Applied Microbiology

Biography

Biography: Suleiman Al-Obeid

Abstract

VISA was first identified in Japan in 1996, it is also termed GISA (Glycopeptides-intermediate Staphylococcus aureus), and these bacterial strains present a thickening of the cell wall, which is believed to reduce the ability of vancomycin to reach there site of action on the level of cytoplasmic membrane D-ala-D-ala. In the Staphylococcus aureus, high level of vancomycin resistance has been rarely reported. In-vivo and in vitro experiments carried out in the year 1992 showed that from Enterococcus faecalis, the vancomycin resistance genes could be transferred by gene transfer to Staphylococcus aureus, granting high level vancomycin resistance to S.aureus. In the year 2002, a VRSA strain was mainly isolated from a patient in Michigan.The definition of hVISA according to Hiramatsu et al. is a strain of Staphylococcus aureus that gives resistance to vancomycin at a frequency of 10-6 colonies or even higher. Strains of hVISA and VISA do not have resistant genes found in Enterococcus and the proposed mechanisms of resistance include the sequential mutations resulting in a thicker cell wall and the synthesis of excess amounts of D-ala-D-ala residues. VRSA strain acquired the vancomycin resistance gene cluster vanA from VRE. An alternative to Vancomycin should be used, specifically for isolates with a Vancomycin MIC>2 mcg/mL. The method is to treat with at least one agent to which VRSA/ VISA is supposed to be susceptible by in vitro lab testing. The agents that are used include linezolid, daptomycin, Ceftaroline, Telavancin, quinupristin–dalfopristin. Use of appropriate infection control practices (such as wearing gloves before and after contact with infectious body substances and adherence to hand hygiene) by healthcare personnel can reduce the spread of VISA and VRSA. Treatment failure under therapeutic levels of vancomycin prompted us to investigate the resistance profile of hVISA D958 strain isolated from blood culture at SFH in KSA.