Armstrong – Table of Contents

geographic areas, having their origin in California, Maryland, District of Columbia,
Illinois, Ohio and Virginia.
After this summary they concluded: 1) the symptom complex was a distinct
disease entity. 2) This condition, by priority, should be called “acute aseptic meningitis”,
but, in view of the recent advance in the knowledge of its etiology, this designation was a
misnomer and they suggested the term “acute lymphocytic choriomeningitis” as a more
accurate designation. 3) The etiological agent was a filterable virus first described by
Armstrong and Lillie. 4) The blood serum of patients recovered from acute aseptic
meningitis protected animals from the virus. This might be used to confirm the diagnosis.
5) Monkeys, mice and guinea pigs were susceptible to the virus, and it was conceivable
that a reservoir of the disease might exist in animals.
Over the course of the next several years, Armstrong and colleagues expanded
their knowledge and concepts of LCM through surveys of various population groups for
the presence of serum neutralizing antibodies (29, 30, 31). The groups included random
samples, outbreaks of febrile central nervous system infections, prison populations,
United States Marine Hospitals and others. They found that white laboratory rats were
susceptible to the virus and provided another experimental host with which to conduct
investigations. Armstrong, in collaboration with Wooley and Onstott (30), using the
practical and reliable serum virus-neutralization test in mice, demonstrated antibodies in
138 of 1,248 sera tested (11 per cent), questionable protection in 131 (10.4 per cent),
while 979 (78.6 per cent) sera provided no protection. Sera from Federal penal
institutions and the beneficiaries of the United States Marine Hospitals gave a higher
incidence of protection than did those from people of comparable ages from other groups