Analysis of clonality and antibiotic resistance among early clinical isolates of Enterococcus faecium in the United States

Abstract

Background: The Enterococcus faecium genogroup, referred to as clonal complex 17 (CC17), seems to possess multiple determinants that increase its ability to survive and cause disease in nosocomial environments.

Methods: Using 53 clinical and geographically diverse US E. faecium isolates dating from 1971 to 1994, we determined the multilocus sequence type; the presence of 16 putative virulence genes (hyl(Efm), esp(Efm), and fms genes); resistance to ampicillin (AMP) and vancomycin (VAN); and high-level resistance to gentamicin and streptomycin.

Results: Overall, 16 different sequence types (STs), mostly CC17 isolates, were identified in 9 different regions of the United States. The earliest CC17 isolates were part of an outbreak that occurred in 1982 in Richmond, Virginia. The characteristics of CC17 isolates included increases in resistance to AMP, the presence of hyl(Efm) and esp(Efm), emergence of resistance to VAN, and the presence of at least 13 of 14 fms genes. Eight of 41 of the early isolates with resistance to AMP, however, were not in CC17.

Conclusions: Although not all early US AMP isolates were clonally related, E. faecium CC17 isolates have been circulating in the United States since at least 1982 and appear to have progressively acquired additional virulence and antibiotic resistance determinants, perhaps explaining the recent success of this species in the hospital environment.

Figure 1

Key events that occurred in the isolates of this study. The MICs listed correspond to the highest ampicillin MIC from each outbreak. The following abbreviations are used in this figure: high-level resistance to streptomycin (STR^HLR), high-level resistance to gentamicin (GEN^HLR), ampicillin resistance (AMP^R) and vancomycin resistance (VAN^R)

Figure 2

A comparison between CC17 isolates and non-CC17 isolates for the presence of ampicillin resistance, vancomycin resistance, the esp_Efm gene, and the hyl_Efm gene. * P < 0.05 against non-CC17 isolates in our study. ** P < 0.005 against non-CC17 isolates in our study. *** P < 0.0005 against non-CC17 isolates in our study

Figure 3

A comparison between CC17 and non-CC17 isolates for the presence of the putative adhesins and pili (fms) genes. fms1-5-9 is the ebp_fm operon while fms11-19-16 and fms 14–17–13 are putative pilus operons. fms21 has been shown to encode pili while fms20 is considered its accessory protein. fms10, also known as scm, is a collagen binding adhesin while fms18 and fms15 are thought to encode putative adhesins. * P < 0.05 against non-CC17 isolates in our study. ** P < 0.005 against non-CC17 isolates in our study. *** P < 0.0005 against non-CC17 isolates in our study