortem lesions      Bones soft and rubbery. calcium carbonate capsules. Paramyxovirus 2 . As birds progressively mobilise skeletal calcium for egg production through lay. Vertical transmission does not usually occur. Epiphyses of long bones enlarged. Beak soft. Transmission is by wild birds and fomites.

occasionally chickens and psittacine cage birds. The infection is transmitted by birds. HI with ND serum or DID (less cross reactions). IFA. High mortality (cage birds). all-in/all-out production. IFA. antibiotics to control secondary bacteria. Differentiate from Infectious bronchitis. antibiotics to control secondary bacteria. Paramyxovirus-3 Introduction Paramyxovirus PMV-3 infects turkeys. EDS-76. biosecurity. Prevention Quarantine. Diagnosis Isolation in CE. haemorrhagic disease. including wild bird contact and fomites. laryngotracheitis. Loss of shell pigment Nervous symptoms (psittacines). HI with ND serum or DID (less cross reactions). Inappetance. Vertical transmission does not usually occur. Drop in egg production (turkeys).Diagnosis Isolation in CE. Treatment No specific treatment. Signs        Depression. HA+. Mortality is usually low in poultry. 112 . Treatment No specific treatment. HA+. Coughing. Post-mortem lesions  No specific lesions.

HA+. Paramyxovirus-6 Introduction Paramyxovirus PMV-6 infection of turkeys. Vertical transmission does not usually occur. The infection is transmitted by birds. Treatment No specific treatment. It is an infectious and transmissible cause of sudden increases in mortality in turkeys between 7 and 28 days of age. Prevention Quarantine. Post-mortem lesions  No specific lesions. Mortality is 0-5%. antibiotics to control secondary bacteria. biosecurity. The infection is inapparent in ducks and geese. In both cases mortality can be high and can be associated with a marked depression in growth. HI with ND serum or DID (less cross reactions). including wild bird contact and fomites. IFA. PEMS and Spiking Mortality of Turkeys Introduction Poult Enteritis and Mortality Syndrome (PEMS) was first identified in high density turkey producing areas of the South Eastern USA in 1991. Vaccination has been used in turkeys but may not be cost-effective. A range of 113 . all-in/all-out production.Prevention Quarantine. all-in/all-out production. Signs   Reduction in egg production. A less acute form of the disease appears to produce more of a lingering mortality. biosecurity. Diagnosis Isolation in CE. Mild respiratory signs.

Emaciation. Signs         Initial hyperactivity and increased vocalisation. Picking at feed. Post-mortem lesions      Dehydration. seeking heat. Liquid intestinal contents. To replicate the condition in full it appears to be necessary to include bacteria in the inoculum. pale brown. Wet litter. Muscle atrophy.mash and poor quality crumbles increase risk. Treatment A range of antibiotics and arsenicals have been used to control the bacterial component of this condition. Increased water consumption. eating litter.viruses have been isolated from affected flocks. Weight loss. 114 . multivitamins and milk replacer products are helpful for nutritional support in the acute phase. Fluoroquinolone antimicrobials appear to be especially effective.5-8% will encourage feed intake and recovery. Increasing weakness. Reduced feed consumption and growth. Good quality diets of a suitable form . All-in/all-out production. Droppings watery. A highly digestible diet with fat at 7. Effective terminal disinfection. This syndrome is clearly distinguished from typical viral enteritis in young turkeys because of the high mortality and severe growth depression. huddling. Pendulous Crop Introduction A complex condition of turkeys and chickens associated with coarse fibrous feed. Diagnosis Signs. Prevention Biosecurity to reduce the introduction of new infections into brooding facilities. lesions. Overdistension of crop in young birds because of an interruption in feed supply may predispose. Caseous cores in bursae (late in the process).

haemorrhage. ulceration. Diagnosis Macroscopic examination of lesions. Diarrhoea. Post-mortem lesions  Inflammation. Infection is by the oral route on exposure to the intermediate hosts. Tetrameres and Cyrnea are nematodes. including crustaceans. Crop contents semi-liquid and foul smelling. if these can be identified. necrosis. Lack of muscle tone. have ulcerations and sometimes mycosis. may be impacted. spiruroid worm parasites of poultry and game birds. lesions. grasshoppers and cockroaches.Signs  Enlargement of crop. Treatment None. and thickening of mucosa of proventriculus. Prevention Remove predisposing factors. Emaciation in heavily infected young chicks (Tetrameres). Proventricular Worms Introduction Dispharynx. identification of worms. Signs    Anaemia. Diagnosis Signs. They are found in the mucosa of crop and proventriculus causing mainly inapparent infections. Post-mortem lesions    Crop distended with feed. 115 .

coccidiosis.Treatment Not usually required. Pseudotuberculosis Introduction An infection of ducks. Prevention Good husbandry and hygiene. adequate protection. Post-mortem lesions  Miliary lesions in a variety of organs but especially in the liver. Differentiate from Duck viral enteritis. Diarrhoea. Signs     Weakness. In peracute disease the only lesion may be enteritis. The disease has a mortality of 5-75%. colibacillosis. isolation. rodents and man with the bacterium Yersinia pseudotuberculosis. Sometimes sudden death. wild birds. duck viral hepatitis. Diagnosis Lesions. Prevention Prevention of access to intermediate hosts. Ruffled feathers. sulphonamides in feed. Treatment Tetracyclines. 116 . other poultry. 'hardening off'. tuberculosis.

lesions. Skin cyanosis of head. hygiene. Pancreas chalky. Watery diarrhoea. antibiotics. Dehydration. diet and water supply. Prevention Good management. Diagnosis History. Loss of appetite. vibriosis. Bluecomb. Crop distension. multivitamins in water. Crop distended. Liver swollen with foci. Kidneys swollen. elimination of other causes. Dark comb and wattles.M. It is associated with hot weather. mucoid casts in intestine.Abubakar. molasses. Signs        Depression. Avian Monocytosis Introduction A sudden onset condition of chickens early in lay with high morbidity and a mortality of 050%. coccidiosis. toxin and possibly a virus infection. capillariasis. 117 . IBD and typhoid. Treatment Adequate water supply. Drop in egg production. Affected birds have an increase in circulating monocytes in their blood. It was commonly reported prior to 1960 but is now rare. Skeletal muscle necrosis. Catarrhal enteritis. Post-mortem lesions         Dehydration. water deprivation.Tahir Pullet disease. Differentiate from fowl cholera.

Treatment Pyrethroids. citrus extracts. 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. May cause anaemia and death in young birds. 118 . Dermanyssus gallinae. mainly at night and may transmit fowl cholera and other diseases.7 mm. vegetable oil and mineralbased products (both liquid sand dusts) have been used to control red mites in the environment. Drop in egg production. which are external parasites of chickens and turkeys. Ornithonyssus bursae. cracks. Birds restless. in nest boxes. Prevention Thorough cleaning. Signs        Presence of grey to red mites up to 0.itching. feeds by sucking blood. Post-mortem lesions  Anaemia. carbamates. fumigation and insecticide treatment at turnaround. Pale comb and wattles. Diagnosis Number and type of mites identified. the Common Red Mite. crevices etc. Loss of condition. Effective monitoring of mite numbers and implementation of control measures before birds are heavily infested improves control. and good design of new equipment to limit harbourages for red mites. Staff complaints . the Northern Fowl Mite spends its entire life cycle on the bird and can multiply more rapidly as a result. Spots on eggs. organophosphates.Red Mite and Northern Fowl Mite Introduction Arachnid mites. For northern fowl mite it is essential to apply approved insecticides to the affected birds. Filling of cracks and crevices.

lesions.M. vaccinal and field strains) and bacteria (Ornithobacterium rhinotracheale. Avian pneumovirus. A number of respiratory viruses (Infectious Bronchitis. ammonia and other gases. The virus grows well in tissue culture (CE kidney. coli) may be involved. Opinions vary as to whether adenovirus can be characterised as a primary respiratory pathogen. Transmission may be vertical and lateral. Respiratory Disease Complex Introduction Respiratory infections in chicken and turkeys are seen worldwide but especially in temperate poultry-producing areas in winter months. E. Diagnosis History. and by fomites. at least 12 sero-types have been described and these may be isolated from healthy chickens. Infected birds may remain carriers for a few weeks. Prevention Quarantine and good sanitary precautions. intranuclear inclusions in liver. Post-mortem lesions  Mild catarrhal tracheitis. formaldehyde and iodides work better. pH). 'Mild Respiratory Disease' Introduction An adenovirus infection of chickens with a morbidity of 1-10% and a mortality of 1-10%. Signs  Mild snick and cough without mortality. may act as 119 .Tahir Respiratory Adenovirus Infection.Abubakar. prevention of immunosuppression. and other factors associated with poor ventilation. CE liver). Lentogenic Newcastle disease virus. It may occur as an exacerbating factor in other types of respiratory disease. Treatment None. The virus is generally resistant to disinfectants (ether. Dust. chloroform. temperature.

mortality 5. Severe airsacculitis of thoracic air sacs in a broiler close to slaughter. Rattling noises. response to environmental changes. Treatment Antimicrobial treatment of specific bacterial infections. Airsacculitis. be challenged by some of these pathogens). of course. Nasal exudate. serology. Sneezing. 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. sanitation of drinking water. Post-mortem lesions    Severe tracheitis with variable exudate . 120 . Head swelling. Prevention Effective ventilation. and have been cut into to reveal a cheesy (caseous) mass of pus. If condemned birds are included mortality may be more than 10%. Figure 29. Differentiate from Chronic Respiratory Disease (Mycoplasmosis). The air sacs are thickened and congested. There is also percarditis evident (at top right).predisposing factors. Morbidity is typically 10-20%. Signs       Snick. carefully applied appropriate viral vaccines. Diagnosis Lesions.10%.catarrhal to purulent. Conjunctivitis. Pericarditis.

spleen and kidney. Diarrhoea. chick inoculation. Treatment None. Reticuloendotheliosis. and quail with morbidity up to 25%.Figure 30. Leg weakness. turkeys. and the infection can be spread by mosquitoes or in contaminated Marek's disease vaccines. ducks. Diagnosis Pathology. 121 . Transmission is lateral and possibly transovarian. A gradual increase in mortality and poor growth in broilers may be the main signs. Marked stunting when Marek's disease vaccine is contaminated. usually higher in females than males. Both tracheas were congested and the upper sample had mucopurulent material in the lumen. Sometimes enteritis and proventriculitis (especially in broilers infected with contaminated Marek's disease vaccine). geese. Sometimes nodules in intestine and caecae. Severe tracheitis is broilers with respiratory disease complex. Post-mortem lesions    Neoplastic lesions in liver. There is an incubation period of 5-15 days. Signs     There may be no obvious signs. Lympoid Tumour Disease Introduction A retrovirus infection of chickens.

Treatment Over-correct ration with three times vitamin D for 2 weeks. Rickets (hypocalcaemic) Introduction Vitamin D deficiency or phosphorus/calcium imbalance is seen in chickens. Beak soft. Prevention Supplementation of vitamin D. turkeys and ducks worldwide. 122 . Growth plates widened and disorganised. Post-mortem lesions       Bones soft and rubbery. antioxidants. Reduction in bodyweight. or Vitamin D or 25-hydroxy vitamin D in drinking water. Birds rest squatting. Differentiate from Encephalomalacia. Avoidance of contamination of live vaccines is the main control measure practised. Diagnosis History. Poor growth. Beading and fracture of ribs.Prevention Formal control programmes have not been documented as the condition is sporadic and relatively self-limiting. lesions. Signs        Lameness. signs. proper calcium and phosphorus levels and ratio. Epiphyses of long bones enlarged. Parathyroids enlarged. Femoral Head Necrosis. Birds go off legs. Soft bones and beak. Hock swelling.

Hock swelling. Even subclinical levels of this condition can predispose to Femoral Head Necrosis. Poor growth. Birds go off legs. lesions (analyse Vitamin A or manganese as a guide to premix inclusion). or vitamin D in drinking water. proper calcium and phosphorus levels and ratio. Some countries have regulations governing the use of phosphorus in fertiliser with a view to reducing water pollution. Signs         Lameness. Growth plates widened and disorganised. Prevention Supplementation of Vitamin D. Birds rest squatting. This has led feed manufacturers to try various approaches to reduce added phosphorus in diets. Intestinal diseases may reduce absorption. Reduction in bodyweight. Post-mortem lesions       Bones soft and rubbery. Treatment Over-correct ration with 3 times vitamin D for 2 weeks. Diagnosis History. turkeys and duck is seen worldwide. Parathyroids enlarged. Beading and fracture of ribs. Beak soft. Enlarged hocks. Epiphyses of long bones enlarged. antioxidants. Soft bones and beak. 123 .M. signs.Abubakar.Tahir Rickets (hypophosphataemic) Introduction Phosphorus deficiency in chickens.

dissimilis in turkeys.Tahir Rotavirus Infection Introduction Rotavirus infection is seen in chickens.5 g faeces). The 124 . partridges and pigeons. large . pheasants. electron microscopy or Elisa on intestinal contents . The parasite species vary: A. seen worldwide. are nematode worm parasites.M. The life cycle is similar to that illustrated in the section on the caecal worm Heterakis. A.submit 6 x . The route of infection is oral and maximum viral excretion occurs 2-5 days post infection. and A. shorter in young birds. Treatment No specific treatment for this infection.Abubakar. It is not known if vertical transmission occurs though virus has been occasionally isolated from embryonated eggs. Control of secondary bacterial enteritis may require antimicrobial medication. columbae in pigeons. The route of infection is oral usually by direct ingestion of the embryonated egg and there is a 5-10-week prepatent period. Use of a good electrolyte solution is beneficial in the acute stage of infection. Roundworm. turkeys. Prevention Good hygiene in brooding areas. Adult birds can tolerate burdens asymptomatically.Ascaridia Introduction Ascaridia sp. Diagnosis Demonstration of virus (PAGE. Signs  Diarrhoea. guinea fowl. galli in fowl. stout white worms up to 12 cms in length. Post-mortem lesions  Viruses replicate mainly in the mature villous epithelial cells. Virus may be found in asymptomatic birds. except that the adults reside in the small intestine and earthworms are not significant paratenic or transport hosts.

Poor growth. Diarrhoea. Wasting. Worms up to 12 cm in length in duodenum and ileum. especially for young birds.parasites may be transported by grasshoppers and earthworms and are resistant to environmental effects. Post-mortem lesions   Enteritis. 125 . In the bottom left quadrant there are also some immature worms. Listlessness. piperazine as locally approved. pasture rotation and regular treatment. levamisole. A collection of mature roundworms (Ascaridia galli) recovered from the small intestine of a layer chicken in rear. mainly in young birds. Signs      Loss of condition. Diagnosis Macroscopic examination with identification of worms. Figure 31. Prevention Prevention of contamination of feeders and drinkers with faeces. oval smooth-shelled nonembryonated eggs in faeces. Treatment Flubendazole.

Abubakar.M. Chickens are most commonly affected but it also infects turkeys. Fowl Typhoid Introduction Disease caused by one of the two poultry-adapted strains ofSalmonella bacteria. sparrows. Histology may be helpful in determining if there is an underlying inflammatory process. Broiler chickens have an avascular area of tendon just above the hock that is the usual site of rupture. Infections still occur worldwide in non-commercial poultry but are rare in most commercial systems now. Salmonella Gallinarum. This can cause mortality in birds of any age. game birds. Signs   Severe lameness. Post-mortem lesions  The fresh lesion contains a haematoma with the end of the ruptured tendon within or adjacent to it. Treatment None. Salmonella Gallinarum. Broiler parents and brown-shell egg layers are especially susceptible. Affected birds should be culled humanely as soon as they are identified. 126 . canaries and bullfinches. The bird may have the hock dropped to the floor.Tahir Ruptured Gastrocnemius Tendon Introduction This is a condition causing severe lameness in roaster type meat chickens and more rarely in turkeys. parrots. guinea fowls. Prevention Establishment of a steady growth profile. Diagnosis Signs and lesions are obvious. Reoviral or staphylococcal arthritis or tenosynovitis may predispose but many cases have no evidence of an inflammatory response. If there is a greenish tinge to the area of swelling it occurred a few days previously. Ruptures of ligaments and joints are also occasionally seen. Avoidance of physical stresses on the musculoskeletal system through careful handling as well as careful design and layout of equipment.

Thirst. Ruffled feathers. tetracylines. LPS-based Elisa assays have been developed but not widely applied commercially. Yellow diarrhoea. The bacterium is fairly resistant to normal climate. Treatment Amoxycillin. mortality is increased in stressed or immunocompromised flocks and may be up to 100%. even in adults. Engorgement of kidneys and spleen. and/or congestion. clean chicks.Morbidity is 10-100%. Prevention Biosecurity. Anaemia. Transmission may be transovarian or horizontal by faecal-oral contamination. egg eating etc. surviving months. McConkey and non-selective agar is advisable. recovered birds are resistant to the effects of infection but may remain carriers. Inappetance. Vaccines for fowl typhoid have been used in some areas. but is susceptible to normal disinfectants. The route of infection is oral or via the navel/yolk. As with other salmonellae. Diagnosis Isolation and identification. fluoroquinolones. Tube and rapid plate agglutination tests have been the standard serological tests for many years but have only been validated for chickens. both live (usually based on the Houghton 9R strain) and bacterins. potentiated sulponamide. Differentiate from Pasteurellosis. Enrichment procedures usually rely on selenite broth followed by plating on selective media. Signs       Dejection. Post-mortem lesions     Bronzed enlarged liver with small necrotic foci. pullorum disease and coli-septicaemia. In clinical cases direct plating on Brilliant Green. Enteritis of anterior small intestine. 127 . Reluctance to move.

in young broiler chickens. The route of infection is oral or via the navel/yolk. Pullorum Disease. White diarrhoea. parrots. pale and shows focal necrosis. Morbidity is 10-80%. usually brown-shell egg layers. surviving months but is susceptible to normal disinfectants. Similar lesions can be seen in Pullorum Disease and with other causes of septicaemia in young chicks. Vent pasting.Figure 32. 'Bacillary White Diarrhoea' Introduction Disease caused by one of the two poultry-adapted strains ofSalmonella bacteria. The bacterium is fairly resistant to normal climate. Loud chirping. It affects chickens most commonly. 128 . Salmonella Pullorum. Transmission may be transovarian or horizontal mainly in young birds and may sometimes be associated with cannibalism. Salmonella Pullorum. The liver on the left is normal. but also infects turkeys. Gasping. Lameness. Bacterial septicaemia caused by Salmonella Gallinarum. Closed eyes. mortality is increased in stressed or immunocompromised flocks and may be up to 100%. guinea fowls. ring doves. Depression. game birds. this usually only causes mortality in birds up to 3 weeks of age. sparrows. Signs          Inappetance. the one on the right is slightly enlarged. Ruffled feathers. ostriches and peafowl. Occasionally it can cause losses in adult birds. It still occurs worldwide in noncommercial poultry but is now rare in most commercial systems.

Urate crystals in ureters. other enterobacteria. are capable of causing enteritis and septicaemia in young birds. and also other than S. S. in the environment or in rodent populations. Montevideo. Intestinal or caecal inflammation. Newport. gizzard wall and heart. tetracylines. They infect chickens. As with other salmonellae. Typhimurium (which are considered separately). S. Splenomegaly. Many species are intestinal carriers and infection is spread by faeces. Regardless of the initial source of the infection. S. Gallinarum. poteniated sulponamide. Caecal cores. The route of infection is oral and transmission may be vertical as a result of shell contamination. fomites and feed (especially protein supplements but also poorly stored grain). Paratyphoid Infections Introduction Salmonellae bacteria other than the species specific sero-typesS. turkeys and ducks worldwide. Salmonellosis. it may become established on certain farms. but S. Enrichment procedures usually rely on selenite broth followed by plating on selective media. Even if these infections do not cause clinical disease. fluoroquinolones. Sero-types vary. Prevention Eradication from breeder flocks. their presence may be significant with respect to carcase contamination as a potential source of human food poisoning. S. paracolon. Differentiate from Typhoid. In clinical cases direct plating on Brilliant Green. Vaccines are not normally used as they interfere with serological testing and elimination of carriers. S. Anatum. McConkey and non-selective agar is advisable. Paratyphoid. Pullorum. Derby. Enteritidis andS.Post-mortem lesions      Grey nodules in lungs. liver. Certain sero- 129 . Bredeney are among the more common isolates. Morbidity is 0-90% and mortality is usually low. Diagnosis Isolation and identification. recovered birds are resistant to the effects of infection but may remain carriers. chilling and omphalitis Treatment Amoxycillin.

Signs        Signs are generally mild compared to host-specific salmonellae. Ruffled feathers. Vent pasting. Senftenberg in hatcheries). Enrichment media such as buffered peptone followed by selective broth or semi-solid media (e. Chemotherapy can prolong carrier status in some circumstances. Cheesy cores in caecae. fluoroquinolones. Post-mortem lesions         In acute disease there may be few lesions. Treatment Sulphonamides. tetracyclines. However this has the potential to reveal the presence of salmonellae that are irrelevant to the clinical problem under investigation. Dejection. other enterobacteria. Enteritis.g. but are susceptible to disinfectants that are suitable for the particular contaminated surfaces and conditions. Foci in liver. The bacteria are often persistent in the environment. In clinical cases direct plating on Brilliant Green and McConkey agar may be adequate. Pericarditis. chilling. Loss of appetite and thirst. especially in dry dusty areas. S. applied at sufficient concentrations. or absent. neomycin. Temperatures of around 80°C are effective in eliminating low to moderate infection if applied for 1-2 minutes. Dehydration. Predisposing factors include nutritional deficiencies. amoxycillin. Closed eyes. Unabsorbed yolk. 130 .g. This approach is often used in the heat treatment of feed. Good management.types are prone to remain resident in particular installations (e. Diarrhoea. Focal necrotic intestinal lesions. Diagnosis Isolation and identification. inadequate water. Differentiate from Pullorum/Typhoid. other bacterial infections and ornithosis (in ducks). Rappaport-Vassiliadis) followed by plating on two selective media will greatly increase sensitivity.

especially in dry dusty areas. has become much more common in both poultry and humans since the early 80s. especially phage type 4. good feed. these bacteria are often specifically cited in zoonosis control legislation. care in avoiding damage to natural flora. applied at sufficient concentrations. Salmonella Enteritidis. inadequate water and other bacterial infections. These are the predominant sero-types associated with human disease in most countries. Feed and feed raw material contamination is less common than for other sero-types. on the one hand. turkeys and ducks cause problems worldwide with morbidity of 0-90% and a low to moderate mortality. competitive exclusion. Typhimurium infections Introduction Salmonella Enteritidis and S. This approach is often used in the heat treatment of feed. clean nests. mills. and. The bacteria are often persistent in the environment. secondly.Prevention Uninfected breeders. The prevalence of S. The route of infection is oral. Salmonellosis. Vertical transmission may be either by shell contamination or internal transovarian contamination of yolk. S. Enteritidis and S. all-in/all-out production. chilling.Typhimurium are presented separately from other sero-types of Salmonella because. fomites and on eggshells.Typhimurium has remained relatively stable though the spread of the highly antibiotic-resistant strain DT104 in various farmed species gives some reason for concern. Infections in chickens. because there are differences in the epidemiology as compared to other salmonellae. Vaccines are not generally used for this group of infections. fumigate eggs. Many infected birds are culled and others are rejected at slaughter. Predisposing factors include nutritional deficiencies. 131 . breeding and grow-out farms. Routine monitoring of breeding flocks. elimination of resident infections in hatcheries. Infection results in a strong immune response manifest by progressive reduction in excretion of the organism and reduced disease and excretion on subsequent challenge. hatcheries and feed mills is required for effective control. but are susceptible to disinfectants that are suitable for the particular contaminated surfaces and conditions. many species are intestinal carriers and infection may be carried by faeces. Temperatures of around 80°C are effective in eliminating low to moderate infection if applied for 1-2 minutes.

Diarrhoea. Prevention Uninfected breeders. Early depletion of infected breeding stock is required in some countries such as those of the European Union. Stunting in older birds. fumigate eggs. elimination of resident infections in hatcheries. Treatment Sulphonamides. other enterobacteria such as E. Misshapen ovules in the ovaries in S. tetracyclines. Unabsorbed yolk. Perihepatitis. mills. Pericarditis. coli. amoxycillin. Good management. 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. Vent pasting. Dehydration. infection Diagnosis Isolation and identification.g. competitive exclusion. all-in/all-out production.Pullorum serum agglutination tests.Enteritidiscauses cross-reactions which may be detected with S. Lost of appetite and thirst.Signs        Dejection. In clinical cases direct plating on Brilliant Green and McConkey agar may be adequate. Cheesy cores in caecae. Enrichment media such as buffered peptone followed by selective broth or semi-solid media (e. However this has the potential to reveal the presence of salmonellae that are irrelevant to the clinical problem under investigation. S. Chemotherapy can prolong carrier status in some circumstances. fluoroquinolones in accordance with the sensitivity. care in avoiding damage to natural flora. Differentiate from Pullorum/Typhoid. hatcheries and feed mills is required for effective control. neomycin. Infection 132 . Rappaport-Vassiliadis) followed by plating on two selective media will greatly increase sensitivity. Routine monitoring of breeding flocks. breeding and grow-out farms. Ruffled feathers. Foci in liver. Post-mortem lesions           In acute disease there may be few lesions. clean nests. good feed.E. Closed eyes. Enteritis.

Bacteriology of oviduct. Typhimurium infection. Vaccines are increasingly being used for S. Diagnosis Use the signs to select birds for culling and post-mortem investigation. Peritonitis. Enteritidis and S. Signs      Sporadic loss of lay. The oviduct is a hollow tube joining the normally sterile environment of the body cavity with the cloaca. Some birds may 'lay' a caseous mass of pus (which may be found in a nest or on the egg belt). leaking urates. or may proceed upwards from the cloaca.). are especially prone to increasing salpingitis. Death. 133 . coliand occasionally Salmonella spp. Systemic viral infections that cause ovarian regression or damage to the oviduct or cloaca. Salpingitis Introduction Salpingitis is an inflammation of the oviduct. which normally has many millions of potentially pathogenic bacteria. Lesions. both inactivated (bacterins) and attenuated live organisms. Post-mortem lesions    Slight to marked distension of oviduct with exudate. Distended abdomen.results in a strong immune response manifest by progressive reduction in excretion of the organism and reduced disease and excretion on subsequent challenge. May form a multi-layered caseous cast in oviduct or be amorphous. It is a complex condition of chickens and ducks associated with various infections including Mycoplasma and bacteria (especially E. Damaged vents. Infection may spread downwards from an infected left abdominal air sac. Anything that damages the epithelium or disturbs normal oviduct motility is likely to increase the likelihood of salpingitis. The control of infection in this area is probably achieved by ciliated epithelium that mostly wafts a carpet of mucus towards the cloaca.

134 . releasing poults into larger areas and in handling heavier birds. Use of a suitable antimicrobial may be beneficial for birds in the early stages and if associated with efforts to minimise risk factors. Prevention Control any septicaemia earlier in life. use healthy parent flocks. Treatment Multivitamins. Morbidity is 10-20%.Treatment Birds with well-developed lesions are unlikely to respond to medication. Signs   Stand on toes shaking. possibly associated with tendon injury. Diagnosis Clinical examination. Shaking or quivering of legs after rising. Post-mortem lesions  None. immunise effectively against respiratory viral pathogens common in the area. aspirin may be helpful if locally approved. exclusion of other problems. Shaky Leg Syndrome Introduction A condition of turkeys with a course of often 3-4 weeks. Prevention Care in transport of brooded poults.

Treatment Leave affected chicks undisturbed. Provide multivitamins. Avoidance of physical stress. typically 7-14day-old. Minimise stress. This appears to be a multifactorial condition. rapidly growing broiler chickens. Excess fluid in lower small intestine and caecae. Birds in good condition die after showing neurological signs. In order to reproduce the typical condition the affected birds are subject to 4 hours without feed and then a mild physical stress such as spraying with cool water. and/or carbohydrate absorption are disturbed resulting in a hypoglycaemia. Orange mucoid droppings. electrolytes and glucose solution to flock. Diagnosis Pattern of mortality. probably because they are growing faster. Mortality drops off as sharply as it started. Dehydration. Males are more susceptible than females. Coma.Spiking Mortality of Chickens Introduction This is a condition characterised by a sudden increase in mortality in young. suggesting a viral component. Signs      Tremor. Feed intake. 135 . Post-mortem lesions    Mild enteritis. Prevention Good sanitation of the brooding house. Avoidance of interruptions in feed supply. Paralysis. Filtered intestinal contents from affected flocks appear to be capable of reproducing the condition. Death. Signs and lesions.

and egg soiling in chickens. geese. Often diarrhoea with excessive urates. Spleen mottled with ecchymotic haemorrhages. ducks. It is transmitted by arthropods. Necrotic foci. 136 . previously known as Serpulina pilosicoli. isolate in chicken eggs or chicks or poults. Brachyspira pilosicoli. Treatment Various antibiotics including penicillin. is an intestinal spirochaete that can be associated with inflammation of the large intestine in a broad range of mammals and birds. Drops in egg production may be seen in both systemic and intestinal forms Post-mortem lesions      Marked splenomegaly. diarrhoea. It has been associated with typhilitis. Prevention Control vectors. Diagnosis Haematology. Signs       Depression. grouse and canaries with morbidity and mortality up to 100%. pheasants. and occasionally by infected faeces. vaccines in some countries. reduced egg production. Liver enlarged with small haemorrhages. Argas persicus.Spirochaetosis Introduction The bacterium Borrelia anserina infects chickens. Weakness and progressive paralysis. Mucoid enteritis. e.g. Thirst. The bacterium is poorly resistant outside host but may be carried by Argas persicus for 430 days. Cyanosis. turkey.

Figure 33. lesions. Use of wings to help in walking. Signs    Sitting on hock or rumps.Tahir Spondylolisthesis. That on the left shows the typical lesion of spondylolisthesis. Kinky-back Introduction A complex condition of broiler chickens with a morbidity of 1-5% and low mortality associated with rapid growth and possibly having a genetic component.M. Prevention Selection for satisfactory conformation in primary breeding. with rotation of the body of the vertebra and the pinching of the spinal column that causes paralysis. These are cross-sections of the spinal column of 4-5-weekold broilers. legs extended forward. 137 . The sample on the right is normal.Abubakar. Post-mortem lesions  Anterior-posterior rotation of the bodies of the last or penultimate thoracic vertebrae resulting in scoliosis just anterior to the kidney. Diagnosis Symptoms. May walk backwards. Treatment None.

Tahir Spraddle Legs or Splay Leg Introduction Occurs in all species in the recent hatchling. Post-mortem lesions  Gross lesions are not usually evident. These include good breeder nutrition. Signs  Legs splay and chick is unable to stand. mainly S. Prevention All measures that improve chick vitality at hatching are beneficial in reducing this problem.Abubakar. Wounds. aureus and seen in chickens and turkeys worldwide. Staphylococcal Arthritis. Treatment None. 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. Diagnosis Clinical signs. Damaged skin due to nutritional deficiencies (such as of biotin) may also be a point of entry. avoidance of excessive hatching egg storage. Staphylococcosis. 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. Bumble Foot Introduction Caused by Staphylococcus bacteria. and toe trimming may be a portal of entry with subsequent spread via the bloodstream to the typical sites of lesions.M. The type of chick box liners and the feeding papers used in the brooding house can also influence the occurrence of the condition. 138 .

and by fomites. Recovered birds may have some immunity but vaccination with staphylococci has not been found to be helpful in preventing the disease to date. Differentiate from septicaemia or tenosynovitis due to Colibacillosis. Treatment Antibiotics. Diagnosis Lesions. most commonly in the plantar area of the foot or just above the hock joint. particularly of parent birds. synoviae. 139 . Predisposing factors include reovirus infection. This condition is a cause of sudden deaths in ducklings of 2-3 weeks of age.g. Competitive exclusion with a non-pathogenic Staphylococcushas been shown to be effective (no commercial products yet available based on this technology). Good management. trauma. Swollen above the hock and around the hocks and feet. Possibly vaccination against reovirus infection. and imunosuppression. the hatchery and in any intervention or surgery (processing. Mycoplasma spp. Low mobility. low stress and prevention of immunosuppression from any cause will all tend to help. Prevention Good hygiene in the nest. Streptococcus bovis Septicaemia Introduction An infection of ducks with the bacterium Streptococcus bovis. toe clipping). isolation and identification of pathogen. in accordance with sensitivity. Infected joints may have clear exudate with fibrin clots.Transmission occurs in the hatchery and in the general farm environment. Some sudden deaths from acute septicaemia if very heavy challenge. Salmonella spp. Signs      Ruffled feathers. Lameness.. especially M. This may progress to abscess formation in these areas. chronic stress. e.. Post-mortem lesions   Tenosynovitis.

). isolation. Sodium deficiency can appear very similar at about the same age . extra care in the immediate post-brooding period. possibly metabolic. Lung congestion and oedema. Post-mortem lesions      Intestine filled with feed. The atria of the heart have blood. Splenic hyperplasia. 140 . Affected well-grown birds may appear to have died from smothering. 'Flipover' Introduction A condition of broiler chickens of unknown cause. Leg weakness or incoordination in a few birds.affected birds respond well to saline injection and will actively seek out salt scattered in the litter. It can be induced by lactic acidosis and about 70% of birds affected are males. Serum accumulation in lung (may be little if examined shortly after death). Prevention Good husbandry and hygiene. Livers heavier than those of pen-mates (as a percentage of bodyweight. lesions. Treatment Amoxycillin. Signs  Sudden death in convulsion.Signs   Sudden deaths. Sudden Death Syndrome. Post-mortem lesions     Beak cyanosis. Diagnosis History. Liver congestion. Haemorrhages in muscles and kidneys. the ventricles are empty. most are found lying on their back.

Prevention Lowering carbohydrate intake (change to mash). Check your local regulations. feed restriction. Diagnosis Identification of the presence of the worms at post-mortem examination. Treatment Flubendazole is effective at a 60 ppm in diet. use of dawn to dusk simulation and avoidance of disturbance. Post-mortem lesions  Occupy space in intestine and create small lesions at point of attachment. Prevention Control the intermediate hosts. Cestodes Introduction Cestodes are tapeworms that are seen in many species. lighting programmes. or birds' access to them. low intensity light.Diagnosis Birds found on back with lack of other pathology. Tapeworms. Treatment None possible. Signs  It is doubtful if any signs are produced under most circumstances. 141 . Most have intermediate invertebrate hosts such as beetles or earthworms. they may not be host specific. however it may not have a zero withdrawal in commercial egg layers.

Tibial Dyschondroplasia. Vitamin D3 supplementation. mild lesions may require histology to distinguish from other problems. Signs    There are usually no signs unless the condition is severe. Swelling and bowing in the region of the knee joints.Figure 34. turkeys and ducks. chloride levels and acid/base balance. Prevention Genetic selection using the Lixiscope to identify bone phenotype. distal tibia. It may be associated with rapid growth and have a nutritional factor. Diagnosis Gross pathology. small ovoid lacunae and more matrix than normal. in decreasing order of frequency. Lixiscope may identify in vivo as early as 2 weeks of age. Microscopically . TD Introduction A complex condition seen in chickens.a mass of avascular cartilage with transitional chondrocytes. Mature tapeworms with their heads (scolices) embedded in the intestine. Treatment None. Differentiate from rickets. 142 . Lameness. and proximal metatarsus. Post-mortem lesions   Plug of cartilage in proximal end of tibia. modifications of calcium and phosphorus ratios.

The infection is seen in turkeys and sometimes pheasants. Weakness. It is more common in warm climates. than in commercial poultry in temperate climates. Transmission is lateral with birds and faeces. Reduced productivity. Treatment Elimination of cracks and crevices in the poultry housing. Bluecomb Introduction Some coronaviruses involved in this condition are considered to be bovine coronaviruses (or closely related thereto). Insecticide sprays in these areas are more likely to be effective than treatment of the birds. with 143 .Abubakar. Prevention As for red mite control. spends little time on host. and may also transmit spirochaetosis and Pasteurella infection. others are avian coronaviruses closely related to infectious bronchitis virus.M. Occasionally paralysis from toxins in the tick saliva. Skin blemishes.Tahir Ticks Introduction Argas persicus is an external parasite of poultry and wild birds. Post-mortem lesions  Anaemia. and is also found on mammals. Morbidity is close to 100% and mortality is 5-100%. Emaciation. These parasites are more likely to be a problem of small scale poultry production in the tropics. Transmissible Enteritis. Diagnosis Identification of the presence of the parasites. Signs       Anaemia.

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.

Post-mortem lesions
       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).

Post-mortem lesions
  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.

Post-mortem lesions
 Emaciation.


 

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.

None recommended.

Market after one season, hygiene, cages, elimination of faeces etc.

Turkey Coryza
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.

Post-mortem lesions
  Excessive mucus in nasal passages and trachea. If there is secondary E. coli infection then pneumonia, airsacculitis and perihepatitis.

Clinical signs, isolation of agent.



possibly involving fomites.live primer followed by inactivated. Sudden drop in production that lasts 2-3 weeks. Eggs depigmented and thin-shelled. Morbidity is 10-100% and mortality 1. Rapid transmission occurs laterally.30%. Signs      Decreased appetite. Post-mortem lesions  Serous rhinitis and tracheitis. isolation of ciliostatic agent. Treatment Antibiotics are not very effective. chlorination of drinking water. maternal antibody may protect. Turkey Rhinotracheitis (Adult) Introduction A disease of turkeys caused by the viruses of the Pneumovirus genus. Paramyxoviridae. control respiratory stressors. Serology. Diagnosis Signs.Antibiotics are not very effective. Loss of voice. Ocular and nasal discharge. vaccination . Prevention All-in/all-out production. chlorinate drinking water. control respiratory stressors. Prevention All-in/all-out production. Good drinking water hygiene. vertical transmission is uncertain. 147 .

Diagnosis Clinical signs. Loss of voice. Morbidity is 10-100% and mortality 1. maternal antibody may protect.30%. coli infection then pneumonia.Abubakar. chlorinate drinking water. control respiratory stressors. Snick. Transmission may be by direct or indirect contact and possibly vertical. isolation and identification of the ciliostatic virus. Conjunctivitis. Morbidity varies. 148 . possibly involving fomites. Vaccination at day-old seems to be most effective. Sinusitis. Ocular and nasal discharge. Turkey Viral Hepatitis Introduction An infection of turkeys caused by an unidentified virus. If there is secondary E. sometimes pus in bronchi. Signs        Decreased appetite.Tahir Turkey Rhinotracheitis (in rear) Introduction A disease of turkeys caused by the viruses of the Pneumovirus genus. Paramyxoviridae. serology (using an Elisa test to demonstrate rising titre). Post-mortem lesions   Serous rhinitis and tracheitis. Prevention All-in/all-out production. airsacculitis and perihepatitis.M. mortality is 1-25%. Dyspnoea. weight gain and feed efficiency. Rapid transmission occurs laterally. vertical transmission is uncertain. Treatment Antibiotics are not very effective. Birds remain carriers for up to 16 days.

Post-mortem lesions       Grey foci (c.Signs   Signs are usually subclinical. Differentiate from histomonosis. environment and high growth rate.no inclusion bodies. Factors involved may include genetics. Valgus/varus. Post-mortem lesions  Linear twisting of growth of long bones. 1 mm) coalescing. Depression and sporadic deaths in birds in good condition. Focal haemorrhage. Diagnosis Isolation in CE. Signs      Lameness. with good management many birds recover. Gastrocnemius tendon may slip. Various angulations of leg. Bile staining. Microscopically . Morbidity is 1-20% and mortality is low. lesions pathognomonic. 149 . Twisted leg Introduction A complex condition seen in chickens and turkeys. Distortion at hock. bacterial and fungal infections. Congestion. Prevention Good sanitation and management. Treatment None. Grey to pink foci in the pancreas. nutrition.

Adoption of optimal nutrition and growth patterns for the economic objectives of the production system. Prevention Selection for good conformation in primary breeding. greater than 20% is abnormal. Differentiate from perosis. but mainly ileum and caecae. Peritonitis (if ulcers penetrate). Predisposing factors include Coccidiosis (especially E. and E. The route of infection is oral and transmission is from faeces of sick or carrier birds or via flies. brunetti). Pale yellow membranes. Diagnosis Symptoms. tenella. Retracted neck. 150 . Watery white faeces (quail). Drooping wings. Quail disease Introduction Ulcerative Enteritis is an acute. Diarrhoea. Partially closed eyes. which may coalesce and may be round or lenticular. lesions. Ruffled feathers. It can start suddenly and cause high mortality: 100% in quail and 10% in chickens. necatrix. The condition occurs worldwide. E.. game birds and pigeons may also be affected. Changed angulation of tibial condyles. Treatment None. highly contagious disease of chickens and quail caused by the bacterium Clostridium colinumand characterised by ulcers of the intestines and caecae. Anaemia. Ulcerative Enteritis. IBDV and overcrowding. Turkeys. The bacterium resists boiling for 3 minutes. intertarsal angulation up to 10% is physiological. Signs         Listlessness. Post-mortem lesions     Deep ulcers throughout intestine. arthritis and synovitis. Blood in intestine.

Treat for coccidiosis if this is a factor. Transmission is by faecal contamination. Figure 35. Wall of the caecum of a chicken suffering from ulcerative enteritis Vibrionic Hepatitis. salmonellosis. Treatment Streptomycin (44 gm/100 litres water). penicillin (50-100 ppm in feed). Inappetance. Diagnosis A presumptive diagnosis may be made on history and lesions. Loss of condition. Prevention Infection-free birds. amoxycillin. birds remaining carriers for months. trichomoniasis. Avian Infectious Hepatitis Introduction An insidious onset disease of chickens caused by Vibrio bacteria. multivitamins. Signs     Dejection. and disease is precipitated by stress. Differentiate from histomonosis ('Blackhead'). necrotic enteritis. Diarrhoea. all-in/all-out production. 151 . Response to treatment should occur in 48 to 96 hours. Bacitracin. possibly probiotics. Morbidity is low. colinum in anaerobic conditions (the agent is often present in pure culture in liver). Confirmation is on absence of other diseases and isolation of Cl. Necrotic foci in liver. low level antibiotics as per treatment. The infective agent is rather resistant to environment and disinfectants. Tetracyclines. coccidiosis.

   

Pale comb and wattles. Scaly comb. Jaundice. Drop in production/weight gain.

Post-mortem lesions
    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.

Erythromycin, fluoroquinolones.

Hygiene, depopulate, obtain birds free of disease, contain stressors.

Viral Arthritis
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.


Post-mortem lesions
     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.

Post-mortem lesions
  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.


155 . Prevention Supplementation of diet with vitamin A.squamous metaplasia of epithelia. lesions. Treatment Vitamin A in drinking water. classic signs of deficiency are very rare in commercial poultry fed complete diets. Pale comb and wattles. Nutritional Roup Introduction Vitamin A deficiency is occasionally seen in chickens and turkeys (insufficient vitamin A during 1-7 weeks of age). infectious sinusitis etc. Poor feathering.Abubakar. feed formulation. Post-mortem lesions     Eyelids inflamed and adhered.M. Nasal and ocular discharge.Tahir Vitamin A Deficiency. antioxidant. Differentiate from Infectious coryza. Signs       Poor growth. Diagnosis Signs. As in the case of other nutritional deficiencies. Microscopically . good quality raw materials. chronic fowl cholera. Excessive urates in kidneys and ureters. Pustules in mouth and pharynx. Drowsiness. Eyelids stuck shut with thick exudate.

Abubakar. damage to the intestine or increased demand for some reason may have an effect. Most will reduce productivity. 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 . They act in a broad range of metabolic pathways. Diagnosis Signs. The embryo is particularly dependent on having adequate supplies of vitamins deposited in the egg. response to supplementation. Some deficiencies induce characteristic microscopic effects. because a continuous supply is required. See the separate discussion under Chondrodystrophy and Fatty Liver and Kidney Syndrome. Simple deficiency is now rare as diets are usually well supplemented. including growth in the young animal.M. Vitamin deficiencies are especially prone to cause problems of hatchability. exclusion of specific diseases.Tahir Vitamin B Deficiencies Introduction The B complex vitamins are water soluble and not stored to any significant extent in the body. and egg production in the layer. 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. However.

seen worldwide. less expensive) to analyse feed for a marker substance such as manganese rather than testing for vitamin levels. Paralysis. Uncontrolled movements. Ventral oedema. Green wings. Post-mortem lesions       Swollen cerebellum with areas of congestion. The problem is associated with feed rancidity typically in diets with high fat. Steatitis. drinking water supplementation with that vitamin is ideal and usually results in a rapid response in birds that are still drinking. Encephalomalacia. Necrosis.may be appropriate (faster. Good quality multivitamin solutions are beneficial in the supportive care of a range of problems characterised by reduced feed intake. Muscular Dystrophy Introduction A spectrum of diseases of chickens and turkeys. The balance of vitamins present should be similar to the daily nutritional requirement of the stock concerned. Vitamin E Deficiency. Exudative Diathesis. characterised by oxidation of various tissues and caused by Vitamin E deficiency. Haemorrhage. Falling over. Muscular dystrophy is seen more frequently in older and mature birds. Staggering. White streaks in muscle. 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. Treatment If a specific vitamin deficiency is suspected. Encephalomalacia and exudative diathesis tends to be seen in young birds of 1-5 weeks of age. Blood-stained or greenish subcutaneous oedema. occasionally ducklings and other birds. Signs        Imbalance. 157 .

especially E . Omphallitis Introduction A condition seen worldwide in chickens. feed rancidity.Proteus. Post-mortem lesions   Enlarged yolk sac with congestion. Differentiate from Encephalomyelitis. use of floor eggs. 'bangers'. turkeys and ducks due to bacterial infection of the navel and yolk sac of newly hatched chicks as a result of contamination before healing of the navel. Morbidity is 1-10% and mortality is high in affected chicks. Signs       Dejection. necrotic dermatitis. Swollen abdomen. Yolk Sac Infection. 158 . 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. Pseudomonas. antioxidant.coli. consistency) that vary according to the bacteria involved. lesions. hatchers or chick boxes.Diagnosis Signs. for example poor hygiene of hatching eggs. Broad-spectrum antibiotics where there are extensive skin lesions. Closed eyes. toxicities. response to medication. It is seen where there is poor breeder farm nest hygiene. Treatment Vitamin E and/or selenium in feed and/or water. Loss of appetite. histopathology. Disease occurs after an incubation period of 1-3 days. inadequate hatchery hygiene or poor incubation conditions. Prevention Proper levels of vitamin E. Abnormal yolk sac contents (colour. selenium. Various bacteria may be involved. and poor hygiene of setters. Vent pasting. Staphylococci. good quality raw materials. Diarrhoea.

exclusion of severely soiled eggs. separate incubation of floor eggs etc.Diagnosis A presumptive diagnosis is based on the age and typical lesions. Confirmation is by isolation and identification of the bacteria involved in the internal lesions.g. Treatment Antibiotics in accordance with sensitivity may be beneficial in the acute stages. sanitation of eggs. frequent collection. most will die before 7 days of age. 159 . Multivitamins in the first few days may generally boost ability to fight off mild infections. clean nests. There should be routine sanitation monitoring of the hatchery. Differentiate from incubation problems resulting in weak chicks. 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.

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