Intracranial inoculation of mouse brain in a dilution of 1:1,000,000 could transmit
infection to mice. A larger dose was necessary following intranasal inoculation for the
disease to develop regularly. Armstrong used this latter route regularly for later studies of
the virus (10, 11). Webster and Fite (9) reported that the virus was readily filterable. They
(9) filtered the virus through graded collodion membranes and estimated the diameter of
the virus particle to be somewhere between 22 and 33 millimicrons. They found that the
virus was neutralized by the serum of individuals convalescent from encephalitis in the
1933 outbreak and was not neutralized by the serum of normal individuals from
uninfected areas (11). The serum of recovered monkeys and mice also neutralized the
virus.
The ready availability of the mouse as a laboratory host enabled Webster and
associates (9) to compare the agent of the 1933 St. Louis outbreak with other viruses.
They reported the absence of cross immunization with the viruses of herpes (simplex),
vesicular stomatitis and equine encephalomyelitis. They also reported that serum
collected from individuals recovered from epidemic (lethargic) encephalitis (von
Economo’s Disease) from one to ten years after the acute attack, from poliomyelitis,
Japanese encephalitis and Australian-X disease did not neutralize the virus.
Armstrong and associates (9) summarized their conclusions as follows: A number
of strains of a virus that seemed to be the etiologic agent of the 1933 epidemic of
encephalitis in St. Louis were isolated in two different laboratories. The virus acted on
monkeys and white mice and was distinct from other previously known viruses. The
number of strains of similar characteristics isolated, and the neutralization of the virus by
serum of individuals convalescent from encephalitis in the epidemic, but not the serum of
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