IMR Press / FBL / Volume 23 / Issue 4 / DOI: 10.2741/4611

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.

Open Access Review

Molecular mechanisms of Chlamydia trachomatis resistance to antimicrobial drugs

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1 Clinical Microbiology and Parasitology Unit, Polyclinic “Dr. Zora Profozic”, Bosutska 19, 10 000 Zagreb, Croatia
2 Department of Biomedical Sciences, University Centre Varazdin, University North, 104. brigade 3, 42 000 Varazdin, Croatia
3 Clinical Microbiology Department, Teaching Institute of Public Health “Dr Andrija Stampar”, Mirogojska cesta 16, 10 000 Zagreb, Croatia
4 Medical Microbiology Department, School of Medicine, University of Zagreb, Salata 3, 10 000 Zagreb, Croatia
Front. Biosci. (Landmark Ed) 2018, 23(4), 656–670; https://doi.org/10.2741/4611
Published: 1 January 2018
(This article belongs to the Special Issue Frontiers in sexually transmitted infections)
Abstract

Chlamydia trachomatis (C. trachomatis) is a leading cause of bacterial sexually transmitted infections in developed and undeveloped countries, and therefore a global public health issue. In an era of increasing bacterial resistance to antibiotics, resistance has been an exceedingly rare phenomenon in C. trachomatis; however, clinical treatment failures attributed to multidrug-resistant C. trachomatis strains have been described on several occasions. Cell culture systems using McCoy cells and subsequent immunofluorescent staining are still the most common methodology used for antimicrobial susceptibility testing, but the presence of resistance markers should be appraised by further genetic analysis. Azithromycin resistance of C. trachomatis is often a result of the mutations in the peptidyl transferase region of 23S rRNA genes, tetracycline resistance is usually linked to the presence of foreign genomic islands integrated in chlamydial chromosome, whereas a predominant mechanism of fluoroquinolone resistance is a point mutation in the gyrA quinolone-resistance-determining region. A nucleotide substitution in rpoB gene is responsible for rifampin resistance, and different mechanisms have been involved in the development of resistance to aminoglycosides, lincomycin and sulphonamide/trimethoprim combinations.

Keywords
Chlamydia trachomatis
Antibiotics
Antimicrobial resistance
Genetics
Mutations
Review
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