Mithali B Jadhav, Geeta Karande, Satish R Patil
(MRSA) is highly prevalent. Although vancomycin has long been a crucial treatment for serious MRSA infections, strains exhibiting reduced susceptibility or complete resistance have emerged due to its extensive use. While VISA arises through a progressive adaptive mechanism marked by cell wall thickening, altered autolytic activity, and mutations in various stress-response regulatory pathways, VRSA typically develops through horizontal transfer of the vanA operon, most frequently from vancomycin-resistant enterococci (VRE). These changes make it harder for vancomycin to reach its intended locations, which could lead to therapy failure and insufficient bacterial eradication. Prolonged use of vancomycin, the existence of chronic ulcers, the use of invasive medical devices, underlying renal illness, and concurrent colonization with MRSA and VRE are factors that contribute to the development of VISA and VRSA. The true incidence of VISA and VRSA is still unclear, despite their clinical significance. Routine susceptibility testing inadequacies, vancomycin's limited agar diffusion, borderline minimum inhibitory concentration values, and the inconsistent dependability of automated systems all contribute to ongoing diagnostic challenges. Underdiagnosis is further brought about by inadequate screening programs. For the purpose of guiding appropriate medication, preventing transmission, and assisting with efficient infection control measures, timely and accurate detection is essential. To address the growing threat of VISA and VRSA, there is an urgent need for continuous surveillance, improved diagnostic techniques, and the development of novel antimicrobial agents, as the availability of effective treatment options continues to decline.