A similar overkill response has been seen in deaths from the ongoing avian flu outbreak that began in Asia. Capable of jumping the species barrier, the H5N1 virus has infected 385 people, killing 243 of them, and scientists fear that it could mutate easily from human to human instead of bird to human.
The two new studies suggest the 1918 virus did induce severe immune reactions, particularly among young adults. But what made the reaction so deadly was that it destroyed the lining of the respiratory system, making it easier for bacteria to infect the lungs.
In most infected populations, Brundage and Shanks found less than 5% of flu deaths occurred within three days of the illness' onset. The median time from the onset of symptoms until death was 7 to 10 days. A significant number died two weeks after their initial symptoms, which is typical of bacterial pneumonia.
Michael Katze, a University of Washington virologist who was a lead scientist in the mice and monkey experiments, said the animals' violent and rapid immune response made it "almost unreasonable" to expect victims of the 1918 virus to live long enough to develop secondary infections.
But he acknowledged the flu pandemic deaths could have been the result of a polymicrobial infection -- a co-infection by multiple microbes.
"Certainly the idea that resident bacteria flora already present could play a role in developing pneumonia is relatively reasonable," he said. "If the 1918 flu had any impact that compromised [immune] function, it could render a normal resident bacteria pathological."
So far, public health officials around the world have focused on stockpiling vast quantities of vaccines and antiviral drugs to combat future pandemic flu strains.
Fauci said scientists also needed to develop new antibiotics as well as vaccines against bacteria, especially against a virulent strain of Staphylococcus aureus that has been linked to seasonal flu deaths and is resistant to many antibiotics.
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mary.engel@latimes.com
