Acinetobacter is a genus of gram-negative bacteria belonging to the Gammaproteobacteria. They are nonmotile, oxidase negative, highly pleomorphic and usually occur in pairs. The genus Acinetobacter has occupied an increasingly important position as an opportunistic pathogen in the hospital environment. The contribution of Acinetobacter spp. to nosocomial infection has increased over the past three decades, and many outbreaks of hospital infection involving Acinetobacter spp. have been reported worldwide [1–3].
Although generally regarded as commensals of human skin and the human respiratory tract, Acinetobacter spp. have also been implicated as the cause of serious infectious diseases such as pneumonia, urinary tract infections, endocarditis, wound infections, meningitis, and septicemia, involving mostly patients with impaired host defenses . Acinetobacter spp. have emerged as particularly important organisms late-onset ventilator associated pneumonia in the in tensive care unit (ICU). This is probably related, at least in part, to the increasingly invasive diagnostic and therapeutic procedures used in hospital ICUs in recent years [4–6].
Acinetobacter spp. have acquired resistance to almost all currently available antimicrobial agents, including the aminoglycosides, the quinolones, and broad-spectrum β-lactams. The spectrum of antibiotic resistance of these organisms, together with their survival capabilities, makes them a threat in hospital environments, as documented by recurring outbreaks both in highly developed countries and elsewhere. Most strains are resistant to cephalosporins, while resistance to carbapenems is being reported increasingly [7, 8]. One particular attribute of these strains is the production of extended-spectrum beta-lactamase (ESBL) enzymes that confer resistance to β-lactams . Guillou et al.  screened 100 isolates of Acinetobacter spp. and found that 81% of the strains produced two types of β-lactamases (TEM and CARB).
Acinetobacter baumannii hospital isolates produce mainly cephalosporinase-type enzyme and are inhibited by 25 mM of clavulanic acid but not by 1 mM EDTA or 100 mM para-chloromercuribenzoate (p-CMB). The β-lactamases produced by Acinetobacter lwoffii ULA-501, A. baumannii ULA-187, and A. baumannii AC-14 strains have been purified and characterized, and their kinetic interactions with several β-lactam molecules, including substrates and inhibitors, have been studied in detail . Three β-lactamase enzymes were identified and appeared to be cephalosporinase-type β-lactamases with different acylation efficiencies (kcat/Km ratio values). Their hydrolytic activities were inhibited by benzylpenicillin, piperacillin, and cefotaxime, none of which behaved as substrates for the enzyme. Carbenicillin was a substrate for the β-lactamase from A. lwoffii ULA-501, although it acted as a transient inactivator of the enzymes produced by the two A. baumannii strains. Clavulanic acid was unable to inactivate the three β-lactamases, whereas sulbactam behaved as an inactivator only at a high concentration (1 mM) that was difficult to achieve during antibiotic therapy .
Kim et al.  studied the prevalence and diversity of carbapenemases among imipenem-nonsusceptible Acinetobacter isolates in Korea. A total of 190 imipenem-nonsusceptible Acinetobacter isolates from 12 Korean hospitals in 2007 were used to determine species, prevalence, and antimicrobial susceptibility of OXA carbapenemase-producing and metallo-β-lactamase-producing isolates. bla
OXA-23 -like and ISAba1-associated bla
OXA-51 -like genes were detected in 80% and 12% of 178 imipenem-nonsusceptible Acinetobacter baumannii isolates, respectively.
Sinha et al.  recovered 150 clinical isolates of Acinetobacter and identified them using various phenotypic tests. Antibiotic susceptibility was determined by the standard disk-diffusion method. Most isolates were resistant to the antibiotics tested, including the third-generation cephalosporins. ESBL production was detected in 28% of the isolates. In the double-disk approximation test, most of the ESBLs in Acinetobacter isolates could be detected with cefepime and cefotaxime.
In one study in the UK, the antimicrobial susceptibility of Acinetobacter obtained from clinical specimens in 54 laboratories was investigated. The majority of the isolates were found to be more resistant to cefotaxime, ceftazidime, piperacillin, piperacillin + tazobactam, gentamicin, and tetracycline than the other gram negative bacteria .
Little information is available on the antibiotic resistance of Acinetobacter spp. isolated from hospitals in Iran. Khosroshahi and Sharifi  recovered 400 isolates from ICU patients in four university hospitals in Isfahan, Iran, of which 15 (3.75%) belonged to A. baumannii. Antibiotic sensitivity testing showed four (26.6%) isolates were resistant to imipenem and meropenem. Similarly, Farhani et al.  recovered 60 isolates of Acinetobacter spp. from Shahid Beheshti Hospital in Kashan, Iran. Among these, 48 were A. baumannii, six were A. lwoffi, and six were other Acinetobacter spp. They were resistant to amikacin, tobramycin, ampicillin + sulbactam, and imipenem.
To assess the level of sensitivity to antibiotics routinely used in the ICU of our hospital and to determine the production of ESBLs, we investigated the antibiotic resistance pattern and ESBL production in Acinetobacter spp. isolated from the ICU of the Afzalipoor Hospital in Kerman, Iran.