A Cellular And Genetic Study On Resistance To Antibiotics Of Chlamydia Trachomatis In Tianjin

In recent years , genital tract infection with Chlamydia Trachomatis is highly prevalent in most areas of the world investigated. C. t can cause urethritis,cervicitis, conjunctivities, pelviperitonitis, lymphogranuloma and accompanied with severe complications and sequelaes, so the treatment of C. t infection is very important. But now more and more cases about resistance to antimicrobial agents have been reported for C. t.Failures of treatments of C. t infection are often seen in clinic, which have caused the attention of many schoolars.Our experiment is based on Chlamydia trachomatis cell culture to detect the in vitro susceptibilities of C. t to Tetracycline, Azithromycine and Moxifloxacin which are now mostly used in clinical. 30 wild C. t isolates were cultured in McCoy cells with drugs of a series of concentrations. MIC was determined as the lowest concentration under which there were no C. t inclusions forming. The resistance wild strains found were detected with PCR(polymerase chain reaction) for resistance gene in order to study the possible mechanism of resistance.The results demonstrated that 2 wild strains were resistant to tetracycline(MIC>5mg/L) and 6 wild strains were high-sensitive to tetracycline(MIC<1 mg/L) and 22 strains were middle-sensitive to tetracycline with MIC between 1-5mg/L. ALL the wild strains detected were sensitive to Azithromycine and Moxif loxacine with MIC<0.5mg/L and MIC<0.12mg/L respectively. Two resistance strains were amplified withthe primers of tetracycline resistant determinant (tetM). The amplified results were positive while four sensitive strains were all negative. We can conclude from the experiment that in Tianjin the clinical wild isolates of Chlamydia trachomatis have already been resistant to tetracycline. The resistant strains were sensitive to Azithromycine and Moxifloxacine, so we can use these two drugs to treat patients failed to recover with tetracyclines. TetM gene segments were amplified from the plasmid DNA of the two resistance strains so the mechanism might be that the transposon carried tetM integrated into the plasmid DNA to express resistance. Further study is needed to support this assumption.