The Great Pneumonia Pandemic of 1918
It is a widespread misconception that millions of Americans died of influenza during the Spanish Flu pandemic of 1918-19. According to a 2008 paper, co-authored by Anthony Fauci, the vast majority of fatalities are now known to have resulted from severe acute bacterial pneumonia caused by the aggressive invasion of phenomenal numbers of bacterial pathogens.
The primary cause of the pandemic remains unidentified and the reasons for its severity are also unknown. Questions arise concerning the current emphasis on responses to coronaviruses when the evidence from all 20th century influenza pandemics suggests that the primary cause of death has been pneumonia arising from bacterial, rather than viral, infection.
What follows is a brief summary of the startling findings of this paper, mostly in the words of the authors themselves.
Article clip from the Houston Post’s newspaper published on October 10, 1918 (University of North Texas Libraries, The Portal to Texas History)
Samples from people who died of influenza during 20th century pandemics exhibited severe changes indicative of bacterial pneumonia, caused by common upper respiratory–tract bacteria. This study examined autopsy specimens from 58 influenza victims in 1918–1919 and reviewed data from published reports from more than 8000 postmortem examinations.
The authors conclude that influenza ‘A’ virus infection, in conjunction with bacterial infection, led to most of the deaths during the 1918–1919 pandemic. The increased fatality rate in the three highest-risk age groups was predominantly due to the increased frequency of bronchopneumonia, not to increased incidence of influenza or an increased bronchopneumonia case-fatality rate.
In virtually all cases, there was compelling evidence of severe acute bacterial pneumonia, either as the predominant pathology or in conjunction with underlying features now believed to be associated with influenza virus infection. Bacteria were commonly observed in massive numbers.
The extraordinary severity of the 1918 pandemic remains unexplained.
Although the cause of influenza was disputed in 1918, there was almost universal agreement among experts that deaths were virtually never caused by the unidentified causative agent itself, but resulted directly from severe secondary pneumonia caused by recognised pathogens – mostly pneumococci, streptococci, and staphylococci. Without this pneumonia, experts generally believed that most patients would have recovered.
Surprising aspects of the influenza-associated pneumonia fatalities included the remarkably high incidence of secondary pneumonia, and the pronounced aggressiveness of bacterial invasion which often resulted in ‘phenomenal’ numbers of bacteria.
Until 1950, most observers believed fatal influenza to be an infection in which an inciting agent of low pathogenicity acted in partnership with known pathogenic bacteria.
An unidentified primary agent was thought to have led to the secondary spread of enormous numbers of bacteria, along the compromised bronchial lining, to every part of the bronchial tree, following which focal infections broke through into the lung.
Automobile-plant workers in Michigan wear masks in 1918 in an effort to protect from the Spanish flu. (Advance Local archive) The Flint Journal
This view was supported in 1917–1918 by measles epidemics in US Army training camps, in which most deaths resulted from streptococcal pneumonia. The pneumonia deaths during the 1918 pandemic proved so highly similar to the then-recent pneumonia deaths from the measles epidemics that noted experts considered them to be the result of one newly emerging disease: epidemic bacterial pneumonia precipitated by prevalent respiratory tract agents.
The question of whether the origins of severe influenza-associated pneumonia were primarily viral or a combination of viral and bacterial agents was carefully considered in 1918–1919, without definitive resolution.
However, in 1935, a study combined human influenza and streptococcal infection in ferrets. Even though neither agent was pathogenic when administered alone, they were highly fatal in combination. During the 1940s, additional studies in ferrets, mice, and rats established that the influenza virus in combination with any of several pneumopathic bacteria acted cooperatively to produce either a higher incidence of disease, a higher death rate, or a shortened time to death.
These effects could be mitigated or eliminated if antibiotics were given shortly after establishment of combined infection. Recent data suggest that influenza vaccination may prevent bacterial disease.
If the next pandemic is caused by a human-adapted virus similar to those recognized since 1918, and if severe pandemic influenza is largely a problem of virus and bacteria arising together, the authors stress the likely importance of new influenza antiviral drugs and vaccines in controlling a future pandemic
In conclusion, prevention, diagnosis, prophylaxis, and treatment of bacterial pneumonia, as well as the stockpiling of antibiotics and bacterial vaccines, should be among the highest priorities in pandemic planning.
The authors, publishing in 2008, were encouraged that such considerations were already being discussed and implemented by those responsible for such plans.
Fauci et al’s paper makes clear that the increased fatalities were due to the increased frequency of pneumonia not to increased incidence of influenza. The pneumonia was sometimes associated with underlying features that are nowadays ‘believed to be’ associated with influenza virus infection. There was a ‘general belief’ that without the pneumonia patients would not have died, and that the unidentified causative agent of the pandemic was not the cause of death.
The authors conclude explicitly that it is the ‘prevention, diagnosis, prophylaxis, and treatment of bacterial pneumonia’ that should be among the highest priorities in pandemic planning. Pandemic mitigation in the 21st century continues instead to focus on the nominal cause of the pandemic rather than on the seldom addressed cause of death. It may be that, not for the first time, Mr Fauci is not following his own best advice.
The illustrations show the widespread use of masks during the 1918-19 pandemic. In this regard, it is interesting to consider that the phenomenal numbers of bacteria encountered during the review were all pathogens associated with the upper respiratory tract. Masks trap bacteria and molds from the out-breath and the bacteria so retained would typically be from the upper respiratory tract.
The origins, severity and lethal nature of the 1918 outbreak remain, apparently, a mystery. It is possible that masks were themselves were perhaps a factor in the eventual scale, scope and aggressiveness of the pathogenic invasions. Until at least the basics are known about the huge tragedy that was the so called ‘spanish flu pandemic’, the precautionary principle commends unobstructed breathing of fresh air.
The 2008 paper is called Predominant Role of Bacterial Pneumonia as a Cause of Death in Pandemic Influenza: Implications for Pandemic Influenza Preparedness
by: David M. Morens, Jeffery K. Taubenberger and Anthony S. Fauci : Oct 1st 2008
The details of Fauci et al’s paper are discussed further in Dr Rock’s Podcast The Great Pneumonia Pandemic of 1918