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.


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

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

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

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

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

 Tremor of head. Brain abscess. the equivalent of the World Health Organisation for animal diseases. signs. Diagnosis A presumptive diagnosis is based on the history. Prevention Vaccination of breeders at 9-15 weeks. Mycotic Encephalitis. Histopathology is usually diagnostic and IFA. Fowl One of only two 'Class A' diseases of poultry targeted for emergency disease control measures by OIE. ducks. neck and wings. Effectively all 9 . especially in turkeys.2 . Microscopic . The embryo protection test has been used in the past. Enterococcus hirae infection. Immunity is long lasting. vitamin deficiency (E. The higher the proportion of the chickens dying or showing signs the higher the IVPI. The cause is a virus. Highly pathogenic forms are usually of the H groups 5 and 7 and may now be identified (if H5 or H7) by the presence of a sequence at the haemagglutinin cleavage site that codes for multiple basic amino acids. The definitive classification of high pathogenicity is an intravenous pathogenicity test (IVPI) in 6-week-old chickens result of greater than 1. Orthomyxovirus type A. In addition official control measures disrupt trade in poultry products from affected areas. A few recovered birds may develop cataracts weeks after infection. partridges. quail. pigeons. and lack of significant lesions. The virus infects chickens. pheasants. attenuated or not. A. EE (especially in pheasant in the Americas). Post-mortem lesions     Gross lesions are mild or absent. Avian Influenza-Highly Plague Introduction Pathogenic (HPAI). This is a test in which the virus is inoculated into susceptible chickens that are then kept under observation. riboflavin). Treatment None. Tremor may be inapparent but is accentuated if chicks are held inverted in the hand. and/or viral isolation may be carried out if required. There may be focal white areas in gizzard muscle (inconstant). This viral disease can cause exceptionally high mortality. turkeys. its pathogenicity is variable. now Elisa is used more commonly. Differentiate from Newcastle disease. and ostriches. toxicities. Marek's disease. and isolates are designated sero-type/ species/location/reference number/year/subtype designation(H/N).nonpurulent diffuse encephalomyelitis with perivascular cuffing.

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

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

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

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

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


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.


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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

while E. 33 . rickets. gallopavonis and E. while E. ruffled feathers. meleagrimitis affects the upper small intestine. Tibia and metatarsus bowed. Lateral slipping of tendon. This disease is not very common in commercially reared turkeys though most turkey growers receive preventative medication for at least part of their lives. of which two are associated with significant disease effects. Signs      Huddling. Diagnosis Lesions. Coccidiosis of Turkeys Introduction Infection of turkeys with Eimeria spp. dispersa is found in the small intestine. choline. ruptured ligaments. infectious synovitis. correct mineral balance. infectious arthritis. Five species of Eimeria have been identified that cause lesions in turkeys. The contents may be haemorrhagic or be watery with white material shed from the mucosa. E.Post-mortem lesions     Shortening and thickening of long bones. analysis of feed. meleagridis affect the lower small intestine rectum and caecae. Shallow trochlea. E. Prevention Addition of manganese. Differentiate from twisted leg. Tucked appearance. Watery diarrhoea that may occasionally be blood stained or contain clumps of mucus or shed mucosa. Post-mortem lesions  The affected area of intestine shows thickening of the wall and dilation. no value to affected bird. adenoides affects the caecae and rectum. Depression. Weight loss. vitamins. Treatment For flock proceed as for prevention.

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

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

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

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

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

Hygiene. Post-mortem lesions    Enlarged kidneys. Kidneys light grey to greyish pink. however this is not routinely practised. Reduced feed intake. Coccidiosis. Prevention Good Hygiene. Diagnosis Lesions.faeces tend to be whitish. Signs     Depression. Tiny white foci and petechiae in the kidneys. presence of coccidial stages in fresh scrapings of kidney lesions. 39 . Treatment Controlled trials of treatments have not been published. Weakness. it can also infect Barbary ducks and swans. Diarrhoea . Kidney Introduction A disease of geese caused by Eimeria truncata that can cause high mortality in geese of 312 weeks of age.Prevention If required coccidiostats could be used in feed.

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

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

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

In general terms a score of 0 indicates no lesions and a score of 4 indicates maximal severity of lesion or death. restricted to upper third of small intestine . Prevention Coccidiostats in feed. Immunity is quite short lived (about 30 days) in the absence of continued challenge.the duodenum and part of the ileum. Diagnosis Signs. hygiene. Petechiae. Moderate Eimeria acervulinainfection (score 2) in chicken duodenum. Amprolium. White spots or bands in the mucosa. vaccination by controlled exposure.     Thickening. Differentiate from necrotic and non-specific enteritis. in severe the entire surface is pale or denuded of epithelium. in feed or water. In milder infections there may be scattered white spots. and other lesions. microscopic exam of scrapings. Sulphonamides. Various publications provide a photographic key to severity of lesion. A detailed description is beyond the scope of this book. Poor absorption of nutrients/pigments. lesions. 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. 43 . Figure 12. Treatment Toltrazuril.

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

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

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

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

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

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

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

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

arching of back.focal necrosis. Differentiate from Duck plague (viral enteritis). in USA since 1967. Treatment Antiserum. Influenza and a 'Type II Variant' hepatitis caused by Astrovirus. coccidiosis. Fall on side. 52 . Duck Virus Enteritis. Kidneys and spleen swollen. A different picornavirus causes a similar condition in North America.survive for ten weeks in brooders and five weeks in faeces. Prevention Vaccination and/or antiserum.5 ml serum of recovered birds given intramuscularly. fomites and arthropods. SN serology. The disease follows a very acute course with a morbidity of 5-100% and mortality of 5-100%. only slightly attenuated vaccine is applied at day old by foot web stab and may be repeated in breeding birds to provide maternal immunity. also the Netherlands and other countries. rapid deterioration and death. Newcastle disease. paddling of legs. All waterfowl are susceptible and the Barbary duck is more susceptible than the Pekin. Depression. Recovered birds may carry the virus for a year. Microscopically . breeder vaccination. lesions. Diagnosis History. Duck Plague Introduction A herpesvirus infection of ducks and geese diagnosed in the UK in 1972. mostly in ornamental collections. Live. Punctate/diffuse haemorrhages. Signs     Sudden death. Transmission is by infected birds. Death in good condition. 0. bile duct proliferation and inflammation. Duck septicaemia (anatipestifer). Post-mortem lesions     Liver swollen. often in opisthotonus. isolation in CE (causes stunting of 9 day embryo).

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

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

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

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

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

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

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

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

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

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

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

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

Morbidity may be up to 50% and mortality is high. Gangrenous skin. Post-mortem lesions    Patches of gangrenous skin with underlying emphysematous and/or sanguinous cellulitis. spleen. Foci in liver. occasionally Staphylococcus aureus. Immunosuppression is therefore a predisposing factor. Necrotic Dermatitis Introduction A bacterial condition seen in chickens and usually caused byClostridium septicum. It occurs due to invasion of 'normal' wounds by 'normal' bacteria in immunosuppressed birds. wattles. penicillin or amoxycillin. 65 . Severe cellulitis especially of thighs. sometimes thighs and other parts. Sudden mortality.Gangrenous Dermatitis. Swelling and infarction of the liver. Signs      Occasionally dejection. especially following congenital Chick Anaemia Virus infection or early Infectious Bursal Disease Virus infection (Gumboro Disease). Treatment Sulphaquinoxaline. The spores of Clostridial bacteria are highly resistant in the environment. rarely Clostridium noyvi / oedematiens. wings. early Infectious Bursal Disease Virus infection). usually over wings and breast. Avoid skin trauma and immunosuppression (congenital CAV infection. Prevention Good hygiene and management. Loss of appetite. Recovery of an abundant growth of causative organism in recently dead birds. Diagnosis Clinical signs and/or lesions.

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

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

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

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

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

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

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

avoid interspecies mixing. Poor growth. This condition has high morbidity and mortality in turkeys. The problem is seen in high-biosecurity facilities. Histamonosis. significant disease has been seen in breeding chickens and free-range layers. Caecal tonsils congested.  First half of intestine inflamed. histomonosis. trichomoniasis. Progressive depression and emaciation. and occasionally chickens. 73 . and mixing groups of different ages. scrapings from fresh material. increase ambient temperature. The effect of antibiotic may be related to the control of secondary bacterial enteritis. Prevention Depopulation. Within a turkey shed transmission is rapid in spite of the fact that it is difficult to infect birds orally with unprotected parasites. Although chickens are relatively resistant to the condition. Outwith earth worms orH. Inappetance. Furazolidone. all-in/all-out production. Blood in faeces (chickens). and also. Histomoniasis. gallinae the parasite is easily destroyed. dimetridazole and ipronidazole have been used in the past. Sulphur-yellow diarrhoea. if possible. Blackhead Introduction Histomonas melagridis is a protozoan parasite of turkeys. The parasite is ingested in the ova ofHeterakis worms or as larvae in earthworms or faeces and there is an incubation period of 15-20 days. Diagnosis Lesions. Cyanosis of head. dimetridazole. hygiene. Treatment Tetracycline. presumably introduced with worm eggs. pheasants and game birds that acts together with facultative bacteria to produce the condition of Blackhead. It has recently been demonstrated that infection occurs readily via the cloaca when birds are on contaminated litter. Signs        Depression. Differentiate from transmissible enteritis. paratyphoid.

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

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

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

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

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

Elisa (both group specific). IB . SN (type specific).antibiotics to control secondary colibacillosis (q. Local immunity is first line of defence. lesions and serology. mycoplasmosis. Muscular shivering.793b Variant Sudden Death Syndrome in Broiler Parents Introduction A Coronavirus infection of chickens with a morbidity of 50-100% and a mortality 0-25%. depending on secondary infections. DID (poor sensitivity.). which may survive 4 weeks in premises. 79 . group specific). heat (56°C for 15 mins). Humoral immunity appears 10-14 days post vaccination.v. Maternal immunity provides protection for 2-3 weeks. flourescent antibody positive and ciliostasis in tracheal organ culture. Avian Influenza and Laryngotracheitis. Definitive diagnosis is based on viral isolation after 3-5 passages in chick embryo. alkalis. Prevention Live vaccines of appropriate sero-type and attenuation. Differentiate from Newcastle disease (lentogenic and mesogenic forms). Poor ventilation and high density are predisposing factors. The infection spreads rapidly by contact. The virus. Infectious Bronchitis. with typical lesions. Infection is via the conjunctiva or upper respiratory tract with an incubation period of 18-36 hours. Cellmediated immunity may also be important. Otherwise as for standard IB. possible reactions depending on virulence and particle size. HA negative. disinfectants (Formal 1% for 3 mins). Some birds/viral strains can be carriers for up to 1 year. Treatment Sodium salicylate 1gm/litre (acute phase) where permitted .Diagnosis Tentative diagnosis is based on clinical sgns. vaccinal reactions. Serology: HI. Signs    Sudden death. fomites or aerosol. is sensitive to solvents. short duration.

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

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

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

Marek's disease and Infectious Bronchitis.Figure 22. 83 . IBD.20% but sometimes up to 60%. In addition to the direct economic effects of the clinical disease. The disease is highly contagious. faeces etc. Mealworms and litter mites may harbour the virus for 8 weeks. seen worldwide. (Turkeys and ducks show infection only. Signs are most pronounced in birds of 4-6 weeks and White Leghorns are more susceptible than broilers and brown-egg layers. but may be via the conjunctiva or respiratory tract. with an incubation period of 2-3 days. The age up to which infection can cause serious immunosuppression varies between 14 and 28 days according to the antigen in question. The route of infection is usually oral. Gumboro Introduction A viral disease. Subclinical infection in young chicks results in: deficient immunological response to Newcastle disease. first identified in the USA in 1962. Flaccid ovarian follicles in a broiler parent chicken undergoing challenge with Infectious Bronchitis virus. Infectious Bursal Disease. which targets the bursal component of the immune system of chickens. susceptibility to Inclusion Body Hepatitis and gangrenous dermatitis and increased susceptibility to CRD. The virus is very resistant. The infective agent is a Birnavirus (Birnaviridae). especially with sero-type 2). persisting for months in houses. the damage caused to the immune system interacts with other pathogens to cause significant effects. and affected birds excrete large amounts of virus for about 2 weeks post infection. There is no vertical transmission. Generally speaking the earlier the damage occurs the more severe the effects. Morbidity is high with a mortality usually 0. Sero-type 1 only.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

        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.


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

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

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

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. It is common to monitor response to vaccination. HI has been used extensively. In some countries it has been customary to provide antibiotics prophylactically during periods of anticipated vaccinal reaction. Use of spray application is recommended but it needs to be applied with care to achieve good protection with minimal reaction. Acute viral infections or heavily contaminated drinking water may have a similar effect to bad management in reducing feed intake. Mortality peaks at 3-5 days for birds that fail to eat at all. and occasionally gasping due to a plug of pus in the lower trachea. which are adequately stored and take into account the local conditions. vaccination. whereas it tends to peak between 6-10 days for chicks that begin eating but then cease. biosecurity. Vaccination programmes should use vaccines of high potency. The LaSota-type vaccine may even repeated at 35-40 days of age if risk is high. and is associated with difficulty maintaining brooding temperature and poor management of feeders and drinkers. 105 . especially in breeding birds by the use of routine serological monitoring. 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. however. To prevent or reduce vaccinal reactions in young chicks it is important that day old have uniform titres of maternal immunity. It is commonest in progeny of young parent flocks (relatively small yolks) or where managers are inexperienced. all-in/all-out production. These tests do not directly evaluate mucosal immunity. Morbidity is up to 10% and mortality close to 100%. A typical programme may involve Hitchner B1 vaccine at day old followed by LaSota-type vaccine at 14 days. snicking.Prevention Quarantine. Vaccinal reactions may present as conjunctivitis. Elisa is now also used. 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). Figure 28.

Signs  Failure to grow. Gall bladder distended. 106 . Because it is enclosed in a relatively unyielding membrane. Poor development. It has since been seen in turkeys. or suffer necrosis. It does not usually cause any mortality or obvious clinical signs and so it is usually identified after slaughter. 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. Differentiate from omphalitis/ yolk sac infection. soluble multivitamin supplementation may help. Oregon Disease . It is caused by a reduction in the blood supply to the deep pectoral muscles. aspergillosis. Diagnosis Based on post-mortem lesions. Prevention Review brooding management. good drinking water hygiene. Treatment Correction of management problems. Most organs normal. bile staining of adjacent tissues. in broiler parent chickens and also in large broiler chickens in various places. Post-mortem lesions      Crop empty. good hygiene and biosecurity in brooding areas to minimise early disease challenges.Deep Pectoral Myopathy Introduction This condition is so named because it was first identified in adult breeding turkeys in Oregon State. any swelling of the muscle tends to cut off the blood supply. nutrition of young parents. Gizzard may be impacted with litter. 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.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

135 . 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. Avoidance of physical stress. Signs and lesions. Dehydration. Feed intake. typically 7-14day-old.Spiking Mortality of Chickens Introduction This is a condition characterised by a sudden increase in mortality in young. probably because they are growing faster. Mortality drops off as sharply as it started. This appears to be a multifactorial condition. Paralysis. Prevention Good sanitation of the brooding house. Signs      Tremor. Filtered intestinal contents from affected flocks appear to be capable of reproducing the condition. Birds in good condition die after showing neurological signs. Diagnosis Pattern of mortality. rapidly growing broiler chickens. electrolytes and glucose solution to flock. Males are more susceptible than females. suggesting a viral component. Death. Treatment Leave affected chicks undisturbed. Post-mortem lesions    Mild enteritis. Coma. Excess fluid in lower small intestine and caecae. Minimise stress. Avoidance of interruptions in feed supply. and/or carbohydrate absorption are disturbed resulting in a hypoglycaemia. Provide multivitamins. Orange mucoid droppings.

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

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

Staphylococcal Arthritis. Staphylococcosis. The type of chick box liners and the feeding papers used in the brooding house can also influence the occurrence of the condition. Prevention All measures that improve chick vitality at hatching are beneficial in reducing this problem. Treatment None. and careful monitoring of incubation conditions. Post-mortem lesions  Gross lesions are not usually evident. 138 . Signs  Legs splay and chick is unable to stand. Infection is usually by the respiratory route with an incubation period of 2-3 days seen after artificial infection. These include good breeder nutrition. avoidance of excessive hatching egg storage. Diagnosis Clinical signs. aureus and seen in chickens and turkeys worldwide. Damaged skin due to nutritional deficiencies (such as of biotin) may also be a point of entry. and toe trimming may be a portal of entry with subsequent spread via the bloodstream to the typical sites of lesions. Wounds.M. Morbidity is usually low and mortality 0-15% though affected birds will often be culled on humane grounds.Tahir Spraddle Legs or Splay Leg Introduction Occurs in all species in the recent hatchling. Bumble Foot Introduction Caused by Staphylococcus bacteria. either accidental or induced by interventions such as beak trimming.Abubakar. mainly S.

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

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

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

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

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

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.



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

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

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

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

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

   

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.


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

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

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

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

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

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