Emergence in vivo resistance to ampicillin in a clinical isolate of Enterococcus hirae.

MASSA R; BANTAR C; MOLLERACH M; NICOLA F; MURRAY B; SMAYEVSKY J; GUTKIND G

JOURNAL OF ANTIMICROBIAL CHEMOTHERAPY

Oxford University Press

Año: 1998 vol. 42 p. 559 - 561

0305-7453

After ten days of ampicillin treatment (1,5 g daily) the Enterococcus hirae responsible for an urinary infection in a male patient with prostaic hyperthropy changed their MICs of penicillin G from 1 to 4 mg/L, imipenem from 0.5 to 4 mg/L and ampicillin from 0.5 to 4 mg/L. A laboratory mutant (EHM) was selected following serial passage in of the penicillin susceptible parent strain (EHS) isolated before ampicillin therapy in tryptic soy broth containing increasing concentrations of penicillin. Mechanism involved in resistance emergence was studied in E. hirae isolated after treatment (EHR) and  EHM mutant. Penicillin Binding Proteins (PBPs) profiles were studied using 125-Iodo as radiotracer. No novel PBP with atypical electrophoretic mobility was detected. The magnitude of the signal attributable to the low affinity PBP 5 was greater in EHM than those detected in EHS and EHR. Western blotting with a polyclonal antibody to the PBP 5 indicated the overproduction of this PBP in EHM, but not in EHR. Resistance in this isolate mat be attributable to a slight decrease in the affinity of B-lactams for one or more PBPs, or to an unidentified mechanism.