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.


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

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

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

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

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

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

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

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

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

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

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


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.


Biotin Deficiency. 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. Thickened skin under foot pad. 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. Treatment No specific treatment known. A RT-PCR test may be used to detect viral RNA in tissues. Sudden deaths in fatty liver and kidney syndrome. Post-mortem lesions   See signs. Prevention Thorough cleaning and disinfection after depletion of an affected flock. Elisa tests have been developed experimentally. Chondrodystrophy. in embryos. Must be confirmed by laboratory tests.    Lung congestion Ovarian regression Yolk peritonitis Pale foci and haemorrhages in pancreas. Scabs around eyes and beak. webbing between toes. 18 . Reduced feed intake and blood sugar can precipitate fatty liver and kidney syndrome. 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. Drinking water which is well chlorinated should be helpful in reducing challenge by this route. Pale livers and kidneys in fatty liver and kidney syndrome. Leg weakness. Viral particles may be demonstrated in bile. Signs       Poor growth. Good biosecurity. Allin/all-out production. Diagnosis Typical signs and lesions.

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

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

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

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

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

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

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

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

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

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

However its main importance is as a cause of condemnation in meat poultry. though most of the birds showing toe scrapes will not go on to develop cellulitis. Prevention Toe scrapes at 15-25 days of age when feather cover is poor are the most likely predisposing factors. 29 . Diagnosis Typical lesions. Careful flock management with a view to reducing toe wounds has the greatest impact in controlling cellulitis. Treatment Treatment would not be possible if the problem is identified at a final depletion. which can replicate in the tissues. skin wounds by particular strains of E. 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'. particularly broiler chickens. 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. often minor. Signs  Affected flocks tend to have poorer than average productivity and uniformity. coli. The condition is caused by infection of.Cellulitis Introduction Cellulitis is literally an inflammation of connective tissues. It typically occurs between skin and muscles and between muscles and may be an incidental finding in a range of conditions. 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. Many meat inspectors become skilled at detecting subtle differences in skin colour in the affected birds. but the affected birds are not readily detectable prior to slaughter.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Haemorrhages in skeletal muscle (especially on thighs).History. Tests used are mainly Elisa. Diagnosis Clinical disease . especially in the Delmarva Peninsula in the USA.4 days. Haemorrhagic syndrome. weights below 0. Antibiotic medication may be indicated if secondary bacterial infection occurs. especially if present prior to 20 days of age. The normal weight of the bursa in broilers is about 0.Signs       Depression. may have haemorrhages. Treatment No specific treatment is available. rapidly proceeds to atrophy. Huddling under equipment. Elisa vaccination date prediction < 7 days). Coccidiosis. Subclinical disease . normal size or reduced in size depending on the stage). Variants: There have been serious problems with early Gumboro disease in chicks with maternal immunity. Diarrhoea with urates in mucus.A history of chicks with very low levels of maternal antibody (Fewer than 80% positive in the immunodifusion test at day old. (previously SN and DID). Post-mortem lesions     Oedematous bursa (may be slightly enlarged. Unsteady gait. Swollen kidneys with urates. Other possible causes of early immunosuppression are severe mycotoxicosis and managment problems leading to severe stress. 84 . Inappetance. Differentiate clinical disease from: Infectious bronchitis (renal). Vent pecking.3% of bodyweight. IBD viruses have been isolated and shown to have significant but not complete cross-protection. lesions. Half-life of maternally derived antibodies is 3. Serology: antibodies can be detected as early as 4-7 days after infection and these last for life. Use of a multivitamin supplement and facilitating access to water may help. This may be confirmed by demonstrating severe atrophy of the bursa. Vaccination date prediction uses sera taken at day old and a mathematical formula to estimate the age when a target titre appropriate to vaccination will occur. Cryptosporidiosis of the bursa (rare).1% are highly suggestive. histopathology. Dehydration. They are all serotype 1.5. subsequent diagnosis of 'immunosuppression diseases' (especially inclusion body hepatitis and gangrenous dermatitis) is highly suggestive.

It is enlarged. 85 . especially nasal and sinus mucosae. Immunity after a live vaccine can be poor if maternal antibody was still high at the time of vaccination. the rectum and the vent. In most countries breeders are immunised with a live vaccine at 6-8 weeks of age and then re-vaccinated with an oil-based inactivated vaccine at 18 weeks. highly infectious disease of chickens. including passive protection via breeders. biosecurity measures may be helpful in limiting the spread between sites. resulting in increased culling. characterised by catarrhal inflammation of the upper respiratory tract. The route of infection is conjunctival or nasal with an incubation period of 1-3 days followed by rapid onset of disease over a 2-3 day period with the whole flock affected within 10 days. This bursa is from an acutely affected broiler. and tracing of contacts may indicate sites on which a more rebust vaccination programme is indicated. occasionally pheasants and guinea-fowl.Prevention Vaccination. This shows the anatomical relationship between the bursa. A strong immunity follows field challenge. turgid and oedematous. Figure 23. Infectious Coryza Introduction A usually acute. It is not egg transmitted. sometimes chronic. When outbreaks do occur. vaccination of progeny depending on virulence and age of challenge. Carriers are important with transmission via exudates and by direct contact. Morbidity is high but mortality low if uncomplicated although it may be up to 20%. Infectious Coryza is caused by the bacterium Haemophilus paragallinarum and is seen in many countries especially in multi-age farms that are never depopulated.

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

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

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

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

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

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

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

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

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

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

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

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

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

        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.


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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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.



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

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

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

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

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

   

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.


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

See the separate discussion under Chondrodystrophy and Fatty Liver and Kidney Syndrome. Diagnosis Signs. and egg production in the layer. However. Vitamin deficiencies are especially prone to cause problems of hatchability.Tahir Vitamin B Deficiencies Introduction The B complex vitamins are water soluble and not stored to any significant extent in the body.Abubakar. They act in a broad range of metabolic pathways. response to supplementation. damage to the intestine or increased demand for some reason may have an effect. If it is suspected that the vitamin premix may not have been included in the ration (or included at too low a level) it 156 . Most will reduce productivity. The embryo is particularly dependent on having adequate supplies of vitamins deposited in the egg.M. because a continuous supply is required. exclusion of specific diseases. Simple deficiency is now rare as diets are usually well supplemented. including growth in the young animal. 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. Some deficiencies induce characteristic microscopic effects.

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

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

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

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