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.
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.
The 5 linezolid-dependent LRSE isolates had 2 potentially relevant amino acid substitutions, G152D (shift from a small amino acid to a negative hydrophilic) and D159Y (shift of hydrophilic to hydrophobic amino acid), and a less significant one (L101V) in L3 protein.
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.