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 because it does not respond to sulfonamides or penicillin (beta-lactams). 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 was first isolated from the sputum of a patient with primary “atypical” pneumonia in 1944. Scientists thought the bacterium was a virus until they observed that antibiotics could be effective against it.
The cell volume of M. pneumoniae is less than 5% of the cell volume of a typical bacillus. The small cellular mass means:
- It can pass through filters typically used to remove bacteria.
- Light microscopy cannot detect it.
- It does not produce visible turbidity in liquid growth media. In order to get a visual confirmation of growth, M. pneumoniae cultures use specialized media.
M. pneumoniae lacks a rigid cell wall, allowing it to alter its size and shape to suit its surrounding conditions. It is also intrinsically resistant to antimicrobials, like beta-lactams, that work by targeting the cell wall. 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 spread through airborne droplets from person to person 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.
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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- Page last reviewed: April 13, 2018
- Page last updated: April 13, 2018
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