Armstrong – Table of Contents

individuals recovered from other diseases, justified the conclusion that it was the
etiologic agent of the recent epidemic.
At the height of the epidemic many observers on the scene described the varied
presentations, the manifestations, and the clinical course of encephalitis as they occurred
in St. Louis in 1933. Dr. James P. Leake provided a brief clinical overview of the illness
in his early report of the outbreak. Dr. Theodore C. Hempelman of the Department of
Pediatrics, Washington University School of Medicine and the St. Louis Children’s
Hospital presented a detailed account of his experience with the illness (12). A major
observation from epidemiological and laboratory studies (13) indicated that, similar to the
situation with poliomyelitis infection, protective antibodies occurred in many people in
the St. Louis who gave no history of prior illness. This observation suggested previous
infections with the virus that produced either mild, non-specific illnesses or completely
inapparent infections. Armstrong (10) devised a method for producing asymptomatic,
non-lethal specific immunity in white mice by infecting them intranasally with St. Louis
encephalitis. He stated that the interest in these findings resided in their possible
relationship to the natural mechanism whereby immunity developed without recognizable
symptoms of the diseases. In order to test the hypothesis of inapparent infections further,
Dr. J. G. Wooley (of the NIH), with mentoring by Armstrong (11), described the
distribution of immunity against St. Louis encephalitis in the United States as determined
by the serum protection (intracerebral) test in white mice. They summarized their
conclusions as follows: 1) Serum protection tests carried out on 524 human sera collected
from 49 cities located in 26 states and the District of Columbia gave definite protection in
158 or 30.1 per cent, questionable protection in 56 or 10.7 per cent and no protection in