Resistance of group B streptococcus (GBS) to antibiotics, particularly erythromycin and clindamycin, was studied. Erythromycin resistance was present in 22% of GBS isolates, and these isolates were constitutively resistant, inducibly resistant, or sensitive to clindamycin. Erythromycin and clindamycin MICs were related to the presence of ermA, ermB, or mefA genes.Group B streptococci (GBS) cause serious, life-threatening infections in the newborn. Mortality of GBS sepsis in neonates is over 50% and is particularly high in preterm infants. Maternal intrapartum prophylaxis for pregnant women colonized with GBS has been recommended for several years (1,2,4,8,9), since clinical trials showed that the administration of antibiotics to women in labor drastically reduced early-onset invasive GBS infection in the neonate.The revised Centers for Disease Control and Prevention guidelines issued in 2002 differ from previous guidelines in that universal culture-based screening for vaginal-rectal colonization with GBS is recommended for all pregnant women at 35 to 37 weeks of gestation. These guidelines recommend susceptibility testing to erythromycin and clindamycin on GBS isolates from penicillin-allergic women at risk for anaphylaxis. The goals of this study were to determine the rate of resistance to erythromycin and clindamycin in GBS colonizing pregnant women and to determine the mechanisms of antibiotic resistance present in the bacteria.Two hundred strains of GBS isolated from vaginal-rectal swabs collected between January 2002 and April 2003 from pregnant women (one isolate per patient) seen in the Family Medicine Department of a teaching community hospital were stored at Ϫ70°C until tested. A single swab was used to collect specimens from the lower vagina and rectum. Standard methods were used to isolate and identify Streptococcus agalactiae (GBS).The Kirby-Bauer disk diffusion susceptibility method was performed for penicillin, vancomycin, tetracycline, erythromycin, and clindamycin according to NCCLS guidelines (13). MICs of erythromycin and clindamycin were determined by E test for all isolates resistant or intermediate to erythromycin. The double disk diffusion test for inducible clindamycin resistance was performed on all isolates resistant to erythromycin but susceptible to clindamycin. Erythromycin and clindamycin disks were placed approximately 16 mm apart on the plate. Inducible clindamycin resistance by erythromycin was detected by a blunting of the clindamycin zone closest to the erythromycin disk, giving the appearance of a "D." Detection of the ermA, ermB, and mefA genes was done using PCR with previously published primers (6).All GBS were susceptible to penicillin and vancomycin, and 30 (15%) were susceptible to tetracycline. Resistance to erythromycin was found in 44 (22%) of the isolates.Resistance genes were detected in 100% of erythromycinresistant isolates (Table 1). Twelve isolates (6%) were resistant to both erythromycin and clindamycin. The MICs of erythromycin and clindamycin for eight of thes...

hMPV is common among young children with apparent respiratory infections, suggesting that it is a significant cause of symptomatic respiratory infections.

Macrolide (including erythromycin and azithromycin) and lincosamide (including clindamycin) antibiotics are recommended for treatment of penicillin-allergic patients with Streptococcus pyogenes pharyngitis. Resistance to erythromycin in S. pyogenes can be as high as 48% in specific populations in the United States. Macrolide and lincosamide resistance in S. pyogenes is mediated by several different genes. Expression of the erm(A) or erm(B) genes causes resistance to erythromycin and inducible or constitutive resistance to clindamycin, respectively, whereas expression of the mef(A) gene leads to resistance to erythromycin but not clindamycin. We studied the resistance of S. pyogenes to erythromycin and clindamycin at an urban tertiarycare hospital. Of 196 sequential isolates from throat cultures, 15 (7.7%) were resistant to erythromycin. Three of these were also constitutively resistant to clindamycin and had the erm(B) gene. Five of the erythromycinresistant isolates were resistant to clindamycin upon induction with erythromycin and had the erm(A) gene. The remaining seven erythromycin-resistant isolates were susceptible to clindamycin even upon induction with erythromycin and had the mef(A) gene. Pulsed-field gel electrophoresis analysis and emm typing demonstrated that the erythromycin-resistant S. pyogenes comprised multiple strains. These results demonstrate that multiple mechanisms of resistance to macrolide and lincosamide antibiotics are present in S. pyogenes strains in the United States.