Armstrong – Table of Contents

and were probably not representative of the general population. Armstrong could only
speculate about reasons for this observation. He and his associates demonstrated
antibodies in protection tests in 90 sera from 481 adults (more than 17-years) or 18.3 per
cent, while only 5 sera from 396 persons under 17-years, or 1.2 per cent, showed
protection. They could not establish the reason for this difference in seroincidence by age
differential. They did show, however, protective antibodies in 17 of 52 sera (32.1 per
cent) from individuals in whom a diagnosis of “aseptic meningitis “ had been made.
Armstrong again reiterated that a positive protection test most likely indicated that the
serum donor had been in contact with the virus of LCM. The occurrence of demonstrable
antibodies in 117 sera from 997 individuals without history of central nervous system or
meningeal involvement suggested to Armstrong that immunity might result not only from
a frank symptomatic attack, but also from either a subclinical infection or a clinical
condition, possibly an upper respiratory symptom complex, unrecognized as due to LCM
virus. The answer came later. Armstrong continued serological testing for the next few
years (31) with basically the same results.
The next major breakthroughs in knowledge about the virus were Armstrong’s
discovery of the host, the common house mouse (Mus musculus) and the presence of
endemicity in the mice (32, 33). Also, in the scientific literature from France, LCM was
becoming known as “La Maladie d’Armstrong” (34). The initial breakthrough occurred
as the result of local environmental investigations related to two patients hospitalized in
the medical service of Dr. Lewis K. Sweet, Chief Medical Officer in Pediatrics at the old
Gallinger Municipal Hospital in Washington, DC. (Later renamed DC General Hospital
and for the past few years operationally defunct). The first patient, who became ill