Influenza infection attracts pneumonia bacteria

SALT LAKE CITY – May 22, 2002 -- Lung cells infected with the influenza A virus are more likely to bind with bacteria that cause pneumonia than uninfected cells, but this phenomenon can be reversed with antiviral treatment. Researchers from the University of Kansas Medical Center present their findings today at the 102nd General Meeting of the American Society for Microbiology. “Bacterial pneumonia caused by Streptococcus pneumoniae can occur secondary to viral infections such as influenza. Previous studies have shown that by treating the influenza virus with Tamiflu, a neuraminidase inhibitor that attacks the influenza virus at the cellular level, secondary complications such as pneumonia can be reduced,” says Dr. Rebecca Horvat, one of the researchers on the study.

Dr. Horvat and her colleagues examined the relationship between the binding of S. pneumoniae bacteria to a lung epithelial cell line (the cells that line the respiratory system) with and without influenza A infection. Preliminary studies showed that after 24, 48 or 72 hours of viral infection, the bacteria bound to the influenza-infected cells 4 to 10 times higher than uninfected cells. When the flu virus was treated with Tamiflu, the increased binding was reversed.

“An influenza-infected lung epithelial cell will bind more S. pneumoniae bacteria than uninfected cells. Treatment with Tamiflu at doses used to treat influenza infections can prevent this increased bacterial binding, and perhaps prevent post-influenza complications, such as pneumonia,” says Dr. Horvat.

S. pneumoniae continues to be the leading cause of community-acquired pneumonia worldwide. Although the ability of bacteria to bind to host cells is the first step in the process of infection, few studies have correlated S. pneumoniae cell binding with the severity of lower respiratory tract infections. Dr. Horvat notes that this study has implications only for influenza A infections and additional research must be done on influenza B infection.

The study was funded by F. Hoffmann-La Roche.

This release is a summary of a presentation from the 102nd General Meeting of the American Society for Microbiology, May 19-23, 2002, in Salt Lake City, Utah. Additional information on these and other presentations at the 102nd ASM General Meeting can be found online at http://www.asmusa.org/pcsrc/gm2002/presskit.htm or by contacting Jim Sliwa (jsliwa@asmusa.org) in the ASM Office of Communications. The phone number for the General Meeting Press Room is (801) 534-4720 and will be active from 10:00 a.m. MDT, May 19 until 12:00 noon MDT, May 23.

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