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Vancomycin-Resistant Organisms on a Burn Unit.

ABSTRACT: The incidence of infections due to vancomycin-resistant organisms has significantly increased during the past several years. This is important because vancomycin has been the drug of choice for treatment of infections due to methicillin-resistant Staphylococcus aureus (MRSA). Enterococci resistant to vancomycin are now emerging, and MRSA organisms with intermediate resistance to vancomycin have been identified in some centers. Cross transfer of resistance will eventually lead to the widespread development of organisms that are more difficult to eradicate. In our burn unit, we have encountered six patients (five with burns, one with necrotizing faciitis) who had wound infections with vancomycin-resistant enterococci. Four patients died, and two recovered after prolonged hospital stays. Attempts to limit development of vancomycin-resistant enterococci are important.

VANCOMYCIN has long been the preferred drug for treating infections due to methicillin-resistant Staphylococcus aureus (MRSA). Rare cases of MRSA with intermediate sensitivity to vancomycin are now being encountered in some institutions. Vancomycin-resistant enterococci (VRE) are becoming more common. Our burn unit has treated six patients, five with acute burns and one with necrotizing fasciitis, whose wounds were infected with VRE.


Bacteriologic records of burn unit patients having cultures positive for VRE were reviewed, and charts of these patients were evaluated. Demographic data, hospital course, and outcomes were recorded.

At our institution, admission topical wound management is initiated at the discretion of the surgeon. Second-degree burns are usually treated by tangential excision or scraping, followed by the application of temporary wound dressing (Biobrane) or porcine xenograft. These dressings are allowed to dry in place (the xenograft after a 24-hour application of silver nitrate). Deeper wounds are usually treated with topical Dakin's solution or 5% mafenide acetate. Excision is done early. Culture data are used to make appropriate changes in topical agents, depending on the organisms identified.

The screening process for VRE used in the microbiology laboratory calls for specimens to be plated, according to their source, in a variety of media, either Baltimore Based Laboratories (BBL) enterococcosel agar or BBL colistin/nalidixic acid agar or both. After incubation, the organism is identified as an enterococcus on the basis of morphology of cultures and a negative catalase test and if esculin hydrolysis and PYR reaction (pyrrolidonyl-[beta]-naphthylamide hydrolysis) are positive. These colonies are also placed in dilution tubes for determination of minimum inhibitory concentration (MIC) read by MicroScan after being plated on BBL vancomycin screen agar (vancomycin 6 mg/L). The MIC and vancomycin screen agar results are read at 24 hours.

During the report period, enterococci were identified as Group D but not further speciated.


The six patients in whom vancomycin-resisrant organisms were encountered ranged from 11 to 84 years of age. Five of the patients were admitted with acute bums, and one patient had necrotizing fasciitis. Bum size ranged from 17% to 96% of total body surface area. Three of the patients with burns died, as well as the one with fasciitis. Two of the patients who died were believed to be preterminal on admission. One patient, 84 years old, whose wounds were essentially healed and whose infection was controlled, died of a heart attack late in his course. In one patient, the group D enterococcal infection was thought to have significantly contributed to the death.

A 41-year-old male patient with bums on 88% of his total body surface and an inhalation injury required a ventilator throughout most of his course and peritoneal dialysis late in his course. He had a wound infection with enterococcus group D sensitive to vancomycin on day 15 after injury. The organism was reported as having become resistant to vancomycin on day 27. A blood culture was positive for this organism on day 51. He was given vancomycin initially and quinupristin/dalfopristin (Synercid) latex; with clearing of the enterococci. While receiving dialysis, he was also treated for several other septic episodes due to various organisms. With gradual improvement, he was weaned off the ventilator; dialysis was also discontinued, lie was discharged to a rehabilitation unit after a hospital stay of 373 days, with 288 days spent on the burn unit.

The sixth patient was an 11-year-old white girl who was burned over 96% of her body and had an inhalation injury, requiring a prolonged course of ventilatory support. She was hospitalized until day 148 on our unit. She had multiple septic episodes and required multiple surgical procedures for debridement and grafting, including the use of cultured epithelial autograft. On postburn day 47, group D enterococcus was cultured from wounds and urine. A 10-day course of vancomycin had been begun on day 35. On day 95, blood cultures for VRE group D were recovered. Quinupristin/dalfopristin (Synercid), given for 1 week and followed by additional vancomycin, controlled the enterococcal infection. The patient was transferred to the Shriners Burns Institute with her wounds essentially grafted, but persistent respiratory problems still necessitated ventilatory support. Subsequently, she returned to Augusta and has been readmitted to the burn unit for numerous re-constructive operations.


The incidence of vancomycin-resistnat infections is increasing. This is especially true of enterococcal organisms. At our institution, during the time frame of this study, enterococci were identified as Enterococcus group D but were not speciated as to type. During this period, vancomycin was the drug of choice for the treatment of MRSA. When an infecting organism was preliminarily identified as a gram-positive coccus, vancomycin was frequently given until the organism was identified. At final identification, the bacterium might eventually be found to be Enterococcus group D, MRSA, or another staphylococcal organism. Treatment with vancomycin might then be continued, or a different antibiotic might be selected. During the report period of this study, quinupristin/dalfoprisitin (Synercid) was available but only on a compassionate use basis. It was not yet available for routine use.

Enterococci are part of normal enteral flora and are not especially pathogenic in humans. They do not usually cause respiratory tract infections. The most frequently encountered enterococcal infections are urinary. Bacteremic extension is not uncommon. These organisms represent a significant nosocomial pathogen in the United States and elsewhere because of their resistance to certain antimicrobial agents, sometimes including the [beta]lactams.

Enterococcal sepsis was a significant cause of morbidity and mortality in our bum unit during a 3-year period from 1989 to 1991. Among 1,146 bum patients admitted, 11% of bacterial infections were found to be enterococcal. In 17 instances, enterococcal septicemia was thought to be a contributory cause of death. In 10 instances, the enterococci were one component of a polymicrobial infection. No cases of VRE were encountered in that series. [1] While infection with VRE can present significant treatment difficulties, the greatest concern is the potential for VRE to transfer their resistance to more pathogenic gram-positive bacteria such as S aureus. [2] The drug of choice for established MRSA infections is vancomycin. The use of this drug when vancomycin is not the only suitable drug may lead to increased risk of future development of vancomycin-resistant organisms, especially Infection surveillance and routine measures for infection control are important in controlling the spread of VRE within the hospiral. [ 3,4]

In a study [5] of 260 patients with enterococcal bacteremia, 72 (28%) had VRE. Risk factors for VRE infection were a high mean number of days of antibiotic therapy, a high mean number of days of vancomycin use, renal insufficiency, and the presence of neutropenia. Mortality was attributed to bacteremia in 96 patients (37%). Vancomycin resistance was not an independent predictor of mortality, but restriction of vancomycin use was recommended. Treatment of MRSA at a hospital in Buffalo, NY, resulted in selection of antibiotics that led to development of a vancomycin-resistant Enterococcus faecium. The importance of selection of antibiotics for patient management and infection control is stressed. [6]

Cases of vancomycin-resistant enterococcal infection appear to be rare. A case of bacteremia due to MRSA with intermediate resistance to vancomycin was reported by Turco et al. [7] The patient was treated with several courses of vancomycin for 18 of 23 hospital weeks. After 6 months, an isolate of MRSA showed an MIC of 8 [micro]g/mL, indicating intermediate resistance to vancomycin. In another isolated case, a patient with endocarditis died of MRSA infection that showed reduced sensitivity to vancomycin. The importance of accurate testing methods to evaluate resistance is stressed by the CD C. [8]

Systemic vancomycin should be reserved for use when no other drug is available. Use of topical vancomycin soaks in bum patients should be avoided unless considered absolutely essential. We have so far identified six VRE infections on our bum unit. Some institutions have reported a few MRSA organisms with intermediate resistance to vancomycin. Because the incidence of infection due to VRE is increasing, the possibility of transfer of resistance from enterococci to other organisms arises. Meticulous attention should be paid to isolation techniques on hospital wards to attempt to prevent interpatient transfer of infections.

From the Joseph M. Still Burn Center, Doctors Hospital, Augusta, Ca.

Reprint requests to Joseph M. Still, MD, Physicians' Multi-specialty Group, PC, 1220 George C. Wilson Dr, Augusta, GA 30909.


(1.) Law E, Belcher K, Still J: Enterococcal infections as a cause of mortality and morbidity in patients with burns. J Burn Care Rehabil 1994;15:236-239

(2.) Moellering R: Vancomycin resistant enterococci. Clin Infect Dis 1998;26:1196-1199

(3.) Holder I, Neely A: Vancomycin resistant enterococci. Burns 1998;24:99-103

(4.) Holder I, Neely A: Antimicrobial resistance. Burns 1999;25:18-23

(5.) Lautenbach E, Bilker w, Brennan P: Enterococcal bacteremia: risk factors for vancomycin resistance and predictors of mortality. Infect Control Hosp Epidemiol 1999;20:318-323

(6.) Schentaj J, Hyatt J, Carr J, et al: Genesis of methicillin resistant Staphylococcus aureus (MRSA). how treatment of MRSA infection had selected for vancomycin resistant Enterococcus faecium and the importance of antibiotic management in infection control. Clin Infect Dis 1998;26:1204-1214

(7.) Turco T, Melko G, Williams J: Vancomycin intermediate/resistant Staphylococcus aureus. Ann Pharmacother 1998;32:758-760

(8.) Kurshid MA: Fourth case of vancomycin-resistant staph infection reported in US. MMWR Morb Mortal Wkly Rep 2000;48:1165-1171


* The incidence of vancomycin-resistant infections is increasing.

* Systemic vancomycin should be reserved for use when no other drug is available.

* Use of topical vancomycin soaks in burn patients should be avoided unless absolutely essential.

* Meticulous attention should be paid to isolation techniques on hospital wards to prevent interpatient transfer of infections.

* The Centers for Disease Control and Prevention stress the importance of accurate testing methods to evaluate resistance.
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Publication:Southern Medical Journal
Geographic Code:1USA
Date:Aug 1, 2001
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