Resistance to Macrolide, Lincosamide and Streptogramin Antibiotics in Staphylococci Isolated in Istanbul, Turkey

  • Aktas, Zerrin (Department of Microbiology and Clinical Microbiology, Medical Faculty of Istanbul, Istanbul University) ;
  • Aridogan, Aslihan (Department of Microbiology and Clinical Microbiology, Medical Faculty of Istanbul, Istanbul University) ;
  • Kayacan, Cigdem Bal (Department of Microbiology and Clinical Microbiology, Medical Faculty of Istanbul, Istanbul University) ;
  • Aydin, Derya (Department of Microbiology and Clinical Microbiology, Medical Faculty of Istanbul, Istanbul University)
  • 발행 : 2007.08.30

초록

The purpose of this study was to investigate the prevalence and genetic mechanisms of erythromycin resistance in staphylococci. A total of 102 erythromycin resistant non-duplicate clinical isolates of staphylococci [78. coagulase negative stapylococci (CNS), 24 Staphylococcus aureus] were collected between October 2003 and August 2004 in Istanbul Faculty of Medicine in Turkey. The majority of the isolates were from blood and urine specimens. Antimicrobial susceptibilities were determined by the agar dilution procedure and the resistance phenotypes by the double disk induction test. A multiplex PCR was performed, using primers specific for erm(A), erm(B), erm(C), and msrA genes.. Among the 78 CNS isolates, 57.8% expressed the $MLS_{B}-constitutive$, 20.6% the $MLS_{B}-inducible$, and 21.6% the $MS_B$ phenotypes. By PCR, 78.2% of these isolates harbored the erm(C) gene, 8.9% erm(A), 6.4% erm(B), and 11.5% msrA genes. In S. aureus, the constitutive $MLS_B$ (58.3 %) was more common than the inducible phenotype (20.8%). erm(A) was detected in 50% and erm(C) in 62.5% of the isolates, while 37.5% contained both erm(A) and erm(C). erm(C)-associated macrolide resistance was the most prevalent in CNS, while ermC) and erm(A, C) was the most prevalent in S. aureus.

키워드

참고문헌

  1. Allignet, J., V. Loncle, and N. Solh. 1992. Sequence of a staphylococcal plasmid gene, vga, encoding a putative ATP-binding protein involved in resistance to virginianmycin A-like antibiotics. Gene. 117, 45-55 https://doi.org/10.1016/0378-1119(92)90488-B
  2. Drinkovic, D., E.R. Fuller, K.P. Shore, D.J. Holland, and R. Ellis- Pegler. 2001. Clindamycin treatment of Staphylococcus aureus expressing inducible clindamycin resistance. J. Antimicrob. Chemother. 48, 315-316 https://doi.org/10.1093/jac/48.2.315
  3. Fiebelkorn, K.R., S.A. Crawford, M.L. McElmeel, and J.H. Jorgensen. 2003. Practical disk diffusion method for detection of inducible clindamycin resistance in Staphylococcus aureus and Coagulase- negative Staphylococci. J. Clin. Microbiol. 41, 4740-4744 https://doi.org/10.1128/JCM.41.10.4740-4744.2003
  4. Leclercq, R. 2002. Mechanisms of resistance to macrolides and lincosamides: Nature of the resistance elements and their clinical implications. Clin. Infect. Dis. 34, 482-492 https://doi.org/10.1086/324626
  5. Levin, T.P., B. Suh, P. Axelrod, A.L. Truant, and T. Fekete. 2005. Potential clindamycin resistance in clindamycin-susceptible, erythromycin- resistant Staphylococcus aureus: Report of a clinical failure. Antimicrob. Agents Chemother. 49, 1222-1224 https://doi.org/10.1128/AAC.49.3.1222-1224.2005
  6. Lim, J.A., A.R. Kwon, S.K. Kim, Y. Chong, K. Lee, and E.C. Choi. 2002. Prevalence of resistance to macrolide, lincosamide and streptogramin antibiotics in Gram-positive cocci isolated in a Korean hospital. J. Antimicrob. Chemother. 49, 489-495 https://doi.org/10.1093/jac/49.3.489
  7. Martineau, F., F.J. Picard, N. Lansac, C. Menard, P.H. Roy, M. Ouellette, and M.G. Bergeron. 2000. Correlation between the resistance genotype determined by multiplex PCR assays and the antibiotic susceptibility patterns of Staphylococcus aureus and Staphylococcus epidermidis. Antimicrob. Agents Chemother. 44, 231-238 https://doi.org/10.1128/AAC.44.2.231-238.2000
  8. National Committee for Clinical Laboratory Standards. 2002. Performance standards for antimicrobial susceptibility tests. Supplement M100-S12. National Committee for Clinical Laboratory Standards, Wayne, Pa, USA
  9. Ozyurt, M., B. Sareyyupoglu, and N. Ardıc. 2004. Erythromycin and tetracycline resistance genes were investigated in methicilline resistant staphylococci isolates by multiplex-PCR. XXX1. TMC Congress Abstr. 262
  10. Schmitz, F.J., R. Sadurski, A. Kray, M. Boos, R. Geisel, K. Kohrer, J. Verhoef, and Ad C. Fluit. 2000. Prevalence of macrolideresistance genes in Staphylococcus aureus and Enterococcus faecium isolates from 24 European university hospitals. J. Antimicrob. Chemother. 45, 891-894 https://doi.org/10.1093/jac/45.6.891
  11. Thakker-Varia, S., W.D. Jenssen, L. Moon-McDermott, M.P. Weinstein, and D.T. Dubin. 1987. Molecular epidemiology of macrolidelincosamide- streptogramin B resistance in Staphylococcus aureus and coagulase-negative staplylococci. Antimicrob. Agents Chemother. 31, 735-743 https://doi.org/10.1128/AAC.31.5.735
  12. Watanakunakorn, C. 1976. Clindamycin therapy of Staphylococcus aureus endocarditis: clinical relapse and development of resistance to clindamycin, lincomycin and erythromycin. Am. J. Med. 60, 419-425 https://doi.org/10.1016/0002-9343(76)90758-0
  13. Weisblum, B. 1995. Erythromycin resistance by ribosome modification. Antimicrob. Agents Chemother. 39, 577-585 https://doi.org/10.1128/AAC.39.3.577
  14. Westh, H., D.M. Hougaard, J. Vuust, and V.T. Rosdahl. 1995. Prevalence of erm gene classes in erythromycin-resistant Staphylococcus aureus strains isolated between 1959 and 1988. Antimicrob. Agents Chemother. 39, 369-373 https://doi.org/10.1128/AAC.39.2.369