Molecular Epidemiology and <i>vanA</i>-Mediated Resistance in Clinical Isolates of <i>Enterococcus faecium</i> and <i>E. faecalis</i> in Iran

AuthorGhazal Zolfagharen
AuthorAbbas Akhavan Sepahien
AuthorMarjan Rahnamaye-Farzamien
AuthorFarzaneh Hosseinien
OrcidAbbas Akhavan Sepahi [0000-0002-4112-8962]en
OrcidMarjan Rahnamaye-Farzami [0000-0001-9745-1657]en
Issued Date2025-10-31en
AbstractBackground: Vancomycin-resistant enterococci (VRE) are critical nosocomial pathogens, particularly Enterococcus faecium and E. faecalis, driven by resistance genes like vanA. Limited data on vanA expression dynamics and strain diversity in Iran necessitate region-specific studies to inform infection control. Objectives: This study investigated the clinical prevalence, resistance patterns, and genetic mechanisms of E. faecalis and E. faecium, focusing on vancomycin resistance mediated by the vanA gene, integron distribution, and strain diversity. Methods: A total of 120 clinical isolates were identified using PCR targeting species-specific D-Ala-D-Ala ligases. Antimicrobial susceptibility was determined by disk diffusion. The vanA gene and its expression were detected via multiplex PCR and real-time RT-PCR, respectively. Integron classes and genetic relatedness were assessed by PCR and pulsed-field gel electrophoresis (PFGE), respectively. Results: Enterococcus faecalis predominated (68.3%, n = 82) over E. faecium (31.6%, n = 38). Enterococcus faecium exhibited significantly higher resistance to ampicillin (89.5%) and penicillin (84.2%) than E. faecalis (5.8% and 7.2%, respectively). The vanA gene was detected in 54.1% of vancomycin-resistant E. faecalis and 69.2% of resistant E. faecium. Vancomycin exposure triggered a significant, species-specific upregulation of vanA expression (8.6-fold in E. faecalis vs. 2.6-fold in E. faecium). Class I integrons were found in 24% of isolates. The PFGE revealed greater genetic diversity in E. faecalis (18 pulsotypes) than in E. faecium (6 pulsotypes, single cluster), with resistance profiles correlating with pulsotypes. Conclusions: The high prevalence of vanA-mediated vancomycin resistance underscores the need for enhanced surveillance. The interplay of genetic adaptation (vanA upregulation), clonal expansion, and antibiotic pressure highlights the need for tailored infection control strategies against VRE.en
DOIhttps://doi.org/10.5812/jjm-164799en
Keyword<i>Enterococcus faecalis</i>en
Keyword<i>E. faecium</i>en
Keyword<i>vanA</i>en
KeywordGene Expressionen
KeywordGenetic Diversityen
PublisherBrieflandsen
TitleMolecular Epidemiology and <i>vanA</i>-Mediated Resistance in Clinical Isolates of <i>Enterococcus faecium</i> and <i>E. faecalis</i> in Iranen
TypeResearch Articleen

Files