What is the pathophysiology of mycoplasmal pneumonia?

Updated: Dec 28, 2018
  • Author: Michael Joseph Bono, MD, FACEP; Chief Editor: Guy W Soo Hoo, MD, MPH  more...
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The organism responsible for mycoplasmal pneumonia, M pneumoniae, is a pleomorphic organism that, unlike bacteria, lacks a cell wall, and unlike viruses, does not need a host cell for replication. The prolonged paroxysmal cough seen in this disease is thought to be due to the inhibition of ciliary movement. M pneumoniae has a remarkable gliding motility and specialized tip organelles that allows it to burrow between cilia within the respiratory epithelium, eventually causing sloughing of the respiratory epithelial cells.

The organism has two properties that seem to correlate well with its pathogenicity in humans. The first is a selective affinity for respiratory epithelial cells and the second is the ability to produce hydrogen peroxide, which is thought to be responsible for much of the initial cell disruption in the respiratory tract and for damage to erythrocyte membranes.

The pathogenicity of M pneumoniae has been linked to the activation of inflammatory mediators, including cytokines. One study reported on an emergence of drug-resistant M pneumoniae infection. However, the study concluded that host immune maturity and not the virulence factor of the organism is a major determinant factor of disease severity. [4] Macrolide-resistant M pneumoniae has emerged in adult community-acquired pneumonia [5] as well as pediatric pneumonia. [6, 7, 8, 9, 10]

Mycoplasma pneumoniae has been identified with an increasing array of illnesses, such as acute hepatitis, [11, 12] immune thrombocytopenic purpura, [13] severe autoimmune hemolytic anemia, [14] Stevens-Johnson syndrome, [15, 16] arthritis, [17] and transverse myelitis. [18, 19]

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