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Chlamydiae that infect humans are divided into three species, Chlamydia trachomatis, Chlamydia pneumoniae, and Chlamydia psittaci, on the basis of antigenic composition, intracellular inclusions, sulfadiazine susceptibility, and disease production. The separation of the genus Chlamydia into the genera Chlamydia and Chlamydophila was controversial; in this chapter, the three chlamydiae that are pathogens of humans are considered to be in the genus Chlamydia in keeping with publications that do not support the new taxonomy. Other chlamydiae infect animals but rarely if ever infect humans. All chlamydiae exhibit similar morphologic features, share a common group antigen, and multiply in the cytoplasm of their host cells by a distinctive developmental cycle. The chlamydiae can be viewed as gram-negative bacteria that lack mechanisms for the production of metabolic energy and cannot synthesize adenosine triphosphate (ATP). This restricts them to an intracellular existence, where the host cell furnishes energy-rich intermediates. Thus, chlamydiae are obligate intracellular pathogens.

Developmental Cycle

All chlamydiae share a common and unique biphasic developmental cycle. The environmentally stable infectious particle (transmissible form) is a small cell called the elementary body (EB). These are about 0.3 μm in diameter (Figure 27-1) with an electron-dense nucleoid. The EB membrane proteins have highly cross-linked membrane proteins. The EBs have a high affinity for host epithelial cells and rapidly enter them. The first step in entry involves interaction between outer membrane proteins of the EB and heparin sulfate proteoglycan of the host cells. The second step involves additional and irreversible binding to a variety of other host cell receptors. There appear to be multiple adhesins, such as OmcB, the major outer membrane protein (MOMP), glycosylated MOMP, and other surface proteins. Following adherence, the mechanisms thought to mediate entry into the host cell also vary and involve cytoskeletal rearrangements and activation of type III secretion systems and other effectors. EBs are usually seen attached near the base of microvilli, where they are subsequently engulfed by the host cell. More than one mechanism appears to be functional: receptor-mediated endocytosis into clathrin-coated pits and pinocytosis via noncoated pits. Lysosomal fusion is inhibited, creating a protected membrane-bound environment around the chlamydiae. Shortly after entry into the host cell, the disulfide bonds of the EB membrane proteins are reduced (no longer cross-linked), and the EB is reorganized into a larger structure called a reticulate body (RB) [replicative form] measuring about 0.5–1 μm (see Figure 27-1) and devoid of an electron-dense nucleoid. Within the membrane-bound vacuole, the RB grows in size and divides repeatedly by binary fission. Eventually, the entire vacuole becomes filled with EBs derived from the RBs to form a cytoplasmic inclusion. The newly formed EBs may be liberated from the host cell to infect new cells. The developmental cycle takes 48–72 hours.


Chlamydiae. A: Thin section electron micrograph of chlamydiae in various stages of ...

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