Abstract
In the United States in the 1930s, although the pathogen was not known, atypical pneumonia was clinically distinguished from pneumococcal pneumonia by its resistance to sulfonamides. Reimann (1938) reported seven patients with an unusual form of tracheo bronchopneumonia and severe constitutional symptoms. He believed the clinical picture of this disease differed from that of the disease caused by influenza viruses or known bacteria and instead suspected “primary atypical pneumonia.” For many years, the responsible infectious agent was tentatively classified as a filterable virus that could pass through a Seitz filter to remove bacteria and was reported to be a psittacosis-like or new virus. After that, Eaton et al. (1942, 1944, 1945) identified an agent that was the principal cause of primary atypical pneumonia using cotton rats, hamsters, and chick embryos. Eaton et al. (1942, 1944, 1945) did not perform an inoculation study in human volunteers. During the 1940s, there were three groups engaged in discovering the etiology of the primary atypical pneumonia. (1) Commission on Acute Respiratory Diseases Diseases directed by John Dingle, (2) Dr. Monroe Eaton’s group, the Virus Research Laboratory of the California State Public Health Department, (3) The Hospital of the Rockefeller Institute for Medical Research directed by Horsfall. During 1940s, the members of the Commission on Acute Respiratory Diseases concluded that the bacteria-free filtrates obtained from the patients, presumably containing a virus, could induce primary atypical pneumonia in human volunteers via Pinehurst trials. During 1950s, serological approaches for identification of the Eaton agent developed such as Fluorescent-Stainable Antibody, and at the beginning of the1960s, the Eaton agent successfully grew in media, and finally accepted as a cause of primary atypical pneumonia. Thus, technical difficulties with visualizing the agent and failure to recognize the full significance of the Pinehurst transmission experiments resulted in a lapse of 20 years before acceptance of the Eaton agent as Mycoplasma pneumoniae. This review describes the history of M. pneumoniae pneumonia with a special focus on the recognition between the 1930 and 1960s of the Eaton agent as the infectious cause.
Highlights
Atypical bacterial pneumonia is caused by atypical organisms that are not detectable on Gram stain and cannot be cultured using standard methods, and characterized by a symptom includes headache, low-grade fever, cough, and malaise
Clyde et al (1961) was able to subculture the tissue culture materials obtained from infected chick embryos into monkey kidney cells and visualized the brightly stained, rounded, granular structures using Liu’s indirect fluorescent antibody procedure (Liu, 1957)
Chanock et al (1960a) revealed evidence that the Eaton agent had developed in 16% of patients with etiologically undiagnosed lower respiratory tract illness using fluorescent-stainable antibody (Eaton antibody)
Summary
Reimann (1938) reported seven patients with an unusual form of tracheo bronchopneumonia and severe constitutional symptoms. He believed the clinical picture of this disease differed from that of the disease caused by influenza viruses or known bacteria and instead suspected “primary atypical pneumonia.”. During 1940s, the members of the Commission on Acute Respiratory Diseases concluded that the bacteria-free filtrates obtained from the patients, presumably containing a virus, could induce primary atypical pneumonia in human volunteers via Pinehurst trials. This review describes the history of M. pneumoniae pneumonia with a special focus on the recognition between the 1930 and 1960s of the Eaton agent as the infectious cause
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