Panel:

Clinical, epidemiological, and pathological similarities between the 1917–18 measles and the 1918–19 influenza epidemics in 39 US army camps^{6,10,13,21,24,28,30,34,37–39,45,51,53,62,63,70,72,82,88}

Shared epidemiological fi ndings

•  Epidemic of high incidence with respiratory and fomite spread

•  High incidence of secondary bacterial pneumonia

•  Mean of 10 days from illness onset to pneumonia death37,38,89

•  High incidence of postpneumonia empyema

•  Severe disease statistically associated with nasopharyngeal carriage of bacterial pathogens

•  Acquisition of bacterial pathogen carriage both before and after viral disease onset*37,38,89

Shared clinical fi ndings

•  Acute laryngotracheobronchitis associated with resultant lung complications

•  Rapid progression of pneumonia to empyema or septic shock

•  Death by sepsis, cardiac failure, acute respiratory distress syndrome, with or without heliotrope cyanosis

Shared pathological and bacteriological fi ndings

•  Strong predominance of bronchopneumonia over lobar pneumonia

•  Bronchopneumonia usually bilateral

•  Bronchopneumonia often ends in septic shock, empyema, cardiac failure, or acute respiratory distress syndrome

•  Evidence of desquamative laryngotracheobronchitis and pan-bronchitis at autopsy

•  Peri-bronchial pattern of lesions evident in early or less involved areas of lung

•  Very extensive neutrophil infi ltration, especially in pneumococcal cases†

•  Extensive necrosis, vasculitis, and haemorrhage in involved lung tissue†

•  Asynchronous changes throughout lung

•  Evidence of repair of (viral) injury

•  Hyaline membranes and ductal dilatation

•  Single or mixed bacterial infection with pneumonia pathogens‡

•  Pneumonia pathogens in fatal cases identical to those causing camp carriage epidemics‡

•  Bacillus (Haemophilus) infl uenzae often found but usually not considered pathogenic

Distinct pathological and bacteriological fi ndings

•  Warthin-Finkeldey cells in lungs only in 1917–18 measles outbreak

^*In 1917, pathologists suspected that both influenza and measles were viral.

^†In measles streptococcal bronchopneumonias, interstitial inflammation was relatively more common and alveolar neutrophilic infiltration less common than in many pandemic influenza bronchopneumonias. Streptococcal bronchopneumonias were also more likely to be haemorrhagic.^24,38,39,63

^‡Mixed bacterial infections at autopsy were common in both post-influenza pneumonia (20%)⁵⁰ and postmeasles pneumonia, although standardised bacteriological data for measles were not collected. The existing measles autopsy data, sparse and often of poor quality, nevertheless suggest that most postmeasles pneumonias were caused by streptococci with or without pneumococci—eg, data from Cumming and colleagues¹⁹ on 18 measles pneumonia autopsies, which show pure streptococci in 15, and streptococci-positive pneumococci in three.²¹ Other bacteria were found less often.