Armstrong – Table of Contents

He considered the virus, possibly either of human or monkey origin, to be of unknown
significance as a cause of disease in nature.
Armstrong maintained a continuing interest in the new virus. Over the next
several years he and collaborating physicians from the United States Naval Medical
Service (23, 24,) and physicians practicing in the local vicinity (22, 25) were able to
establish the virus as the etiology of a specific medical entity including its various clinical
presentations. In April 1935 (26) he recovered LCM from the central nervous system of a
patient from Maine who died with an illness characterized by meningeal signs. He also
demonstrated spontaneous infection among some of the laboratory’s stock monkeys by
isolation of virus and detection of antibody development. During this same period he also
noted a “grippe-like” illness without central nervous system involvement in a laboratory
attendant who developed potent neutralizing antibodies during convalescence. This latter
case led Armstrong to suggest that immunity might develop in the absence of
recognizable central nervous system involvement. He also indicated that laboratory
observations in experimental animals showed that the virus was distributed widely
throughout the various organs, that there was no marked neurotropism, and he speculated
that it was conceivable that immunity might result from systemic infection without
central nervous system involvement (27). This was indeed shown to be the case with
observation of future additional cases.
In June 1935 Armstrong and Paul F. Dickens, United States Navy Medical Corps
collaborated on several almost simultaneous reports (23, 24) entitled “Benign
Lymphocytic Choriomeningitis (Acute Aseptic Meningitis) – A New Disease Entity”.
They included 4 detailed case reports, including one seen and reported by Dr. Walter