Pathogenesis:

The pathogenesis of the microorganism has two properties: 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. Colonization of the respiratory tract by M. pneumoniae results in the cessation of ciliary movement. The normal clearance mechanisms of the respiratory tract do not function, resulting in contamination of the respiratory tract and the development of a dry cough.

Mycoplasma pneumonia cause infection primarily as extracellular parasites, attaching to the surface of ciliated and nonciliated epithelial cells. This is done by the P1 adhesin protein that localizes themselves at the tips of the bacterial cells and binds to sialic acid residues on host epithelial cells. The attachment site, or receptor, is a complex carbohydrate structurally akin to antigen I of red blood cells. Following attachment, mycoplasmal organisms may cause direct cytotoxic damage to epithelial cells because of hydrogen peroxide generation or cytolysis via an inflammatory response mediated by mononuclear cells or antigen-antibody reactions.

Mycoplasma pneumoniae is also thought to be involved in mediating other diseases and infections in its monopolization of the immune response. Some patients have developed severe bacterial and viral infections just after or during a M. pneumoniae infection. This is thought to occur by the creation of an environment that is anatomically, physiologically, and/or immunologically conducive to other organisms for invasion as well as for cellular damage.

The diagram above illustrates mycoplasmas (red) infecting epithelial cells (black). The mycoplasmas form a small structure called a "tip" by which they adhere to the epithelial cells. If the mycoplasmas are prevented from adhering to the epithelial cells, they are avirulent.