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Somerson et al., 1963
Mycoplasma pneumonia is caused by Mycoplasma pneumoniae, a very small bacterium that lacks cell wall and periplasmic space. On Gram-stain, Mycoplasma stains pink, i.e. it is Gram-negative by staining. However, it is structurally different from other Gram-negative organisms because it lacks a cell wall.
M. pneumoniae is the bacterium responsible for Mycoplasma pneumonia, an atypical pneumonia common in children and young adults.
- Bacteria; Firmicutes; Mollicutes; Mycoplasmatales; Mycoplasmataceae; Mycoplasma pneumoniae
- The term Mycoplasma (“mykes”, meaning fungus and “plasma”, meaning formed) is derived from the fungal-like growth of some mycoplasma species.
- Mycoplasma is the smallest self-replicating organism. They are bacteria that lack a cell wall and periplasmic space, have reduced genomes, and limited metabolic activity.
- Mycoplasma pneumoniae cells have an elongated shape that is approximately 1-2 µm in length and 0.1–0.2 µm in width.
- The extremely small cell size means they are incapable of being examined by light microscopy; a stereomicroscope is required for viewing the morphology of M. pneumoniae colonies, which are usually less than 100 µm in length. The inability to synthesize a peptidoglycan cell wall is due to the absence of genes encoding its formation and results in an increased importance in maintenance of osmotic stability to avoid desiccation. The lack of a cell wall also calls for increased support of the cell membrane, which includes a rigid cytoskeleton composed of an intricate protein network and, potentially, an extracellular capsule to facilitate adherence to the host cell.
- M. pneumoniae are the only bacterial cells that possess cholesterol in their cell membrane (obtained from the host) and possess more genes that encode for membrane lipoprotein variations than other mycoplasmas, which are thought to be associated with its parasitic lifestyle. M. pneumoniae cells also possess an attachment organelle, which is used in the gliding motility of the organism by an unknown mechanism.
- The absence of a peptidoglycan cell wall results in 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.
- On Gram-stain, Mycoplasma stains pink, i.e. it is Gram-negative by staining. However, it is structurally different from other Gram-negative organisms because it lacks a cell wall.
- Sequencing of the M. pneumoniae genome in 1996 revealed it is 816,394 bp (approximately 800 kb) in size. The genome contains 687 genes that encode for proteins, of which about 56.6% code for essential metabolic enzymes; notably those involved in glycolysis and organic acid fermentation.
- M. pneumoniae is consequently very susceptible to loss of enzymatic function by gene mutations, as the only buffering systems against functional loss by point mutations are for maintenance of the pentose phosphate pathway and nucleotide metabolism.
- Loss of function in other pathways is suggested to be compensated by host cell metabolism.
- In addition to the potential for loss of pathway function, the reduced genome of M. pneumoniae outright lacks a number of pathways, including the TCA cycle, respiratory electron transport chain, and biosynthesis pathways for amino acids, fatty acids, cholesterol and purines and pyrimidines.
- These limitations make M. pneumoniae dependent upon import systems to acquire essential building blocks from their host or the environment that cannot be obtained through glycolytic pathways.
- Along with energy costly protein and RNA production, a large portion of energy metabolism is exerted to maintain proton gradients (up to 80%) due to the high surface area to volume ratio of M. pneumoniae cells. Only 12 – 29% of energy metabolism is directed at cell growth, which is unusually low for bacterial cells, and is thought to be an adaptation of its parasitic lifestyle. Unlike other bacteria, M. pneumoniae uses the codon UGA to code for tryptophan rather than using it as a stop codon.
- Ken; Waites, B; Deborah, F. Talkington (2004). "Mycoplasma pneumoniae and Its Role as a Human Pathogen". Clin. Microbiol. Rev. 17 (4): 697–728. doi:10.1128/CMR.17.4.697-728.2004.
- Romero-Arroyo, C. E.; Jordan, J.; Peacock, S. J.; Willby, M. J.; Farmer, M. A.; Krause, D. C. (1994). "Mycoplasma pneumoniae protein P30 is required for cytadherence and associated with proper cell development". J. Bacteriol. 181: 1079–1087. doi:10.1128/CMR.17.4.697-728.2004.
- S. Dallo, and J. Baseman "Intracellular DNA replication and long-term survival of pathogenic mycoplasmas" Microb. Pathog. 2000; 29, 301–309. Template:10.1006/mpat.2000.0395
- Wodke, J. A. H.; Puchałka, J.; Lluch-Senar, M.; Marcos, J.; Yus, E.; Godinho, M.; Gutiérrez-Gallego, R.; Serrano, L.; Klipp, E.; Maier, T. "Dissecting the energy metabolism in Mycoplasma pneumoniae through genome-scale metabolic modeling". Mol. Syst. Biol. 2010: 9. doi:10.1038/msb.2013.6.