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Distribution of Virulence Determinants (esp, cylA, and gelE) Among Clinical Enterococcus Isolates: A Molecular Study
Bhawani Shankar Verma1, Prashanth K Guddeti2, Ramanath Karicheri3
1Microbiology, Prince Medical College and Hospital, Sikar, IND.
Background:
The genus Enterococcus contains gram-positive cocci. Before the widespread use of antibiotics, enterococci were known causes of endocarditis, urinary tract infections (UTIs), and intra-abdominal infections. The three most important enterococcal virulence agents discovered are cytolysin (cylA), enterococcal surface protein (esp), and gelatinase (gelE). Serious concerns about infectious illnesses are raised by the increasing number of genes for antibiotic resistance.
Materials And Methods:
The study was granted permission by the Institutional Ethical Committee (MU/Research/EC/Ph.D./2021/58), and every single sample was taken from patients who were hospitalized at the Index Medical College Hospital and Research Center in Indore, India. One hundred and six enterococcal isolates were collected between December 2021 and August 2024, and their species distribution was examined. Standard molecular techniques were used to identify virulence genes, such as cytolysin (cylA), enterococcal surface protein (esp), and gelatinase (gelE).
Results:
Among 106 Enterococcus isolates analyzed by reverse transcription polymerase chain reaction (RT-PCR), the esp gene was the most prevalent (74.53%), followed by cylA (55.66%) and gelE (45.28%). Enterococcus faecalis showed higher frequencies of virulence genes compared to Enterococcus avium. High resistance was observed to erythromycin, penicillin, chloramphenicol, and tetracycline, whereas most isolates remained sensitive to linezolid and vancomycin. These findings indicate the presence of virulence-associated genes and variable antimicrobial resistance patterns among the Enterococcus isolates.
Conclusion:
The study reveals a significant pathogenic potential of Enterococcus strains, evidenced by the high prevalence of major virulence genes (esp, cylA, and gelE).
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