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.


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

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

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

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

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

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

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

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

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

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

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


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.


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

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

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

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

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

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

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

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

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

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

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

However its main importance is as a cause of condemnation in meat poultry. Post-mortem lesions  Typically it presents as exudate ranging from liquid and pale cream pus to yellowish solid plaques of caseous material under the skin of the abdomen and/or in the leg. It typically occurs between skin and muscles and between muscles and may be an incidental finding in a range of conditions. often minor. which can replicate in the tissues. The condition is caused by infection of.Cellulitis Introduction Cellulitis is literally an inflammation of connective tissues. Prevention Toe scrapes at 15-25 days of age when feather cover is poor are the most likely predisposing factors. Careful flock management with a view to reducing toe wounds has the greatest impact in controlling cellulitis. Diagnosis Typical lesions. Signs  Affected flocks tend to have poorer than average productivity and uniformity. 29 . If identified at a thinning there may be time for antibacterial treatment to have some benefit for those birds in the early stages of the problem. Many affected birds have no other lesions and are reasonably well grown. but the affected birds are not readily detectable prior to slaughter. coli. 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. skin wounds by particular strains of E. Treatment Treatment would not be possible if the problem is identified at a final depletion. particularly broiler chickens. Routine monitoring of skin damage at about 25 days of age may be helpful in fostering good practices. In the USA it is called 'Inflammatory Process'.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

The cause has been identified as Adenovirus BC14. Diagnosis Signs. Prophylactic antimicrobial medication may be necessary in some circumstances. 127. Post-mortem lesions    Excessive fluid content throughout the small intestine. especially where treatment is initiated early. Germany. Argentina. Treatment should coincide with good relittering and it is important to provide fresh sanitary drinking water. lesions. Water intake may be increased or irregular. Feed acidification may be helpful in some circumstances. feed interruptions and subclinical coccidiosis may be contributory factors. No single bacterium appears to be responsible. Mortality is usually negligible. Prevention Competitive exclusion ('normal adult flora') use in day-old chicks reduces the risk of this condition. Voluminous caecae. England. Peru. In the autumn of 1976 a distinct egg drop syndrome was first identified in Northern Ireland. Treatment Amoxycillin and tylosin treatment appear to be beneficial. first isolated in Northern Ireland in 1976. Careful choice of any feed enzymes and their matching with local raw materials can have an impact on substrates made available to intestinal bacteria.Dietary changes. often with gas bubbles. France. Signs   Diarrhoea. Uruguay. microscopic examination of scrapings from the wall of the small intestine (to exclude coccidiosis and perhaps to assess the bacterial flora). Good control of coccidiosis. rather we are dealing with a disruption in the normal flora of the gut. Spain. Wet faeces in the rectum. Circumstantial evidence suggests that the main route of transmission is through the eggs (vertical transmission) 54 . Brazil. Apparently a similar disease had been seen over a 4-year period in broiler parents in Holland. Holland. Egg Drop Syndrome 76 Introduction Egg drop may be defined as a sudden drop in egg production or a failure to achieve a normal peak in production. It affects chickens and has occurred in Ireland.

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

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

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

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

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

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

FHN is the commonest infectious cause of lameness in broilers in the UK. Post-mortem studies of birds culled due to lameness and of birds found dead. turkeys. Pasteurellosis Introduction Fowl Cholera is a serious. rickets. indicated that 0. Signs   Lameness.75% of all male broilers placed had lesions in the hip bone. Post-mortem lesions  Degeneration of the epiphyses of long bones with thinning of the cortex and tendency to break when force is applied. Fowl Cholera. arthritis. coli. highly contagious disease caused by the bacterium Pasteurella multocida in a range of avian species including chickens. It is seen worldwide and was one of the first infectious 61 . staphylococci. especially hypophosphataemic. Differentiate from synovitis.FHN Introduction A condition of chickens and turkeys that may be associated with several different bacterial infections e. Treatment Antibiotic therapy in accordance with sensitivity is likely to be beneficial only for birds in the early stage of this process and may not be economically justifiable.Femoral Head Necrosis . Prevention Exclusion of floor eggs and dirty eggs from the hatchery. (increasing order of susceptibility). and water fowl. spondylolisthesis. Diagnosis Base on post-mortem lesions and isolation of a causative organism. Predisposing factors include immunosuppresive viruses such as Infectious Bursal Disease Virus and Chicken Anaemia Virus and non-infectious bone pathologies such as hypophosphaetamic rickets.g. E. Careful attention to mineral and Vitamin D nutrition to avoid subclinical. streptococci. Use of a wing for support during walking and hip flexion.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

        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.


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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Treatment Antibiotics. 139 . Mycoplasma spp. and imunosuppression. Some sudden deaths from acute septicaemia if very heavy challenge. especially M. Prevention Good hygiene in the nest. Lameness. e. This may progress to abscess formation in these areas. Good management. and by fomites. Signs      Ruffled feathers. Possibly vaccination against reovirus infection. Differentiate from septicaemia or tenosynovitis due to Colibacillosis. Recovered birds may have some immunity but vaccination with staphylococci has not been found to be helpful in preventing the disease to date. Predisposing factors include reovirus infection. particularly of parent birds. trauma. most commonly in the plantar area of the foot or just above the hock joint. Swollen above the hock and around the hocks and feet. Salmonella spp. Diagnosis Lesions. This condition is a cause of sudden deaths in ducklings of 2-3 weeks of age. Infected joints may have clear exudate with fibrin clots.. Post-mortem lesions   Tenosynovitis. low stress and prevention of immunosuppression from any cause will all tend to help. synoviae. Low mobility. isolation and identification of pathogen. toe clipping).Transmission occurs in the hatchery and in the general farm environment. in accordance with sensitivity. chronic stress.. 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). Streptococcus bovis Septicaemia Introduction An infection of ducks with the bacterium Streptococcus bovis.g.

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

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

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

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

rapid spread. The course of the disease is about 2 weeks and birds then remain carriers for months. The viruses survive in frozen faeces for months.

       Anorexia. Depression. Frothy diarrhoea. Subnormal body temperature. Darkening of the head. Loss of weight. Huddling.

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.



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

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

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

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

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

   

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

Post-mortem lesions
    Focal hepatic necrosis in 10% of affected. Foci often stellate, or there may be a cauliflower-like 'spotty liver'. Haematocysts under capsule. Swelling of organs. Catarrhal enteritis.

History, lesions, isolation of infective agent from bile. Differentiate from leukosis, histomonosis, ulcerative enteritis, fowl cholera, and typhoid.

Erythromycin, fluoroquinolones.

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

Viral Arthritis
Viral Arthritis is the classic, but by no means the only, manifestation of reovirus infection of chickens; at least 5 sero-types of virus occur. Morbidity is high but mortality is usually low. Transmission is by faecal contamination, and good both laterally and vertically. Birds remain carriers for over 250 days. The virus is resistant to heat, ether, chloroform, pH and environmental factors. Reoviruses vary markedly in pathogenicity and the tissue damaged. Some can cause other disease syndromes such as early chick mortality and malabsorption syndrome. Some strains have shown severe systemic disease including pericarditis in chickens. Others have caused immunosuppression by damaging the cloacal bursa in ducks.

       Lameness. Low mobility. Poor growth. Inflammation at hock. Swelling of tendon sheaths. Unthriftiness. Rupture of gastrocnemius tendons.


Post-mortem lesions
     Swelling and inflammation of digital flexor and metatarsal extensor tendon sheaths. Foot pad swelling. Articular cartilages may be ulcerated. Haemorrhage in tissues. Fibrosis in chronic cases.

Diagnosis may be based on the history, lesions, IFA and rising antibody titre. Isolation may be readily achieved in CE yolk sac and CAM and also cell cultures (CE kidney or liver cells). Serology may be by DID, FAT or Elisa. 'Silent' infections (not associated with obvious disease) are common. Differentiate from mycoplasmosis, salmonellosis, Marek's, Pasteurella, erysipelas.


Vaccination is ideally carried out by administering a live vaccine in rear followed by an inactivated vaccine prior to coming into lay. Most vaccines are based on strain 11/33. Rear birds in all-in/all-out production systems.

Visceral Gout, Nephrosis, Baby Chick Nephropathy
Visceral gout is the deposition of white urates, which are normally excreted as a white cap on well formed faeces, in various tissues. Urates are also often deposited in joints and in the kidney. This condition can occur as an individual problem at any age. Outbreaks are seen in young chicks in the first week of life (baby chick nephropathy) or in flocks suffering kidney damage, or reduced water intake. All poultry species are susceptible. The kidney damage can arise from infection with certain strains of Infectious Bronchtiis virus, exposure to some mycotoxins or inadequate water intake (often because the birds have not adapated to a new type of drinker). Baby Chick Nephropathy can be due to inappropriate egg storage conditions, excessive water loss during incubation or during chick holding/transport, or inadequate water intake during the first few days of life. Very low humidity in brooding will also increase the likelihood of this problem. The timing of mortality is a reasonable guide as to the source of the problem. In Pekin/mallard ducks the condition is almost always due to inadequate water intake, whereas in muscovy ducks it is seen in breeders allowed to continue laying for over 24 weeks without a rest.


  Depression. Low feed intake and growth.

Post-mortem lesions
  Chalky white deposits on pericardium, liver, air sacs, peritoneum. Similar deposits may be present in joints and are usually present in the kidney.


This is based on correcting any management errors and encouraging water intake. Avoid any intentional or unintentional restriction in water intake. Sodium bicarbonate at 1g/litre water is mildly diuretic, however it could be counter-productive if water intake is in any way restricted.

Careful monitoring of the conditions of hatching egg storage and incubation with a view to achieving a standard egg weight loss profile. Humidification of holding rooms and chick transporters may also be beneficial. Humidifiers in chick brooding areas are being used increasingly, especially where whole house hot air brooders are in use. Ample supplies of drinkers should be available and filled with water at house temperature prior to the arrival of the chicks.

Figure 36. Severe visceral gout in a young chick. There are white chalky deposits around the heart (in the pericardium) on all major abdominal organs, including liver, gizzard and intestines, and even in the tissues of the thigh.


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

M. Signs These may be summarised:                     Perosis Curled Toe Paralysis Paralysis/'Stargazing' Dermatitis/Scaly Skin Mouth Lesions Conjunctivitis Anaemia Fatty Liver and Kidney Syndrome Poor Feathering Loose feathers Hatchability problems Embryo with clubbed down Thiamine (B1) Riboflavin (B2) Pantothenic acid Pyridoxine (B6) Niacin Folic Acid Cyanocobalmin (B12) Biotin Post-mortem lesions   Usually the gross lesions are non-specific. Most will reduce productivity. They act in a broad range of metabolic pathways. However. Vitamin deficiencies are especially prone to cause problems of hatchability. response to supplementation. 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 . damage to the intestine or increased demand for some reason may have an effect. and egg production in the layer. See the separate discussion under Chondrodystrophy and Fatty Liver and Kidney Syndrome.Tahir Vitamin B Deficiencies Introduction The B complex vitamins are water soluble and not stored to any significant extent in the body. The embryo is particularly dependent on having adequate supplies of vitamins deposited in the egg. because a continuous supply is required. Some deficiencies induce characteristic microscopic effects. Simple deficiency is now rare as diets are usually well supplemented. Diagnosis Signs. exclusion of specific diseases.Abubakar. including growth in the young animal.

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

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

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

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