V. Fernandez-baca et al., Molecular epidemiological typing of Enterobacter cloacae isolates from a neonatal intensive care unit: three-year prospective study, J HOSP INF, 49(3), 2001, pp. 173-182
Since 1992, there has been an increase in the incidence of Enterobacter sep
sis in the neonatal intensive care unit (NICU) of the authors' hospital. Fr
om 1995 to 1997, a prospective molecular epidemiological survey of the colo
nizing and infecting strains isolated from neonates was conducted. Enteroba
cter cloacae was the most frequent cause of neonatal sepsis, accounting for
19.2% of all neonatal infections, reaching a peak incidence of 2.2/1000 du
ring 1996. Fifty isolates from the NICU and four epidemiologically unrelate
d strains were characterized by pulse-field gel electrophoresis (PFGE), rib
otyping, enterobacterial repetitive intergenic consensus (ERIC)-PCR and pla
smid profiling. PFGE was the most discriminatory technique and identified 1
3 types (two of them classified into two and three subtypes) compared with
ERIC-PCR, plasmid profiling and ribotyping that identified 11, 11 and seven
types, respectively. A good correlation was found between all techniques.
Five different clones caused 15 cases of sepsis. Clones A and B were preval
ent in 1995 and 1996, but they were not isolated in 1997, An outbreak cause
d by clone G in 1997 was controlled by cohort nursing and hygienic measures
, without changing the antibiotic policy. Strains were characterized by the
ir antibiotic resistance pattern and divided into three groups. Group I cor
related with PFGE types A, B1 and B2, which hyperproduced Bush type 1 chrom
osomal beta -lactamase and expressed extended-spectrum beta -lactamases (ES
BLs). Group 11 only hyperproduced Bush type 1 chromosomal beta -lactamase a
nd correlated with PFGE-types DI, D2, D3 and 1. Finally, Group III, with in
ducible P-lactamases, correlated with the rest of PFGE types. The sudden di
sappearance of E. cloacae after reinforcement of hygienic measures confirms
the importance of patient-to-patient transmission. (C) 2001 The Hospital I
nfection Society.