Prolonged Outbreak of Infection Due to TEM-21-Producing Strains ofPseudomonas aeruginosaand Enterobacteria in a Nursing Home

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Abstract
Over a 6-year period, 24 extended-spectrum β-lactamase (ESBL)-producing isolates ofPseudomonas aeruginosawere collected from 18 patients living in a nursing home. These isolates had a delayed development of a red pigment and exhibited a similar antibiotype (resistance to all β-lactams except for imipenem and to gentamicin, tobramycin, netilmicin, ciprofloxacin, and rifampin) associated with the production of the TEM-21 β-lactamase and a type II 3′-N-aminoglycoside acetyltransferase [AAC(3)-II] enzyme. Surprisingly, serotyping showed that these isolates belonged to four successive serotypes (P2, P16, P1, and PME), although molecular typing by PCR methods and pulsed-field gel electrophoresis yielded identical or similar profiles. Moreover, in all isolates theblaTEM-21gene was part of a chromosomally located Tn801transposon truncated by an IS6100element inserted within the resolvase gene, and theaac(3)-IIgene was adjacent to this structure. During the same period, 17 ESBL-producing isolates of enterobacteria were also collected from 10 of these patients. These isolates harbored a similar large plasmid that contained theblaTEM-21and theaac(3)-IIgenes and that conferred additional resistance to sulfonamides and chloramphenicol, as well as to kanamycin, tobramycin, netilmicin, and amikacin, conveyed by an AAC(6′)-I enzyme. TheblaTEM-21gene was part of the Tn801transposon disrupted by IS4321. Thus, a single clone ofP. aeruginosathat had undergone a progressive genetic drift associated with a change in serotype appeared to be responsible for an outbreak of nosocomial infections in a nursing home. This strain has probably acquired theblaTEM-21-encoding plasmid that was epidemic among the enterobacteria at the institution, followed by chromosomal integration and genomic reorganization.

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