Armstrong – Table of Contents

310 or 50.1 per cent. 2) Sera giving definite protection were collected from 32 cities
located in 21 states and the District of Columbia. 3) Of sera from 39 clinically definite
encephalitis cases from the St. Louis epidemic (1933), collected 4 to 10 months following
the attack, 37 or 94.8 per cent showed protection. Among 113 normal controls having no
known exposure to encephalitis cases, there were 11, or 9.4 per cent, whose sera gave
protection, while among 56 normal controls who had been in contact with cases, there
were 20, or 35.7 per cent whose sera showed definite protection. 5) A positive serum
protection test was believed to be evidence that the serum donor had been in contact with
the virus of encephalitis and had suffered either a clinical or sub-clinical type of
infection. 6) They also stated that the serum-protection test they reported indicated that
the St. Louis type of encephalitis was immunologically distinct from encephalitis
lethargica (von Economo’s Disease), poliomyelitis and the post-infectious encephalitides.
A particularly vexing problem was trying to determine how the virus spread. The early
epidemiological data exonerated the water and milk supply. Despite a superficial
epidemiological resemblance to poliomyelitis because of its similar seasonal incidence in
late summer and early fall, St. Louis encephalitis differed from poliomyelitis in its
predominant clinical presentation and its major incidence in the elderly. The epidemic
occurred in a drought-like period that had been preceded by a heavy rainy season. The
result was scattered pools of stagnant water that were ideal areas for the luxuriant
proliferation of mosquito larvae. Suspicion then focused on mosquitoes as possible
vectors from an unknown host or reservoir. In 1930 Dr. K. F. Meyer et al. (14) isolated
Western equine encephalomyelitis (WEE) from horses in California and in 1933 Kelser
(15) showed that Aedes aegypti mosquitoes could transmit WEE experimentally. Based