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.


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

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

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

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

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

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

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

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

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

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

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


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.


webbing between toes. 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. Elisa tests have been developed experimentally. Viral particles may be demonstrated in bile. Sudden deaths in fatty liver and kidney syndrome. It may be helpful to control other conditions which may be occurring at the same time. Biotin Deficiency. 18 . Chondrodystrophy. Treatment No specific treatment known. Pale livers and kidneys in fatty liver and kidney syndrome. Diagnosis Typical signs and lesions.    Lung congestion Ovarian regression Yolk peritonitis Pale foci and haemorrhages in pancreas. 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. in embryos. Thickened skin under foot pad. Signs       Poor growth. Leg weakness. Post-mortem lesions   See signs. Good biosecurity. Scabs around eyes and beak. Drinking water which is well chlorinated should be helpful in reducing challenge by this route. Must be confirmed by laboratory tests. 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. Allin/all-out production. Prevention Thorough cleaning and disinfection after depletion of an affected flock. Reduced feed intake and blood sugar can precipitate fatty liver and kidney syndrome.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

FHN Introduction A condition of chickens and turkeys that may be associated with several different bacterial infections e.Femoral Head Necrosis . turkeys.g. highly contagious disease caused by the bacterium Pasteurella multocida in a range of avian species including chickens. coli. Diagnosis Base on post-mortem lesions and isolation of a causative organism. Careful attention to mineral and Vitamin D nutrition to avoid subclinical. indicated that 0.75% of all male broilers placed had lesions in the hip bone. and water fowl. staphylococci. E. (increasing order of susceptibility). Predisposing factors include immunosuppresive viruses such as Infectious Bursal Disease Virus and Chicken Anaemia Virus and non-infectious bone pathologies such as hypophosphaetamic rickets. Pasteurellosis Introduction Fowl Cholera is a serious. Signs   Lameness. Prevention Exclusion of floor eggs and dirty eggs from the hatchery. Treatment Antibiotic therapy in accordance with sensitivity is likely to be beneficial only for birds in the early stage of this process and may not be economically justifiable. arthritis. Post-mortem studies of birds culled due to lameness and of birds found dead. rickets. FHN is the commonest infectious cause of lameness in broilers in the UK. Post-mortem lesions  Degeneration of the epiphyses of long bones with thinning of the cortex and tendency to break when force is applied. especially hypophosphataemic. streptococci. Differentiate from synovitis. Fowl Cholera. It is seen worldwide and was one of the first infectious 61 . spondylolisthesis. Use of a wing for support during walking and hip flexion.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

        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.


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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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.



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

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

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

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

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

   

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

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

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

Erythromycin, fluoroquinolones.

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

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

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


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

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


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

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


  Depression. Low feed intake and growth.

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


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

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

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


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

They act in a broad range of metabolic pathways. including growth in the young animal. However. Most will reduce productivity. response to supplementation. and egg production in the layer.Tahir Vitamin B Deficiencies Introduction The B complex vitamins are water soluble and not stored to any significant extent in the body. The embryo is particularly dependent on having adequate supplies of vitamins deposited in the egg. Simple deficiency is now rare as diets are usually well supplemented. damage to the intestine or increased demand for some reason may have an effect. Vitamin deficiencies are especially prone to cause problems of hatchability. Diagnosis Signs. See the separate discussion under Chondrodystrophy and Fatty Liver and Kidney Syndrome. Some deficiencies induce characteristic microscopic effects. exclusion of specific diseases.Abubakar. 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.M. If it is suspected that the vitamin premix may not have been included in the ration (or included at too low a level) it 156 . because a continuous supply is required.

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

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

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

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