1918

Outbreak of influenza pandemic (erroneously called “Spanish influenza” because it was first reported from neutral Spain), first in Camp Funston (Kansas), then to other army camps, thence to France (via troops disembarking at Brest) and the rest of Europe. During Germany’s final Hundred Days Offensive in March, 1918, American Expeditionary Force alone reported approximately 360,000 cases of influenza (Hallett, 229). In U.S., spring (March-April) first wave was mild; virus adapts to humans via “passage,” abetted by tightly packed trenches and transport trains, which left infected, but not yet symptomatic soldiers in the trenches to pass the virus on to healthy replacements. In U.S., epidemic likely originated in the military installations, viz, Camp Funston in March and Camp Devens (north of Boston) in September (Byerly II, 79. 93-94). The second wave (beginning in August) was deadly (Barry, 169-184). Philadelphia authorities refused to cancel Liberty Loan Parade of September 28; in three days all hospital beds in Phila’s 31 hospitals were filled; in 10 days the epidemic there had exploded to hundreds of thousands ill and hundreds of deaths each day (Hallett, 221ff.). In 25 of the 40 largest army training camps, at least one quarter of soldiers reported sick with influenza and pneumonia, and eight camps reported more than 500 deaths. Unlike regular influenza, Spanish flu could produce fevers up to 106 degrees that led to delirium or lethargy to the point of prostration. Patient bled from the nose and ears and coughed up bloody sputum . . . Medical officers found cyanosis from lack of oxygen among most alarming symptoms (Byerly II, 77-78). Outbreak at Camp Devens (north of Boston) on 8 September, with 6,000 patients crammed into a 2,000-bed hospital. It led to inspection by William Welch, Rufus Cole (Rockefeller Institute), Victor Vaughan, and Simeon Walbach (Harvard) (Barry, 188ff.; Byerly II 74-75; Crosby, chap 1); Welch sent for Rockefeller Institute’s Oswald Avery, who found Pfeiffer’s B. influenzae, but pneumococcus, hemolytic streptococcus, and staphylococcus aureus as well, and remained unconvinced B. influenzae was root cause (Hallett, 288ff.). His research tended to finding that an antipneumococcus serum, rather than a vaccine against B. influenzae, addressed the primary infection (296). During autopsies, Welch could not believe the condition of the lungs resulted from flu, and speculated the disease was a new kind of infection or return of the plague. By end of October, 17,000 had contracted influenza and/or pneumonia, one-third of the command (Crosby, chap 1). During 1918-1919 epidemic, 47% of all deaths in U.S. were from influenza and its complications, with death toll in excess of 675,000 and – unlike typical influenza -- with young adults 20-40 the most likely to die (Hallett, 238-239). Data from 10 American cities showed an average influenza sickness rate of 28%, comparable to that in the army training camps. In the camps, the average was at least 20-30% sick rates, but they only capture soldiers who reported sick and received medical attention (Byerly I, 79, 86). The lungs of victims resembled those of only one known disease: a virulent form of bubonic plague known as pneumonic plague (241). “In 1918 the immune systems of young adults mounted massive responses to the virus. That immune response filled the lungs with fluid and debris, making it impossible for the exchange of oxygen to take place. The immune response killed” (249-50). In 1918, ARDS (following from a violent infection of the influenza virus itself) had virtually a 100% mortality rate, though doctors could treat the pneumonia caused by secondary bacterial infections (via Avery & Cole’s serum for Types I & II pneumococcus; surgical draining of empyemas; drugs; x-rays; oxygen), though the resources were scarce and unavailable to doctors in Public Health Service. Out of 100,000 civilian doctors, 72,000 joined the Volunteer Medical Service, but only 1,045 enlisted in the PHS (Hallett, 316ff). Death toll estimated at 50-100 million; up to 5% of world population (Hallett, 397). In research beginning in 1919, Park & Williams reversed their position on causal role of B. influenzae; many researchers moved to filterable virus as the cause, though the only evidence was negative evidence as to a bacterial cause (Hallett, 415-417).