The relationship between virulence factors and vancomycin resistance among Enterococci collected from food and human samples in Southern Turkey


Terkuran M. , Erginkaya Z. , Ünal E., Güran M., Kızılyıldırım S., Uğur G., et al.

ANKARA UNIVERSITESI VETERINER FAKULTESI DERGISI, cilt.61, ss.133-140, 2014 (SCI İndekslerine Giren Dergi) identifier identifier

  • Cilt numarası: 61 Konu: 2
  • Basım Tarihi: 2014
  • Doi Numarası: 10.1501/vetfak_0000002617
  • Dergi Adı: ANKARA UNIVERSITESI VETERINER FAKULTESI DERGISI
  • Sayfa Sayısı: ss.133-140

Özet

The aims of this research were to study the prevalence of potential virulence factors, vancomycin resistance and also to evaluate a possible correlation that can exist between vancomycin resistance and potential virulence factors between 51 Enterococcus spp. isolated from food and 50 Enterococcus faecium strains from human in southern Turkey. Identification of the isolates was determined by Vitek-II system. Antimicrobial susceptibility tests were performed by Vitek-II system and disc diffusion method. The presence of vanA and vanB as well as enterococcal virulence genes of cytolysin (cylA), the aggregation substance (asa1), gelatinase (gelE), enterococal surface protein (esp), hyaluronidase (hyl) were investigated by Polymerase Chain Reaction (PCR) method. Haemolysin production was also studied phenotypic method. Apart from one isolate, none of the food originated enterococci were resistant to vancomycin, and none carried vanA and vanB resistance genes. All clinical isolates were resistant to vancomycin and 84% of them carried vanA; 2%, vanB; and 14%, neither vanA nor vanB genes. Except for the cylA gene, all other virulence genes and vancomycin resistance were higher in human strains, and a positive correlation was observed between multivirulence genes and hemolytic activity. For all strains, a positive correlation existed between the esp gene positivity and vancomycin resistance, while for only E. faecium, esp, hyl gene positivity and vancomycin resistance a positive correlation could be seen. Furthermore, "silent cylA" genes were found in two food and one intestinal strains. Based on our findings, we can suggest that virulence increases in parallel to vancomycin resistance, and food may be a potential source for dissemination of gelE, asa1 and hyl virulence genes. Finally, esp and hyl genes presence should carefully be monitored in food originated enterococci.

The aims of this research were to study the prevalence of potential virulence factors, vancomycin resistance and also to evaluate a possible correlation that can exist between vancomycin resistance and potential virulence factors between 51 Enterococcus spp. isolated from food and 50 Enterococcus faecium strains from human in southern Turkey. Identification of the isolates was determined by Vitek-II system. Antimicrobial susceptibility tests were performed by Vitek-II system and disc diffusion method. The presence of vanA and vanB as well as enterococcal virulence genes of cytolysin (cylA), the aggregation substance (asa1), gelatinase (gelE), enterococal surface protein (esp), hyaluronidase (hyl) were investigated by Polymerase Chain Reaction (PCR) method. Haemolysin production was also studied phenotypic method. Apart from one isolate, none of the food originated enterococci were resistant to vancomycin, and none carried vanA and vanB resistance genes. All clinical isolates were resistant to vancomycin and 84% of them carried vanA; 2%, vanB; and 14%, neither vanA nor vanB genes. Except for the cylA gene, all other virulence genes and vancomycin resistance were higher in human strains, and a positive correlation was observed between multivirulence genes and hemolytic activity. For all strains, a positive correlation existed between the esp gene positivity and vancomycin resistance, while for only E. faecium, esp, hyl gene positivity and vancomycin resistance a positive correlation could be seen. Furthermore, "silent cylA" genes were found in two food and one intestinal strains. Based on our findings, we can suggest that virulence increases in parallel to vancomycin resistance, and food may be a potential source for dissemination of gelE, asa1 and hyl virulence genes. Finally, esp and hyl genes presence should carefully be monitored in food originated enterococci.