Epidemiological typing of klebsiellae with extended-spectrum beta-lactamases from European intensive care units.
Extended-spectrum beta-lactamases (ESBLs) are an increasing cause of resistance to oxyimino-aminothiazolyl cephalosporins, especially in klebsiellae. In a recent survey we detected ESBLs in 220 (23%) of 966 consecutive klebsiellae from 35 intensive care units (ICUs) in southern and western Europe. The present study examined the extent to which this distribution reflected epidemic strain spread, as against the distribution of ESBL genes into unrelated strains. All 220 ESBL producers were subjected to capsular serotyping and pulsed-field gel DNA electrophoresis (PFGE). Beta-Lactamases were typed for strains isolated on three or more occasions, with the emphasis on SHV enzymes, as these were commoner than TEM variants. Serotyping and PFGE typing defined 85 distinct strains, from 23 of the 35 participating centres. Of 14 centres that contributed five or more ESBL producers, all sent representatives of more than one strain, and two centres sent members of ten or more different strains in contributions of 17-21 ESBL-producing isolates. Nevertheless, epidemic strains-defined as those represented by three or more isolates-accounted for a majority (61%) of the collection. Fifty-two isolates of the same serotype K25 (occasionally acapsular) strain with SHV-4 beta-lactamase were recovered at two French hospitals and one in Belgium. This strain has been found by others in France, and has become particularly widespread. Another single strain was found in two separate Portuguese centres, and many individual hospitals had one or more epidemic strain(s), as well as a scatter of diverse ESBL producers. Major variation in antibiogram and plasmid profile was apparent within strains, with some intra-strain variation in beta-lactamase type. These data imply a fluid situation, with resistance determinants being gained, modified or lost. The endemicity of ESBL producers is disturbing since it limits the potential for control by blocking strain spread, while the diversity within strains is disturbing because it complicates the design of antibiotic policies even during 'single strain' outbreaks.
Yuan
M
M
Antibiotic Group, Department of Medical Microbiology, St Bartholomew's and the Royal London School of Medicine and Dentistry, Whitechapel Site, London, UK.
Aucken
H
H
Hall
L M
LM
Pitt
T L
TL
Livermore
D M
DM
D000900:Anti-Bacterial Agents / Q000494:pharmacology; D015169:Colony Count, Microbial; D004269:DNA, Bacterial / Q000235:genetics; D004352:Drug Resistance, Microbial; D016521:Electrophoresis, Gel, Pulsed-Field; D005060:Europe / Q000453:epidemiology; D006801:Humans; D007362:Intensive Care Units; D007709:Klebsiella / Q000145:classification* / Q000187:drug effects / Q000201:enzymology / Q000235:genetics; D007710:Klebsiella Infections / Q000188:drug therapy / Q000453:epidemiology / Q000382:microbiology; D010641:Phenotype; D010957:Plasmids; D016133:Polymerase Chain Reaction; D012703:Serotyping; D001618:beta-Lactamases / Q000145:classification* / Q000235:genetics
D000900:Anti-Bacterial Agents; D004269:DNA, Bacterial; D001618:beta-Lactamases