Interactions between influenza and bacterial respiratory pathogens: implications for pandemic preparedness

Abstract

It is commonly believed that the clinical and epidemiological characteristics of the next influenza pandemic will mimic those of the 1918 pandemic. Determinative beliefs regarding the 1918 pandemic include that infections were expressed as primary viral pneumonias and/or acute respiratory distress syndrome, that pandemic-related deaths were the end states of the natural progression of disease caused by the pandemic strain, and that bacterial superinfections caused relatively fewer deaths in 1918 than in subsequent pandemics. In turn, response plans are focused on developing and/or increasing inventories of a strain-specific vaccine, antivirals, intensive care beds, mechanical ventilators, and so on. Yet, there is strong and consistent evidence of epidemiologically and clinically important interactions between influenza and secondary bacterial respiratory pathogens, including during the 1918 pandemic. Countermeasures (eg, vaccination against pneumococcal and meningococcal disease before a pandemic; mass uses of antibiotic(s) with broad spectrums of activity against common bacterial respiratory pathogens during local epidemics) designed to prevent or mitigate the effects of influenza-bacterial interactions should be major focuses of pandemic-related research, prevention, and response planning.

The frequency of influenza and bacterial coinfection: a systematic review and meta‐analysis

“…Consistent with the prior literature,55, 62 we found that S. pneumoniae was the most frequent bacterial coinfection; however, both S. aureus and other bacterial coinfections were also quite common. This diverse profile of coinfecting pathogens confirms current Infectious Disease Society of America (IDSA) recommendations for broad‐spectrum antibiotic coverage for influenza‐related pneumonia 63.…”

Influenza Infection Leads to Increased Susceptibility to Subsequent Bacterial Superinfection by Impairing NK Cell Responses in the Lung

“…Earlier reports suggest that influenza virus can cause epithelial damage and/or surface receptor changes, which may increase bacterial colonization (17,18). In contrast, altered tneutrophil functions and excessive production of immunosuppressive IL-10 have been implicated in flu infection-increased susceptibility to secondary streptococcal infection in the lung (19)(20)(21)(22). Recently, IFN-g-mediated macrophage functional depression (23) or macrophage desensitization to bacterial ligand-triggered TLR signaling (20) was also found to play a role in this process.…”

Temporal cross‐correlation between influenza‐like illnesses and invasive pneumococcal disease in The Netherlands

“…Histopathological studies in deceased and severe human influenza cases during a pandemic outbreak14, 15, 16 attribute a substantial fraction of influenza deaths to secondary pneumococcal infection. The strength of the interaction between influenza or influenza‐like illness (ILI) and IPD at population level, however, varies across studies from non‐existent to significant 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27.…”