Jcs. De Azavedo et al., Prevalence and mechanisms of macrolide resistance in invasive and noninvasive group B streptococcus isolates from Ontario, Canada, ANTIM AG CH, 45(12), 2001, pp. 3504-3508
Macrolide resistance has been demonstrated in group B streptococcus (GBS),
but there is limited information regarding mechanisms of resistance and the
ir prevalence. We determined these in GBS obtained from neonatal blood cult
ures and vaginal swabs from pregnant women. Of 178 isolates from cases of n
eonatal GBS sepsis collected from 1995 to 1998, 8 and 4.5% were resistant t
o erythromycin and clindamycin, respectively, and one isolate showed interm
ediate penicillin resistance (MIC, 0.25 mug/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 hig
h (> 80%) among both groups of isolates. Of 32 erythromycin-resistant isola
tes, 28 possessed the erm methylase gene (7 ermB and 21 ermTR/ermA) and 4 h
arbored the mefA gene; one isolate harbored both genes. One isolate which w
as susceptible to erythromycin but resistant to clindamycin (MIC, 4 mug/ml)
was found to have the linB gene, previously identified only in Enterococcu
s faecium. The mreA gene was found in all the erythromycin-resistant strain
s as well as in 10 erythromycin-susceptible strains. The rate of erythromyc
in resistance increased from 5% in 1995-96 to 13% in 1998-99, which coincid
ed with an increase in macrolide usage during that time.