Objectives:

Recently PER-1 extended-spectrum b-lactamase (ESBL) was discovered in a Peudomonas aeruginosa strain in France and was subsequently detected in Acinetobacter spp. and Pseudomonas aeruginosa in other countries including Turkey. The purpose of this study was to clarify the molecular epidemiology of infection caused by a strain of cefepime-resistant A. baumannii and also to determine the mechanism of drug resistance.

Methods:

Cefepime-resistant A. baumannii strains were isolated from clinical specimens of nine patients hospitalised in an intensive care unit in Busan, Korea. Antimicrobial susceptibilities were determined by the disk diffusion and agar dilution methods. The double disk synergy (DDS) test was performed for screening of ESBL production. Isoelectric focusing and conjugation experiments were performed. blaPER-1 and blaPER-2 alleles were detected by PCR, and sequences of amplified products were determined by using the dideoxy-chain termination method. Pulsed-field gel electrophoresis (PFGE) was performed for molecular typing of isolates.

Results:

The isolates showed same antimicrobial susceptibility pattern, positive DDS results and PFGE patterns. The isolates contained three b-lactamase bands: pI 5.3, 7.9, and 9.4. PCR-based experiments detected blaPER-1 genes. MICs of ampicillin, piperacillin, cephalothin, cefoxitin, cefoperazone, ceftazidime, cefotaxime, cefepime, and aztreonam to these isolates were >=256 mg/L, respectively, and those of imipenem were 8–16 mg/L. Despite repeated attempts, the resistance to cefepime of A. baumannii isolates was not transferred to the recipient.

Conclusions:

A. baumannii isolates from clinical specimens of nine patients hospitalised in a same intensive care unit were shown to be of the same clone. All these isolates contained blaPER-1 gene which caused resistance to cefepime. To the best of our knowledge, outbreaks caused by PER-1 ESBL-producing A. baumannii have not previously been described.