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Staphylococcus aureus  is a Gram-positive bacterium causing a wide range of infections ranging from cutaneous infections to endocarditis and bacteremia. Beta-lactamases such as penicillin and, subsequently, methicillin have been used in the treatment of  S. aureus infections . With the emergence of methicillin-resistant  Staphylococcus aureus  (MRSA), vancomycin, a bacterial cell wall synthesis inhibitor, has been used as the treatment of choice for MRSA infections.  However, over the past few decades, there have been reports of reduced susceptibility and resistance of  S. aureus  to vancomycin globally, most recently from Michigan, United States, in July 2021. Based on the minimum inhibitory concentration (MIC) of the antibiotic against  S. aureus , there are three strains of resistance, vancomycin-intermediate  Staphylococcus aureus  (VISA), vancomycin-resistant  Staphylococcus aureus  (VRSA), and heterogeneous vancomycin-intermediate  Staphylococcus aureus  (hVISA).  The increasing prevalence of VISA and VRSA infections is a cause of global concern. This qualitative review of peer-reviewed research publications aims to describe the cases of VISA and VRSA reported in the literature globally and summarizes the genetic mechanisms implicated in their resistance. The most common mechanism implicated in VRSA infections is the vanA operon, while cell wall thickening is responsible for VISA infections. This review aims to perform a global comparison between the MIC corresponding to the strength of resistance to vancomycin and the presence of the vanA operon. In this review, VISA and VRSA are noted to be most susceptible to quinupristin-dalfopristin and linezolid, respectively. Maintaining active systemic surveillance for such infections, employing strict infection control measures, and continuing to mitigate indiscriminate and irrational use of antibiotics are some of the actions that can be undertaken to reduce the incidence and transmission of VISA, VRSA, and hVISA infections worldwide.

Reduced Susceptibility and Resistance to Vancomycin of Staphylococcus aureus: A Review of Global Incidence Patterns and Related Genetic Mechanisms