62159343 Poultry Diseases and Their Treatment | Public Health | Infection

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.


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

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

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

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

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

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

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

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

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

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

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


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.


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

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

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

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

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

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

and response to treatment. Campylobacter jejuni infection is not currently considered to be pathogenic in poultry though a Campylobacter-like organism is considered to be the cause of 'Vibrionic Hepatitis'. All campylobacters are delicate organisms that survive for relatively short periods outside the host unless protected by organic material. The reason for this is unclear. managing birds for maximum uniformity. Prevention Keep pullet flocks on low calcium diet until 5% production hen/day. pets and wild animals. biofilm or engulfed by protozoa. There are indications that plantar pododermatitis. Infected poultry are a potential reservoir of this zoonosis. Congested lungs. Active ovary with egg in oviduct. Diagnosis This is made on signs. principally in the caecae. In poultry they tend to multiply in large numbers in the hindgut. are bacteria that commonly infect a broad range of livestock species. Campylobacter Infection Introduction Campylobacter spp. There is an annual cycle with increased risk of infection in the summer months in some countries. It may be that management that favours dry litter reduces the risk of infection and/or transmission within the flock. Campylobacters are a significant cause of enteritis in man. 24 . other acute infections and other causes of sudden death. lack of other significant lesions. Treatment Provide 5 gm of oyster shell per hen on 3 successive days along with vitamin D in drinking water. Differentiate from IB 793b. Campylobacter jejuni is the commonest species found in poultry. lesions.Post-mortem lesions    Cyanosis. carcase quality and litter quality are better on farms which tend to have Campylobacter-negative stock.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

They are all serotype 1. Dehydration. Huddling under equipment. Haemorrhagic syndrome. especially in the Delmarva Peninsula in the USA. subsequent diagnosis of 'immunosuppression diseases' (especially inclusion body hepatitis and gangrenous dermatitis) is highly suggestive. lesions. This may be confirmed by demonstrating severe atrophy of the bursa. normal size or reduced in size depending on the stage). Half-life of maternally derived antibodies is 3.5. Use of a multivitamin supplement and facilitating access to water may help. Diarrhoea with urates in mucus.3% of bodyweight.4 days. Tests used are mainly Elisa. Haemorrhages in skeletal muscle (especially on thighs). Variants: There have been serious problems with early Gumboro disease in chicks with maternal immunity. 84 . Cryptosporidiosis of the bursa (rare). weights below 0.A history of chicks with very low levels of maternal antibody (Fewer than 80% positive in the immunodifusion test at day old. Treatment No specific treatment is available. Other possible causes of early immunosuppression are severe mycotoxicosis and managment problems leading to severe stress. The normal weight of the bursa in broilers is about 0. Elisa vaccination date prediction < 7 days). rapidly proceeds to atrophy. Serology: antibodies can be detected as early as 4-7 days after infection and these last for life. Post-mortem lesions     Oedematous bursa (may be slightly enlarged. IBD viruses have been isolated and shown to have significant but not complete cross-protection. histopathology. Inappetance. Differentiate clinical disease from: Infectious bronchitis (renal). especially if present prior to 20 days of age. Diagnosis Clinical disease . Subclinical disease .1% are highly suggestive. Swollen kidneys with urates. (previously SN and DID). Vent pecking. 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.History. Antibiotic medication may be indicated if secondary bacterial infection occurs. Coccidiosis. may have haemorrhages. Unsteady gait.Signs       Depression.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Diagnosis Symptoms. 137 . Treatment None. Use of wings to help in walking. Signs    Sitting on hock or rumps.Tahir Spondylolisthesis. lesions. Figure 33.M. 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. 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. legs extended forward.Abubakar. These are cross-sections of the spinal column of 4-5-weekold broilers. Prevention Selection for satisfactory conformation in primary breeding. The sample on the right is normal. with rotation of the body of the vertebra and the pinching of the spinal column that causes paralysis. May walk backwards.

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

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

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

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

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

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

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

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

Post-mortem lesions
       Dehydration. Emaciation. Enteritis with petechial haemorrhages. Froth ingesta. Sometimes casts. Pancreas chalky. Urates in kidneys/ureters.

Reproduction with filtered contents, isolation in turkey eggs, electron microscopy, immunofluorescence, Elisa. Commercial M4I IB Elisa will detect some infections.

Warmth and good management, antibiotics, milk replacer, potassium chloride. Disinfect and rest houses for 3-4 weeks.

All-in/all-out production, good hygiene and biosecurity, good management.

Trichomoniasis, Canker, Frounce
Trichomonas gallinae is a protozoan parasite of pigeons and doves (canker), raptors (frounce), turkeys and chickens. It has variable pathogenicity. Morbidity is high and mortality varies but may be high. Transmission is via oral secretions in feed and water, and crop milk.


     Mouth open. Drooling and repeated swallowing movements. Loss of conditon. Watery eyes in some birds. Nervous symptoms (rare).

Post-mortem lesions
  Yellow plaques and raised cheesy masses in mouth, pharynx, oesophagus, crop and proventriculus. Raptors may have liver lesions.

Lesions, large numbers of protozoa in secretions. Differentiate from Pox and candidiasis.

Previously approved products included dimetridazole, nithiazide, and enheptin. Organic arsenical compounds (where approved) and some herbal products may be of some benefit in managing this problem in food animals.

Eliminate stagnant water, eliminate known carriers, add no new birds.

A bacterial infection, caused by Mycobacterium avium, of poultry, game birds, cage birds etc. Morbidity and mortality are high. Transmission is via faecal excretion, ingestion, inhalation, offal and fomites. The disease has a slow course through a flock. The bacterium resists heat, cold, water, dryness, pH changes and many disinfectants.

     Severe loss of weight with no loss of appetite. Pale comb. Diarrhoea. Lameness. Sporadic deaths.

Post-mortem lesions
 Emaciation.


 

Grey to yellow nodules attached to intestine. Granulomas in liver, spleen and many other tissues, even bone marrow.

Isolation, acid-fast stain in tissues, TB test. Differentiate from Lymphoid leukosis.

None recommended.

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

Turkey Coryza
A condition of turkeys possibly associated with Bordetella avium(previously designated Alkaligenes faecalis) infections. This bacterium usually causes mild respiratory disease in only a proportion of the flocks, and low mortality. It can be synergistic with other respiratory pathogens such as Ornithobacterium,Pasteurella spp, Mycoplasma spp. and pneumoviruses.

      Decreased appetite, weight gain and feed efficiency. Loss of voice. Ocular and nasal discharge. Conjunctivitis. Snick. Dyspnoea.

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

Clinical signs, isolation of agent.



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

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

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

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

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

   

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

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

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

Erythromycin, fluoroquinolones.

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

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

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


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

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


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

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


  Depression. Low feed intake and growth.

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


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

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

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


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

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

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

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

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

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