Mycoplasma pneumonia pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Mycoplasma pneumoniae is transmitted through airborne droplets from person-to-person. M. pneumoniae is primarily an extracellular pathogen that has evolved a specialized attachment organelle for close association with host cells. The organism's tropism for respiratory epithelial cells and its synthesis of hydrogen peroxide aid in the pathogenesis of Mycoplasma. Additionally, Mycoplasma produces community acquired respiratory distress syndrome (CARDS) toxin, a unique virulence factor which activates the host's inflammatory pathways and airway dysfunction.
Pathophysiology
Transmission
- Mycoplasma is thought to be exclusively a human pathogen.[1]
- Mycoplasma pneumoniae is transmitted through airborne droplets from person-to-person.
- Incubation period ranges from 1 to 4 weeks.[1]
Host Invasion
- M. pneumoniae is primarily an extracellular pathogen that has evolved a specialized attachment organelle for close association with host cells.[1]
- M. pneumoniae’s uses sialoglycoproteins or sialoglycolipid receptors for attachment.
- The close association between M. pneumoniae and the host cells prevents the bacterium from being eliminated by the host’s mucociliary clearance mechanisms.
- Following attachment, Mycoplasma uses adhesion proteins to adhere to the host cell. Adhesion proteins include P1 and P30.
- Once adhered to the mucosa of a host organism, M. pneumonia extracts nutrients, grows and is then able to undergo binary fission to reproduce.
- Mycoplasma damages the respiratory epithelial cells at the base of cilia, activating the innate immune response and producing local cytotoxic effects.[1]
- While M. pneumoniae primarily lives on the surface of the respiratory epithelial cells, it has also been shown to invade tissues and replicate intracellularly.
- The endocytosis of M. pneumoniae by the host cells could aid in the establishment of a latent or chronic disease state, facilitate the bacterium in evading an immune response, or interfere with the efficacy of certain drug therapies.[1]
- M. pneumoniae has the following features which aid in its pathogenesis:[1]
- Tropism for respiratory epithelial cells
- Production of hydrogen peroxide, which results in the production of reactive oxygen species and subsequent damage to the respiratory tract and membranes of red blood cells
- Attachment sites include the upper and lower respiratory tract, causing pharyngitis, bronchitis and pneumonia.
- Pneumonia results from the host's production of macrophages, immunoglobulins (IgA, IgG, and IgM).
Virulence Factor - CARDS Toxin
- M. pneumoniae produces community acquired respiratory distress syndrome (CARDS) toxin, a unique virulence factor.[1]
- The CARDS toxin most likely aids in the colonization and pathogenic pathways of M. pneumoniae, leading to activation of cytokines, inflammation, and airway dysfunction.[1]