A total of 55 Enterococcus faecalis and 21 Enterococcus faecium non-replica
te isolates were obtained from routine clinical specimens, during a 1 year
period, in a tertiary care hospital in Athens, Greece. The most common isol
ation site was the urinary tract (44% of E. faecalis and 33% of E. faecium
isolates). No vancomycin resistance was detected. Ampicillin-resistant isol
ates did not produce beta-lactamase. High-level gentamicin resistance was d
etected in 22% and 0% of E. faecalis and E. faecium isolates, respectively.
The corresponding figures for high-level streptomycin resistance were 40%
and 33%. The aminoglycoside-modifying enzyme gene aac(6')+aph(2 ") was dete
cted by PCR in 10 of 12 high-level gentamicin-resistant E faecalis Isolates
, and the ant(6)-I gene in all high-level streptomycin-resistant isolates o
f both species. DNA fingerprinting by PFGE grouped 31 of 55 E. faecalis iso
lates into 10 clusters, end 10 of 21 E. faecium isolates into two clusters,
containing two to seven isolates each. Two E. faecalis PFGE types, compris
ing isolates expressing high-level aminoglycoside resistance, and not obser
ved among non-high-level aminoglycoside-resistant strains, were disseminate
d in building A of the hospital. In contrast, high-level aminoglycoside res
istance seemed to have been acquired nosocomially by a number of genotypica
lly different E. faecium types. Molecular typing was therefore instrumental
in understanding the differences in the mode of spread and acquisition of
high-level aminoglycoside resistance among these two different enterococcal
species.