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.


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

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

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

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

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

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

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

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

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

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

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


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.


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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

coccidiosis. rapid deterioration and death. often in opisthotonus. isolation in CE (causes stunting of 9 day embryo). 0.survive for ten weeks in brooders and five weeks in faeces. Duck septicaemia (anatipestifer). Microscopically . Prevention Vaccination and/or antiserum. mostly in ornamental collections. Treatment Antiserum. bile duct proliferation and inflammation. All waterfowl are susceptible and the Barbary duck is more susceptible than the Pekin. fomites and arthropods. Influenza and a 'Type II Variant' hepatitis caused by Astrovirus.focal necrosis. Depression. arching of back. lesions. Post-mortem lesions     Liver swollen. Live. Diagnosis History. SN serology. paddling of legs. Differentiate from Duck plague (viral enteritis). A different picornavirus causes a similar condition in North America. breeder vaccination. also the Netherlands and other countries. only slightly attenuated vaccine is applied at day old by foot web stab and may be repeated in breeding birds to provide maternal immunity. Kidneys and spleen swollen. Duck Plague Introduction A herpesvirus infection of ducks and geese diagnosed in the UK in 1972.5 ml serum of recovered birds given intramuscularly. Signs     Sudden death. The disease follows a very acute course with a morbidity of 5-100% and mortality of 5-100%. Duck Virus Enteritis. 52 . Fall on side. Recovered birds may carry the virus for a year. Newcastle disease. Transmission is by infected birds. Death in good condition. Punctate/diffuse haemorrhages. in USA since 1967.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

        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.


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

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

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

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

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

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

Growth is more rapid and consistent in an anaerobic jar. Cultures from the trachea of birds showing typical signs are preferred.Ornithobacterium Infection. The organism grows slowly producing tiny colonies on blood agar. age at infection etc. This was first identified as a new disease syndrome of turkeys in Germany in the early 1990s. Important cofactors may include respiratory viral vaccines (Newcastle disease. Most isolates are oxidase positive and galactosidase positive Serology using Elisa tests has been used. severe bronchopneumonia. Reduced weight gain. Confirmation is by isolation of the organism. Inoculation of fresh material from a case can reproduce lung lesions similar to those caused by Pasteurella multocida infection in previously uninfected turkeys over 10 weeks of age. The infection is common in chickens and turkeys. preferably as a flock test comparing results before and after the challenge. ORT Introduction Ornithobacterium Infection is an infection of chickens and turkeys with the bacterium Ornithobacterium rhinotracheale(ORT). field challenge with respiratory viruses. The slow-growing bacterium was named in 1994. Bordetella aviuminfection. Within the poultry house it is likely to be by aerosols. Post-mortem lesions  Airsacculitis. Infectious Bronchitis). It is a Gram-negative pleomorphic organism. Signs    Coughing. Reduced egg production. A range of sero-types have been identified. tracheitis. The severity of its effects depends on the pathogenicity of the particular strain and other risk factors such as viral infections. E. In broiler chickens its main importance seems to be as a cause of airsacculitis in apparently healthy flocks that is only identified at slaughter. direct contact and drinkers. sneezing. coli overgrowth may occur. coli infections. Diagnosis Clinical signs and lesions. It had been previously isolated in a number of other countries. It commonly exacerbates respiratory disease caused by pneumovirus infections in turkeys. Some uncertainty exists about mechanisms of transmission. This can cause significant losses through condemnations. The range occurring in turkeys is wider than that seen in chickens. There is some evidence that hatcheries may play a role in the epidemiology. 108 . ventilation problems. perhaps through survival of the organism on shell surfaces or shell membranes. and E.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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.



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

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

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

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

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

   

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.


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

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

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

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

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

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