Control of glycopeptide-resistant enterococci in an oncology unit

Enterococci are responsible for 10-12% of nosocomial infections. Since 1987 the incidence of glycopeptide-resistant enterococci (GRE; termed vancomyci n-resistant enterococci in the United States) has increased dramatically. T he mechanism of GRE is well understood and involves mutation of a single te rminal amino acid in a peptidoglycan precursor leading to reduced vancomyci n affinity. Studies implicated antibiotic selection pressure as a major ris k factor for GRE infection and colonization. In the hematology unit of a Lo ndon hospital, GRE emerged in December 1993, with 38% of patients positive in a point prevalence study. Between December 1993 and June 1995, 13 patien ts acquired GRE bacteremia, five of whom died. Between 1995 and 1996 a pros pective sequential study was undertaken to determine the effect of changing antibiotic treatment of febrile neutropenia (FN). All patients admitted to the hematology unit were enrolled in the study. In phase 1, treatment cont inued with ceftazidime monotherapy. Tn phase 2, piperacillin-tazobactam rep laced ceftazidime, and enhanced infection control measures were encouraged. In phase 3, therapy returned to ceftazidime. In phase 1, 57% of patients b ecame colonized or infected with GRE. Phase 2, which was divided into two 4 -month cohorts, showed a significant reduction in GRE acquisition, falling to 8% colonization and no clinical infections in the second 4 months. In ph ase 3, despite heightened infection control procedures, the acquisition rat e rose to 36%.