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Chlamydiae are eubacteria that are currently separated into four species: Chlamydia psittaci and Chlamydia pecorum, which are important animal pathogens, and Chlamydia trachomatis and Chlamydia pneumoniae, which are significant agents of sexually transmitted, ocular, respiratory, and other infections in humans. Chlamydiae possess several intriguing features that are unique among eubacteria. One such feature is their unique developmental cycle, which takes place entirely within a cytoplasmic inclusion vacuole in a eucaryotic host cell (recently reviewed in references 7 and 33). The cycle is initiated when an elementary body (EB) is taken into a host cell by receptormediated endocytosis. Extracellular EBs are very small cocci (about 0.3 mm in diameter) that are metabolically inert and osmotically stable. Within minutes after an EB enters a host cell, its dormancy is broken and it commences a lengthy reorganization process which converts it into the reticulate body (RB) form. The RBs are about 1 mm in diameter, divide by binary fission, and are osmotically fragile. RBs divide logarithmically from about 6 h to about 20 h postinfection. The cycle becomes asynchronous by 20 h, with some RBs continuing to divide while others begin to reorganize into the infectious EB form. Generally, the host continues to support chlamydial growth until 30 to 72 h postinfection before it lyses and a mixture of several hundred RBs, EBs, and intermediate forms is released. At least one reason for the restriction of chlamydiae to an intracellular environment for growth is their apparent inability to generate ATP by respiratory or fermentative metabolism. To compensate for this deficiency, RBs scavenge host-supplied NTPs by translocation mechanisms. Another unusual feature of chlamydiae is their cell envelope structure, a subject recently reviewed by Raulston (40). The envelope is gram negative in that it includes an inner membrane and a lipopolysaccharide-containing outer membrane. Unique features include 18 to 22 regularly-spaced domeshaped surface projections, which are observed by scanning electron microscopy on only one hemisphere of both EBs and RBs (17, 29). Transmission electron microscopic studies suggest that fibrillar projections extend through these domes and possibly through the vacuolar membrane within which RBs divide (27, 28, 39). Neither the function nor the chemical composition of these structures is known. Perhaps the most striking feature of the chlamydial envelope is its apparent lack of peptidoglycan (PG), although chlamydiae possess penicillinbinding proteins (3) and are sensitive to drugs that inhibit PG synthesis, such as penicillin G and D-cycloserine. The conclusion that chlamydiae lack PG is based largely on the failure to detect muramic acid in chlamydiae (3, 16). Supporting observations include the failure to detect a PG layer by electron microscopy and the failure of antibodies directed against PG to react with chlamydiae (24). When infected cells are incubated with suitable concentrations of penicillin or D-cycloserine, cell division is inhibited, abnormal RB forms accumulate in the inclusion vacuole, and the development of infectious EBs does not occur. The abnormal forms are many times the size of normal RBs and contain internal membranous structures resembling miniature chlamydiae (30, 36). Generation of normal RBs and reorganization of RBs to EBs occurs upon the removal of penicillin or D-cycloserine. Morphologically similar abnormal forms can be induced in infected cells by treatment with interferon-g and starvation of amino acids (6, 10).

Disulfide cross-linked envelope proteins: the functional equivalent of peptidoglycan in chlamydiae?