Outbreak of (OXA-66 carbapenemase) multidrug-resistant Acinetobacter baumannii in a Spanish tertiary-care hospital: Epidemiology and study of patient movements

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Background: Acinetobacter baumannii is an increasingly common nosocomial pathogen. Carbapenems have been the agents of choice for severe Acinetobacter infections. We describe an outbreak of multidrug-resistant (MDR) A. baumannii that produced OXA-66 carbapenemase and was resistant to imipenem. We also analyze the relationship between the spread of this strain and patients’ movements within the hospital.

Methods: Thirty-one isolates of A. baumannii with very similar susceptibility patterns from 15 patients, recovered in a 2 months period, were studied. We analyzed 8 more isolates recovered during the following year. ERIC-PCR and RAPD genotyping methods were used to define clusters of clonally related isolates. PFGE was used to confirm the results and to check the maintenance of the epidemic strain over the following year. Patterns of possible transmission were analyzed by recording patient movements within the hospitals. Antibiotic susceptibility testing to 28 agents was performed by microdilution and by E-test. The isolates were screened by PCR analysis with primers specific for 6 carbapenemase genes. Amplification products were sequenced to determine the gene present.

Results: Twelve of the 15 patients studied were hospitalizated at the ICU. The most frequent sites of isolation were the respiratory tract (16) and the blood (11). With the exception of colistin (0% resistance) there were no antibiotics with good activity against these isolates. Of the other antibiotics tested, tigecycline showed the best activity with an MIC90 value of 2 mg/L. The genotypic study revealed that the same strain was responsible for all the infections. All the isolates harboured the bla-OXA-51–like gene and the 6 of them chosen to sequence the gene were identical and 100% homologous with the bla-OXA-66 gene. PCR showed that the insertion sequence ISAba1 was present upstream of the oxacillinase gene in all the isolates.

Conclusion: a) Molecular typing revealed that the outbreak detected in our hospital was due to a single A. baumannii clonal group. b) The epidemic strain of A. baumannii produces an OXA-66-ISAba1 carbapenem-hydrolyzing oxacillinase. c) Even though the outbreak was controlled, and the number of isolates decreased significantly, the clone responsible of the outbreak persisted at the hospital during the following year.