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62159343 Poultry Diseases and Their Treatment

62159343 Poultry Diseases and Their Treatment

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  • By
  • Paul McMullin
  • M.Abubakar.Tahir
  • M.Sc.(Hons) Animal Nutrition
  • University of Agriculture Faisalabad
  • Amyloidosis
  • Anatipestifer Disease, New Duck Syndrome, Duck Sepicaemia
  • Arizona infection, Arizonosis
  • Ascites
  • Aspergillosis
  • Avian Encephalomyelitis Egg Drop
  • Avian Encephalomyelitis, Epidemic Tremors
  • AvianInfluenza-Highly Pathogenic (HPAI), Fowl Plague
  • Avian Leukosis (Serotype J), Myelocytomatosis
  • Avian Leukosis, Lymphoid Leukosis, Leukosis/Sarkoma Group
  • Avian Rhinotracheitis 'Swollen Head Syndrome'
  • Beak Necrosis
  • Bedbug Infestation
  • Big Liver and Spleen Disease
  • Biotin Deficiency, Including Fatty Liver and Kidney Syndrome
  • Biting Lice
  • Blackfly Infestation
  • Botulism
  • Breast Blister
  • Caecal Worm
  • Calcium Tetany
  • Campylobacter Infection
  • Candidiasis, Moniliasis, Thrush
  • Cannibalism, Feather pecking
  • Capillariasis-Hairworm Infection
  • Cellulitis
  • Chicken Anaemia
  • Chlamydiosis, Psittacosis, Ornithosis
  • Chondrodystrophy, Slipped Tendon or Perosis
  • Coccidiosis of Turkeys
  • Coccidiosis, Caecal, E tenella
  • Coccidiosis, E mitis
  • Coccidiosis, Ileorectal, E brunetti
  • Coccidiosis, Intestinal, of Ducks and Geese
  • Coccidiosis, Kidney
  • Coccidiosis, Mid-intestinal, E maxima
  • Coccidiosis, Mid-intestinal, E necatrix
  • Coccidiosis, Upper Intestinal, E acervulina
  • Colibacillosis, Colisepticemia
  • Contact Dermatitis, Hock Burn, Pododermatitis
  • Cropworms
  • Cryptosporidiosis
  • Dactylariosis
  • Degenerative Joint Disease
  • Depluming and Scaly Leg Mites
  • Dissecting Aneurysm, Aortic Rupture
  • Duck Viral Hepatitis
  • Duck Virus Enteritis, Duck Plague
  • Dysbacteriosis, Non-specific Bacterial Enteritis
  • Egg Drop Syndrome 76
  • Endocarditis
  • Epiphysiolysis
  • Equine Encephalitis (EEE, WEE, VEE)
  • Erysipelas
  • Fatty Liver Haemorrhagic Syndrome
  • Favus
  • FemoralHead Necrosis-FHN
  • Fowl Cholera, Pasteurellosis
  • Fowl Pox, Pox, Avian Pox
  • Gangrenous Dermatitis, Necrotic Dermatitis
  • Gape
  • Gizzard worms-Chickens
  • Gizzard worms-Geese
  • Goose Parvovirus (Derzsy's Disease)
  • Haemorrhagic Disease, Aplastic Anaemia, Haemorrhagic Anaemia
  • Haemorrhagic Enteritis
  • Heat Stress
  • Hexamitiasis
  • Histamonosis, Histomoniasis, Blackhead
  • Hydropericardium-Hepatitis Syndrome, Angara Disease
  • Impaction and Foreign Bodies of Gizzard
  • Inclusion Body Hepatitis
  • Infectious Bronchitis, IB
  • Infectious Bronchitis, IB-793b Variant Sudden Death Syndrome in Broiler Parents
  • Infectious Bronchitis, IB Egg-layers
  • Infectious Bursal Disease, IBD, Gumboro
  • Infectious Coryza
  • Infectious Laryngotracheitis, ILT
  • Intussusception
  • Leukocytozoonosis
  • Lymphoproliferative Disease (LPD)
  • Malabsorption Syndrome, Runting/Stunting
  • Marek's disease
  • Mycoplasma gallisepticum infection, M.g., Chronic Respiratory Disease-Chicken
  • Mycoplasma gallisepticum infection, M.g., Infectious Sinusitis-Turkeys
  • Mycoplasma immitans infection
  • Mycoplasma iowae infection, M.i
  • Mycoplasma meleagridis infection, M.m
  • Mycoplasma synoviaeinfection, M.s. Infectious Synovitis
  • Mycotoxicosis
  • Necrotic Enteritis
  • Newcastle Disease (Paramyxovirus 1)
  • Non-starter and 'Starve-out's
  • Oregon Disease-Deep Pectoral Myopathy
  • Ornithobacterium Infection, ORT
  • Osteomyelitis Complex, Turkey
  • Osteoporosis, Cage Fatigue
  • Paramyxovirus 2-Yucaipa Disease
  • Paramyxovirus-3
  • Paramyxovirus-6
  • PEMS and Spiking Mortality of Turkeys
  • Pendulous Crop
  • Proventricular Worms
  • Pseudotuberculosis
  • Pullet disease, Bluecomb, Avian Monocytosis
  • Red Mite and Northern Fowl Mite
  • Respiratory Adenovirus Infection, 'Mild Respiratory Disease'
  • Respiratory Disease Complex
  • Reticuloendotheliosis, Lympoid Tumour Disease
  • Rickets (hypocalcaemic)
  • Rickets (hypophosphataemic)
  • Rotavirus Infection
  • Roundworm, large-Ascaridia
  • Ruptured Gastrocnemius Tendon
  • Salmonella Gallinarum, Fowl Typhoid
  • Salmonella Pullorum, Pullorum Disease, 'Bacillary White Diarrhoea'
  • Salmonellosis, Paratyphoid Infections
  • Salmonellosis, S. Enteritidis and S. Typhimurium infections
  • Salpingitis
  • Shaky Leg Syndrome
  • Spiking Mortality of Chickens
  • Spirochaetosis
  • Spondylolisthesis, Kinky-back
  • Spraddle Legs or Splay Leg
  • Staphylococcosis, Staphylococcal Arthritis, Bumble Foot
  • Streptococcus bovis Septicaemia
  • Sudden Death Syndrome, 'Flipover'
  • Tapeworms, Cestodes
  • Tibial Dyschondroplasia, TD
  • Ticks
  • Transmissible Enteritis, Bluecomb
  • Trichomoniasis, Canker, Frounce
  • Tuberculosis
  • Turkey Coryza
  • Turkey Rhinotracheitis (Adult)
  • Turkey Rhinotracheitis (in rear)
  • Turkey Viral Hepatitis
  • Twisted leg
  • Ulcerative Enteritis, Quail disease
  • Vibrionic Hepatitis, Avian Infectious Hepatitis
  • Viral Arthritis
  • Visceral Gout, Nephrosis, Baby Chick Nephropathy
  • Vitamin A Deficiency, Nutritional Roup
  • Vitamin B Deficiencies
  • Yolk Sac Infection, Omphallitis

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.


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

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

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

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

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

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

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

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

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

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

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


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.


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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

recumbency. Torticollis. Swollen sinuses.g.Signs      Snick. Signs     Incoordination. Airsacculitis. There are no effective preventative medicines or feed additives. Prevention The oocysts of cryptosporidia are extremely resistant to chemical disinfection. Circling. coli-septicaemia) there may be benefit in medicating for these. Low weight gain. Cough. If other disease processes are complicating the situation (e. It is becoming increasingly common for water companies to screen water supplies for cryptosporidia because of the human health implications of mammalian strains. Post-mortem lesions    Sinusitis. Diagnosis Identification of the parasites attached to the epithelium by microscopic examination (smears histopathology acid-fast staining). 48 . Treatment Unfortunately there is currently no known effective treatment in poultry. Steam cleaning is effective in reducing infection as oocysts are inactivated above about 65°C Dactylariosis Introduction A rare fungal disease of chickens and turkeys caused byDactylaria gallopava. Tremors. Pneumonia. Diarrhoea.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

subsequent diagnosis of 'immunosuppression diseases' (especially inclusion body hepatitis and gangrenous dermatitis) is highly suggestive. Use of a multivitamin supplement and facilitating access to water may help. Elisa vaccination date prediction < 7 days).A history of chicks with very low levels of maternal antibody (Fewer than 80% positive in the immunodifusion test at day old.1% are highly suggestive. Inappetance. Post-mortem lesions     Oedematous bursa (may be slightly enlarged.3% of bodyweight. Dehydration.4 days. lesions. histopathology. Diarrhoea with urates in mucus. Vent pecking. Cryptosporidiosis of the bursa (rare). Antibiotic medication may be indicated if secondary bacterial infection occurs. Subclinical disease . Unsteady gait. Serology: antibodies can be detected as early as 4-7 days after infection and these last for life. especially if present prior to 20 days of age. 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. weights below 0.5. IBD viruses have been isolated and shown to have significant but not complete cross-protection. Other possible causes of early immunosuppression are severe mycotoxicosis and managment problems leading to severe stress. They are all serotype 1. Haemorrhagic syndrome. Half-life of maternally derived antibodies is 3. Diagnosis Clinical disease . Huddling under equipment. 84 . especially in the Delmarva Peninsula in the USA. This may be confirmed by demonstrating severe atrophy of the bursa.Signs       Depression. Swollen kidneys with urates. Treatment No specific treatment is available. The normal weight of the bursa in broilers is about 0.History. rapidly proceeds to atrophy. (previously SN and DID). Tests used are mainly Elisa. normal size or reduced in size depending on the stage). Coccidiosis. Differentiate clinical disease from: Infectious bronchitis (renal). may have haemorrhages. Haemorrhages in skeletal muscle (especially on thighs). Variants: There have been serious problems with early Gumboro disease in chicks with maternal immunity.

sometimes chronic. especially nasal and sinus mucosae. Carriers are important with transmission via exudates and by direct contact. It is not egg transmitted. biosecurity measures may be helpful in limiting the spread between sites. occasionally pheasants and guinea-fowl. and tracing of contacts may indicate sites on which a more rebust vaccination programme is indicated. Figure 23. In most countries breeders are immunised with a live vaccine at 6-8 weeks of age and then re-vaccinated with an oil-based inactivated vaccine at 18 weeks. turgid and oedematous. Infectious Coryza Introduction A usually acute. highly infectious disease of chickens. Morbidity is high but mortality low if uncomplicated although it may be up to 20%. It is enlarged. Infectious Coryza is caused by the bacterium Haemophilus paragallinarum and is seen in many countries especially in multi-age farms that are never depopulated. The 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. vaccination of progeny depending on virulence and age of challenge. characterised by catarrhal inflammation of the upper respiratory tract. resulting in increased culling. 85 . the rectum and the vent. This bursa is from an acutely affected broiler.Prevention Vaccination. When outbreaks do occur. A strong immunity follows field challenge. This shows the anatomical relationship between the bursa. including passive protection via breeders. Immunity after a live vaccine can be poor if maternal antibody was still high at the time of vaccination.

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

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

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

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

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

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

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

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

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

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

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

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

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

        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.


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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

May cause anaemia and death in young birds. Diagnosis Number and type of mites identified. which are external parasites of chickens and turkeys. Birds restless. Filling of cracks and crevices. Dermanyssus gallinae. Staff complaints . and good design of new equipment to limit harbourages for red mites. Post-mortem lesions  Anaemia. citrus extracts. Loss of condition. For northern fowl mite it is essential to apply approved insecticides to the affected birds. Pale comb and wattles. Prevention Thorough cleaning. fumigation and insecticide treatment at turnaround. 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. Treatment Pyrethroids. crevices etc.Red Mite and Northern Fowl Mite Introduction Arachnid mites. vegetable oil and mineralbased products (both liquid sand dusts) have been used to control red mites in the environment. Signs        Presence of grey to red mites up to 0.7 mm. 118 . cracks. feeds by sucking blood. Effective monitoring of mite numbers and implementation of control measures before birds are heavily infested improves control. the Northern Fowl Mite spends its entire life cycle on the bird and can multiply more rapidly as a result. Drop in egg production. Spots on eggs. mainly at night and may transmit fowl cholera and other diseases. carbamates. the Common Red Mite. organophosphates. Ornithonyssus bursae. in nest boxes.itching.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

   

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.


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

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

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

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

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

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