The American Centers for Disease Control and Prevention (CDC) recognizes Acinetobacter baumannii as a source of global outbreaks and epidemics especially due to its increasing resistance to commercially available antibiotics. In this study, 69 single patient multidrug resistant isolates collected from all over Palestine, except Gaza, were studied. All the isolates were resistant to all the β–lactam antibiotics including the carbapenems. Of the 69 isolates, 82.6% were positive for blaOXA-23, 14.5% were positive for blaOXA-24, and 3% were positive for blaOXA-58. None were positive for blaOXA-143 and blaOXA-235. In addition, 5.8% and 0% were positive for blaNDM and blaKPC, respectively. Of the 69 isolates, none were positive for the aminoglycoside aphA6 gene while 93% were positive for the aphA1 gene. The acetyltransferases aacC1 and aacA4 genes tested positive in 22% and 13% of the isolates, respectively. The ompA biofilm-producing virulence gene was detected in all isolates. Finally, Multilocus Sequence Typing (MLST) of 13 isolates revealed that more than one strain of A. baumannii was circulating in Palestinian hospitals as results revealed that 7 isolates were of ST208, 2 isolates ST218, 1 isolate ST231, 1 isolate ST348, and 2 new Sequence Types. The detection of these drug resistant pathogens is a reminder of the importance of active surveillance for resistant bacteria in order to prevent their spread in hospital settings.
A cinetobacter species are a major cause of hospital-acquired infections, especially in intensive care units (ICUs) (1). This, in part, is due to the bacteria's ability to survive long-term on hospital environment surfaces and their ability to acquire antibiotic resistance genes (2). One of the Acinetobacter species most often associated with high morbidity and mortality is A. baumannii (1). However, other Acinetobacter species have also been associated with acquiring broad-spectrum antibiotic resistance genes and causing severe disease (3-6). Here we report the isolation of an A. junii strain that was resistant to all -lactam antibiotics, including the carbapenems, and the aminoglycosides. This isolate's carbapenem resistance mechanism was a result of acquiring two carbapenem resistance genes, bla NDM-1 and bla OXA-58. To our knowledge, this is the first report of the coexistence of bla NDM-1 and bla OXA-58 in A. junii. The A. junii strain was isolated from surveillance swabs collected from a 5-day-old baby girl who was referred to Caritas Baby Hospital (CBH) on 9 October 2012 from another hospital located in the northern part of Palestine. Upon admission to CBH's pediatric ward, surveillance (nose, rectal, and umbilical) swabs were collected from the patient on Copan Transystem swabs (Copan Diagnostics, Corona, CA) and transferred to the clinical laboratory within 30 min. This is part of the infection control policies that were followed at CBH to evaluate the presence of bacteria resistant to broad-spectrum antibiotics in high-risk patients referred from other medical institutions. The Caritas Baby Hospital Medical Research Committee approved the study (MRC-14). The specimens were inoculated on a selective agar medium (MacConkey-cefotaxime [10 g/ml] and MacConkey-meropenem [0.5 g/ml]) and incubated for 24 h at 37°C as previously described (7, 8). A weakly lactose-fermenting, oxidase-negative, Gram-negative coccobacillus was isolated on both selective media and was presumptively identified as Acinetobacter species. The identification of the isolate as A. junii was obtained after sequencing the first 500 bp of the amplified 16S rRNA gene as previously described (9). Antimicrobial susceptibility testing was performed by disk diffusion (Oxoid, United Kingdom) according to the standards of the Clinical and Laboratory Standards Institute (10). For the antimicrobial agent colistin, we used the Etest (AB Biodisk; bioMérieux, France) to determine its MIC. The antibiogram showed a total resistance to all -lactam antibiotics and the aminoglycosides (Table 1). On the other hand, the isolate was susceptible to the fluoroquinolones, tetracyclines, trimethoprim-sulfamethoxazole, and colistin (Table 1). In order to identify the carbapenem resistance mechanism that mediated A. junii's resistance, PCR using primers for the class A carbapenemases (bla NCM , bla SME , bla IMI , bla GES , and bla KPC), the class D oxacillinases (bla OXA-58-like , bla OXA-23-like , bla OXA-24-like , bla OXA-51-like , bla OXA-23 , bla OXA-24 , bla ...
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