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The 1918-21 influenza pandemic was the most lethal natural event in recent history. In the Pacific region, the pandemic's effects varied greatly across different populations and settings. In this region, the pandemic's lethal effects extended over 3 years, from November, 1918, in New Zealand to as late as July, 1921, in New Caledonia. Although a single virus strain probably affected all the islands, mortality varied from less than 0·1% in Tasmania, to 22% in Western Samoa. The varied expressions of the pandemic across the islands reflected the nature and timing of past influenza epidemics, degrees of social isolation, ethnicity and sex-related effects, and the likelihood of exposures to pathogenic respiratory bacteria during influenza illnesses. The high case-fatality rate associated with this pandemic seems unlikely to recur in future influenza pandemics; however, understanding the critical determinants of the mass mortality associated with the 1918-21 pandemic is essential to prepare for future pandemics., (Copyright © 2018 Elsevier Ltd. All rights reserved.)

During the 1918-1919 pandemic, influenza mortality widely varied across populations and locations. Records of U.S. military members in mobilization camps (n = 40), military academies, and officer training schools were examined to document differences in influenza experiences during the fall 1918. During the fall-winter 1918-1919, mortality percentages were higher among soldiers in U.S. Army mobilization camps (0.34-4.3%) than among officer trainees (0-1.0%). Susceptibility to infection and clinical expressions of 1918 pandemic influenza varied largely based on host epidemiological characteristics rather than the inherent virulence of the virus., (Reprint & Copyright © 2016 Association of Military Surgeons of the U.S.)

The reasons for the unprecedented mortality during the 1918 influenza pandemic remain poorly understood. We examined morbidity records from three military cohorts from years prior to and during the 1918 pandemic period to assess the effects of previous respiratory illnesses on experiences during the pandemic. Clinical registers and morbidity lists were examined to identify all medical encounters for acute respiratory illnesses in students at two U.S. military officer training academies and Australian soldiers deployed in Europe. Influenza-like illness prior to the major pandemic wave of 1918 predisposed Australian soldiers [relative risk (RR) 1·37, 95% confidence interval (CI) 1·18-1·60, P < 0·0001] and US officer trainees at West Point (RR 3·10, 95% CI 2·13-4·52, P < 0·0001) and Annapolis (RR 2·03, 95% CI 1·65-2·50, P < 0·0001) to increased risks of medically treated illnesses in late 1918. The findings suggest that susceptibility to and/or clinical expressions of the 1918 pandemic influenza virus depended on previous experiences with respiratory infectious agents. The findings are consistent with observations during the 2009 pandemic in Canada and may reflect antibody-dependent enhancement of influenza infection.

Very few Pacific islands escaped the 1918-1919 influenza pandemic. Subsequent influenza epidemics in the established colonial outposts of American Samoa and New Caledonia infected many but killed very few persons whereas the extraordinarily isolated Niue, Rotuma, Jaliut and Yule islands experienced high mortality influenza epidemics (>3% of population) following 1918. These dichotomous outcomes indicate that previous influenza exposure and degree of epidemiological isolation were important mortality risk factors during influenza epidemics on Pacific islands.

Background: During the 1918 pandemic period, influenza-related mortality increased worldwide; however, mortality rates varied widely across locations and demographic subgroups. Islands are isolated epidemiological situations that may elucidate why influenza pandemic mortality rates were so variable in apparently similar populations., Objectives: Our objectives were to determine and compare the patterns of pandemic influenza mortality on islands., Methods: We reviewed historical records of mortality associated with the 1918-1920 influenza pandemic in various military and civilian groups on islands., Results and Conclusions: Mortality differed more than 50-fold during pandemic-related epidemics on Pacific islands [range: 0.4% (Hawaii) to 22% (Samoa)], and on some islands, mortality sharply varied among demographic subgroups of island residents such as Saipan: Chamorros [12%] and Caroline Islanders [0.4%]. Among soldiers from island populations who had completed initial military training, influenza-related mortality rates were generally low, for example, Puerto Rico (0.7%) and French Polynesia (0.13%). The findings suggest that among island residents, those who had been exposed to multiple, antigenically diverse respiratory pathogens prior to infection with the 1918 pandemic strain (e.g., less isolated) experienced lower mortality. The continuous circulation of antigenically diverse influenza viruses and other respiratory infectious agents makes widespread high mortality during future influenza pandemics unlikely., (© 2012 Blackwell Publishing Ltd.)

Purulent bronchitis was a distinctive and apparently new lethal respiratory infection in British and American soldiers during the First World War. Mortality records suggest that purulent bronchitis caused localized outbreaks in the midst of a broad epidemic wave of lethal respiratory illness in 1916-1917. Probable purulent bronchitis deaths in the Australian Army showed an epidemic wave that moved from France to England. Purulent bronchitis may have been the clinical expression of infection with a novel influenza virus which also could have been a direct precursor of the 1918 pandemic strain., (© 2011 Blackwell Publishing Ltd.)

Of the unexplained characteristics of the 1918-19 influenza pandemic, the extreme mortality rate among young adults (W-shaped mortality curve) is the foremost. Lack of a coherent explanation of this and other epidemiologic and clinical manifestations of the pandemic contributes to uncertainty in preparing for future pandemics. Contemporaneous records suggest that immunopathologic responses were a critical determinant of the high mortality rate among young adults and other high-risk subgroups. Historical records and findings from laboratory animal studies suggest that persons who were exposed to influenza once before 1918 (e.g., A/H3Nx 1890 pandemic strain) were likely to have dysregulated, pathologic cellular immune responses to infections with the A/H1N1 1918 pandemic strain. The immunopathologic effects transiently increased susceptibility to ultimately lethal secondary bacterial pneumonia. The extreme mortality rate associated with the 1918-19 pandemic is unlikely to recur naturally. However, T-cell-mediated immunopathologic effects should be carefully monitored in developing and using universal influenza vaccines.

In 1918, two waves of epidemic influenza arose with very different clinical phenotypes. During the first wave, infection rates were high but mortality was low. During the second wave, high numbers of deaths occurred and mortality differed 30-100 times among seemingly similar groups of affected adults, but the reason for this variation is unclear. In 1918, the crews of most warships and some island populations were affected by influenza during both waves of infection and had no or very few deaths during the second wave. However, some warships and island populations were not affected during the first wave of infection and had high mortality during the second wave. These findings suggest that infection during the first wave protected against death, but not infection, during the second wave. If so, the two waves of infection were probably caused by antigenically distinct influenza viruses--not by one virus that suddenly increased in pathogenicity between the first and second waves. These findings are relevant to modern concerns that the 2009 influenza A H1N1 virus could suddenly increase in lethality., (Copyright © 2011 Elsevier Ltd. All rights reserved.)

Background: During the 1918-1919 influenza pandemic, nurses and physicians were intensively exposed to the pandemic A/H1N1 strain. There are few published summaries of the mortality experiences of nurses and physicians during the pandemic., Methods: Mortality records from U.S. and British Armies during the First World War and obituary notices in national medical association journals were reviewed to ascertain death notices of nurses and physicians likely to have died of influenza., Results: Illness-related mortality among U.S. military nurses (1·05%) was one and one-half times higher than among U.S. medical officers (0·68%), nearly two times higher than among British medical officers (0·55%), and nine times higher than among British nurses (0·12%). Among U.S. nursing officers, mortality was approximately twice as high among those assigned in the United States than in Europe. Among civilian physicians, mortality during the influenza pandemic was markedly increased in Canada, New Zealand, South Africa and the United States but not Australia., Conclusions: During the 1918 pandemic, mortality among nurses and physicians was relatively low compared to their patients and significantly varied across locations and settings. Medical-care providers (particularly U.S. nursing officers) who were new to their assignments when pandemic-related epidemics occurred may have had higher risk of influenza-related mortality because of occupational exposures to bacterial respiratory pathogens that they had not previously encountered., (© 2011 Blackwell Publishing Ltd.)

Background: Understanding the risk of mortality during the 1918-1919 influenza pandemic could inform preparations for a future pandemic., Methods: Prospectively collected demographic, hospitalization, and death data from all individuals who served in the Australian Imperial Force from 1914 through 1919 in Europe and the Middle East were abstracted from archived records. Analyses were conducted to determine mortality risk factors., Results: Hospitalization with a respiratory illness during the spring-summer of 1918 protected soldiers from death (odds ratio, 0.37 [95% confidence interval, 0.25-0.53]; P < .001) but not from hospitalization during the fall-winter of 1918-1919. During the fall-winter of 1918-1919, there was a strong inverse relationship between risk of dying of pneumonia-influenza and time in military service. The pneumonia-influenza death rate among men who enlisted in 1918 (6.33 deaths per 100 person-years) was 9 times higher than that among the 1917 enlistment cohort (0.72 deaths per 100 person-years) and >14 times higher than that among the 1916 cohort (0.43 deaths per 100 person-years), 1915 cohort (0.29 deaths per 100 person-years), and 1914 cohort (0.28 deaths per 100 person-years)., Conclusion: There was a strong inverse relationship between length of service in the Australian Imperial Force and mortality risk from pneumonia-influenza during the fall-winter of 1918-1919. The protective effect of increased service likely reflected increased acquired immunity to influenza viruses and endemic bacterial strains that caused secondary pneumonia and most of the deaths during the 1918-1919 influenza pandemic.

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.

Objective: To assess how numbers and age distributions of cases and deaths during an influenza pandemic in the United States would potentially vary from those during the 1918-1919 pandemic, given the same virulence of the pandemic strain., Methods: Influenza cases and deaths in two referent populations (U.S. residents in 1917 and 2006) were calculated using clinical case rates from three pandemics (1918-like, 1957-like, and 1968-like) and case fatality rates from the 1918-1919 pandemic., Results: Across pandemic scenarios, overall case ("attack") rates ranged from 24.7% to 34.2%, and overall death rates ranged from 4.4 to 6.7 per 1000. In both referent populations, total cases and deaths were significantly higher when using 1957-like and 1968-like, compared to 1918-like, case rates. Under all pandemic scenarios, the most deaths occurred among those aged 25 to 29 years. However, in the 2006 referent population, there were large numbers and high proportions of deaths in middle-aged and elderly adults (unlike during the 1918-1919 pandemic)., Conclusions: Numbers and distributions of cases and deaths during influenza pandemics depend on numbers of individuals, clinical case rates, and case fatality rates in relation to age. During a future pandemic in the United States, influenza deaths will likely not be as sharply focused in young adults as in 1918-1919 (even if case fatality rates are similar) because of larger proportions of middle-aged and elderly adults and potentially higher case rates among adults older than 30.

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.