[Detection of inducible resistance to clindamycin in cutaneous isolates of Staphylococcus spp. by phenotypic and

Laura Merino-Díaz1, Angel Cantos de la Casa, María José Torres-Sánchez

  • 1Servicio de Microbiología, Hospitales Universitarios Virgen del Rocío, Sevilla, España.

Abstract

Insights

Mechanisms of macrolide, lincosamide, and streptogramin B (MLSB) resistance in Staphylococcus were investigated. The MSB efflux mechanism was most common, with inducible MLSB resistance more prevalent than constitutive MLSB resistance.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Antimicrobial Resistance

Background:

  • Staphylococcus isolates exhibit resistance to macrolides, lincosamides, and streptogramins B (MLSB) via efflux (MSB phenotype) or target modification (MLSB phenotype).
  • MLSB resistance can be constitutive (cMLSB) or inducible (iMLSB), impacting treatment strategies.

Purpose of the Study:

  • To determine the prevalence of different MLSB resistance mechanisms in erythromycin-resistant Staphylococcus clinical isolates.
  • To correlate phenotypic resistance patterns with genotypic detection of resistance genes.
  • To provide insights into the distribution and prediction of antimicrobial resistance.

Main Methods:

  • 117 erythromycin-resistant Staphylococcus spp. clinical isolates from cutaneous samples were analyzed.
  • Phenotypic resistance was assessed using the double disk diffusion test.
  • Real-time PCR was employed to detect ermA, ermC, ermB, and msrA genes.

Main Results:

  • The MSB phenotype was the most frequent resistance mechanism (11.2% of isolates).
  • Inducible MLSB resistance (iMLSB) was more common than constitutive MLSB resistance (cMLSB).
  • The msrA gene correlated with the MSB phenotype, and ermC was prevalent in MLSB-resistant strains.

Conclusions:

  • Phenotypic and genotypic methods show good correlation for predicting resistance mechanisms.
  • Understanding these mechanisms aids in predicting epidemiological trends of resistance.
  • This knowledge supports the selection of appropriate antimicrobial therapies.

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