"The origin of this pandemic has always been disputed and may never be resolved. However, the observations of trained observers at that time are worth noting because they may bear on later genomic analysis of the recently resurrected 1918 virus nucleotide fragments and the abortive "swine flu" epidemic of 1976. In Richard Shope's Harvey lecture of 1936, he reviews evidence that in the late summer or early autumn of 1918, a disease not previously recognized in swine, and closely resembling influenza in humans, appeared in the American Middle West. Epidemiologic-epizootiologic evidence strongly suggested that the causative virus was moving from humans to swine rather than in the reverse direction. Similar observations were made on the other side of the world and reported in a little-known paper in the National Medical Journal of China. In the spring of 1918, influenza in humans spread rapidly all over the world and was prevalent from Canton, China, to the most northern parts of Manchuria and from Shanghai to Szechuan. In October 1918, a disease diagnosed as influenza appeared in Russian and Chinese pigs in the area surrounding Harbin. Thus, epidemiologic evidence, fragmentary as it is, appears to favor the spread of virus from humans to swine, in which it remained relatively unchanged until it was recovered more than a decade later by Shope in the first isolation of influenza virus from a mammalian species. The virus of 1918 was undoubtedly uniquely virulent, although most patients experienced symptoms of typical influenza with a 3- to 5-day fever followed by complete recovery. Nevertheless, although diagnostic virology was not yet available, bacteriology was flourishing and many careful postmortem examinations of patients by academic bacteriologists and pathologists disclosed bacterial pathogens in the lungs. However, this was a time when bacterial superinfection in other virus diseases could lead to death; for example, measles in military recruits was often fatal. This information is important in considering the question of "will there ever be another 1918." To the degree that secondary bacterial infection may contribute to influenza death rates, it should at least be partially controllable by antimicrobial agents, as indeed was the case in 1957."