Nearly all Avian Influenza viruses isolated from wild birds are low-pathogenic and cause no clinical problems in these birds. Often, high-pathogenicity mutants emerge in poultry from a low-pathogenicity virus introduced into this poultry some time earlier. Possible routes of introduction of wild-bird AI viruses into poultry farms, and the design of biosecurity measures to block these routes, are discussed by Koch and Elbers [NJAS-Wageningen Journal of Life Sciences 54-2, 2006].
In poultry dense areas, epidemic spread of HPAI between farms has been observed to continue despite animal movement bans and biosecurity measures. Mechanisms of between-farm transmission are not well understood at present. However, modelling analyses of data from past epidemics enable estimation of the transmission risk as a function of between-farm distance. This in turn allows the construction of risk maps for between-farm spread, and a calculation of the expected effect of ring culling and ring vaccination strategies [Boender et al, PLoS Comput. Biol. 3(4): e71.]
This question can not be answered with any useful precision, even if country X has encountered one or a few HPAI introductions in the past. This is in contrast to the quantitative estimation of between-farm spread, in the event HPAI has been introduced into this country, which may well be possible if past epidemic data on between-farm spread is available [Boender et al (2007), PLoS Comput. Biol. 3(4): e71; Meuwissen et al (2006), NJAS-Wageningen Journal of Life Sciences 54-2, 195-206].
Avian influenza (AI) is a contagious viral disease of birds caused by influenza A viruses which may also infect mammals. On rare occasions some types of avian influenza viruses have infected humans, but usually without involving human to human spread.
Influenza A virus is a member of the family Orthomyxoviridae and contains eight segments of linear negative sense RNA. Two of these genes, the haemagglutinin (HA) and neuraminidase (NA), encode surface glycoproteins associated with virulence. The HA protein is the most abundant and is responsible for attachment of the virus to host cell membranes whilst NA is a host cell receptor destroying enzyme thereby facilitating release of progeny virions. Antibody responses to these two proteins form the basis for the division of influenza A viruses into their antigenic subtypes. So far 16 HA and 9 NA subtypes have been detected in birds and mammals worldwide and these occur in a number of different combinations. Only two types of AI viruses, H5 and H7, are known to include highly pathogenic viruses. However, not all H5 and H7 influenza viruses are highly pathogenic.
Wild waterfowl are considered the natural reservoir of all influenza A viruses whereas relatively few subtypes have been recorded from mammals. Wild waterfowl have probably carried influenza viruses, with no apparent harm, for centuries. They are known to carry viruses of the H5 and H7 subtypes, but usually in the low pathogenic form. On present understanding, H5 and H7 viruses may be introduced to poultry flocks in their low pathogenic form (LPAI) by wild birds. When allowed to circulate in poultry populations, the viruses can mutate, usually within a few months, into the highly pathogenic form (HPAI) which may in turn be transported by migrating birds over large distances. LPAI strains commonly cause only mild symptoms (ruffled feathers, a drop in egg production) and may easily go undetected. HPAI strains may spread rapidly through poultry flocks, causing disease affecting multiple internal organs, and may cause mortality that can approach 100% often within 48 hours. This is why the presence of an H5 or H7 virus in poultry is always cause for concern, even when the initial signs of infection are mild.
The incubation period is the time between infection and the appearance of signs of disease. "Shedding," as it applies to viruses, means that the animal's secretions and/or droppings contain viral particles that may infect other animals or people. Some birds (e.g., growing poultry) rapidly show clinical signs of disease and simultaneously shed virus. Other infected birds, including some species of waterfowl, may appear clinically healthy whilst shedding the virus. The incubation and shedding periods for AI virus in many species are not known.
Avian influenza viruses are sensitive to most detergents and disinfectants, heating and desiccation will inactivate them. However, AI viruses may persist in soil, faeces and pond water for varying amounts of time, depending on environmental conditions. The ability of AI viruses to survive in the environment depends on temperature and humidity. According to a 1998 study, the stability of the Hong Kong H5N1 (HPAI) virus in wet faeces in the environment was more than 40 days at 4°C. The virus becomes less stable as the temperature increases and at 25°C the virus was stable for 8 days and at 35°C the virus was stable for only 2 days. The same study reported that H5N1 HPAI virus in dry faeces at 25°C was stable for only 1 day.
The current outbreaks of H5N1 HPAI, which began in South-East Asia in 2003, are the largest and most severe on record. Never before in the history of this disease have so many countries been simultaneously affected, resulting in the loss of so many birds. Despite the death or destruction of over many millions of birds, the virus is now considered endemic in many parts of Indonesia, Viet Nam, Cambodia, China and Thailand. During 2008 outbreaks of H5N1 HPAI have occurred in 27 countries throughout Asia, Africa, Europe and the Middle East and control of the disease in poultry is expected to take many years. The H5N1 virus is also of particular concern for public health and human cases of infection have been reported in Azerbaijan, Bangladesh, Cambodia, China, Djibouti, Egypt, Indonesia, Iraq, Lao People's Democratic Republic, Myanmar, Nigeria, Pakistan, Thailand, Turkey, and Vietnam.
No. Of the very few avian influenza viruses that have infected humans, the current H5N1 strain of avian influenza virus is the most pathogenic and has caused more than 240 human deaths in central and Southeast Asia, the Middle East, and Africa. This is a small number compared with the huge number of birds affected and the numerous associated opportunities for human exposure, especially in areas where backyard flocks are common. It is not presently understood why some people, and not others, become infected following similar exposures. Unlike normal seasonal influenza, where infection causes only mild respiratory symptoms in most people, the disease caused by H5N1 follows an unusually aggressive clinical course, with rapid deterioration and high fatality. Primary viral pneumonia and multi-organ failure are common.
Direct contact with infected poultry, or surfaces and objects contaminated by their faeces, is presently considered the main route of human infection by the avian H5N1 virus. To date, most human cases have occurred in rural or urban fringe areas where many households keep small poultry flocks, which often roam freely, sometimes entering homes or sharing outdoor areas where children play. As infected birds shed large quantities of virus in their faeces, opportunities for exposure to infected droppings or to environments contaminated by the virus are abundant under such conditions. Moreover, because many households in Asia depend on poultry for income and food, many families sell or slaughter and consume birds when signs of illness appear in a flock, rather than disposing of the birds safely, and this practice has proved difficult to change. Exposure is considered most likely during slaughter, defeathering, butchering, and preparation of poultry for cooking. There is no evidence that properly cooked poultry or eggs can be a source of infection.
The H5N1 virus that has caused human illness and death in Asia is resistant to amantadine and rimantadine, two antiviral medications commonly used for influenza. Limited evidence suggests that some antiviral drugs, notably oseltamivir (commercially known as Tamiflu), can reduce the duration of viral replication and improve prospects of survival, provided they are administered within 48 hours following symptom onset. However, prior to the recent outbreak of H5N1 HPAI in Turkey, most patients have been detected and treated late in the course of illness. For this reason, clinical data on the effectiveness of oseltamivir are limited. In suspected cases, ideally oseltamivir should be prescribed as soon as possible to maximize its therapeutic benefits. However, given the significant mortality currently associated with H5N1 infection and evidence of prolonged viral replication in this disease, administration of the drug should also be considered in patients presenting later in the course of illness. The recommended dose of oseltamivir for the treatment of influenza, in adults and adolescents 13 years of age and older, is 150 mg per day, given as 75 mg twice a day for five days. Oseltamivir is not indicated for the treatment of children younger than one year of age. In cases of severe infection with the H5N1 virus, an increase to the daily recommended dose or the duration of treatment should be considered although doses above 300 mg per day are associated with increased side effects. Due consideration should be given to patients who are severely ill with H5N1 infection and especially those with gastro intestinal symptoms as drug absorption may be impaired.
The OIE has a list of international reference experts
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