Impact of influenza and other community-acquired viruses

The incidence of community-acquired pneumonia peaks during the winter season each year. Increases in mortality from these pneumonias and influenza-like illnesses (P&I) above an "epidemic threshold" for 2 or more weeks generally signify increased numbers of influenza virus infections in the community, although peaks in P&I mortality typically lag a few weeks behind peaks in influenza virus activity. Most of the pneumonias cases found during influenza virus epidemics are due to secondary bacterial infections, with an increase in the frequency of Staphylococcus aureus over that seen in nonepidemic periods. One interaction between bacteria and influenza viruses that may increase disease severity by increasing growth of the virus is proteolytic cleaving of the hemagglutinin mediated directly or indirectly by bacterial products. Influenza virus infections also have many effects on the host that can enhance secondary bacterial infections; included are impairments of mucus clearance and T cell, polymorphonuclear cell and macrophage functions, as well as alterations in respiratory epithelium that can enhance adherence of bacteria. Recent studies indicate that the role of respiratory syncytial virus infections in causing acute pulmonary syndromes in elderly individuals, including secondary bacterial pneumonia, is essentially equivalent to that of influenza A viruses during years when there is not a severe influenza epidemic. Although other respiratory viruses can occasionally cause or facilitate the development of community-acquired pneumonia, currently available epidemiological data do not support significant roles for them relative to those of influenza and respiratory syncytial viruses.