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Pregled bibliografske jedinice broj: 1250174

Molecular mechanisms of Chlamydia trachomatis resistance to antimicrobial drugs


Meštrović, Tomislav; Ljubin-Sternak, Sunčanica
Molecular mechanisms of Chlamydia trachomatis resistance to antimicrobial drugs // Frontiers in bioscience-Landmark, 23 (2018), 4; 656-670 doi:10.2741/4611 (međunarodna recenzija, pregledni rad, znanstveni)


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Naslov
Molecular mechanisms of Chlamydia trachomatis resistance to antimicrobial drugs
(Molecular mechanisms of Chlamydia trachomatis resistance to antimicrobial drugs)

Autori
Meštrović, Tomislav ; Ljubin-Sternak, Sunčanica

Izvornik
Frontiers in bioscience-Landmark (2768-6701) 23 (2018), 4; 656-670

Vrsta, podvrsta i kategorija rada
Radovi u časopisima, pregledni rad, znanstveni

Ključne riječi
chlamydia trachomatis ; antimicrobial resistance ; antibiotics

Sažetak
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.

Izvorni jezik
Engleski

Znanstvena područja
Temeljne medicinske znanosti, Kliničke medicinske znanosti



POVEZANOST RADA


Ustanove:
Medicinski fakultet, Zagreb,
Nastavni zavod za javno zdravstvo "Dr. Andrija Štampar",
Sveučilište Sjever, Koprivnica

Poveznice na cjeloviti tekst rada:

doi

Citiraj ovu publikaciju:

Meštrović, Tomislav; Ljubin-Sternak, Sunčanica
Molecular mechanisms of Chlamydia trachomatis resistance to antimicrobial drugs // Frontiers in bioscience-Landmark, 23 (2018), 4; 656-670 doi:10.2741/4611 (međunarodna recenzija, pregledni rad, znanstveni)
Meštrović, T. & Ljubin-Sternak, S. (2018) Molecular mechanisms of Chlamydia trachomatis resistance to antimicrobial drugs. Frontiers in bioscience-Landmark, 23 (4), 656-670 doi:10.2741/4611.
@article{article, author = {Me\v{s}trovi\'{c}, Tomislav and Ljubin-Sternak, Sun\v{c}anica}, year = {2018}, pages = {656-670}, DOI = {10.2741/4611}, keywords = {chlamydia trachomatis, antimicrobial resistance, antibiotics}, journal = {Frontiers in bioscience-Landmark}, doi = {10.2741/4611}, volume = {23}, number = {4}, issn = {2768-6701}, title = {Molecular mechanisms of Chlamydia trachomatis resistance to antimicrobial drugs}, keyword = {chlamydia trachomatis, antimicrobial resistance, antibiotics} }
@article{article, author = {Me\v{s}trovi\'{c}, Tomislav and Ljubin-Sternak, Sun\v{c}anica}, year = {2018}, pages = {656-670}, DOI = {10.2741/4611}, keywords = {chlamydia trachomatis, antimicrobial resistance, antibiotics}, journal = {Frontiers in bioscience-Landmark}, doi = {10.2741/4611}, volume = {23}, number = {4}, issn = {2768-6701}, title = {Molecular mechanisms of Chlamydia trachomatis resistance to antimicrobial drugs}, keyword = {chlamydia trachomatis, antimicrobial resistance, antibiotics} }

Časopis indeksira:


  • Web of Science Core Collection (WoSCC)
    • Science Citation Index Expanded (SCI-EXP)
    • SCI-EXP, SSCI i/ili A&HCI
  • Scopus
  • MEDLINE


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