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Notes from the Field: Vancomycin-Resistant Staphylococcus aureus — Delaware, 2015

Maroya Spalding Walters, PhD1; Paula Eggers2; Valerie Albrecht, MPH1; Tatiana Travis1; David Lonsway, MMSc1; Greg Hovan, MBA3; Debra Taylor, MPH1; Kamile Rasheed, PhD1; Brandi Limbago, PhD1; Alexander Kallen, MD1

Vancomycin-resistant Staphylococcus aureus (VRSA) is a rare, multidrug-resistant bacterium of public health concern that emerged in the United States in 2002. VRSA (S. aureus with vancomycin minimum inhibitory concentration [MIC] ≥16 µg/mL) arises when vancomycin resistance genes (e.g., the vanA operon, which codes for enzymes that result in modification or elimination of the vancomycin binding site) from vancomycin-resistant enterococci (VRE) are transferred to S. aureus (1). To date, all VRSA strains have arisen from methicillin-resistant S. aureus (MRSA). The fourteenth VRSA isolate (VRSA 14) identified in the United States was reported to CDC in February 2015.

VRSA 14 was cultured from the chronic toe wound of a patient in Delaware with diabetes mellitus and end-stage renal disease requiring hemodialysis; vancomycin-resistant Enterococcus faecalis was also isolated from this culture. The wound was first noted during an inpatient admission in April 2014. MRSA was isolated in August and October 2014, and MRSA and VRE were isolated in January 2015; these isolates are not available for further characterization. No antibiotic use was reported in the 4 months before VRSA isolation.

The VRSA and VRE toe wound isolates (February 2015) and an MRSA isolate from a nasal swab from the patient (March 2015) were sent to CDC for further characterization. The VRSA and VRE were confirmed to be resistant to vancomycin (MICs = 512 µg/mL for both); polymerase chain reaction testing confirmed the presence of vanA in both isolates. Pulsed-field gel electrophoresis and S. aureus protein A (spa) typing identified both the VRSA and MRSA as types USA100 and t002, placing them in staphylococcal clonal complex 5. This indicates that VRSA 14 has a health care–associated strain background, as do VRSA 1–12. Among VRSA isolated in the United States, only VRSA 13 had a community-associated strain background (2).

Persons considered to be at increased risk for VRSA acquisition were health care providers at the wound clinic and the dialysis clinic and dialysis patients sharing the same dialysis shift as the VRSA patient. Three of six wound clinic health care workers, all 13 dialysis clinic workers, and the three health care providers who evaluated the wound at an outpatient clinic consented to groin and nasal swab surveillance cultures. Twelve of 13 patients who shared a dialysis shift with the VRSA patient consented to nasal swabs. No MRSA, VRSA, or VRE were cultured from the health care workers or dialysis patients, indicating that close contacts did not share precursor organisms or VRSA with the patient. To facilitate immediate use of contact precautions in the event the patient presented for care, Delaware public health authorities notified facilities where the patient routinely sought health care. Notably, the last four VRSA isolates confirmed by CDC have been isolated from patients in Delaware.

All 14 VRSA identified in the United States appear to have independently acquired the vanA operon. Transmission of VRSA beyond the index patients has not been detected. However, VRSA arise from highly transmissible MRSA progenitor strains, and a robust public health response to all reported VRSA is recommended. Guidelines for VRSA investigation were revised in 2015 and are available at Isolation of suspected or confirmed VRSA should be reported immediately through state and local health departments (e.g., the state antibiotic resistance program coordinator) to CDC's Division of Healthcare Quality Promotion (

1Division of Healthcare Quality Promotion, National Center for Emerging and Zoonotic Infectious Diseases, CDC; 2Delaware Division of Public Health; 3Delaware Public Health Laboratory.

Corresponding author: Maroya Spalding Walters,, 404-639-3539.


  1. Zhu W, Clark N, Patel JB. pSK41-like plasmid is necessary for Inc18-like vanA plasmid transfer from Enterococcus faecalis to Staphylococcus aureus in vitro. Antimicrob Agents Chemother 2013;57:212–9.
  2. Limbago BM, Kallen AJ, Zhu W, Eggers P, McDougal LK, Albrecht VS. Report of the 13th vancomycin-resistant Staphylococcus aureus isolate from the United States. J Clin Microbiol 2014;52:998–1002.

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