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| Fowl Plague, Avian Influenza-Highly Pathogenic | |||
| Introduction | One of only 2 ''Class A'' diseases of poultry targeted for emergency disease control measures by OIE. This viral disease can cause exceptionally high mortality. In addition official control measures disrupts trade in poultry products from affected areas. | ||
| Cause | Orthomyxovirus type A, pathogenicity variable, designated serotype/species/location/reference number/year/sub-type 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 which code for multiple basic amino acids. The definitive classification of high pathogenicity is an intravenous pathogenicity test in 6 week old chickens result of greater than 1.2 . | ||
| Agent Type | Virus | Morphology | 80-120 nm diameter, may be filamentous, contains 8 strands of RNA, facilitating reassortments when single cells are infected with 2 viruses. |
| Species | chicken, turkey, ducks, partridge, pheasant, quail,
pigeon, ostriches, etc.etc. Effectively all birds are
considered to be at risk of infection. Man and pigs may become infected. |
Age | 1 week+ |
| Distribution | Apathogenic and mildly pathogenic influenza A viruses occur worldwide. Highly pathogenic avian influenza A (HPAI) viruses of the H5 and H7 HA subtypes have been isolated occasionally from free-living birds. Outbreaks due to HPAI were recorded in the Pennsylvania area, USA, in the years 1983-84. More recently outbreaks have occurred in Australia, Pakistan, Mexico and, from December 1999, in northern Italy, Chile in 2002, The Netherlands and Belgium in 2003. H5 viruses of low pathogenicity may become highly pathogenic usually after circulating in poultry flocks for a time (Pennsylvania, Italy). See current OIE records for up to date information on distribution e.g. the OIE Page | ||
| Signs | Sudden death, depression, coughing, nasal and ocular discharge, swollen face, cyanosis of comb/wattles,diarrhoea (often green), nervous signs such as paralysis. Sudden, almost complete, cessation of feed consumption may be the most obvious sign in some outbreaks. | ||
| Lesions | With sudden deaths lesions may be restricted to organ swelling, with some petechiae of spleen and heart. Inflammation of sinuses, trachea, air-sacs and conjunctiva, ovarian regression or haemorrhage, necrosis of skin of comb and wattles, sub cutaneous oedema of head and neck, dehydration, muscles congested, haemorrhage in proventricular and gizzard mucosae and lymphoid tissue of intestinal tract. Turkey lesions tend to be less marked than those of chickens, while ducks may be symptomless, lesionless carriers of highly pathogenic virus. During a multi-species outbreak distinct patterns of lesions may be evident in differing species or classess (rear vs lay, meat vs laying birds). | ||
| Morbidity | High | Mortality | 5-100, low in ducks |
| Differential Diagnosis | Newcastle disease, fowl cholera, infectious laryngotracheitis, other respiratory infections, bacterial sinusitis in ducks | ||
| Diagnosis | Presumptive History, lesions Confirmation Viral isolation in chick embryo, HA+, NDV-, DID+ | ||
| Transmission | Direct contact with secretions from infected birds, especially faeces. Rate varies,waterfowl,equipment,clothing, drinking water,vertical possible? carriers ? Virus replicates mainly in respiratory tissues of chickens and turkeys but in intestinal tract of clinically normal waterfowl. Avirulent in one species may be virulent in others. Broken contaminated eggs may infect chicks in the incubator simulating vertical transmission. | ||
| Agent Survival | Moderately resistant, can survive 4 days in water at 22 C., over 30 days at 0 C. Temperature:Inactivation by 56°C/3 hours; 60°C/30 min pH: Inactivated by acid pH Chemicals: Inactivated by oxidising agent Disinfectants: Inactivated by formalin and iodine compounds Survival: Remains viable for long periods in tissues | ||
| Route of Infection | Probably oral initially, possibly by conjunctiva or respiratory route | ||
| Predisposing Factors | Infections with other pathogens (e.g. Pasteurella) may increase mortality, even with ''low pathogenicity'' strains | ||
| Incubation Period | 3-5 days | ||
| Prevention | Hygiene, quarantine, all in/all out etc., minimize contact with wild birds, controlled marketing of recovered birds. Vaccination is not normally recommended because, although it may reduce losses initially, since vaccinated birds may remain carriers if exposed to the infection. Vaccines have been used in recent outbreaks in Mexico and Pakistan. Inactivated vaccines to be effective must be to the right subtype for the particular situation (H5 will not protect against H7 and vice-versa). In outbreaks, slaughter correct disposal of carcases, cleaning, disinfection, isolation, 21 day interval to re-stocking. | ||
| Treatment | None, but good husbandry, nutrition and antibiotics may reduce losses. Eradication by slaughter is usual in chickens and turkeys | ||
| Immunity | Survivors can be expected to have a high degree of immunity but may harbour virulent virus | ||
| Serology | Commercial Elisa test kits are now available. As with many such tests occasional false positive reactions occur. The agar gel precipitation test is non-group-specific and is used to confirm any positives. | ||
| Further Information | |||