Turkey: the possibilities
Turkey continues to worry health authorities, although they are trying to put the best face on it they can. But it remains a scary face. Despite official declarations that "nothing has changed" in the virus, the four official, and ten unofficial WHO cases is a large number to have appeared in such a short space of time. In addition, dozens of others are under observation in various hospitals for symptoms compatible with avian influenza in widely scattered locations in eastern, central and northern Turkey (The Globe and Mail)
What are the possibilities?
First possibility, this is no different than other human cases in southeast asia and China, because all the victims had heavy exposures to infected poultry. But a history of heavy exposure is not known with certainty in all of the cases and I consider the proposition doubtful.
Second possibility, with exposure more widespread than previous years, we are seeing the usual seasonal pattern of influenza A, which peaks in the wintertime as temperatures plunge. The reason for the seasonality is elusive and many explanations have been given. The US is currently experiencing a typical upsurge of seasonal flu (not human bird flu), and the Turkish cases could be simply the avian version's counterpart in Turkey. This explanation is given additional credence by a paper published today in the Archives of Internal Medicine by Anna Thorson and colleagues at Stockholm's Karolinska Institute. Their symptom prevalence survey of over 45,000 Vietnamese revealed a substantial risk of Influenza Like Illness (ILI) in people living in households where poultry became sick and died or were slaughtered when they became ill. The population lived in a region with documented H5N1 poultry infection. Based on these data Thorson et al. estimated between 650 and 750 people with poultry-associated ILI in the study period of April to June 2004. ILI might have been even higher in the winter months preceding the study period. This finding lends weight to the seasonal explanation of the Turkish cases.
Third possibility, the virus may have changed in ways to make transmission from birds to humans easier. This would indicate an intermediate stage in full adaptation to humans, perhaps with a virus that has predilections for both human and avian receptors (see previous post). This would be a very worrisome development suggesting transition to pandemic potential was imminent.
Fourth possibility, and worst of the them, is that the virus has attained a limited capability of person to person transmission. The evidence either for or against this is slim at the moment, but clearly any of the previous explanations makes this transition more likely by varying amounts.
We have been saying here for a year or more that we believed there were many mild or inapparent infections with H5N1, something given greater weight (but not proved) by Thorson's paper. If true (and we strongly believe it is), this means the virus has considerably less case fatality than the official 50%, which includes only the most seriously ill. How much less is difficult to say, but I would not be surprised if it were below 10% or even 5%. This is only small consolation, however, because the great Spanish Flu of 1918 had an estimated mortality of only 2% - 3%.
The next (and long overdue) step is a seroprevalence survey in poultry-infected areas to see the prevalence of antibodies to H5N1 in the population.
What are the possibilities?
First possibility, this is no different than other human cases in southeast asia and China, because all the victims had heavy exposures to infected poultry. But a history of heavy exposure is not known with certainty in all of the cases and I consider the proposition doubtful.
Second possibility, with exposure more widespread than previous years, we are seeing the usual seasonal pattern of influenza A, which peaks in the wintertime as temperatures plunge. The reason for the seasonality is elusive and many explanations have been given. The US is currently experiencing a typical upsurge of seasonal flu (not human bird flu), and the Turkish cases could be simply the avian version's counterpart in Turkey. This explanation is given additional credence by a paper published today in the Archives of Internal Medicine by Anna Thorson and colleagues at Stockholm's Karolinska Institute. Their symptom prevalence survey of over 45,000 Vietnamese revealed a substantial risk of Influenza Like Illness (ILI) in people living in households where poultry became sick and died or were slaughtered when they became ill. The population lived in a region with documented H5N1 poultry infection. Based on these data Thorson et al. estimated between 650 and 750 people with poultry-associated ILI in the study period of April to June 2004. ILI might have been even higher in the winter months preceding the study period. This finding lends weight to the seasonal explanation of the Turkish cases.
Third possibility, the virus may have changed in ways to make transmission from birds to humans easier. This would indicate an intermediate stage in full adaptation to humans, perhaps with a virus that has predilections for both human and avian receptors (see previous post). This would be a very worrisome development suggesting transition to pandemic potential was imminent.
Fourth possibility, and worst of the them, is that the virus has attained a limited capability of person to person transmission. The evidence either for or against this is slim at the moment, but clearly any of the previous explanations makes this transition more likely by varying amounts.
We have been saying here for a year or more that we believed there were many mild or inapparent infections with H5N1, something given greater weight (but not proved) by Thorson's paper. If true (and we strongly believe it is), this means the virus has considerably less case fatality than the official 50%, which includes only the most seriously ill. How much less is difficult to say, but I would not be surprised if it were below 10% or even 5%. This is only small consolation, however, because the great Spanish Flu of 1918 had an estimated mortality of only 2% - 3%.
The next (and long overdue) step is a seroprevalence survey in poultry-infected areas to see the prevalence of antibodies to H5N1 in the population.
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