Fowl Plague is an infectious disease of fowls, characterised by a variety of disease syndromes ranging from sub clinical to mild upper respiratory loss of egg production to acute generalised fatal disease.
Distribution
Perroncito first described the disease in Italy in 1878. Avian influenza is distributed throughout the world. There are three incidences of fowl plaques in North America, after the last fowl plague outbreak in 1929. There are reports of influenzas infections in several countries like Belgium, Scotland, Italy, Russia, Australia, Hong Kong, France and Israel. Influenzas in turkeys have been reported in Hungary, France, Holland, Italy, Ireland, England, Canada, USA and Israel. Avian Influenza is not an important disease in India.
Aetiology
Avian influenza virus along with all other influenza viruses constitute the Orthomyxoviridae family. This is a RNA virus and the viral envelop has haemagglutination and neuraminidase activity. There is three antigenically distinct types of influenza virus: Type A, Type B and Type C. Till date, influenza type A virus has been isolated from birds. Influenza type A virus also found in human, swine, horse and in other mammals. Type B and C found only in humans. Influenza A viruses are subtyped on the basis of haemagglutination and neuraminidase antigens. Virus is relatively sensitive to detergents and virus is rapidly destroyed by formalin, ether, dilute acids and ammonium ions. Virus is inactivated by heat, high pH and dryness. Virus can thrice well in faecal material for 30-35 days and at 4° C and 7 days at 20° C.
Susceptible Hosts
The disease is observed mainly in poultry, ducks, quail, pheasants and turkey. The viral strains are highly pathogenic to chicken and turkey. The disease is also reported from geese, Muscovy ducks, guinea fowl, partridges, chukars, ostriches and other ratites. Virus also replicate in ferrets, cats, hamsters, mice, monkey, mink and pigs after experimental inoculation.
Mode of Transmission
Virus is excreted in the respiratory tract, conjunctiva, faeces from the infected birds. Transmission can occur through direct contact between infected and susceptible birds.
Main route of transmission is faeco-oral route through contaminated feed and water.
Bird to bird transmission also occurs through droplets or aerosol route.
Contaminated equipment’s, supplies, cages, clothes, delivery vehicles may also act as source of infection.
Insects play a role in mechanical transmission of the disease.
Several reports have been published in favour of concurrent infection in domestic poultry birds with the arrival of migratory birds.
Reports are available that turkeys become infected with viruses from pigs.
Virus can also be transmitted vertically through eggs, as evidenced in Pennsylvania outbreak.
Pathogenicity
Incubation period of the disease varies from few hours to 3 days. It depends on virulency of virus, species exposed and route of exposure. Morbidity of the disease may extend up to 100% but mortality is up to 70% or as low as 0%. Viral multiplication occurs in the respiratory tract and in the conjunctiva. There is development of pneumonia and conjunctivitis.
Clinical Findings
Clinical signs depend on the strain of the virus, age and species of the host, immune status of the host, other concurrent infections, deficiency conditions and environmental conditions such as excess ammonia and dust. In per acute case, the birds may die without showing any sign and symptom. Clinically there is decreased feed conversion, emaciation, increased broodiness of hens, decreased egg production, mild to severe respiratory signs like coughing, sneezing, rales, lacrimation, huddling, oedema of head and face, cyanosis of featherless parts of the skin, subcutaneous haemorrhage, nervous disorders and even diarrhoea. In some cases, there may be complete caseation of egg laying.
Lesions
In acute case, there is haemorrhagic lesions found in the skin, liver, spleen, myocardium of heart, kidneys and lungs. These lesions are usually absent in per acute cases. Mild lesions are found in sinuses, characterized by catarrhal, fibrinous, sero-fibrinious, mucopurulent or caseous inflammation. Air sacs may be thickened and have a fibrinous or caseous exudate. Catarrhal peritonitis and ‘egg peritonitis’ may be found. Yellowish grey necrotic foci are seen in spleen, kidneys, liver, lungs and pancreas. Spleen of chicken may be enlarged to its double in size. Crop and proventriculus are distended. Crop is filled with watery fluid and proventriculus with greenish fluid.
Histologically highly pathogenic strain produces oedema, hyperaemia, haemorrhage and degenerative necrotic foci in visceral organs. Myocardial necrosis and myocarditis are frequently noticed. Perivascular cuffing of lymphocytes are evident in different visceral organs. There is wide spread perivascular lymphoid cuffing, glial foci, vascular proliferation and various neuronal changes are observed in brain. Histopathological section of kidney shows dilated collecting ducts and medullary loops filled with heterophilic epithelial and urate crystalline cast.
Diagnosis
- History and clinical signs.
- Gross and histological necropsy changes.
- Isolation of virus: Nasopharyngeal swab may be collected from trachea and cloaca and chicken embryos 10-11 days old are inoculated with the material via allantoic cavity. Death of embryo occurs within 24 hours. After 72 hours or at death the eggs should be removed from incubator, chilled and allantoic fluid is collected. Viral replication is demonstrated by chicken erythrocyte haemagglutinating activity in the allantoic fluid.
- Haemagglutination test: The virus haemagglutinates RBC, specially of rabbit but the elution process is very slow.
- Immuno diffusion test: This test using a nucleocapsid protein rich extract from infected chorio-allantoic membrane has been used successfully.
- Agar gel precipitation test.
- Fluorescent antibody technique
- Complement fixation test
- ELISA
- Now a days various molecular diagnostic techniques are being rewarded for quick and successful diagnosis of the disease.
Treatment
There is no practical and specific treatment for the disease. However, studies conducted by Beard (1987) showed that Amantadine hydrochloride and Rimantadine hydrochloride administered in drinking water reduce the mortality. In India, amantadine has been used successfully in field cases. But soon resistant strain evolved.
Control
- When an outbreak is evident, all the affected birds should be segregated, preferably to be disposed off.
- Premises should be disinfected properly.
- Feed and water troughs are to be cleaned regularly and supply of pure and clean drinking water should be maintained.
- Strict hygienic measures in house should be adopted and no outsider should be allowed in farm.
- Provision of foot-dip must be arranged.
- Persons working in farm should be medically checked and those showing influenza type symptoms should not be allowed to work in the house at any ground as the disease can be propogated from human beings.
- Pigs and other animals should not be allowed to graze in the surrounding area.
- Vaccination: Inactivated oil emulsion vaccine may protect the birds. But, in India no commercial vaccine is available.
