BACKGROUND: Recently, Acinetobacter emerged as an important pathogen and the prevalence of isolation has increased since the last two decades worldwide. AIMS:To determine Acinetobacter incidence, their clinical demography, antibiotyping and speciation. SETTINGS AND DESIGN: A study of the clinical samples submitted to microbiology laboratory of a teaching hospital over a period of 3 years (December 1994 through November 1997. MATERIALS AND METHODS: Identification, speciation and antibiotyping were performed for the isolates of Acinetobacter recovered from infective samples. Clinical demographic characteristics were studied retrospectively. RESULTS: Total 510 of 5391 (9.6%) of isolates were Acinetobacter, responsible for 71.2% (363 of 510) monomicrobial and 28.8% (147 of 510) polymicrobial infections. The organism was responsible for 156 (30.6%) cases of urinary tract infection and 140 (27.5%) cases of wound infection and was most prevalent in the intensive care unit (30.8%, 140 of 455). The crude mortality rate due to multi-drug resistant Acinetobacter septicemia was 7.9% (36 of 455). The isolates could be classified into 7 species, with A. baumannii being most predominant. No peculiar pattern during antibiotyping was observed, but most of them were multi-drug resistant. CONCLUSION: Multi-drug resistant Acinetobacter nosocomial infection has emerged as an increasing problem in intensive care units of the hospital, responsible for 7.9% deaths. The analysis of risk factors and susceptibility pattern will be useful in understanding epidemiology of this organism in a hospital setup.

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Clinical Laboratory Standards Institute (CLSI) recommends two-step approach for extended-spectrum-β-lactamase (ESBL) detection which includes the screening of recommended agents and the phenotypic confirmation of ESBL using a combination of screening agent and β-lactamase inhibitor. To investigate this approach, we screened 145 β-lactamase-producing Acinetobacter baumannii isolates for ESBL from tracheal secretions using double disk synergy test (DDST) and phenotypic confirmatory disc diffusion test (PCDDT), the determination of minimum inhibitory concentration (MIC) for ceftazidime and cefotaxime (with/without clavulanic acid), and the unique disc placement scheme. Eighteen of 145 (12.4%) isolates showed ESBL production. All 18 isolates showed positive PCDDT. MIC of these isolates were extremely high (>512 µg/ml), and eight fold decrease in MIC was shown by only one isolate. The unique disc placement scheme detected 13 (72.2%) and 3 (16.7%) of ESBL producers and ampC producers, respectively. High level resistance to cefoxitin and cefotaxime among these isolates is suggestive of the derepressed mutants. The PCDDT was most effective ESBL detection method while the unique disc placement scheme showed advantage of detection of ampC β-lactamase, derepressed mutants and multiple β-lactam resistance mechanism in these isolates. This is a rare report comparing different tests for phenotypic ESBL detection in clinical isolates of A. baumannii.