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Glenn R. Hodges, MD; Robert J. Fass, MD; Samuel Saslaw, MD, PhD

Arch Intern Med. 1972;130(2):277-282.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

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 . . . [Full Text PDF of this Article]

Author Affiliations
Columbus, Ohio

From the Division of Infectious Diseases, Department of Medicine, the Ohio State University College of Medicine, Columbus.

Footnotes
Received for publication April 6, 1971; accepted May 28.

Reprint requests to University Hospital, 410 W Tenth Ave, Columbus, Ohio 43210 (Dr. Hodges).

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