The global increase in multidrug resistance of Acinetobacter spp. has created widespread problems in the treatment of patients in intensive care units (ICUs) of hospitals. To assess the sensitivity of Acinetobacter isolates to antibiotics routinely used in ICUs, we investigated antibiotic resistance patterns and extended-spectrum β-lactamase (ESBL) production among Acinetobacter spp. isolated from the ICU of a university hospital in Kerman, Iran.
Fifteen isolates of Acinetobacter spp. were recovered from one hundred clinical specimens collected from the ICU of Afzalipoor Hospital in Kerman, Iran, from October 2010 to June 2011. Preliminary antibiotic sensitivity testing was carried out using the disk-diffusion breakpoint assay, and MICs of different antibiotics were determined using the E-test. ESBL production was detected by a double-disk synergy test and confirmed by a phenotypic confirmatory test. Substrate hydrolysis in the presence and absence of the following inhibitors was carried out using the rapid fixed-time method: para-chloromercuribenzoate (p-CMB), clavulanic acid, sulbactam, and NaCl.
Overall, 73.3% of the isolates were resistant to imipenem (MIC range 240-128 µg/mL) and 66% to ciprofloxacin (MIC range 240-64 ± 0.08 µg/mL). All of the isolates were fully resistant (MIC 240 µg/mL) to piperacillin, while 93.3%, 53.3%, and 93.3% were resistant to piperacillin + tazobactam (MIC 240 µg/mL), amikacin (MIC range 128-16 µg/mL), and cefepime (MIC range 240-60 µg/mL), respectively. The isolates were also resistant to chloramphenicol and tetracycline: MICs of these two agents were ≥ 240 µg/mL. The test for ESBL production was positive for only three isolates (nos. 1, 10, and 15). The rate of substrate hydrolysis was highest in the presence of p-CMB (80.2 ± 0.02) and lowest in the presence of NaCl (2.1 ± 0.01) (P ≤ 0.05).
Many isolates of Acinetobacter spp. are resistant to almost all antibiotics routinely used in the ICU of our hospital, including imipenem, ciprofloxacin, and piperacillin + tazobactam. Three isolates were ESBL producers. The other isolates exhibited high resistance to β-lactams, but they did not produce any ESBL enzymes.