Mechanisms of Spread

Asian influenza was truly the Phineas Fogg of diseases, spreading around the world in less than twice eighty days with a rapidity to delight the most sanguine of Jules Verne virologists. This global dissemination has been attributed to the capacity of Asian virus to infect a highly susceptible population (1, 2). Beyond belaboring the obvious, what more needs to be said about how Asian influenza spread ? Students of past epidemics and pandemics have noted that clinical influenza spread rapidly even before the advent of fast transportation (3) and that dates of maximal incidence did not provide good evidence of routes of spread ( 4). Such discrepancies spoiled the case-to-case transfer explanation, and prompted several suggestions as to how a new antigenic strain of virus could appear within a short space of time in widely separated countries: (1) mutation on a single occasion followed by rapid spread; (2) widespread preof virus in masked form, with its almost provocation to infectivity (3); (3) stmultaneous mutations in multiple foci (5). The abundance of data collected as Asian virus extended throughout the world in 1957 established direct lines of transmission from one focus to another, and makes it unnecessary to invoke multiple mutations to explain pandemic occurrence (6). Do the data also disprove the suggestion regarding pre-seeding of virus and provocation to infectivity? Not necessarily. On the contrary, the behavior of Asian influenza lends support to this concept. How else can we explain the fact that after the introduction and multiple seeding of in the United States during the summer, outbreaks were consistently limited to situations in which large numbers of people were crowded together (7) ? How else can we explain the almost simultaneous outbreaks in the fall in Arizona, Cleveland, Oregon, Florida, and New York? These are some of