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.


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

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

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

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

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

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

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

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

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

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

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


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.


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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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.



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

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

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

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

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

   

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

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

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

Erythromycin, fluoroquinolones.

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

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

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


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

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


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

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


  Depression. Low feed intake and growth.

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


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

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

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


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

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

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

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

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

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