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Influenza infection can enhance the ability of the bacterium Streptococcus pneumoniae to cause ear and throat infections, according to research published ahead of print in the journal Infection and Immunity. In the study, the investigators infected mice with either influenza alone, pneumococci alone, or both at once, and then monitored the populations of bacteria and virus over time. They also monitored the mice for development of middle ear infection. Influenza infection enhanced the bacterium's ability to colonize the nasopharynx, and to infect the normally sterile middle ear.
"We learned that once influenza virus is introduced, all of the "rules" regarding phase variants are out the window," says corresponding author W. Edward Swords of Wake Forest University in Winston-Salem, N.C. Phase variation refers to the fact that the colonizing bacteria have transparent cell surfaces, while those that spread within the host have opaque surfaces.
"However, in the presence of influenza, opaque variants can readily colonize the nasopharynx, and transparent variants can persist in the ear," says Swords. "This indicates that the host environs are more permissive for infection by the entire bacterial population."
Furthermore, recent research had shown that influenza interferes with innate immunity in a way that enables pneumococci to flourish. In this research, Swords shows that that interference manifests as increased inflammatory responses at the mucosal surface in the influenza-infected mice, such as within the middle ear, and in the nasopharynx.
"As with most pneumococcal infections, it should be appreciated that localized nonlethal infections are much more common than the rapidly lethal presentations," says Swords. "For example, influenza is a contributing factor in otitis media in children."
"If we can understand why and how viral infection causes bacteria to colonize privileged sites like the middle ear, we will better know what aspects of disease to focus on with preventive or therapeutic treatments," says Swords.
The final version of the article is scheduled for the November 2014 issue of Infection and Immunity.
Source: American Society for Microbiology (ASM)