title: Prevalence and mechanisms of macrolide resistance in invasive and noninvasive group B streptococcus isolates from Ontario, Canada.
abstract: Macrolide resistance has been demonstrated in group B streptococcus (GBS), but there is limited information regarding mechanisms of resistance and their prevalence. We determined these in GBS obtained from neonatal blood cultures and vaginal swabs from pregnant women. Of 178 isolates from cases of neonatal GBS sepsis collected from 1995 to 1998, 8 and 4.5% were resistant to erythromycin and clindamycin, respectively, and one isolate showed intermediate penicillin resistance (MIC, 0.25 microg/ml). Of 101 consecutive vaginal or rectal/vaginal isolates collected in 1999, 18 and 8% were resistant to erythromycin and clindamycin, respectively. Tetracycline resistance was high (>80%) among both groups of isolates. Of 32 erythromycin-resistant isolates, 28 possessed the erm methylase gene (7 ermB and 21 ermTR/ermA) and 4 harbored the mefA gene; one isolate harbored both genes. One isolate which was susceptible to erythromycin but resistant to clindamycin (MIC, 4 microg/ml) was found to have the linB gene, previously identified only in Enterococcus faecium. The mreA gene was found in all the erythromycin-resistant strains as well as in 10 erythromycin-susceptible strains. The rate of erythromycin resistance increased from 5% in 1995-96 to 13% in 1998-99, which coincided with an increase in macrolide usage during that time.
authors.affiliation: Department of Microbiology, Toronto Medical Laboratories and Mount Sinai Hospital, Toronto, ON, Canada. jdeazavedo@mtsinai.on.ca
authors.forename: J C
authors.initials: JC
authors.lastname: de Azavedo
authors.forename: M
authors.initials: M
authors.lastname: McGavin
authors.forename: C
authors.initials: C
authors.lastname: Duncan
authors.forename: D E
authors.initials: DE
authors.lastname: Low
authors.forename: A
authors.initials: A
authors.lastname: McGeer
mesh_terms: D000328:Adult; D000900:Anti-Bacterial Agents / Q000494:pharmacology*; D002981:Clindamycin / Q000494:pharmacology; D004352:Drug Resistance, Microbial; D004917:Erythromycin / Q000494:pharmacology; D005260:Female; D005798:Genes, Bacterial / Q000235:genetics; D005838:Genotype; D006801:Humans; D007231:Infant, Newborn; D055231:Lincosamides; D018942:Macrolides; D008826:Microbial Sensitivity Tests; D009864:Ontario / Q000453:epidemiology; D010641:Phenotype; D011247:Pregnancy; D020133:Reverse Transcriptase Polymerase Chain Reaction; D018805:Sepsis / Q000453:epidemiology; D013290:Streptococcal Infections / Q000453:epidemiology* / Q000382:microbiology*; D013292:Streptococcus agalactiae / Q000187:drug effects* / Q000472:pathogenicity
chemical_list: D000900:Anti-Bacterial Agents; D055231:Lincosamides; D018942:Macrolides; D002981:Clindamycin; D004917:Erythromycin