Related Experiment Video

Updated: Aug 13, 2026

Antimicrobial Synergy Testing by the Inkjet Printer-assisted Automated Checkerboard Array and the Manual Time-kill Method
12:03

Antimicrobial Synergy Testing by the Inkjet Printer-assisted Automated Checkerboard Array and the Manual Time-kill Method

Published on: April 18, 2019

Frequent resistance of clinical group B streptococci isolates to clindamycin and erythromycin

M D Pearlman1, C L Pierson, R G Faix

  • 1Department of Obstetrics and Gynecology, The University of Michigan Health System, Ann Arbor 48109-0276, USA. pearlman@umich.edu

Obstetrics and Gynecology
|August 12, 1998
PubMed
Abstract

Insights

High rates of group B streptococcus resistance to clindamycin and erythromycin were observed. This is concerning for penicillin-allergic patients requiring alternative intrapartum antibiotics.

Area of Science:

  • Obstetrics and Gynecology
  • Infectious Diseases
  • Microbiology

Background:

  • Group B Streptococcus (GBS) is a significant cause of neonatal infections.
  • Penicillin is the preferred antibiotic for intrapartum prophylaxis, but penicillin allergy is common.
  • Alternative antibiotics like clindamycin and erythromycin are used for penicillin-allergic patients.

Purpose of the Study:

  • To determine the prevalence of reported penicillin allergy in parturients.
  • To assess the in vitro resistance rates of clinical GBS isolates to clindamycin and erythromycin.

Main Methods:

  • One hundred clinical GBS isolates were tested for resistance to clindamycin, erythromycin, penicillin G, vancomycin, and cefazolin.
  • The frequency of reported beta-lactam allergy was recorded for all laboring women over a 4-month period.

Main Results:

  • Fifteen percent of GBS isolates were resistant to clindamycin, and 16% were resistant to erythromycin.
  • No GBS isolates showed resistance to penicillin G, vancomycin, or cefazolin.
  • Twelve percent of 963 women reported a penicillin allergy, with only 30% able to describe their reaction.

Conclusions:

  • Frequent in vitro resistance of GBS to clindamycin and erythromycin raises concerns for intrapartum prophylaxis in penicillin-allergic patients.
  • The findings suggest a potential for inadequate GBS prophylaxis with current alternative antibiotic recommendations.
  • Thorough questioning regarding penicillin allergy history may help optimize antibiotic selection for intrapartum prophylaxis.

More Related Videos

Antibiotic Dereplication Using the Antibiotic Resistance Platform10:49

Antibiotic Dereplication Using the Antibiotic Resistance Platform

Published on: October 17, 2019

Antibiotic Efficacy Testing in an Ex vivo Model of Pseudomonas aeruginosa and Staphylococcus aureus Biofilms in the Cystic Fibrosis Lung09:26

Antibiotic Efficacy Testing in an Ex vivo Model of Pseudomonas aeruginosa and Staphylococcus aureus Biofilms in the Cystic Fibrosis Lung

Published on: January 22, 2021

Related Concept Videos

Development of Antibiotic Resistance01:30

Development of Antibiotic Resistance

Antibiotic resistance is a major public health concern that arises when bacteria evolve mechanisms to withstand the effects of antibiotic treatments. This resistance can be intrinsic, acquired through genetic mutations, or transferred between bacteria via horizontal gene transfer. The development of antibiotic resistance poses significant challenges in treating bacterial infections and necessitates ongoing research to develop new therapeutic strategies.Intrinsic resistance occurs when bacterial...
Mechanism of Antibiotic Resistance in MRSA01:25

Mechanism of Antibiotic Resistance in MRSA

Antibiotic resistance in bacteria arises when microorganisms evolve the ability to withstand drugs designed to kill them or inhibit their growth, rendering once-effective treatments useless. This phenomenon, driven by genetic change and selection under antibiotic exposure, poses a profound threat to modern medicine. Mechanisms include drug-inactivating enzymes (e.g., β-lactamases), efflux pumps that eject antibiotics, mutations altering antibiotic targets, decreased drug uptake, and acquisition...
Inhibitors of Gram-positive Cell Wall Synthesis01:23

Inhibitors of Gram-positive Cell Wall Synthesis

Bacterial cell walls are typically rigid structures composed mainly of peptidoglycan, a mesh-like polymer that provides mechanical strength and maintains cell shape. The synthesis of peptidoglycan is a crucial process in bacterial growth and serves as a primary target for many antibiotics.Mechanism of Action of Beta-Lactam AntibioticsBeta-lactam antibiotics, such as penicillin, inhibit peptidoglycan synthesis in actively growing cells. These antibiotics share a characteristic four-membered...
Inhibitors of Bacterial Protein Synthesis01:25

Inhibitors of Bacterial Protein Synthesis

Aminoglycosides constitute a highly potent class of bactericidal antibiotics that exert their antimicrobial effects by targeting the bacterial ribosome, specifically disrupting protein synthesis. These polycationic molecules consist of amino-modified sugars linked via glycosidic bonds to an aminocyclitol core such as 2-deoxystreptamine or streptamine. Their strong positive charges facilitate tight binding to the negatively charged phosphate backbone of ribosomal RNA (rRNA), primarily at the 16S...
Inhibitors of Bacterial DNA Synthesis01:28

Inhibitors of Bacterial DNA Synthesis

Bacterial pathogens depend on precise and efficient DNA replication to sustain infection. Two type II topoisomerases—DNA gyrase and topoisomerase IV—are critical to this process, as they resolve DNA supercoiling and unlink chromosomes during replication. Fluoroquinolones, synthetic derivatives of quinolones, exploit this mechanism by stabilizing the transient DNA–enzyme cleavage complex, preventing strand religation, and causing lethal double-strand breaks. These antibiotics are selectively...
Clinical Significance of Antibiotic Resistance01:25

Clinical Significance of Antibiotic Resistance

Methicillin-resistant Staphylococcus aureus (MRSA) presents a critical public health threat, arising from its capacity to resist β-lactam antibiotics due to acquisition of the mecA gene within the staphylococcal cassette chromosome mec (SCCmec). This gene encodes penicillin-binding protein 2a (PBP2a), which impairs binding efficacy of methicillin and other β-lactams. MRSA has evolved into distinct clonal lineages impacting humans and animals alike, reinforcing its significance within the One...