Abstract
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.
Highlights
BackgroundStaphylococcus aureus, a Gram-positive bacterium, has been responsible for both community-acquired and hospital-acquired infections
Methicillin, a semi-synthetic beta-lactam antibiotic, was first used in the late 1950s as a treatment for the new penicillin-resistant Staphylococcus aureus (PRSA) infections (PRSA) [4]. This antibiotic covalently binds penicillin enzymes like carboxypeptidases and transpeptidases, which inhibits the synthesis of the bacterial cell wall [3]
Further studies indicated that the resistance to both these classes of antibacterial agents was due to a low-affinity penicillin-binding protein (PBP) called the PBP2a [5]
Summary
Staphylococcus aureus, a Gram-positive bacterium, has been responsible for both community-acquired and hospital-acquired infections This bacterium is found on the skin and the mucosal membranes of healthy individuals. Penicillin is a beta-lactam antibiotic that covalently binds to various penicillin-binding enzymes, known as penicillin-binding proteins This leads to the inhibition of biosynthesis of the cell wall, causing a bactericidal effect on S. aureus [3]. Methicillin, a semi-synthetic beta-lactam antibiotic, was first used in the late 1950s as a treatment for the new penicillin-resistant Staphylococcus aureus (PRSA) infections (PRSA) [4]. This antibiotic covalently binds penicillin enzymes like carboxypeptidases and transpeptidases, which inhibits the synthesis of the bacterial cell wall [3]. The MRSA isolates were reported to contain a genetic element known as SCCmec within which a specific gene known as mecA was responsible for encoding PBP2a
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