In 8 LRSE isolates representing all PFGE types, genes encoding the L3, L4, and L22 ribosomal proteins that factor in ribosome assembly were sequenced to identify mutations conferring linezolid resistance (6).
The 27 LRSE isolates were tested by pulsed-field gel electrophoresis (PFGE) as described (12) and screened for cfr gene (7).
Growth curves were conducted in the presence and absence of linezolid for the above 8 LRSE isolates, 1 clinical LSSE isolate (A1521, linezolid MIC 2 [micro]g/mL), and the ATCC 29213 S.
We retrospectively examined medical records (anonymized demographic data, clinical characteristics, comorbidities, prior linezolid treatment for [greater than or equal to]3 days, and in-hospital deaths) of the 27 patients harboring LRSE to ascertain factors influencing resistance acquisition and outbreak persistence.
Linezolid MICs were >256 [micro]g/mL for 23 LRSE isolates and 8-32 [[micro]]g/mL for 4 LRSE isolates.
Most of the LRSE isolates were clonally related, but 3 distinct PFGE types were detected, implying that linezolid resistance emerged in at least 3 different strains, which subsequently spread between patients.
Characteristics of the 8 LRSE isolates tested by growth analysis are shown in Table 2; curves of the 5 highly LRSE isolates at 0, 32, and 128 [micro]g/mL linezolid and of the 3 low-level LRSE and controls at half-MIC linezolid are shown in Figures 1 and 2.