Mycoplasma pneumoniae

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Mycoplasma pneumoniae
Scientific classification
Domain:	Bacteria
Phylum:	Mycoplasmatota
Class:	Mollicutes
Order:	Mycoplasmatales
Family:	Mycoplasmataceae
Genus:	Mycoplasma
Species:	M. pneumoniae
Binomial name
Mycoplasma pneumoniae Somerson et al., 1963

Mycoplasma pneumoniae is a species of very small-cell bacteria that lack a cell wall, in the class Mollicutes. M. pneumoniae is a human pathogen that causes the disease Mycoplasma pneumonia, a form of atypical bacterial pneumonia related to cold agglutinin disease.

It is one of the smallest self-replicating organisms and its discovery traces back to 1898 when Nocard and Roux isolated a microorganism linked to cattle pneumonia. This microbe shared characteristics with pleuropneumonia-like organisms (PPLOs), which were soon linked to pneumonias and arthritis in several animals. A significant development occurred in 1944 when Monroe Eaton cultivated an agent thought responsible for human pneumonia in embryonated chicken eggs, referred to as the "Eaton agent." This agent was classified as a bacteria due to its cultivation method and because antibiotics were effective in treating the infection, questioning its viral nature. In 1961, a researcher named Robert Chanock, collaborating with Leonard Hayflick, revisited the Eaton agent and posited it could be a mycoplasma, a hypothesis confirmed by Hayflick’s isolation of a unique mycoplasma, later named Mycoplasma pneumoniae. Hayflick’s discovery proved M. pneumoniae was responsible for causing human pneumonia.

Taxonomically, Mycoplasma pneumoniae is part of the Mollicutes class, characterized by their lack of a peptidoglycan cell wall, making them inherently resistant to antibiotics targeting cell wall synthesis, such as beta-lactams. With a reduced genome and metabolic simplicity, mycoplasmas are obligate parasites with limited metabolic pathways, relying heavily on host resources. This bacterium uses a specialized attachment organelle to adhere to respiratory tract cells, facilitating motility and cell invasion. The persistence of M. pneumoniae infections even after treatment is associated with its ability to mimic host cell surface composition.

Pathogenic mechanisms of M. pneumoniae involve host cell adhesion and cytotoxic effects, including cilia loss and hydrogen peroxide release, which lead to respiratory symptoms and complications such as bronchial asthma and chronic obstructive pulmonary disease. Additionally, the bacterium produces a unique CARDS toxin, contributing to inflammation and respiratory distress. Treatment of M. pneumoniae infections typically involves macrolides or tetracyclines, as these antibiotics inhibit protein synthesis, though resistance has been increasing, particularly in Asia. This resistance predominantly arises from mutations in the 23S rRNA gene, which interfere with macrolide binding, complicating management and necessitating alternative treatment strategies.