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Biomed J. 2015 May-Jun;38(3):215-20. doi: 10.4103/2319-4170.138306.

Serotype distribution and resistance genes associated with macrolide and fluoroquinolone resistance in Streptococcus agalactiae isolates from a hospital in southern Taiwan.

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Department of Microbiology, Immunology, and Biopharmaceuticals, National Chiayi University, Chiayi, Taiwan.
Graduate Institutes of Clinical Medical Sciences, College of Medicine, Chang Gung University; Molecular Infectious Diseases Research Center, Chang Gung Memorial Hospital at Linkou; Division of Pediatric Infectious Diseases, Chang Gung Children's Hospital at Linkou, Chang Gung University College of Medicine, Taoyuan, Taiwan.



Antimicrobial resistance of Streptococcus agalactiae (Group B Streptococcus, GBS) has been emerging worldwide. We aimed to examine the correlation of drug-resistant genes with serotypes and with the mutations of the quinolone resistance-determining region (QRDR) in GBS isolates.


A total of 323 human GBS isolates were collected from a hospital in southern Taiwan. Laboratory investigation included serotyping by a multiplex polymerase chain reaction (PCR) method, antimicrobial susceptibility testing by a disc diffusion method, and mechanism analysis of the resistance to macrolides and fluoroquinolones by PCR and sequencing methods.


Multiplex PCR showed that the most prevalent serotypes were Ib, III, V, and VI, mostly isolated from urine. The ermB gene was highly prevalent in serotypes Ib and V and was associated with clindamycin and macrolide resistance. GBS with a serine-to-leucine mutation at codon 81 in GyrA and with a serine-to-phenylalanine or -tyrosine mutation at codon 79 in ParC had a higher minimum inhibitory concentration of levofloxacin than isolates with only an aspartic acid-to-tyrosine mutation at codon 83 (>32 μg/ml vs. 16 μg/ml) in GyrA.


The most prevalent GBS serotypes were Ib, III, V, and VI. The ermB and mefE genes carried in serotypes Ib and V were highly associated with the resistance to macrolides and clindamycin. Mutations at codon 79 and codon 83 of ParC were the major determining factors for high-level fluoroquinolone resistance.

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