Mycoplasma pneumoniae

Mycoplasma pneumoniae
Mycoplasma pneumoniae
Scientific classification
Kingdom: Bacteria
Division: Firmicutes
Class: Mollicutes
Order: Mycoplasmatales
Family: Mycoplasmataceae
Genus: Mycoplasma
Species: M. pneumoniae
Binomial name
Mycoplasma pneumoniae
Somerson et al., 1963

Mycoplasma pneumoniae is a very small bacterium in the class Mollicutes. It causes the disease mycoplasma pneumonia, a form of atypical bacterial pneumonia, and is related to cold agglutinin disease.

Contents

Cell wall/Treatment

This species lacks a peptidoglycan cell wall, like all Mollicutes. Instead, it has a cell membrane that incorporates sterol compounds, similar to eukaryotic cells. It obtains these sterols from the host serum, allowing it to retain a simple structure. Lacking a cell wall, these organisms are resistant to the effects of penicillins and other beta-lactam antibiotics, which act by disrupting the bacterial cell wall. Antibiotics with activity against these organisms include certain macrolides (erythromycin, azithromycin, clarithromycin), fluoroquinolones and their derivatives (e.g., ciprofloxacin, levofloxacin), and tetracyclines (e.g., doxycycline). The outer most boundary is three layered plasma membrane called trilaminar unit membrane.

Genome

M. pneumoniae has one of the smallest genomes known, with 816 kilobase pairs (kbs). Its genome and proteome have been fully characterized. It uses some unique genetic code, making its code more similar to mitochondria than to other bacteria. Thus it is said that Mycoplasma pneumoniae has a degenerate genome. It lacks the cellular machinery for making many essential compounds, including new purines and pyrimidines. It also has no tri-carboxylic acid cycle and an incomplete electron transport chain. Because of this, it is an obligate parasite and is never found free-living.

History

M. pneumoniae was historically known as "Eaton's agent."[1]

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."[2] This agent could be grown in chicken embryos and passed through a filter that excluded normal bacteria. However, it could not be observed by high magnification light microscopy, and it caused a pneumonia that could not be treated with the antimicrobials sulphonamides and penicillin.[2] Eaton suggested the possibility that the disease was caused by a mycoplasma, but the agent did not grow on the standard 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.[3] 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 compounds (e.g., organic gold salt).[4]

In the early 1960s, Leonard Hayflick, then at the Wistar Institute in Philadelphia, was first to isolate and cultivate the causative agent of primary atypical pneumonia (the Eaton Agent). He identified the agent as a mycoplasma and named it Mycoplasma pneumoniae.[5] The ability to grow Eaton's agent, now known as Mycoplasma pneumoniae, in cell-free media allowed an explosion of research into what had overnight become the most medically important mycoplasma and what was to become the most studied mycoplasma.

References

  1. ^ Dajani, A.S.; W.A. Clyde Jr. and F.W. Denny (1965). "EXPERIMENTAL INFECTION WITH MYCOPLASMA PNEUMONIAE (EATON'S AGENT)". The Journal of Experimental Medicine 121 (6): 1071–1086. doi:10.1084/jem.121.6.1071. PMC 2138014. PMID 14319403. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2138014. 
  2. ^ a b Eaton MD, Meiklejohn G, van Herrick W, Corey M (1945). "STUDIES ON THE ETIOLOGY OF PRIMARY ATYPICAL PNEUMONIA : III. SPECIFIC NEUTRALIZATION OF THE VIRUS BY HUMAN SERUM". J. Exp. Med. 82 (5): 329–42. doi:10.1084/jem.82.5.329. PMC 2135563. PMID 19871504. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2135563. 
  3. ^ Marmion BP (1990). "Eaton agent—science and scientific acceptance: a historical commentary". Rev. Infect. Dis. 12 (2): 338–53. doi:10.1093/clinids/12.2.338. PMID 2109871. 
  4. ^ Marmion BP, Goodburn GM (January 1961). "Effect of an organic gold salt on Eaton's primary atypical pneumonia agent and other observations". Nature 189 (4760): 247–8. doi:10.1038/189247a0. PMID 13767007. 
  5. ^ Proceedings of the US National Academy of Sciences, 1962, 48, 41-49.

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