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Commentary
Abysmal Maine
trH3N2 Testing Raises Concerns
Recombinomics Commentary 13:00
November 21, 2011
Sears said there is no thought at this point that the virus is spreading from person to person and there were no reports of flu among members of either child's family.
The above comments are from a media report widely distributed in Canada, as well as ProMED which distributed the report worldwide. Although the two cases in Maine had swine “exposures”, there is little data to support the role of these exposures in the infection of these two cases. However, the exposure did lead to sophisticated testing leading to the identification of trH3N2, including the second case which was represent by a sample with a low level of RNA and produced a profile consistent with seasonal H3N2. The swine exposure led to sequencing by the CDC which confirmed trH3N2.
The USDA has released sequences from the first swine isolate, A/swine/NY/A01104005/2011, identified with the novel, trH3N2 found in all seven of the human cases. This isolate matched the human cases in all eight gene segments to produce an unambiguous match. However, this isolate was from a September 13 sample, confirming a failure of the USDA to find this novel virus in swine prior to the spread in humans in July and August, as seen in the isolates from Indiana and Pennsylvania.
In contrast to the enhanced screening of swine by the USDA and associated academic institutions, the test of human cases has been abysmal. In Maine only two positives have been reported for the 2011/2012 season, which were the two trH3N2 cases (A/Maine/06/2011 and A/Maine/07/2011). Similarly, Indiana has reported 3 influenza cases since the summer of 2011 and two of the three (A/Indiana/08/2011 and A/Indiana/10/2011) were trH3N2 cases. Pennsylvania has not filed a weekly report for the entire 2011/2012, but the CDC has released sequences from 5 influenza A cases, and three (A/Pennsylvania/09/2011, A/Pennsylvania/10/2011, A/Pennsylvania/11/2011) were trH3N2 cases. Thus, in spite of the identification of 7 cases in these three states, the human testing has been minimal, which is due in part to statements such as those cited above, as well as a Maine CDC advisory claiming all prior 2011 trH3N2 cases had a swine exposure, or the CDC early release MMWR, which requested samples from patients with a swine exposure.
Although the two cases in Maine had extensive swine exposures, there is little evidence that these exposures are the cause of the infections. Both cases attended the Fryeburg fair, where symptomatic swine were identified, and the second case also participated in a pig scramble at the fair and had swine exposures after the fair. However, the symptomatic swine tested negative for SOIVs, and the swine exposure after the fair for the second cases were asymptomatic. Moreover, the time gap between the end of the fair on October 9, and the initial symptoms on October 22, eliminated the swine exposures at the fair as a cause of the infection in the second case.
However, the CDC put out two November 4 reports on the second case to create the illusion that there was an exposure to sick pigs in the week prior to symptoms for the second case. One report was written for health professionals, which noted exposure to “live” pigs in the week prior to symptoms (because the pis were asymptomatic), and the report for the news media cited exposure to “sick” pigs, but failed to include the time frame because the “sick” pigs were at the fair, which ended two weeks prior to disease onset.
Thus, the Maine cases, like the here cases in Pennsylvania and the two cases in Indiana have failed to link the cases to symptomatic swine, other than the first case in Maine, although these symptomatic swine tested negative for SOIVs.
Thus, the above comments on swine exposure limit testing on cases without swine exposure, leading to a rate of trH3N2 in human cases in Maine of 100%.
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