Staphylococcus aureus with Reduced Susceptibility to Vancomycin -- Illinois, 1999

Staphylococcus aureus is one of the most common causes of hospital- and community-acquired infections. Nosocomial methicillin-resistant S. aureus (MRSA) infections have become common, and cases of community-acquired MRSA infections also have occurred (1,2). Since 1996, vancomycin-intermediate S. aureus (VISA; vancomycin minimum inhibitory concentration [MIC]=8-16 µg/mL) has been identified in Europe, Asia, and the United States (3-5). The emergence of reduced vancomycin susceptibility in S. aureus increases the possibility that some strains will become fully resistant and that available antimicrobial agents will become ineffective for treating infections caused by such strains. This report describes the fourth case of confirmed VISA from a patient in the United States.

In April 1999, a 63-year-old woman with MRSA bacteremia (MIC less than 1 µg/mL) was transferred from a long-term-care facility to an Illinois hospital (hospital A). The patient had a history of frequent hospitalizations for complications of hemodialysis-dependent, end-stage renal disease, and intravascular access, including two failed arteriovenous grafts, multiple central venous catheter-associated infections, and intermittent receipt of vancomycin therapy through June 1998. Thirteen days after hospital admission and 25 days after initiating vancomycin therapy (median vancomycin serum concentration=12.7 µg/mL; range: 12.1 µg/mL-20.9 µg/mL), a culture from her blood grew S. aureus with an MIC of 4 µg/mL; the blood culture was tested using the Vitek® system (bioMerieux; Hazelwood, Missouri)*. Three subsequent blood specimens drawn within the next 3 days grew S. aureus with MICs of 8 µg/mL on confirmatory testing. The isolates, identical by pulsed-field gel electrophoresis, were resistant to penicillin, oxacillin, clindamycin, erythromycin, ciprofloxacin, and rifampin but susceptible to trimethoprim-sulfamethoxazole, tetracycline, gentamicin, and had intermediate susceptibility to chloramphenicol. No VISA strains were recovered from other body sites. An echocardiogram demonstrated a mitral valve vegetation but the patient declined surgical intervention. Despite treatment with intravenous vancomycin, rifampin, and tobramycin, the patient died 10 days after the first VISA blood specimen was drawn; the cause of death was endocarditis.

The VISA isolate was interpreted as "susceptible" at 4 µg/mL by the Vitek system. Because of the increased awareness of VISA strain emergence, according to laboratory protocol at hospital A, confirmatory testing was performed on all strains of S. aureus with Vitek (MIC greater than or equal to 4 µg/mL) using three additional independent methods: the Pasco Gram Positive Microtiter Panel (Pasco Laboratories, Wheatridge, Colorado), MIC=8 µg/mL; the Etest (AB Biodisk North America, Inc., Piscataway, New Jersey), MIC=6 µg/mL; and inoculation into brain heart infusion (Remel, Lenexa, Kansas) agar with 6 µg/mL of vancomycin (e.g., a vancomycin screen plate indicated growth). Susceptibility results were confirmed by CDC.

After identifying the VISA isolate, hospital A's infection-control department implemented CDC's Interim Guidelines for Prevention and Control of Staphylococcal Infection Associated with Reduced Susceptibility to Vancomycin (6) and began an epidemiologic investigation to evaluate potential transmission. None of 10 family members or 171 health-care workers screened by nares culture was colonized with VISA. No other VISA isolates were identified in other hospitalized patients.

Reported by: MA Khurshid, MD, T Chou, MPH, R Carey, PhD, R Larsen, Chicago; C Conover, MD, SL Bornstein, MD, Acting State Epidemiologist, Illinois Dept of Public Health. Hospital Infections Program, National Center for Infectious Diseases; and an EIS Officer, CDC.

Editorial Note:

Since the emergence of nosocomial MRSA infections in the 1980s, and more recently the emergence of community-acquired MRSA infections, vancomycin is being used increasingly as therapy for treating suspected S. aureus infections. Because few therapies are available to treat MRSA, the confirmed reports of VISA strains demonstrating reduced susceptibility to vancomycin, which has been the drug of last resort to treat MRSA, is of concern.

The acronyms "VISA" and "GISA" (glycopeptide-intermediate S. aureus) have been used in the United States to describe S. aureus isolates with reduced susceptibility to vancomycin. The National Committee for Clinical Laboratory Standards published interpretive criteria defining both (7). The term "GISA" is a technically more accurate description of VISA strains, because all isolates have shown intermediate level MICs to the glycopeptide drugs, vancomycin and teicoplanin. However, clinicians may not recognize the term glycopeptide, and the acronym VISA is used more frequently.

Laboratorians may not be aware of proper methods for accurately identifying VISA (8). Hospital A's laboratory described in this report properly identified this VISA-infected patient by using a confirmatory testing protocol consistent with CDC's interim guidelines (6). This protocol included an algorithm to identify candidate strains (i.e., vancomycin MIC greater than or equal to 4 µg/mL) for confirmatory testing. At hospital A's laboratory, the Vitek system is not used only to detect intermediate resistance of S. aureus isolates but also to detect candidate strains for confirmatory susceptibility testing. Correct and prompt identification of VISA is critical in preventing transmission.

If candidate strains are detected, CDC is available to perform expedited confirmatory susceptibility testing. CDC is seeking laboratory reports of confirmed cases of VISA infection for an ongoing nationwide epidemiologic study. Information on confirmatory testing, investigation therapy, and infection-control guidelines can be obtained from CDC's Hospital Infections Program, National Center for Infectious Diseases, telephone (404) 639-6413; World-Wide Web site, http://www.cdc.gov/ncidod/hip/vanco/vanco.htm, or e-mail SEARCH@cdc.gov. The recovery of S. aureus with reduced susceptibility to vancomycin (e.g., MIC greater than or equal to 4 µg/mL) should be reported promptly to local and state health departments and to CDC, infection-control precautions should be implemented (6), and an epidemiologic investigation should be conducted.

References

1. Herold B, Immergluck LC, Maranan MC, et al. Community-acquired methicillin-resistant Staphylococcus aureus in children with no identified predisposing risk. JAMA 1998;279:593-8.
2. CDC. Four pediatric deaths from community-acquired methicillin-resistant Staphylococcus aureus--Minnesota and North Dakota, 1997-1999. MMWR 1999;48:707-10.
3. CDC. Reduced susceptibility of Staphylococcus aureus to vancomycin--Japan, 1996. MMWR 1997;46:624-6
4. Smith TL, Pearson ML, Wilcox KR, et al. Emergence of vancomycin resistance in Staphylococcus aureus. N Engl J Med 1999;340:493-501.
5. Rotun SS, McMath V, Schoonamker DJ, et al. Staphylococcus aureus with reduced susceptibility to vancomycin isolated from a patient with fatal bacteremia. Emerg Infect Dis 1999;5:147-9.
6. CDC. Interim guidelines for prevention and control of staphylococcal infection associated with reduced susceptibility to vancomycin. MMWR 1997;46:626-8,656.
7. National Committee for Clinical Laboratory Standards. Approved standard M7-A4:methods for dilution antimicrobial susceptibility tests for bacteria that grow aerobically. 4th ed. Wayne, Pennsylvania: National Committee for Clinical Laboratory Standards, 1997.
8. CDC. Laboratory capacity to detect antimicrobial resistance, 1998. MMWR 2000;48:1167-71.

* Use of trade names and commercial sources is for identification only and does not imply endorsement by CDC or the U.S. Department of Health and Human Services.

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