Primary atypical pneumonia (PAP) was first described as a clinical entity distinct from bacterial and influenzal pneumonia in 1938.1 Central nervous system (CNS) complications, including meningoencephalitis, transverse myelitis, hemiplegia, ascending paralysis, and cranial nerve palsy were described in the initial and subsequent reports but little could be concluded about their pathogenesis since the etiology of PAP was unknown.2 In 1944, Eaton isolated a filterable agent from clinical cases of PAP and experimentally infected hamsters and cotton rats.3 It was a number of years, however, before the Eaton agent was generally recognized to be of etiologic significance. This occurred when Eaton agent isolates were visualized in chick-embryo lung tissue by immunofluorescent techniques and rises in fluorescent antibody titers were measured in the patients from whom the isolates were obtained.4,5 In 1962, the Eaton agent was cultured on artifical media, identified as a mycoplasma, and named Mycoplasma pneumoniae
Hodges GR, Fass RJ, Saslaw S. Central Nervous System Disease Associated With Mycoplasma pneumoniae Infection. Arch Intern Med. 1972;130(2):277–282. doi:10.1001/archinte.1972.03650020097018
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