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Atypical pneumonia in humans is most often caused by Mycoplasma pneumoniae.
It spreads mainly through respiratory droplets.
M. pneumoniae initiates infection in the respiratory tract by attaching to the apical surface of the ciliated epithelial cells.
It uses a specialized surface protein called P1 adhesin to bind to glycoprotein receptors on the epithelial cells.
Once attached, the bacteria halt ciliary movement of epithelial cells. This prevents clearance of mucus and traps inhaled particles in the airways.
The bacteria also release virulence factors, such as the CARDS toxin, which damage epithelial cells and lead to cell death.
The accumulation of mucus and cellular debris results in airway inflammation.
This environment supports further growth of M. pneumoniae and may enable secondary infections.
Clinically, atypical pneumonia presents with a persistent dry cough, sore throat, and low-grade fever.