CHLAMYDIAL INFECTIONS: INTRODUCTION
Three chlamydial species cause human infections: Chlamydia trachomatis, Chlamydophila psittaci, and Chlamydophila pneumoniae. C. psittaci is widely distributed in nature, producing genital, conjunctival, intestinal, or respiratory infections in many mammalian and avian species. Genital infections with C. psittaci have been well characterized in several species and cause abortion and infertility. Although mammalian strains of C. psittaci are not known to infect humans, avian strains occasionally do so, causing pneumonia and the systemic illness known as psittacosis. C. pneumoniae is a fastidious chlamydial species that appears to be a common cause of upper respiratory tract infection and pneumonia, primarily in children and young adults, and is a cause of recurrent respiratory infections in older adults. Studies have also linked C. pneumoniae infection to atherosclerotic cardiovascular disease and perhaps to asthma. No animal reservoir has been identified for C. pneumoniae; it appears to be an exclusively human pathogen spread via the respiratory route through close personal contact. C. trachomatis is also an exclusively human pathogen and was identified as the cause of trachoma in the 1940s. Since then, C. trachomatis has been recognized as a major cause of sexually transmitted and perinatal infection.
Chlamydiae are obligate intracellular bacteria that are classified in their own order, Chlamydiales (Fig. 169-1). They possess both DNA and RNA, have a cell wall and ribosomes similar to those of gram-negative bacteria, and are inhibited by antibiotics such as tetracycline. A unique feature of all chlamydiae is their complex reproductive cycle (Fig. 169-2). Two forms of the microorganism—the extracellular elementary body (EB) and the intracellular reticulate body (RB)—participate in this cycle. The EB is adapted for extracellular survival and is the infective form transmitted from one person to another. EBs attach to susceptible target cells (usually columnar or transitional epithelial cells) and enter the cells inside a phagosome. Within 8 h of cell entry, the EBs reorganize into RBs, which are adapted to intracellular survival and multiplication. They undergo binary fission, eventually producing numerous replicates contained within the intracellular membrane-bound “inclusion body,” which occupies much of the infected host cell. Chlamydial inclusions resist lysosomal fusion until late in the developmental cycle. After 24 h, the RBs condense and form EBs still contained within the inclusion. The inclusion then lyses, releasing EBs from the cell to initiate infection of adjacent cells or transmission to another person. Under some conditions [e.g., exposure to interferon γ (IFN-γ) or antibiotics], an altered life cycle is induced in which large, metabolically inactive RBs persist but do not replicate. Removal of the IFN-γ or antibiotics is followed by restoration of the normal life cycle.
Studies with monoclonal antibodies and nucleotide sequencing of the major outer-membrane protein have delineated at least 20 serotypes of
C. trachomatis. According to the classification of Wang and Grayston, strains associated with trachoma are generally of the A, B, Ba, and C serovars, while serovars D through K are largely associated with sexually transmitted and perinatally acquired infections. Serovars L
1, L
2, and L
3 produce lymphogranuloma venereum (LGV) and hemorrhagic proctocolitis. The LGV strains exhibit unique biologic behavior in that they are more invasive than the other serovars, produce disease in lymphatic tissue, grow readily in cell culture systems and macrophages, and are lethal when inoculated intracerebrally into mice and monkeys. Non-LGV strains of
C. trachomatis characteristically produce infections involving the superficial columnar epithelium of the eye, genitalia, and respiratory tract.
C. trachomatis is an infrequent cause of endocarditis, peritonitis, pleuritis, and possibly periappendicitis and occasionally causes respiratory infections in older children and adults. Some immunosuppressed patients with pneumonia have had either serologic or cultural evidence of
C. trachomatis infection, but more data are necessary to define a pathogenic role for this organism in these patients.
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