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Biosensor for Detection of Antibiotic Resistant Staphylococcus Bacteria
Published on: May 8, 2013
Detection of multiple macrolide- and lincosamide-resistant strains of Streptococcus pyogenes from patients in the
Meredith E Hasenbein1, John E Warner, Kathleen G Lambert
1Department of Laboratory Medicine, Children's Hospital Boston and Harvard Medical School, Massachusetts 02115, USA.
Abstract:
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 tertiary-care 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 erythromycin-resistant 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.
Insights
Streptococcus pyogenes resistance to erythromycin and clindamycin is a growing concern. Multiple resistance genes, including erm(A), erm(B), and mef(A), contribute to macrolide and lincosamide antibiotic resistance in S. pyogenes strains.
Area of Science:
- Microbiology
- Infectious Diseases
- Pharmacology
Background:
- Macrolide and lincosamide antibiotics are alternatives for penicillin-allergic patients with Streptococcus pyogenes pharyngitis.
- Erythromycin resistance in S. pyogenes can be high, up to 48% in some US populations.
- Resistance mechanisms involve various genes, including erm(A), erm(B), and mef(A).
Purpose of the Study:
- To investigate the prevalence and mechanisms of erythromycin and clindamycin resistance in S. pyogenes.
- To characterize the genetic basis of antibiotic resistance in clinical isolates.
Main Methods:
- Analysis of 196 S. pyogenes isolates from throat cultures.
- Phenotypic testing for erythromycin and clindamycin resistance (constitutive and inducible).
- Molecular methods including PCR for resistance genes (erm(A), erm(B), mef(A)), pulsed-field gel electrophoresis, and emm typing.
Main Results:
- 15.3% (15/196) of S. pyogenes isolates were resistant to erythromycin.
- Erythromycin-resistant isolates harbored erm(B) (3 isolates, constitutive clindamycin resistance), erm(A) (5 isolates, inducible clindamycin resistance), or mef(A) (7 isolates, clindamycin susceptible).
- Pulsed-field gel electrophoresis and emm typing indicated the presence of multiple S. pyogenes strains exhibiting resistance.
Conclusions:
- Multiple genetic mechanisms contribute to macrolide and lincosamide resistance in S. pyogenes.
- The study highlights the presence of diverse resistance patterns in clinical isolates.
- Understanding these resistance mechanisms is crucial for effective treatment of S. pyogenes infections.
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