Study: Deaths From Bacterial Pneumonia During 1918-1919 Influenza Pandemic
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Suggested citation for this article: Brundage JF, Shanks GD. Deaths from bacterial pneumonia during 1918–19 influenza pandemic. Emerg Infect Dis. 2008 Aug; [Epub ahead of print]
For nearly 90 years, the debate over why the Spanish Flu of 1918-1919 was so deadly has raged. Estimates put the number of deaths well in excess of 20 million worldwide, with some studies suggesting twice or three times that number.
Survival rates varied immensely from one region to another, and even among disparate ethic groups in the same area.
In New Zealand, as this study points out, death rates were ≈7× higher for indigenous (Maori) populations (influenza deaths 2,160, mortality rate 42.3/1,000) than for other residents (influenza-related mortality rate 4.5/1,000).
In the United States, the overall case fatality ratio (CFR) was roughly 2%, but that wasn't the whole story. Among indigenous peoples, that number was many times higher.
Here is how the authors of this study. appearing in the August edition of the Journal of Emerging Infectious Diseases, describe their hypothesis. (Reparagraphed for readability)
Deaths from Bacterial Pneumonia during 1918–19 Influenza Pandemic
John F. Brundage* and G. Dennis Shanks†
*Armed Forces Health Surveillance Center, Silver Spring, Maryland, USA; and †Australian Army Malaria Institute, Enoggera, Queensland, Australia
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.
In other words, the authors believe the high death rates encountered in the 1918 pandemic were caused primarily by secondary bacterial pneumonias, not by the inherent pathogenicity of the pandemic virus.
Much of this study is based on contemporaneous reports from doctors treating patients in 1918-1919. Bacterial pneumonia was often cited as the cause of death in pandemic victims.
The authors postulate that those who initially developed bacterial pneumonia became `superspreaders' - via paroxysms of coughing in enclosed areas - of common colonizing strains of bacteria, such as pneumococci, hemolytic streptococci, H. influenzae, and S. aureus.
Quoting from the study:
Finally, for brief periods and to varying degrees, affected hosts became “cloud adults” who increased the aerosolization of colonizing strains of bacteria, particularly pneumococci, hemolytic streptococci, H. influenzae, and S. aureus (39).
For several days during local epidemics—particularly in crowded settings such as hospital wards, military camps, troop ships, and mines—some persons were immunologically susceptible to, infected with, or recovering from infections with influenza virus. Persons with active infections were aerosolizing the bacteria that colonized their noses and throats, while others—often, in the same “breathing spaces”—were profoundly susceptible to invasion of and rapid spread through their lungs by their own or others’ colonizing bacteria.
The authors present a good deal of data in support of their theory, including the two following charts.
Here we see the attack rate, by age, of the Influenza virus. Notice that the most commonly affected age group are children aged 5 to 9.
This second chart tracks the incidence of pneumonia by age, along with the overall excess deaths by age. The CFR closely matches the rate of pneumonia, and does not follow the first chart, which is attack rate by age.
If virulence of the virus were the causative agent in most deaths, then the authors argue that 5 to 9 year-olds should have experienced a higher fatality ratio than victims in their mid-20's.
This is a fascinating study, reasonably easy to read, and worth taking the time to review in detail. I've just selected a few of the highlights.
While it may not completely answer the question as to the causes of the virulence of the 1918 pandemic, it does provide plenty of food for thought.
Based on this study, the authors have proposed the following recommendations (again, Reparagraphed for readability):
We suggest that preparations for the next influenza pandemic should focus on more than preventing and treating influenza virus infections. A modified influenza pandemic plan might include the following components:
1) Before a pandemic, expand indications for and decrease barriers to receipt of vaccination against S. pneumoniae (36–38,40).
2) During a pandemic, in communities not yet affected, universally vaccinate with a safe and effective strain-specific influenza vaccine, if available.
3) During local epidemics, treat all serious clinical cases with an antibacterial agent that is effective against S. pneumoniae, S. pyogenes, H. influenzae, and S. aureus (including methicillin-resistant S. aureus); isolate patients with clinical cases from other patients and as many others as possible (35,37–39).
4) Conduct pandemic-related surveillance that tracks the incidence, nature (e.g., species, affected sites, antimicrobial drug sensitivities), and outcomes of bacterial infections that complicate influenza cases.
