VISA infection involves S. aureus strains with intermediate vancomycin susceptibility, generally produced by accumulation of mutations such as cell-wall thickening and excess D-Ala-D-Ala residues, rather than by vanA acquisition [1][2]. hVISA is a related heterogeneous phenotype that can contribute to vancomycin treatment failure [4][1]. VRSA is distinct, usually acquiring plasmid-mediated vanA from enterococci [2].
Disease overview
BacterialVancomycin-intermediate Staphylococcus aureus infection
万古霉素中介金黄色葡萄球菌感染
Evidence-backed informationEN 6/7 applicable sections · ZH 6/7 applicable sectionsUpdated Sep 3, 2026
Vancomycin-intermediate Staphylococcus aureus (VISA) and heterogeneous VISA (hVISA) are S. aureus phenotypes with reduced vancomycin susceptibility, arising mainly through accumulated mutations rather than vanA acquisition [1][2]. They are clinically relevant in healthcare-associated sterile-site and bloodstream infections, with reported increasing incidence and prevalence among MRSA isolates [3][4]. Public-health relevance centers on vancomycin treatment failure and nosocomial spread, while distinguishing these phenotypes from VRSA [4][2].
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Reported VISA infections include sterile-site disease, and related hVISA disease is more frequently detected in bloodstream infections than in other specimens [3][4]. In a VISA/MRSA sterile-site cohort, pneumonia, unknown source, higher severity, solid-organ malignancy, and admission from skilled care facilities were associated with mortality, while VISA status itself did not show excess mortality compared with non-VISA S. aureus [3]. hVISA has been linked to vancomycin treatment failure and increased hospitalization, costs, and mortality in bacteraemic patients [4].
VISA infection incidence has been described as increasing, with a single-center cohort identifying MRSA and VISA sterile-site infections over several years [3]. A meta-analysis estimated hVISA prevalence among MRSA isolates at about 6% in Asia and Europe/America, with higher detection in bloodstream infections than other infections (9.4% vs 5.5%) [4]. The distribution points to healthcare-associated and nosocomial settings, with concern that increasing hVISA prevalence may reduce vancomycin effectiveness [4].
Resistant Staphylococcus aureus, including VISA, can spread through close physical contact with infected patients and through exposure to contaminated wound material such as bandages, particularly in healthcare settings where close contact between caregivers, visitors, and hospitalised patients is common [5]. Transmission has not been documented in the United States for VRSA, but the same routes of spread as for methicillin-resistant S. aureus (MRSA) are considered plausible for VISA/VRSA, including person-to-person contact and contact with contaminated surfaces or wound dressings [5].
The supplied evidence identifies medically complex patients with persistent bacteremia or native mitral valve endocarditis due to daptomycin non-susceptible VISA, including an elderly patient not considered an operative candidate [6]. Patients with MRSA bacteremia in the setting of vancomycin failure, or isolates with vancomycin MIC greater than 2 µg/mL, are also identified as relevant groups in the evidence [2].
Hand hygiene and adherence to healthcare infection-control precautions are the principal measures recommended to limit the spread of vancomycin-intermediate Staphylococcus aureus (VISA), given that resistance in S. aureus remains exceptionally rare and transmission principally occurs in healthcare settings through close physical contact or contaminated wound material [5]. Caregivers, visitors, and anyone having close physical contact with hospitalized patients infected with VISA should observe the same protective measures applied to other antimicrobial-resistant staphylococci [5]. Healthcare providers are specifically advised to wear gloves before and after contact with infectious body substances and to maintain rigorous hand hygiene, consistent with core infection-control practices intended to reduce transmission of these resistant organisms to other patients [5]. Avoiding direct contact with wounds or contaminated material further reduces opportunities for spread in both clinical and community settings [5].
- 1Hiramatsu K et al. Vancomycin-intermediate resistance in Staphylococcus aureus. J Glob Antimicrob Resist. 2014 Dec. PMID: 27873679. doi: 10.1016/j.jgar.2014.04.006.PubMed: https://pubmed.ncbi.nlm.nih.gov/27873679/
- 2Wikipedia contributors. Vancomycin-resistant Staphylococcus aureus - Wikipedia [Internet]. Wikipedia. cited 2 Sept 2026.Available from: https://en.wikipedia.org/wiki/Vancomycin-resistant_Staphylococcus_aureus
- 3Burnham JP et al. Impact of Time to Appropriate Therapy on Mortality in Patients with Vancomycin-Intermediate Staphylococcus aureus Infection. Antimicrob Agents Chemother. 2016 Sep. PMID: 27401565. doi: 10.1128/AAC.00925-16.PubMed: https://pubmed.ncbi.nlm.nih.gov/27401565/
- 4Keikha M et al. Global distribution of heterogeneous vancomycin-intermediate Staphylococcus aureus strains (1997-2021): a systematic review and meta-analysis. J Glob Antimicrob Resist. 2024 Jun. PMID: 38336227. doi: 10.1016/j.jgar.2024.02.002.PubMed: https://pubmed.ncbi.nlm.nih.gov/38336227/
- 5US Centers for Disease Control and Prevention. About Vancomycin-resistant Staphylococcus aureus | S. aureus | CDC [Internet]. cited 3 Sept 2026.Available from: https://www.cdc.gov/staphylococcus-aureus/about/vancomycin-resistant-staph.html
- 6Baxi SM et al. Daptomycin non-susceptible, vancomycin-intermediate Staphylococcus aureus endocarditis treated with ceftaroline and daptomycin: case report and brief review of the literature. Infection. 2015 Dec. PMID: 25805524. doi: 10.1007/s15010-015-0763-0.PubMed: https://pubmed.ncbi.nlm.nih.gov/25805524/
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