Figure 1. Proposed schematic pathomechanisms in M. pneumoniae encephalitis.

(Left) Respiratory tract infection. M. pneumoniae resides mostly extracellularly on epithelial surfaces. Its close association allows the production of direct injury by a variety of local cytotoxic effects. Furthermore, it can induce inflammatory responses, elicited by both adhesion proteins and glycolipid epitopes that result in pneumonia. (Right) Encephalitis. Extrapulmonary disease of the CNS is characterized by systemic dissemination with resultant direct infection and local tissue injury (A) or immune-mediated injury (B,C). The latter may occur as a result of cross-reactive antibodies against myelin components, e.g., gangliosides and galactocerebroside C. These antibodies could theoretically have originated from intrathecal synthesis (B) or from outside the CNS (C). Figure adapted from [1]; see references in the text.