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.


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

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

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

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

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

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

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

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

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

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

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


Post-mortem lesions
  Serous rhinitis and tracheitis, sometimes pus in bronchi. If secondary invasion byE. coli then pneumonia, airsacculitis and perihepatitis. Congestion, oedema and pus in the air space of the skull occurs in a proportion of affected birds due to secondary bacterial infections.

Clinical signs, serology, isolation of ciliostatic agent. Differentiate from Infectious Bronchitis, Lentogenic Newcastle disease, low virulence avian influenza,Ornithobacterium rhinotracheale. Serology - Elisa normally used, not all commercial kits are equally sensitive to response to both A and B challenge viruses.

Antibiotic not very effective. Control respiratory stressors, chlorination of drinking water, multivitamins.

All-in/all-out production, vaccination (degree of cross protection between A and B types remains to be established). Live vaccines can reduce clinical signs and adverse effects, inactivated vaccines may be used in breeders prior to lay.

Figure 10. Pus in skull bones. This is a common sequel to avian pneumovirus infection in both chickens and turkeys.


Beak Necrosis
A condition seen in chickens and turkeys caused by excessively fine mashed feeds.

   Feed accumulates along edges of lower beak leading to distortion and necrosis of horny tissue. Has been associated with curled tongue in turkeys in the past. This may also be associated with ulcers in the roof of the mouth (palate) which can be confused with some forms of mycotoxicosis.

Post-mortem lesions
 See signs.

Clinical signs, exclusion of other causes of similar signs.

Not usually sufficiently severe to justify medication. Mild water sanitation may help control secondary infections in the affected tissues.

Check feed particle size by granulometry, grind less finely.

Bedbug Infestation
A condition of poultry, pigeons (and mammals) caused by infestation with the external parasite Cimex lectularius. The parasites are up to 5 mm long and feed at night. It occurs mainly in subtropical and some temperate areas. Adult parasites can survive for 1?12 months in the environment without feeding. Eggs laid by the adult parasites hatch in 4?20 days, there are five nymphal stages each of which feed on birds. Growth to adult parasite takes 1?3 months, depending on temperature.

   Lack of thrift. Anaemia. Reduced production when infestation is serious.


Post-mortem lesions
 Anaemia.

Identification of the parasite. Differentiate from other blood sucking parasites.

Appropriate insecticide treatment of the environment, in particular the cracks and crevices where the parasites hide during the daytime.

Thorough treatment of the empty building at turn-around with an appropriate insecticide. Fumigation is also helpful.

Big Liver and Spleen Disease
This condition was first seen in Australia in 1980. It is now known to be caused by an Avian Hepevirus. Related viruses have been reported to cause a hepatitis/splenomegaly syndrome in the USA, sub-clinical infection in pigs and Type E Hepatitis in man. The pig origin virus can cause disease in man, but avian hepeviruses are believed not to be zoonotic. The lesions are associated with deposition of antigen/antibody complexes in tissues. Only chickens are known to be naturally affected, most commonly broiler parents in lay. Natural infections have only been demonstrated in chickens over 24 weeks of age though it is possible that vertical transmission and/or infection in rear occurs with a subsequent period of latency. Transmission is usually by the faecal/oral route. Faecal contamination of drinking water is likely to be an efficient means of spread of this infection. Embryos inoculated intravenously become persistently antigen positive.

    Chronic under production or egg drops of up to 20%. Mortality of up to 1% per week for 3-4 weeks. Anaemia. Premature moulting.

Post-mortem lesions
  Enlarged spleen (over 1gm/kg bodyweight, often with pale foci). Liver usually enlarged, sometimes with subcapsular Affected birds may also have: haemorrhage.


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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Cyanosis of head. Progressive depression and emaciation. paratyphoid. Histomoniasis. and mixing groups of different ages. Treatment Tetracycline. Histamonosis. scrapings from fresh material. This condition has high morbidity and mortality in turkeys. if possible. dimetridazole. Caecal tonsils congested. and occasionally chickens.  First half of intestine inflamed. Prevention Depopulation. Poor growth. significant disease has been seen in breeding chickens and free-range layers. The parasite is ingested in the ova ofHeterakis worms or as larvae in earthworms or faeces and there is an incubation period of 15-20 days. hygiene. It has recently been demonstrated that infection occurs readily via the cloaca when birds are on contaminated litter. Sulphur-yellow diarrhoea. Inappetance. Differentiate from transmissible enteritis. presumably introduced with worm eggs. 73 . histomonosis. gallinae the parasite is easily destroyed. avoid interspecies mixing. Within a turkey shed transmission is rapid in spite of the fact that it is difficult to infect birds orally with unprotected parasites. trichomoniasis. Blackhead Introduction Histomonas melagridis is a protozoan parasite of turkeys. Furazolidone. Although chickens are relatively resistant to the condition. Signs        Depression. all-in/all-out production. increase ambient temperature. Blood in faeces (chickens). dimetridazole and ipronidazole have been used in the past. The problem is seen in high-biosecurity facilities. and also. Outwith earth worms orH. pheasants and game birds that acts together with facultative bacteria to produce the condition of Blackhead. The effect of antibiotic may be related to the control of secondary bacterial enteritis. Diagnosis Lesions.

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

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

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

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

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

Poor ventilation and high density are predisposing factors. 79 . Avian Influenza and Laryngotracheitis. Muscular shivering. depending on secondary infections. Definitive diagnosis is based on viral isolation after 3-5 passages in chick embryo. Cellmediated immunity may also be important. disinfectants (Formal 1% for 3 mins). Differentiate from Newcastle disease (lentogenic and mesogenic forms). heat (56°C for 15 mins). DID (poor sensitivity. fomites or aerosol. Signs    Sudden death.793b Variant Sudden Death Syndrome in Broiler Parents Introduction A Coronavirus infection of chickens with a morbidity of 50-100% and a mortality 0-25%. The virus. with typical lesions. short duration. IB . The infection spreads rapidly by contact. Infection is via the conjunctiva or upper respiratory tract with an incubation period of 18-36 hours. Serology: HI. mycoplasmosis.antibiotics to control secondary colibacillosis (q. Prevention Live vaccines of appropriate sero-type and attenuation. SN (type specific). alkalis. Maternal immunity provides protection for 2-3 weeks. Some birds/viral strains can be carriers for up to 1 year.). is sensitive to solvents. HA negative. Otherwise as for standard IB. vaccinal reactions. Treatment Sodium salicylate 1gm/litre (acute phase) where permitted . which may survive 4 weeks in premises. flourescent antibody positive and ciliostasis in tracheal organ culture. Local immunity is first line of defence. Humoral immunity appears 10-14 days post vaccination. possible reactions depending on virulence and particle size. Infectious Bronchitis. lesions and serology.v. group specific). Elisa (both group specific).Diagnosis Tentative diagnosis is based on clinical sgns.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

        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.


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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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.



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

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

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

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

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

   

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.


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

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

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

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

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

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