Vancomycin resistant enterococcus (VRE) is a common cause of hospital acquired infection with significant patient morbidity and mortality. DNSE and LNSE appear to becoming an emerging drug resistant pathogen.
We performed a retrospective chart review of all DNSE and LNSE isolates from January 1, 2011 to December 31, 2013. DNSE was defined as a daptomycin MIC >4, LNSE as a linezolid MIC >2, and VRE as a vancomycin MIC >4.
116 isolates were identified and included: DNSE alone, n = 74 (63.8%); LNSE alone, n = 2 (1.7%); both DNSE/LNSE, n = 40 (34.5%). Of these isolates, 75 (65%) were VRE, and 41 (35%) were VSE. In VRE isolates 56% were DNSE-alone, 2.7% were LNSE-alone, and 41% were DNSE/LNSE. In VSE isolates, 85% were DNSE-alone, 0% were LNSE alone, 15% were DNSE/LNSE. There were 96 (83%) E. faecium isolates, and 20 (17%) E. faecalis; both DNSE and LNSE were seen in E. faecium isolates, whereas only DNSE was seen in E. faecalis isolates. Of the DNSE, the proportion with antibiotic exposure in the preceding 6 months was seen with vancomycin, 57%; daptomycin, 25%, and linezolid 7%; and of the LNSE, vancomycin, 57%; linezolid, 2.4%; and daptomycin, 21.4%; for all comparisons, the proportion of DNSE and LNSE isolates with prior exposure to either vancomycin, daptomycin or linezolid was not statistically significant from the proportion of isolates that did not have prior exposure (p > 0.255). Prior enterococcal isolation in the preceding 6 months did not have an association with the development of DNSE, OR 0.73, p = 1; or LNSE, OR 1.5, p = 0.301. VRE vs. non-VRE was associated with a 4.38 higher odds of having LNSE, p = 0.002. Of the DNSE isolates, 65% were susceptible to linezolid, and of the LNSE isolates, 5% were susceptible to daptomycin. 15/19 (78.9%) of the bloodstream infection (BSI) isolates also exhibited vancomycin resistance and this carried a 53% mortality. All deaths due to enterococcus BSI were VRE (8/8), 25% (2/8) of these were both DNSE and LNSE.
DNSE and LNSE may be emerging as important causes of healthcare associated infections. The evolution of this resistance pattern may not be adequately explained by prior antibiotic exposure.
S. Kon, None
G. Balba, None
R. Teran, None
L. Duong, None
P. Kumar, None
S. Ajluni, None
J. Timpone, None
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