Aetiology

Humans are the only hosts for Mycoplasma pneumoniae.[4] Transmission of M pneumoniae occurs from human to human via aerosols.[4][16][17]

Pathophysiology

Mycoplasma pneumoniae is mainly a mucosal pathogen, but during disease it may have a systemic spread.[4][18][19]

M pneumoniae disease is initiated by its attachment to the respiratory epithelium via a unique tip organelle. This organelle contains P1 adhesin and facilitates adherence and gliding motility. Following cytoadherence in the respiratory tract, M pneumoniae induces localised tissue disruption and cytotoxicity through production of hydrogen peroxide and other free radicals. The subsequent immune response, mediated by macrophages and lymphocytes, exacerbates clinical illness and contributes to pulmonary injury. Damage to epithelial cilia is associated with severe and persistent cough.[4][20]

M pneumoniae may have an intracellular lifestyle enabling it to escape from the immune system.[21] It may produce toxins that cause persistent cough, and the immunological response to M pneumoniae, particularly the release of pro-inflammatory cytokines, rarely also promotes acute exacerbations of asthma.[4][20][22][Figure caption and citation for the preceding image starts]: Proposed pathophysiologic cascade of Mycoplasma pneumoniae pneumonia in humansSaraya T, Kurai D, Nakagaki K, et al. Novel aspects on the pathogenesis of Mycoplasma pneumoniae pneumonia and therapeutic implications. Front Microbiol. 2014;5:410. (CC BY 2.0). [Citation ends].com.bmj.content.model.Caption@839f11e

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