File:12035 2012 8320 Fig3 HTML.webp

English: Chlamydiae are Gram-negative bacteria. They are obligate intracellular parasites because their multiplication depends on the host cell for energy and various nutrients. Chlamidiae have evolved a unique biphasic developmental cycle in which they alternate two distinct morphological forms: the elementary body (EB) and the reticulate body (RB). EBs are small tight bodies and represent the metabolically inactive form of bacteria, which can resist environmental stress and survive outside a host for a limited time. Infection begins with the attachment of the EB to the surface of susceptible host cells, followed by its internalization by endocytosis and the formation of phagosomes (Chlamydia inclusions) that are heavily modified by chlamydial proteins which prevent their fusion with lysosomes. Shortly after uptake, EBs differentiate into the metabolically active form of RB and begin to replicate within the phagosomes. RBs replicate by binary fission that, after 24–72 h, becomes asynchronous, with some RBs converting back to EBs. Finally, EBs are released from infected cells, often after causing the death of the host cells, and can infect new cells, either in the same organism or in a new host. C. pneunoniae was classified as the third species of Chlamidia and was associated in humans with acute infections of the lower respiratory tract. It is recognized as a common cause of mild pneumonia in children and young adults. It infects both epithelial cells and macrophages within the lungs and may be disseminated to sites outside of the lungs by infected monocytes and macrophages. Infection may also persist or, alternatively, the bacterium may be present in asyntomatic patients. Recently, a large volume of research showed evidence that C. pneumoniae may contribute directly and indirectly (immuno-mediated) to atherosclerosis. Indeed, it was one of the few infectious agents that have been found within and isolated from cells of human atherosclerotic plaques