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Contrary to what many might conclude because of its recent headline status, avian influenza is not a new disease. Fowl Plague was first described in Italy in 1878 and reported to be caused by a filterable virus in 1900. It was later determined in 1955 that Fowl Plague was actually one of the group of avian influenza (AI) viruses, commonly called “bird flu.”
This group of viruses has migratory waterfowl, seabirds, and shorebirds as their natural hosts and usually does not cause them severe disease. This almost perfect host-parasite relationship, where the highly mobile hosts are not significantly impaired, greatly facilitates the worldwide distribution of the AI viruses. It is when these viruses, which are present in the intestinal tract of the hosts, are shed in the feces to infect domestic poultry species such as chickens, turkeys, or quail that problems can result.
The genetic portion of the influenza viruses is an eight-piece, segmented genome. Each independent segment codes for the production of a protein which is part of the structure of the virus or for an enzyme necessary for the formation of the virus. Two very important surface structures are the hemagglutinin (H), which attaches the virus to the cell so that penetration may occur, and the Neuraminidase (N), which is important for cell penetration and for release of the newly formed virus from the infected cell. These two major structures are assigned numerical identifiers which differ from other Hs and Ns antigenically. There are known to be 15 Hs and 9 Ns that can be distinguished by a variety of tests using specific antibodies.
The AI viruses range widely in their ability to cause disease, all the way from infected birds showing no disease signs at all to flocks that experience essentially 100% mortality. The viruses that cause this high rate of death in poultry have been either H5 or H7 viruses. Not all of the AI viruses that possess these two Hs are killers; some cause no serious disease at all. However, AI viruses are prone to mutate, and many of the H5 and H7 viruses that are at first very mild (“low path”) change and become highly lethal (“high path”) AI viruses, especially when allowed to persist and circulate in poultry. In fact, such changes in pathogenicity with H5s and H7s have been so common on the world scene that the international animal disease regulatory body (OIE) is considering a plan to call for the eradication of all H5 or H7 infected flocks, even if they are not currently causing severe disease. In fact, the U.S. Dept. of Agriculture’s Animal and Plant Health Inspection Service is currently developing a United States surveillance/control program specifically directed at these two H serotypes in both commercial and backyard poultry, scheduled to be underway in 2005.
The greatest concern by influenza experts is that the segmented nature of the influenza genome may allow for the development of a “new” reassortant (exchanged gene segments) influenza virus that has the H5 lethality being seen in individuals in southeast Asia with the contagious character of the current H3 human strains of influenza. This would likely occur in a human co-infected with both viruses, but there is also the possibility of other animals such as pigs serving as mixing vessels. It should be noted that both the “1957 Asian influenza” and the “1968 Hong Kong flu” emerged from the same area of the world as new reassortant viruses and caused severe worldwide pandemics because none of us had antibodies against the H2 Asian and the H3 Hong Kong hemagglutinins. We also need to remember that the 1918 pandemic of H1 influenza is estimated to have killed 20–50 million people at a time when the world population was much less dense and not nearly so rapidly mobile as today.
Reports from Vietnam and Thailand indicate that of the 44 individuals known to be infected with the current H5N1 virus, about 70% have died of the disease. There is apparently only one possible case of human-to-human transmission so far, and that was from a sick daughter to her caretaker mother. Based on all the recent developments, however, there is epidemiological evidence that the disease was acquired by individuals coming in contact with infected live poultry, not by consuming poultry products. Additionally, in countries with slaughter inspection programs, there is very little chance of flocks infected with these rapidly lethal infections successfully making it to the processing plant and passing inspection. That may not be the situation in developing countries relying on backyard flocks and live poultry market slaughter systems.
While some antiviral medications may provide help in special situations like nursing homes, hopefully those charged with the heavy responsibility of determining which influenza H subtypes will be included in the human vaccine for the upcoming years will make the right decision on whether to include an H5. Only time will tell if they will be right or wrong. A recent report indicates that there will be at least some H5 human vaccine available by 2006 or 2007. With all the uncertainties associated with future H5 vaccine production, testing, and availability, it seems clear that the world’s regulatory officials need to intensify their efforts to make the needed changes in the way the live poultry markets operate so they will no longer serve as distribution centers for influenza viruses, to poultry or to people.
by Charles W. Beard, DVM, Ph.D., is Vice President for Research & Technology, U.S. Poultry & Egg Association, Tucker, GA 30084-7303, [email protected].