Re: Ecologic Immunology of Avian Influenza (H5N1) in Migratory Birds
Yes, they don't say it, but others do (for example Gauthier-Clerc et al.). The precise pattern of spread places an evidentiary burden on people claiming that migrants are the vectors (especially if this precise pattern does not match any known migratory pattern). A match of the broad pattern is not good enough.
And of course it is possible that it is x% migrants and 100-x% trade. I think it would be constructive to return from time to time to the issues raised by the Weber-Stilianakis-paper (ands as niman has admitted of not having read it I will completely ignore his comments). It is still largely unknown how heavy exercise and infections interact in migrants. Current knowledge makes it worthwhile to consider the hypothesis that heavy exercise and infection with HPAI don't go together very well...
I just think that there so many doubts that the role of migrants should still be treated as an open question.
The problems with most of these "papers" really stems from the fact that the authors have no background in infectious disease. Most have some affiliation with bird watchers or wetlands groups and they view H5N1 from the point of view of the bird.
However, H5N1 is not linked to an individual bird, individual species, or individual pathway. In fact the nature reserves offer an opportunity for the H5N1 to hitch a ride on multiple species and move from one flyway to another.
That is why these conversations are such a waste of time. Those with these religious convictions create straw men, such as the demand that an individual species or flyway explain all of the data. It is not reality based.
The facts on the Qinghai strain are quite simple. It was first identified in May, 2005 at Qinghai Lake. At that time it was possible to argue that the strain would burn itself out at Qinghai Lake. Sequence data said otherwise, but those who couldn't read a sequence could use the dead birds don't fly argument.
However, by the summer of 2005, that argument was not viable. Prior to Qinghai Lake, the Asian version of H5N1 had never been reported in wild birds or poultry west of China. Russia, Kazakhstan, and Mongolia all reported H5N1 for the first time ever in the summer of 2005, and all involved the Qinghai strain. H5N1 was isolated and sequenced, including H5N1 from a healthy crested grebe, and the story was over.
The presence of Qinghai H5N1 in Siberia predicted movement into Europe, the Middle East, and Africa because of overlapping flyways. Those predictions were confirmed in 2005 with Qinghai H5N1 isolations in all three regions. Many more countries (over 50 in total) reported H5N1 in early 2006 and again ALL were the Qinghai strain, which was found primarily in wild birds, especially in Europe, but was also in a small number of poultry outbreaks in Europe, as well as human cases in Turkey, Iraq, Azerbaijan, Egypt, and Djibouti. Although the sequences signaled independent introductions of various sub-clades, ALL were Qinghai.
Moreover, the evidence against smuggling or trade was also OVERWHELMING. Although poor biosecurity will lead to local spread, the spread into these new areas was almost exclusively via wild birds. The only credible example of H5N1 movement over long distances via poor biosecurity was the H5N1 in Hungary and the UK this year. Although wild birds could have been involved in the spread, the linkage of both location to the same company and the close similarity (99.96%) between isolates from the two sites suggests the H5N1 may have been trucked from Hungary to the UK by a turkey distibutor. However, the 99.96% match identified what kind of of matches would be expected in farm to farm or farm to wild bird transmissions, and such matches was not evident in the multiple introductions.
The country with the largest number of positive wild birds in 2006 and again in 2007 was Germany. In 2006 there were three distinct introductions. One was in northern Germany, where there were ZERO reported outbreaks on farms. The northern Germany sequences matched southern Denmark, where there were also no reported outbreaks on farms. A second subclade was in southern Germany where there were no reported outbreaks in poultry. These sequences matched Switzerland isolates, where there were no reported outbreaks on farms. A third subclade was in southern German and matched sequences that had a wider distribution (Italy, the Czech Republic, and Ukraine).
Although the outbreaks were regionally distinguishable by sequence, the H5N1 was not limited to a given species. The same sequences in northern Germany that were in MANY wild bird species were also found in a cat and a stone martin. Similarly, sequences from Austria that matched a healthy teal in Egypt in 2005 were found in a goose and cat in Austria.
Thus, H5N1 moves from flyway to flyway and from species to species and attempts to pin H5N1 down to a given species or flyways are at best uniformed.
These facts are quite public and fully supported by public sequences and peer reviewed journal articles, bird watcher fairy tales not withstanding.
The sequence analysis also discredits reports of trade and smuggling. In 2004 H5N1 was smuggled into Belgium. The H5N1 was clade 1 out of Thailand. The number of clade 1 infections reported in poultry or wild birds in Europe is ZERO. The number in the Middle East is ZERO. The number in Africa is ZERO. The number anywhere other than southeast Asia is ZERO. The same is true for H5N1 found in quarantined exotic birds from Taiwan. The H5N1 was the Fujian strain (clade 2.3). The birds died in quarantine in the UK in early 2006. The number of Fujian isolates from farms or wild birds in Europe is ZERO. The number in the Middle East is ZERO. The number in Africa is ZERO. In fact the number outside of eastern China and southeast Asia is ZERO.
ALL of the reported infections in wild birds (dozens of species), domestic poultry, people, and various mammals such as cats, stone martins, dogs, foxes have been Qinghai (clade 2.2).
The DATA could not be clearer.
