Yamuna Devi, Punithavathy PM, Sangeeta Thomas and Balaji Veeraraghavan
MRSA is a public health threat and significant cause of health care-associated and community-associated infections. Vancomycin is considered as gold standard in treating life-threatening infections. Recently, reduced vancomycin susceptibility has been reported across the world. However, infection with S. aureus resistant to vancomycin is clinically rare and less relevant in causing infections. The clinical failure of vancomycin therapy is being increasingly reported with vancomycin intermediate S. aureus (VISA) and hetero-resistant vancomycin intermediate S. aureus (hVISA). The therapeutic option in treating hVISA and VISA remains uncertain. Extensive use of vancomycin over a period of time leads to generation of selective pressure and emergence of resistance. In addition, vancomycin has low tissue penetration, slow bactericidal activity and risk of nephrotoxicity. Although, phenotypic feature of VISA and hVISA were well known, their genetic basis remains unknown. VISA and hVISA is generated by the accumulation of mutation leads to thickening of cell wall. Trapping of vancomycin molecule occurs due to the presence of false targets D-ala D-ala residues in the cell wall, before reaching its target site in cytoplasmic membrane. Despite, it is difficult to detect hVISA using standard susceptibility testing methods. Treatment failure is common among patients with high bacterial load infections. Treating of patients with hVISA/ VISA infections is of great challenge for clinicians.