You know what we’re not getting from the mainstream media coverage of the H1N1 flu? Insights like this one from ProMed:
I have been following the ProMed “swine flu” updates and noticed an interesting omission. I am a virologist who works on RNA viruses
(including flu), and I feel that the reports are “viro-centric,” i.e., heavily biased towards blaming everything on influenza and not enough speculation about co-infections. I certainly agree that there should be more funding for basic respiratory disease research and am pleased that President Obama asked for an additional USD 1.5 billion to help out, but I do not think spending it all on influenza vaccine trials is wise.Three observations make it highly likely that the “flu” fatalities are due to bacterial co-infections. First, a study from Baylor (Ramilio et al, Blood, 2007) profiling humans with flu symptoms found that greater than 30 percent of the fatalities were in people with bacterial-influenza co-infections. Knowing the inadequacy of the diagnostics, I would assume the number of co-infections is much higher than 30 percent, possibly even 90 percent in fatalities.
Second, the index case in Mexico was a small boy who got severely sick, but his doctor gave him an antibiotic (usually for bacterial infections) and he survived. The fact that he got better two days after an antibiotic may indicate that he had a bacterial infection in addition to a flu infection.
Third, one of the earliest Mexican deaths was a diabetic woman in her 40s. A lung biopsy contained influenza. Several people around her had respiratory diseases, but none of them were positive for influenza! This means that it was possible she too had both flu and bacterial infections that led to her death.
It is well known that flu infections make it easier to maintain respiratory bacterial infections and vice versa. To safeguard against flu-related deaths, doctors should prescribe more antibiotics. However, since the cost of antibiotics is high and since over-prescribing antibiotics is dangerous, diagnostics that
discriminate between viral and bacterial infections should be used.For example, there is already an FDA-approved pregnancy-test-type device [produced by Rapid Pathogen Screening (RPS) Inc.] that determines whether teardrops from a person with conjunctivitis arise from bacterial or viral infection (it uses antibodies to MxA and C-reactive proteins, which are early host responses to either viral or bacterial infections). I have no personal interest in that company, but I have strong interests in exploiting the host’s responses to disease in detection.
It is not surprising to me that molecular biologists are now finding changes in circulating H3N2 viruses as well as H1N1. The currently available diagnostics are poor, and much of what was blamed on H1N1 could have been H3N2 or another virus or bacteria or a co-infection. Much more funding should go to developing host-response diagnostics, since there are about 100 known host proteins that can discriminate acute bacterial from acute viral infections. Expression of those proteins in the plasma should allow first responders to discriminate the serious cases from the light ones.
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Communicated by:
Maria Salvato, PhD
Professor, Institute of Human Virology
University of Maryland School of Medicine
Baltimore, Md.







