Antimicrobial Susceptibility Patterns and Macrolide Resistance Genes of beta-Hemolytic Viridans Group Streptococci in a Tertiary Korean Hospital.
10.3346/jkms.2007.22.5.791
- Author:
Young UH
1
;
Gyu Yel HWANG
;
In Ho JANG
;
Ohgun KWON
;
Hyo Youl KIM
;
Kap Jun YOON
Author Information
1. Department of Laboratory Medicine, Yonsei University Wonju College of Medicine, Wonju, Korea. u931018@yonsei.ac.kr
- Publication Type:Original Article
- Keywords:
Streptococcus;
erm(B);
mef(A);
Macrolides;
Drug Resistance
- MeSH:
Ceftriaxone/pharmacology;
Chloramphenicol/pharmacology;
Clindamycin/pharmacology;
Cross Infection/*genetics;
*Drug Resistance, Bacterial;
Erythromycin/pharmacology;
Humans;
Immunoenzyme Techniques;
Korea;
Macrolides/*pharmacology;
Penicillin G/pharmacology;
Phenotype;
Polymerase Chain Reaction;
Tetracycline/pharmacology;
Vancomycin/pharmacology;
Viridans Streptococci/*genetics/*metabolism
- From:Journal of Korean Medical Science
2007;22(5):791-794
- CountryRepublic of Korea
- Language:English
-
Abstract:
The aim of this study was to investigate antimicrobial susceptibilities and macrolide resistance mechanisms of beta-hemolytic viridans group streptococci (VGS) in a tertiary Korean hospital. Minimum inhibitory concentrations (MICs) of seven antimicrobials were determined for 103 beta-hemolytic VGS isolated from various specimens. The macrolide resistance mechanisms of erythromycin-resistant isolates were studied by the double disk test and polymerase chain reaction (PCR). The overall resistance rates of beta-hemolytic VGS were found to be 47.5% to tetracycline, 3.9% to chloramphenicol, 9.7% to erythromycin, and 6.8% to clindamycin, whereas all isolates were susceptible to penicillin G, ceftriaxone, and vancomycin. Among ten erythromycin-resistant isolates, six isolates expressed a constitutive MLSB (cMLSB) phenotype, and each of the two isolates expressed the M phenotype, and the inducible MLSB (iMLSB) phenotype. The resistance rates to erythromycin and clindamycin of beta-hemolytic VGS seemed to be lower than those of non-beta-hemolytic VGS in our hospital, although cMLSB phenotype carrying erm(B) was dominant in beta-hemolytic VGS.
