Influenza Circulation in United States Army Training Camps Before and During the 1918 Influenza Pandemic: Clues to Early Detection of Pandemic Viral Emergence

Abstract

Background. Surveillance for respiratory diseases in domestic National Army and National Guard training camps began after the United States’ entry into World War I, 17 months before the “Spanish influenza” pandemic appeared.Methods. Morbidity, mortality, and case-fatality data from 605 625 admissions and 18 258 deaths recorded for 7 diagnostic categories of respiratory diseases, including influenza and pneumonia, were examined over prepandemic and pandemic periods.Results. High pandemic influenza mortality was primarily due to increased incidence of, but not increased severity of, secondary bacterial pneumonias.Conclusions. Two prepandemic incidence peaks of probable influenza, in December 1917–January 1918 and in March–April 1918, differed markedly from the September–October 1918 pandemic onset peak in their clinical-epidemiologic features, and they may have been caused by seasonal or endemic viruses. Nevertheless, rising proportions of very low incidence postinfluenza bronchopneumonia (diagnosed at the time as influenza and bronchopneumonia) in early 1918 could have reflected circulation of the pandemic virus 5 months before it emerged in pandemic form. In this study, we discuss the possibility of detecting pandemic viruses before they emerge, by surveillance of special populations.

A Missed Summer Wave of the 1918–1919 Influenza Pandemic: Evidence From Household Surveys in the United States and Norway

“…In the Northern hemisphere, recent literature has documented prepandemic herald waves in both the United States and Norway during the spring of 1918 (February–April). This wave was mild with low mortality; it often started in military populations and did not always spread to the civil populations [ 1 – 6 ].…”

The 1918 Influenza Pandemic and Its Legacy

“…Epidemiological and clinical data from the U.S. Army training camps in 1917-1918 showed three peaks of acute respiratory disease incidence before and during the 1918 pandemic (Chertow et al 2015). Low-incidence influenza outbreaks in December 1917 and in April 1918 were associated with case-fatality ratios fivefold lower than during the 1918 fall peak.…”

“…The majority of people presenting with clinical illness in the 1918 pandemic had typical, self-limiting influenza, but a disproportionate number developed lower respiratory involvement and died of the consequences of pneumonia (Morens et al 2008). Case-fatality ratios in the United States were ∼0.5%-1.0% (Viboud et al 2013), but case fatality was much higher in many developing countries (Chandra et al 2012;Chandra 2013), and in many crowded environments, from inner cities (Mamelund 2006) to military training camps set up during World War I (Chertow et al 2015). The global mortality estimates range from 50 million to as high as 100 million in the first pandemic year (Johnson and Mueller 2002).…”

“…The decreased mortality in the elderly could be attributed to nineteenth century exposure to then-prevalent influenza A viruses either containing an H1 HA or an N1 neuraminidase (NA), or to other conserved antigens in common with the 1918 virus (Taubenberger and Morens 2006;Viboud et al 2013). Although the 1918 virus was pathogenic for persons of all ages, the disproportionate increase in frequency of secondary bacterial pneumonias in healthy young adults might be an additional manifestation of viral pathogenicity related to differential host immune responses (Xiao et al 2013;Kash et al 2014;Chertow et al 2015;Kash and Taubenberger 2015;Walters et al 2016).…”

“…These secondary infections in 1918-1919 were most frequently associated with the pneumopathogens Streptococcus pneumoniae, Streptococcus pyogenes, and Staphylococcus aureus (Morens et al 2008). Had it not been for secondary bacterial pneumonias caused by these and other pneumopathogens, the 1918 pandemic likely would have been associated with a far lower mortality (Chertow et al 2015). Increased incidence of secondary bacterial pneumonias in persons with influenza may be thus considered an intrinsic property of viral pathogenicity, and this is likely to be the case for other pathogenic influenza viruses.…”