Erythromycin and Clindamycin Resistance in Group B Streptococcal Clinical Isolates

Abstract

Erythromycin (EM) and clindamycin (CM) susceptibility testing was performed on 222 clinical isolates of group B Streptococcus. A multiplex PCR assay was used to detect the ermB, ermTR, and mefA/E antibiotic resistance genes. These results were compared to the phenotypes as determined by the standard EM/CM double disk diffusion assay.Group B Streptococcus (GBS) is one of the leading causes of neonatal bacterial infection. This type of infection commonly leads to pneumonia, septicemia, or meningitis. Because of the serious nature of neonatal GBS infections, the suggested standard protocol for the obstetrician/gynecologist is that pregnant women should be tested for the presence of GBS at 35 to 37 weeks of gestation (7,15). Once GBS colonization is diagnosed, the typical treatment for these patients is penicillin, to which there is no known resistance. However, there is a significant population of penicillin-allergic patients, a reported 12% of pregnant women (12), for whom the macrolide (erythromycin [EM]) or lincosamide (clindamycin [CM]) class of drugs needs to be administered, in particular, for those patients who are at high risk for anaphylactic shock. Previous reports have cited resistance of GBS to EM and CM of up to 37% and 17%, respectively (7). The resistance is commonly caused by three genes: ermB, ermTR, and mefA/E (1, 9, 10). The ermB and ermTR genes encode 23S rRNA methylases, which alter the binding of the antibiotic target site. The expression of these genes leads to the constitutively expressed and the erythromycin-induced macrolide, lincosamide, and streptogramin B (cMLS and iMLS, respectively) resistance phenotypes (9). The mefA and mefE genes, which are 90% identical, encode 14-and 15-member macrolide efflux pumps and lead to the macrolide only (M) resistance phenotype (1). Because of the presence of ermB, ermTR, mefA/E, and other antibiotic resistance genes on plasmids and/or transposons, these genes can pass from organism to organism, and the monitoring of the antibiotic resistance of GBS should occur regularly (13). We used a multiplex PCR assay to screen for the prevalence of the ermB, ermTR, and mefA/E genes in GBS clinical isolates from 222 patients for whom physicians ordered GBS testing. The samples, representing 20 states in the United States and 60% of which were from Florida, New Jersey, and Texas, were chosen at random. Patient ages ranged from 15 to 82 years, with an average of 31.3 Ϯ 11.8 years. These results were compared to the antibiotic resistance phenotypes as determined by the standard EM/CM double disk diffusion assay (3,11,15)

Intrapartum GBS screening and antibiotic prophylaxis: a European consensus conference

“…In Belgium, as determined by the National Reference Centre for GBS, macrolide resistance increased from 10.4% in the early 2000s to 33% among invasive strains isolated from 2008 to 2011 [59]. These figures are consistent with similar reports from Europe [61][62][63][64][65], North America [60,[66][67][68][69][70], and Asia [71,72], except some surveillance studies in Sweden reported 510% [73], thus showing some geographical differences. Different mechanisms account for the acquired resistance to macrolides in streptococci [74].…”

Serotype, Genotype, and Clinical Manifestations of Group B Streptococcus (GBS) Isolated from Neonates in China

“…For patients allergic to β-lactam antibiotics, macrolide antibiotics are used as alternatives. Gygax et al reported that resistance to macrolide antibiotics is an increasing problem for the treatment of GBS infections (20). In the present study, we found that all GBS strains were susceptible to penicillin, ceftriaxone, and cefepime, suggesting that penicillin should remain the first-line antibiotic for the treatment of GBS infection.…”

Prevalencia de portación vaginal-anal de Streptococcus agalactiae en el tercer trimestre de gestación y susceptibilidad a macrólidos y lincosamidas, en mujeres embarazadas de Clínica Alemana Temuco, Chile

“…En los últimos años se ha reportado un aumento significativo de cepas de S. agalactiae resistentes a eritromicina y clindamicina, en diversas partes del mundo. En nuestra experiencia, en la Región Metropolitana de Santiago, luego de una década de pesquisa universal de S. agalactiae, en un hospital universitario, también se observó este aumento significativo de resistencia a macrólidos y lincosamida [14][15][16][17][18][19] . La vigilancia de resistencia antimicrobiana se hace indispensable para definir los fármacos de elección y alternativas, en un centro que aplique protocolos de prevención, como es el caso de Clínica Alemana Temuco.…”