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.


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

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

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

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

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

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

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

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

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

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

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


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.


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

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

Weekly treatments are required. Diagnosis Anaemia. Eggs and larvae survive through the winter to cause new infestations in the following year. 5 mm long and found in North and South America that are external parasites of birds and mammals. Treatment Treatment is difficult. although these insects can travel up to 15 miles. 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. especially in autumn and winter and treat if required. The flies transmit leucocytozoonosis and also a filarial parasite in ducks. 20 . The condition tends to occur near to rapidly flowing streams. Examine for lice regularly. Blackfly Infestation Introduction Grey-black hump-backed flies. Post-mortem lesions  Anaemia.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. Swarms of flies. season. local history. Prevention Similar measures as for mosquito control. It is usually necessary to treat twice at a 7-10 day interval to fully control the condition. Signs   Anaemia in young birds.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Ulcers. scrapings from fresh material. Prevention Good sanitation. possibly in combination with an RNA virus and immunosuppression caused by Chick Anaemia Virus or Infectious Bursal Disease. Regular worming to help control the intermediate hosts. Hydropericardium-Hepatitis Syndrome. The disease is readily reproduced by inoculating birds with a bacteria-free filtrate of a liver extract from an affected bird. caseous cores with yellow. 74 . Having both chickens and turkeys on the same property is likely to increase the risk of this disease in turkeys.g. especially in chickens. Mortality may reach 60% but more typically 10-30%.g. Arsenicals are less effective in treatment than they are in prevention. dimetridazole). grey or green areas. and only nitarsone is approved in the USA. nitrofurans (e. nifursol) and arsenicals (e. 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.Abubakar. avoid mixing species. It affects mainly broilers and broiler parents in rear and has also been seen in pigeons. concrete floors. however they may not be present in the early stages. 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. Use of an anti-histomonas product in feed where such products are approved but due care with respect to residue avoidance would be required.g. Treatment Historically nitro-imidazoles (e. furazolidone. Some herbal products based on the essential oils (e.g. given recent new knowledge on the mechanism of transmission.M.Tahir Post-mortem lesions    Enlargement of caeca. usually grey in colour. Liver may have irregular-round depressed lesions. Diagnosis Lesions. It is a condition caused by an adenovirus. 'Herban)' have been used with some apparent success though controlled trials and formal approval for this purpose are not recorded.nitarsone) have been used to treat this important disease of poultry. Angara Disease Introduction This condition was first identified in broilers in Pakistan in 1987.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

        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.


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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

response to environmental changes. If condemned birds are included mortality may be more than 10%. be challenged by some of these pathogens). carefully applied appropriate viral vaccines. 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. Morbidity is typically 10-20%. Prevention Effective ventilation. 120 . Diagnosis Lesions. There is also percarditis evident (at top right).predisposing factors. The air sacs are thickened and congested. Nasal exudate. Rattling noises. Post-mortem lesions    Severe tracheitis with variable exudate . and have been cut into to reveal a cheesy (caseous) mass of pus. Signs       Snick. Conjunctivitis. Head swelling. Figure 29.10%. of course. Sneezing. Pericarditis.catarrhal to purulent. Differentiate from Chronic Respiratory Disease (Mycoplasmosis). sanitation of drinking water. Treatment Antimicrobial treatment of specific bacterial infections. Severe airsacculitis of thoracic air sacs in a broiler close to slaughter. Airsacculitis. serology. mortality 5.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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.



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

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

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

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

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

   

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.


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

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

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

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

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

Sign up to vote on this title
UsefulNot useful