![]() In the wake of its worldwide spread, the number of deaths was unprecedented. ![]() Undoubtedly, the 1918–19 pandemic strain of influenza had unique pathophysiologic effects. However, healthcare providers, medical experts, and published data from the 1918 period suggest that most deaths were caused by secondary bacterial pneumonias ( 5 – 12) hemorrhagic pneumonitis that rapidly progressed to death was considered an alarming but uncommon clinical manifestation ( 8, 11– 13). Not surprisingly, plans and resources to respond to the next influenza pandemic focus almost exclusively on the virus, i.e., preventive vaccines and antiviral treatment of infections with a novel influenza strain ( 4). Many influenza experts, policy makers, and knowledgeable observers believe that a novel influenza A (H1N1) strain directly caused most deaths during the 1918–19 pandemic, often from a hemorrhagic pneumonitis that rapidly progressed to acute respiratory distress syndrome and death ( 1 – 3). ![]() This hypothesis suggests opportunities for prevention and treatment during the next pandemic (e.g., with bacterial vaccines and antimicrobial drugs), particularly if a pandemic strain–specific vaccine is unavailable or inaccessible to isolated, crowded, or medically underserved populations. This sequential-infection hypothesis is consistent with characteristics of the 1918–19 pandemic, contemporaneous expert opinion, and current knowledge regarding the pathophysiologic effects of influenza viruses and their interactions with respiratory bacteria. ![]() However, we hypothesize that infections with the pandemic strain generally caused self-limited (rarely fatal) illnesses that enabled colonizing strains of bacteria to produce highly lethal pneumonias. ![]() Hence, preparations for the next pandemic focus almost exclusively on vaccine prevention and antiviral treatment for infections with a novel influenza strain. Deaths during the 1918–19 influenza pandemic have been attributed to a hypervirulent influenza strain. ![]()
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