To the Editor: Previous articles in the Journal have described the emergence of Staphylococcus aureus with reduced susceptibility to vancomycin (also known as heteroresistant vancomycin-intermediate Staphylococcus aureus, or hVISA) in populations where methicillin-resistant S. aureus (MRSA) is endemic in healthcare settings.1,2 We describe a case of infection caused by hVISA from a region where healthcare-associated MRSA infection is relatively uncommon.3

A 79-year-old woman with an extensive medical history, including type 2 diabetes mellitus and multiple bypass procedures for lower-limb ischaemia, presented with critical ischaemia of the right lower leg. After above-knee amputation, she developed a discharge from the stump wound from which multiresistant MRSA was cultured. Despite receiving several courses of intravenous vancomycin (a total of 25 days of therapy over 5 months), the infection did not resolve.

Extensive debridement surgery, with removal of multiple grossly infected vascular grafts, was performed, and MRSA was cultured from the graft material. Subsequently, the patient developed a discharging sinus from which MRSA with reduced susceptibility to glycopeptide antibiotics was cultured (vancomycin minimal inhibitory concentration [MIC], 8 mg/L; teicoplanin MIC, 24 mg/L). This isolate was shown to be hVISA by population analysis profiling (PAP). When the original MRSA isolate was subsequently tested by PAP, heterogenous subpopulations of bacteria with reduced susceptibility to vancomycin were present which had not been detected by routine susceptibility testing (ie, the isolate was already hVISA).

Review of the patient’s medical records from other Perth healthcare institutions revealed no evidence of vancomycin administration before the initial isolation of MRSA, or contact with known MRSA-colonised patients or healthcare workers. Multilocus sequence typing and staphylococcal cassette chromosome mec allotyping identified the MRSA strain as ST239-MRSA-III, a multiresistant “international” MRSA clone frequently isolated in Australia, mainly on the east coast.4

Despite further surgery and institution of alternative antimicrobial therapy (initially rifampicin and fusidic acid and subsequently linezolid), the patient died of ongoing ischaemia and uncontrolled infection.

Prolonged or repeated use of vancomycin in patients with implanted prostheses that are infected with MRSA should be discouraged, not only because it is commonly futile, but also because it may promote the emergence of subpopulations of S. aureus with reduced susceptibility to vancomycin, as occurred in this case. The fact that these resistant subpopulations were detected in an isolate before the commencement of vancomycin therapy (and then only with specialised testing) reinforces our recommendation.