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Infections Due to Beta-Lactamase-producing, High-Level Gentamicin-resistant Enterococcus faecalis

Virginia D. Wells, MD; Edward S. Wong, MD; Barbara E. Murray, MD; Philip E. Coudron, PhD; Denise S. Williams, MT; and Sheldon M. Markowitz, MD
[+] Article and Author Information

Affiliations: From the Department of Veterans Affairs Medical Center and the Medical College of Virginia, Richmond, Virginia; and the University of Texas Health Sciences Center, Houston, Texas.

Requests for Reprints: Sheldon M. Markowitz, MD, Infectious Diseases Section (111-C), Department of Veterans Affairs Medical Center, 1201 Broad Rock Boulevard, Richmond, VA 23249.

Current Author Addresses: Dr. Wells: Division of Infectious Diseases, Box 49-MCV Station, Medical College of Virginia, Richmond, VA 23298.

Drs. Wong and Markowitz, and Ms. Williams: Infectious Diseases Section (111-C), Department of Veterans Affairs Medical Center, 1201 Broad Rock Boulevard, Richmond, VA 23249.

Dr. Coudron: Pathology Service (113), Department of Veterans Affairs Medical Center, 1201 Broad Rock Boulevard, Richmond, VA 23249.

Dr. Murray: Program in Infectious Diseases and Clinical Microbiology, The University of Texas Health Science Center at Houston, P.O. Box 20708, Houston, TX 77225.


Ann Intern Med. 1992;116(4):285-292. doi:10.7326/0003-4819-116-4-285
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Objective: To investigate the risk factors, clinical features, molecular epidemiology, and treatment outcomes associated with an outbreak of infections due to beta-lactamase-producing, high-level gentamicin-resistant Enterococcus faecalis.

Design: Case-control and molecular genetics study.

Setting: Tertiary care Veterans Affairs hospital.

Patients: Sixty-five patients infected or colonized with beta-lactamase-producing high-level gentamicin-resistant E. faecalis (case patients) were matched and compared with 65 randomly selected patients infected or colonized with beta-lactamase-negative, gentamicin-susceptible E. faecalis.

Measurements and Main Results: During the 20-month study period, 124 of 1506 isolates (8.2%) of E. faecalis from 70 patients were found to produce beta-lactamase. Univariate analysis showed older age, higher APACHE II score, nosocomial acquisition, recent surgical procedure, total parenteral nutrition, and antibiotic treatment to be significantly associated with the acquisition of beta-lactamase-producing, high-level gentamicin-resistant E. faecalis. A multivariate analysis, done using stepwise multiple logistic regressions, showed that only two variables remained significant: an APACHE II score > 6 (odds ratio, 9.5; 95% Cl, 4.4 to 20.3) and antibiotic treatment (odds ratio, 10.2; Cl, 4.5 to 23.2). The mortality rate for case patients was 7.7% (5 of 65 patients; Cl, 1.2% to 14.2%); no control patient died. Of 23 infections occurring in case patients, 13 were treated with "inappropriate" antibiotics (regimens that included a beta-lactamase-unstable antibiotic); 2 patients improved and 11 had complete resolution of disease. "Appropriate" treatments (regimens that included a beta-lactamase-stable antibiotic) were used in 10 patients; 5 of 10 infections were fatal. Restriction enzyme digests of total chromosomal DNA showed nearly identical patterns for selected isolates of beta-lactamase-producing, high-level gentamicin-resistant E. faecalis, suggesting dissemination through the hospital of a single strain of E. faecalis.

Conclusions: Fatal infections were observed despite treatment with beta-lactamase-stable antibiotics. The risk for infection or colonization with beta-lactamase-producing, high-level gentamicin-resistant E. faecalis was strongly associated with severe underlying disease (acute physiology and chronic health evaluation [APACHE] II score, > 6) and previous antibiotic treatment. These results may be useful in targeting high-risk patients for infection-control interventions.

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