Imp-1-producing carbapenem-resistant acinetobacter ursingii from Japan

Abstract

Sir, Acinetobacter baumannii represents the most clinically important and frequently detected Acinetobacter species. There has been concern about the possible emergence of carbapenem resistance in A. baumannii by acquisition of OXA-type carbapenemases or metallo-β-lactamases, since few effective antimicrobial agents are available. Several mechanisms could lead to carbapenem resistance in A. baumannii, including β-lactamases capable of hydrolysing carbapenems, loss of porins and up-regulation of efflux pumps. Currently, 33 genomic species have been identified by molecular methods in the genus Acinetobacter. A. baumannii is generally the most frequent pathogen among clinical isolates, although it is difficult to perform accurate species identification at many institutions. Recently, sequencing has provided reliable species identification of Acinetobacter isolates at some laboratories, and severe infections caused by species other than A. baumannii have been reported.1 Little is known about carbapenem resistance among non-A. baumannii species. With respect to Acinetobacter ursingii, there have been a few reports about bacteraemia due to this pathogen,2 but no mention of carbapenem resistance. We isolated carbapenem-resistant A. ursingii from a Japanese patient with a bloodstream infection. To our knowledge, this is the first reported clinical isolate of carbapenem-resistant A. ursingii. During the past 6 years (January 2005 to May 2011), we detected six A. ursingii isolates from blood cultures at our hospital, which has 1300 beds and is located in northern Japan. Of these six isolates, only one strain (isolated from the blood cultures of an inpatient) was carbapenem resistant. The patient was admitted to our hospital with rupture of an infected aortic aneurysm in 2010. He had several underlying diseases, including diabetes, hypertension and oropharyngeal carcinoma, and was on haemodialysis for chronic renal failure. Emergency aortic replacement was performed on the day of admission. Six days after surgery, carbapenem-resistant A. ursingii was isolated from a blood culture taken in the intensive care unit. Because of the antibiotic susceptibility profile, ciprofloxacin was administered intravenously. The patient had a central venous catheter, peripheral catheter, urethral catheter, thoracostomy tube and endotracheal tube. The patient continued to receive antibiotic therapy for 2 weeks, after which laboratory parameters normalized. Acinetobacter species were identified by the VITEK 2 bacterial identification system and genomic species identification was done by partial sequencing of the RNA polymerase β-subunit (rpoB) gene.3 MICs were determined by the agar dilution method of the CLSI.4 PCR was done to detect the OXA-51-like, OXA-23-like, OXA-24-like and OXA-58-like carbapenemase genes, as well as the IMP-1, IMP-2, VIM-1, VIM-2, SIM and NDM-1-type metallo-β-lactamase genes.5,6 Proximity of ISAba1, ISAba2, ISAba3 and IS18 to blaOXA-58-like genes6 and the carO (outer membrane protein) gene7 was also investigated by PCR. In addition, the OXA-type carbapenemase and metallo-β-lactamase genes were sequenced. The MICs of the patient's carbapenem-resistant A. ursingii isolate were as follows: piperacillin ≥256 mg/L; ceftazidime ≥256 mg/L; cefepime ≥256 mg/L; imipenem 32 mg/L; meropenem; 32 mg/L; levofloxacin 0.5 mg/L; and colistin 0.5 mg/L. PCR revealed that this isolate possessed both IMP-1 and OXA-58-like genes, with no other carbapenem resistance genes being detected. The OXA-58-like carbapenemase gene was not linked to ISAba1, ISAba2, ISAba3 or IS18. Sequencing of the blaOXA-58-like and blaIMP-1 genes yielded OXA-58 and IMP-1, respectively. The isolate also showed a loss of carO genes. Thus, the mechanism of resistance could have involved a synergistic interaction between IMP-1 expression and a loss of this outer membrane protein. Our findings are in accordance with a recent study from South Korea,7 where the blaIMP-1 gene was detected in several carbapenem-resistant non-A. baumannii isolates. Three Acinetobacter isolates with imipenem MICs ≥8 mg/L have been detected in blood cultures at our hospital over the past 6 years, and one of these isolates was identified as A. ursingii by partial rpoB gene sequencing. The remaining two isolates were identified as Acinetobacter soli. Use of molecular methods for identification of Acinetobacter genomic species has revealed the prevalence of various species. A recent study has shown that bacteraemia due to A. baumannii but also due to non-A. baumannii species may be associated with poor outcome.8 Our findings indicate that carbapenem resistance may exist among clinical isolates of A. ursingii and emphasize the importance of accurate epidemiological investigation of non-A. baumannii species, including A. ursingii. This study was supported by internal funding. None to declare. We obtained written informed consent to release clinical information regarding the patient. We thank our laboratory staff for their technical support.

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