Mycoplasma pneumoniae infections have a wide spectrum of clinical symptoms and disease manifestations. Pneumonia caused by M. pneumoniae is a type of atypical bacterial pneumonia. Before tests to diagnose M. pneumoniae were available, pneumonia caused by M. pneumoniae was considered “atypical” given the differences in clinical presentation and response to treatment used for “typical” pneumonia. The varied presentation and limited diagnostic methods available present unique challenges for accurately identifying M. pneumoniae cases and appropriately treating patients.
The true magnitude of this health issue in the United States is unknown. However, an estimated 2 million cases of M. pneumoniae infections occur each year. Experts estimate that M. pneumoniae infections account for between 1 and 10 in every 50 cases of community-acquired pneumonia
M. pneumoniae lacks a rigid cell wall, allowing it to alter its size and shape to suit its surrounding conditions. Therefore, antimicrobials that work by targeting the cell wall, like beta-lactams, do not work against these bacteria. Due to its lack of a cell wall, M. pneumoniae is extremely susceptible to desiccation. Thus, bacterial transmission from person to person by airborne droplets only occurs through close contact.
M. pneumoniae bacteria spread from person-to-person contact by respiratory droplets. and is exclusively a human pathogen. M. pneumoniae is primarily an extracellular pathogen that has evolved a specialized attachment organelle for close association with host cells. This attachment is critical to the bacteria’s survival and ability to infect. The close association between M. pneumoniae and the host cells prevents the host’s mucociliary clearance mechanisms from removing the bacterium. The bacterium attaches to and damages the respiratory epithelial cells at the base of cilia. This activates the innate immune response and produces local cytotoxic effects.
Role of toxin production
M. pneumoniae produces a unique virulence factor known as Community Acquired Respiratory Distress Syndrome (CARDS) toxin. The CARDS toxin most likely aids in the colonization and pathogenic pathways of M. pneumoniae, leading to inflammation and airway dysfunction. While M. pneumoniae primarily lives on the surface of the respiratory epithelial cells, it can 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
- Interfere with the efficacy of certain drug therapies
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