Background Vancomycin‑resistant Staphylococcus aureus (VRSA) is a serious public health challenging concern worldwide. Objectives Therefore, the objective of present study of 62 published studies was to evaluate the prevalence of VRSA based on different years, areas, isolate source, antimicrobial susceptibility testing, and the genetic determinants. Methods We searched the relevant articles that focused on the prevalence rates of VRSA in PubMed, Scopus, Embase, and Web of Science from 2000 to 2019. Statistical analyses were conducted using STATA software (version 14.0). Results The prevalence of VRSA was 2% before 2006, 5% in 2006–2014, and 7% in 2015–2020 that showed a 3.5-fold increase in the frequency of VRSA between before 2006 and 2020 years. The prevalence of VRSA was 5% in Asia, 1% in Europe, 4% in America, 3% in South America, and 16% in Africa. The frequencies of VRSA isolated from clinical, non-clinical, and mixed samples were 6%, 7%, and 14%, respectively. The prevalence of VRSA was 12% using disk diffusion agar method, 7% using MIC-base methods, and 4% using mixed-methods. The prevalence of vanA, vanB, and vanC1 positive were 71%, 26%, and 4% among VRSA strains. The most prevalent genotype was staphylococcal cassette chromosomemec (SCCmec) II, which accounted for 57% of VRSA. The most prevalent staphylococcal protein A (spa) types were t002, t030, and t037. Conclusion The prevalence of VRSA has been increasing in recent years particularly in Africa/Asia than Europe/America. The most prevalent of genetic determinants associated with VRSA were vanA and SCCmec II. This study clarifies that the rigorous monitoring of definite antibiotic policy, regular surveillance/control of nosocomial-associated infections and intensive surveillance of vancomycin-resistance are required for preventing emergence and further spreading of VRSA.

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Background Biofilm is a community of bacteria embedded in an extracellular matrix, which can colonize different human cells and tissues and subvert the host immune reactions by preventing immune detection and polarizing the immune reactions towards an anti-inflammatory state, promoting the persistence of biofilm-embedded bacteria in the host. Main body of the manuscript It is now well established that the function of immune cells is ultimately mediated by cellular metabolism. The immune cells are stimulated to regulate their immune functions upon sensing danger signals. Recent studies have determined that immune cells often display distinct metabolic alterations that impair their immune responses when triggered. Such metabolic reprogramming and its physiological implications are well established in cancer situations. In bacterial infections, immuno-metabolic evaluations have primarily focused on macrophages and neutrophils in the planktonic growth mode. Conclusion Based on differences in inflammatory reactions of macrophages and neutrophils in planktonic- versus biofilm-associated bacterial infections, studies must also consider the metabolic functions of immune cells against biofilm infections. The profound characterization of the metabolic and immune cell reactions could offer exciting novel targets for antibiofilm therapy.