Molecular Studies on Resistance and Virulence Determinants Among Clinical Isolates of Enterococcus Species

Abstract

Enterococci, intestinal commensal bacteria, emerged as a serious nosocomial pathogen in the recent years, causing mild urinary tract infections to severe infections like endocarditis. Enterococcal pathogenicity may be attributed to large array of virulence factors and multidrug resistance. Hence the present study aimed at the identification of enterococci, detection of various virulence factors and antibiotic resistance and their molecular characterization among clinical isolates of enterococci. Also, the study was intended to detect CRISPR distribution as well as alternative drug of choice for effective treatment of multi drug resistant enterococcal infections. Phenotypically identified and genotypically confirmed enterococci (n = 151) were screened for the presence of various virulence factors and the virulence genes (cylA, esp, gelE, asa1 and hyl) and antibiotic resistance profile was assessed phenotypically by Kirby Bauer disk diffusion and Minimum inhibitory concentration (MIC) determination and screened further for the presence of antibiotic resistance coding genes (Genes encoding Aminoglycoside Modifying Enzymes, Vancomycin Resistant genes). CRISPR distribution among the clinical enterococcal isolates was assessed and was correlated with the antibiotic resistance profile. Metallic oxides such as Zinc oxide and Magnesium oxide were screened for the anti-enterococcal activity. Virulence genes are predominant among E. faecalis (97.75%) than E. faecium (61.54%) and other species of enterococci (68%). Multidrug resistance was observed more among E.faecium (94.87%) while all the multidrug resistant E.faecium lacked CRISPR components. Susceptibility profiling showed that (94.20%) fosfomycin susceptibility among urinary E.faecalis. Only 2 E. faecium isolates were found to be VRE of which 1 had vanA phenotype with vanA gene while the other had vanB phenotype with vanA gene. Prudent use of antibiotics can limit the emergence of multidrug resistance among the clinical isolates of enterococci.