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H1N1 in Swine in Iceland Raises Pandemic Concerns
Recombinomics Commentary 21:17
October 29, 2009

Clinical signs commenced on 24 Oct 2009 with 10 sows off feed, temperature greater than 40 C, some were coughing, and 2 aborted. Two workers had had flu-like symptoms for a few days prior to the clinical signs in the pigs.

The above comments are from an OIE report on an H1N1 outbreak at a farm in Iceland.  As was reported in prior outbreaks in swine in Canada, Argentina, Australia, UK, Ireland, Norway, Japan, Indonesia, and the United States, the swine infection was thought to be linked to infected workers.  However, the detection of H1N1 swine in Iceland suggests that such infections worldwide are much higher than reported.

In the US, only one such outbreak has been reported.  H1N1 was found in swine at a Minnesota Fair, so the number of reported outbreaks on farms remains at zero, even though the United States has reported the highest number of human cases, and outbreaks in swine producing states had been widespread and growing dramatically since the start of the new school year.

Although the USDA has chided reporters for calling swine flu swine flu, and assuring the public that the swine food supply is safe, they have provided no reports on the detection of H1N1 in swine, and unlike the above countries, have failed to file OIE reports.  Reports by others have described a relative mild condition in swine, which rapidly spreads through herds and is eventually controlled through extensive culling.  The failure to detect H1N1 in swine raises concerns that surveillance is minimal, which was clear in the spring when the human H1N1 sequences were released.

Those sequences clearly demonstrated that the H1N1 originated in swine.  In addition to the 5 swine flu genes, there were two avian genes (PB2 and PA) and one human gene (PB1).  The PB1 gene was introduced into swine in 1993, along with human H3 and N2.  Subsequent H1N1 isolates swapped out the human H3 and N2 for swine H1 and N1 or human H1 and N1.  Those with swine H1N1 subsequently acquired the avian PA and PB2 in the late 90's.  These triple reassortants have been circulating in swine for over a decade. 

However, the triple reassortants isolated from humans had evolved away from most of the sequences in American swine, reflecting the poor surveillance and limited sequence database for swine H1N1 in North America.  The absence of reports of H1N1 in swine on farms in the US reflects a continuing poor surveillance of swine in the US, which provides little support for assurances that the H1N1 is not in the US swine food supply.

The same concerns exist for turkeys.  H1N1 has been reported in turkeys in Chile and Canada, but there have not been reports of H1N1 in turkeys in the US, even though human cases have been high in turkey raising states.  These surveillance failures also raise concerns about H1N1 in US turkeys.

Although the vast majority of human cases of swine flu come from humans, the lack of surveillance in two well described hosts, swine and turkeys, raises concerns of silent evolution and transmission in the hosts.

A more robust surveillance system, especially in US swine, is long overdue.

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