A forgotten epidemic that changed medicine: measles in the US Army, 1917-18

Abstract

A US army-wide measles outbreak in 1917-18 resulted in more than 95,000 cases and more than 3000 deaths. An outbreak investigation implicated measles and streptococcal co-infections in most deaths, and also characterised a parallel epidemic of primary streptococcal pneumonia in soldiers without measles. For the first time, the natural history and pathogenesis of these diseases was able to be well characterised by a broad-interdisciplinary research effort with hundreds of military and civilian physicians and scientists representing disciplines such as internal medicine, pathology, microbiology, radiology, surgery, preventive medicine, and rehabilitation medicine. A clear conceptualisation of bronchopneumonia resulting from viral-bacterial interactions between pathogens was developed, and prevention and treatment approaches were developed and optimised in real time. These approaches were used in the 1918 influenza pandemic, which began as the measles epidemic waned. The outbreak findings remain relevant to the understanding and medical management of severe pneumonia.

Figure 1:. Admissions to hospital for selected diagnoses, and number of troops in the US Army

Data for 39 US army mobilisation camps combined, by month, from April 1, 1917, to Dec 31, 1919.

Figure2:. Images of the 1917–18 army measles epidemics

(A) Measles isolation ward, Camp Zachary Taylor, Louisville (KY, USA), in winter 1917–18; army isolation principles and practices during the epidemic were often elaborate.^,,– (B–E) Thousands of surgically thoracotomised soldiers who survived postviral bacterial empyema, especially those associated with Streptococcus haemolyticus, had severe and permanent disabilities.

Figure3:. Postmeasles streptococcal complications

(A) Typical streptococcal bronchopneumonia, with early stage micronodular consolidation extending along and around the bronchioles, and sometimes extending to the lung periphery to break out as subpleural abscesses potentially leading to empyemas. Near universal early laryngitis and tracheitis suggested infectious spread in a distal direction along the bronchial tree. (B) Bilateral postmeasles streptococcal bronchopneumonia. A bronchus is filled with purulent exudate, with transmural inflammation and necrosis of the bronchial wall (right side of bronchus). In the pulmonary tissue, bacteria were concentrated more in the interstitium than in alveoli,^, and pathologists claimed “an apparent inability [of Streptococcus haemolyticus] to enter the tissue proper.” (C) Interstitial bronchopneumonia with bilateral empyema and fibrinous pericarditis due to S haemolyticus. (D) Patient with air-filled empyema cavity, its walls indicated by arrows, and a tube entering the cavity at the bottom. (E) The same patient treated with repeated drainage followed by irrigation with Dakin’s solution; after negative pressure suction, the thickened visceral pleura lies against the chest wall.