[Clinical aspects, diagnosis and treatment of urogenital Chlamydia infection].
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Chlamydia pneumoniae is associated with several chronic human diseases, including chronic obstructive pulmonary disease and atherosclerotic cardiovascular disease. During chronic disease, organisms are believed to exist in a persistent phase that is not well understood at the genetic level. Long-term in vitro continuous infections are spontaneously persistent and are less susceptible than in vitro acute infections to treatment with antibiotics, and are therefore particularly relevant as an in vitro model of in vivo chronic disease. Real-time reverse transcriptase-PCR (r-t RT-PCR) was used to quantitate transcript copy numbers of 13 genes in continuous and acute infections with C. pneumoniae. The set of genes studied encodes proteins with known or predicted functions in the cell membrane, the inclusion membrane, cell division, metabolism, and immunopathology. Significant upregulation was seen for five genes (CPn0483, nlpD, ompA, pmp1 and porB) in continuous cultures. The genes omcB, pmp1, and porB, all of which encode membrane proteins, shared similar patterns of expression over both acute and continuous profiles. These results show that Chlamydia in the long-term continuous model of persistence have a unique transcription profile, adding to our knowledge of regulation of this important stage of chlamydial growth.
Chlamydia trachomatis has been recognized as a pathogen of trachoma, nongonococcal urethritis, salpingitis, endocervicitis, pelvic inflammatory disease, inclusion conjunctivitis of neonates, follicular conjunctivitis of adults, infantile pneumonia and associated conditions. Chlamydial infections during pregnancy may also cause a variety of perinatal complications. Different antigenic strains of C. trachomatis from endocervical, nasopharyngeal and conjunctival origins have been associated with different clinical conditions. Control programs emphasizing early diagnosis, targeted screening, and effective treatment will lead to an eventual decline in the incidence of perinatal chlamydial infection. This review focuses on current problems of perinatal C. trachomatis infections in the aspects of microbiological and immunological pathogenesis.
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This is a screening study for chlamydial infections (1153 patients females). In the number of 272 cases (23.59%) chlamydial infection was confirmed by ELISA blood tests. We purpose to determine the risk factors for tubal infertility, because Chlamydia trachomatis (CT) is the most important cause of pelvic inflammatory disease (PID) and permanent tubal damage. High correlations (correlation coefficient-"r") of chlamydial infection with hygienic level (r=0.51), avoided use of condoms (r=0.58) or number of abortions (r=0.65) were noticed. Results with primary prevention through sexual education have been disappointing, so is necessary preventing or limiting sequelae of chlamydial infection, such as PID and tubal infertility.
Chlamydia pneumoniae is an obligate intracellular human pathogen that causes acute respiratory diseases such as pneumonia and bronchitis. Previous studies have established that C. pneumoniae can induce cytokines in mouse and/or human cells, but little information is available on the cytokine response of respiratory epithelial cells, a first line of infection. In this study, heparin treatment of C. pneumoniae significantly reduced its ability to induce interleukin 8 (IL-8) and tumor necrosis factor alpha (TNF-alpha) mRNA in human lung carcinoma cells, indicating that cytadherence is an important early stimulus for induction of proinflammatory mediators. Although the IL-8, gamma interferon, and TNF-alpha message was consistently induced by infection of A549 cells not treated with heparin, only an elevation of IL-8 protein was detected in A549 supernatants. A549 IL-beta and IL-6 mRNA and supernatant protein profiles were not significantly changed by infection. Heat or UV inactivation of C. pneumoniae only partially reduced the cytokine response, and inhibition of C. pneumoniae protein or DNA synthesis did not affect its ability to induce cytokine gene expression. To prevent stress-induced cytokine release by the A549 cells, centrifugation was not utilized for infection experiments. These experiments establish the importance of cytadherence in cytokine release by cells of respiratory epithelial origin and suggest that further work in the area of cytokine mediators is warranted to gain valuable pathogenic and therapeutic insights.
OBJECTIVE: The possibility that some bacterial-specific factor(s) may play a role in triggering Chlamydia trachomatis reactive arthritis was investigated. METHODS: Since the variable domains of the major outer membrane protein (MOMP) contain the serovar-determining epitopes of C. trachomatis, the ability of serum IgG to recognize peptides mimicking these epitopes was determined in 2 groups of infected patients, one with and the other without reactive arthritis. Because asymptomatic C. trachomatis infections are frequent, and nonspecific reactions due to inflammation could be observed, this study was also performed with samples from healthy blood donors and from patients with inflammatory arthritis unrelated to C. trachomatis infection. RESULTS: A predominant reactivity against peptides duplicating the J serovar-specific epitopes was only observed in the group of patients with reactive arthritis. For positive samples, differences between the two groups of C. trachomatis-infected patients were clearly observed. The mean numbers of positive responses obtained for each of the 7 peptides of the MOMP domain I or each of the 8 peptides of the MOMP domain IV were significantly higher for samples from patients with reactive arthritis (4.7 and 6) than for those from patients with only C. trachomatis urogenital infection (1.3 and 2.9). CONCLUSION: Patients with reactive arthritis had a pattern of reactivities that was compatible with infection by several serotypes of bacteria. Repeated exposures to C. trachomatis might therefore be involved in the development of the disease.
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