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      Deaths from Bacterial Pneumonia during 1918–19 Influenza Pandemic

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          Abstract

          A sequential-infection hypothesis is consistent with characteristics of this pandemic.

          Abstract

          Deaths during the 1918–19 influenza pandemic have been attributed to a hypervirulent influenza strain. Hence, preparations for the next pandemic focus almost exclusively on vaccine prevention and antiviral treatment for infections with a novel influenza strain. 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. 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. 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.

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          Transmissibility of 1918 pandemic influenza

          Christina E Mills, James M. Robins, Marc Lipsitch (2004)
          The 1918 influenza pandemic killed 20–40 million people worldwide 1 , and is seen as a worst-case scenario for pandemic planning. Like other pandemic influenza strains, the 1918 A/H1N1 strain spread extremely rapidly. A measure of transmissibility and of the stringency of control measures required to stop an epidemic is the reproductive number, which is the number of secondary cases produced by each primary case 2 . Here we obtained an estimate of the reproductive number for 1918 influenza by fitting a deterministic SEIR (susceptible-exposed-infectious-recovered) model to pneumonia and influenza death epidemic curves from 45 US cities: the median value is less than three. The estimated proportion of the population with A/H1N1 immunity before September 1918 implies a median basic reproductive number of less than four. These results strongly suggest that the reproductive number for 1918 pandemic influenza is not large relative to many other infectious diseases 2 . In theory, a similar novel influenza subtype could be controlled. But because influenza is frequently transmitted before a specific diagnosis is possible and there is a dearth of global antiviral and vaccine stores, aggressive transmission reducing measures will probably be required. Supplementary information The online version of this article (doi:10.1038/nature03063) contains supplementary material, which is available to authorized users.
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            Insights into the interaction between influenza virus and pneumococcus.

            Jonathan A. McCullers (2006)
            Bacterial infections following influenza are an important cause of morbidity and mortality worldwide. Based on the historical importance of pneumonia as a cause of death during pandemic influenza, the increasingly likely possibility that highly pathogenic avian influenza viruses will trigger the next worldwide pandemic underscores the need to understand the multiple mechanisms underlying the interaction between influenza virus and bacterial pathogens such as Streptococcus pneumoniae. There is ample evidence to support the historical view that influenza virus alters the lungs in a way that predisposes to adherence, invasion, and induction of disease by pneumococcus. Access to receptors is a key factor and may be facilitated by the virus through epithelial damage, by exposure or up-regulation of receptors, or by provoking the epithelial regeneration response to cytotoxic damage. More recent data indicate that alteration of the immune response by diminishing the ability of the host to clear pneumococcus or by amplification of the inflammatory cascade is another key factor. Identification and exploration of the underlying mechanisms responsible for this synergism will provide targets for prevention and treatment using drugs and vaccines.
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              Influenza virus neuraminidase contributes to secondary bacterial pneumonia.

              V Peltola, K Murti, Jonathan A. McCullers (2005)
              Secondary bacterial pneumonia is a common cause of death during influenza epidemics. We hypothesized that virus-specific factors could contribute to differences in annual excess mortality. Recombinant influenza viruses with neuraminidases from representative strains from the past 50 years were created and characterized. The specific level of their neuraminidase activity correlated with their ability to support secondary bacterial pneumonia. Recombinant viruses with neuraminidases from 1957 and 1997 influenza strains had the highest level of activity, whereas a virus with the neuraminidase from a 1968 strain had the lowest level of activity. The high level of activity of the neuraminidase from the 1957 strain, compared with that of other neuraminidases, more strongly supported the adherence of Streptococcus pneumoniae and the development of secondary bacterial pneumonia in a mouse model. These data lend support to our hypothesis that the influenza virus neuraminidase contributes to secondary bacterial pneumonia and subsequent excess mortality.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Emerg Infect Dis
                Journal ID (publisher-id): EID
                Title: Emerging Infectious Diseases
                Publisher: Centers for Disease Control and Prevention
                ISSN (Print): 1080-6040
                ISSN (Electronic): 1080-6059
                Publication date (Print): August 2008
                Volume: 14
                Issue: 8
                Pages: 1193-1199
                Affiliations
                [* ]Armed Forces Health Surveillance Center, Silver Spring, Maryland, USA
                [† ]Australian Army Malaria Institute, Enoggera, Queensland, Australia
                Author notes
                Address for correspondence: John F. Brundage, Armed Forces Health Surveillance Center, 2900 Linden Ln, Rm 216, Silver Spring, MD 20910, USA; email: john.brundage@ 123456na.amedd.army.mil
                Article
                Publisher ID: 07-1313
                DOI: 10.3201/eid1408.071313
                PMC ID: 2600384
                PubMed ID: 18680641
                SO-VID: 7cc9b008-3b37-402b-a4d5-6b5816da8c4b
                History
                Categories
                Subject: Historical Review

                ScienceOpen disciplines: Infectious disease & Microbiology
                Keywords: influenza,epidemiology,mass immunization,history,pandemic,historical review,infection control,bacterial pneumonia,public health practice,opportunistic infections
                Data availability:
                ScienceOpen disciplines: Infectious disease & Microbiology
                Keywords: influenza, epidemiology, mass immunization, history, pandemic, historical review, infection control, bacterial pneumonia, public health practice, opportunistic infections

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