Mycoplasma pneumoniae is a very small bacterium in the class Mollicutes. It is a human pathogen that causes the disease mycoplasma pneumonia, a form of atypical bacterial pneumonia related to cold agglutinin disease. M. pneumoniae is characterized by the absence of a peptidoglycan cell wall and resulting resistance to many antibacterial agents. The persistence of M. pneumoniae infections even after treatment is associated with its ability to mimic host cell surface composition.

Discovery and History

In 1898, Nocard and Roux were the first to isolate a mycoplasma species in culture from bovine, however it was not until 1944 when Mycoplasma pneumoniae, known then as Eaton’s agent, was isolated and described from a patient with primary atypical pneumonia.

First M. pneumoniae was considered as a virus rather than a bacterium, when Eaton and colleagues cultured the causative agent of human primary atypical pneumonia (PAP) or “walking pneumonia“.[3] The terms ‘walking pneumonia and ‘atypical pneumonia’ were coined to describe the unresponsiveness of pneumonia inducing mycoplasma infections to antibiotics like penicillin. Eaton’s agent could be grown in chicken embryos and passed through a filter that excluded normal bacteria. Eaton suggested the possibility that the disease was caused by a mycoplasma, but the agent did not grow on the standard pleuropneumonia-like organism (PPLO) media of the time. These observations led to the conclusion that the causative agent of PAP is a virus. Researchers at that time showed that the cultured agent could induce disease in experimentally infected cotton rats and hamsters. In spite of controversy whether the researchers had truly isolated the causative agent of PAP (based largely on the unusual immunological response of patients with PAP), in retrospect their evidence along with that of colleagues and competitors appears to have been quite conclusive.[4] There were reports linking Eaton’s Agent to the PPLOs or mycoplasmas, well known then as parasites of cattle and rodents, due to sensitivity to antimicrobial. Studies that followed until 1963 determined that Eaton’s agent was a bacterium that caused human lower respiratory tract infections.

Symptoms of Infection

M. pneumoniae is known to cause a host of symptoms such as primary atypical pneumonia, tracheobronchitis, and upper respiratory tract disease. Primary atypical pneumonia is one of the most severe types of manifestation, with tracheobronchitis being the most common symptom and another 15% of cases, usually adults, remain asymptomatic.


Diagnosis of Mycoplasma pneumoniae infections is complicated by the delayed onset of symptoms and the similarity of symptoms to other pulmonary conditions. Often, M. pneumoniae infections are diagnosed as other conditions and, occasionally, non-pathogenic mycoplasmas present in the respiratory tract are mistaken for M. pneumoniae. Historically, diagnosis of M. pneumoniae infections was made based on the presence of cold agglutinins and the ability of the infected material to reduce tetrazolium. Presently, causative diagnosis is dependent upon laboratory testing, however these methods are more practical in epidemiological studies than in patient diagnosis.[2] Culture tests are rarely used as diagnosic tools; rather immunoblotting, immunofluorescent staining, hemadsorption tests, tetrazolium reduction, metabolic inhibition tests, serological assays, and polymerase chain reaction (PCR) are used for diagnosis and characterization of bacterial pneumonic infections.

Treatment and Prevention

The difficulty in eradicating Mycoplasma pneumoniae infections is due to the ability of the bacterium to persist within an individual, as well as the lack of cell wall in M. pneumoniae, which renders multiple antibiotics directed at the bacterial cell wall ineffective in treating infections.[2] M. pneumoniae therefore displays resistance to antimicrobials such as β-lactams, glycopeptides, sulfonamides, trimethoprim, polymixins, nalidixic acid, and rifampin.[2][13] The majority of antibiotics used to treat M. pneumoniae infections are targeted at bacterial rRNA in ribosomal complexes, including macrolides, tetracycline, ketolides, and fluoroquinolone, many of which able to be administered orally.


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