Interactions between influenza and bacterial respiratory pathogens: implications for pandemic preparedness

Abstract

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.

Figure 1

Examples of pathophysiological interactions between influenza and bacterial respiratory pathogens and various clinical expressions

Figure 2

Faces of “influenzo-pneumonic septicaemia” (A) “An early case in which the facial colour is frankly red, and the patient might not appear ill were it not for the drooping of the upper eye-lids and a half-closed appearance to the eyes.” (B) “Cyanosis in which the colour of the lips and ears arrests attention in contrast to the relative pallor of the face. The patient may yet live for twelve hours or more.” (C) “The heliotrope cyanosis. The patient is not in physical distress, but the prognosis is almost hopeless.” Reproduced from reference 32.

Figure 3

Hospitalisations for, deaths due to, and variability of case fatality of pneumonia and influenza at 40 large US army camps during the autumn of 1918

Figure 4

Between Sept 15 and Oct 20, 1918, there were approximately 7–10 day lags between the epidemic curves of “influenza/bronchitis” and “pneumonias” at Camp Pike, AR, and “influenza/pneumonia” and associated “fatalities” at Camp Grant, IL