Infl uenza pandemics occur as a result of two different mechanisms: novel emergence of an avian descendent virus (as in the 1918 virus) or a modifi cation of a human adapted virus by genetic mixing as in the reassortment of novel hemagglutinin (HA) with or without non-committent neuraminidase, (NA) as in the 1968 H3N2 strain [19] . The pandemics of 1948, 1957 and 1968 were caused by variations of the infl uenza virus resulting from this shuffl ing of the eight gene pairs within the virus. Infl uenza pandemics occur in three waves. The typical fi rst wave or initial outbreak, as in the spring of 1918, was relatively mild, starting from the Midwest and spreading along the rail lines with soldiers from Ft. Funston, Kansas, modern day Ft. Riley [2, 3, 14, 16] . The novel H1N1 discovered in Mexico also had such a humble origin. Both patient zeros reported little problems and made complete recoveries. Unlike the Mexican outbreak, the 1918 spring outbreak was not even noted in the index in the 1918 volumes of the Journals of the American Medical Association. Infl uenza was not a reportable disease until 1925 in the United States: the only evidence of the early occurrence was the registration of deaths reported as uncomplicated cases of pneumonia by physicians to various public health departments [3, 8, 9] .