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Background: In this study we describe the clinical and molecular characteristics of an outbreak due to carbapenem-resistant Klebsiella pneumoniae (CR-KP) producing CTX-M-15 and OXA-48 carbapenemase. Isogenic strains, carbapenem-susceptible K. pneumoniae (CS-KP) producing CTX-M-15, were also involved in the outbreak., Results: From October 2010 to December 2012 a total of 62 CR-KP and 23 CS-KP were isolated from clinical samples of 42 patients (22 had resistant isolates, 14 had susceptible isolates, and 6 had both CR and CS isolates). All patients had underlying diseases and 17 of them (14 patients with CR-KP and 3 with CS-KP) had received carbapenems previously. The range of carbapenem MICs for total isolates were: imipenem: 2 to >32 μg/ml vs. <2 μg/ml; meropenem: 4 to >32 μg/ml vs. <2 μg/ml; and ertapenem: 8 to >32 μg/ml vs. <2 μg/ml. All the isolates were also resistant to gentamicin, ciprofloxacin, and cotrimoxazole. Both types of isolates shared a common PFGE pattern associated with the multilocus sequence type 101 (ST101). The bla CTX-M-15 gene was detected in all the isolates, whereas the bla OXA-48 gene was only detected in CR-KP isolates on a 70 kb plasmid., Conclusions: The clonal spread of K. pneumoniae ST101 expressing the OXA-48 and CTX-M-15 beta-lactamases was the cause of an outbreak of CR-KP infections. CTX-M-15-producing isolates lacking the bla OXA-48 gene coexisted during the outbreak.

Acinetobacter baumannii is an emerging multidrug-resistant pathogen and very little information is available regarding its imipenem resistance in Latin American countries such as Bolivia. This study investigated the antimicrobial resistance profile of 46 clinical strains from different hospitals in Cochabamba, Bolivia, from March 2008 to July 2009, and the presence of carbapenemases as a mechanism of resistance to imipenem. Isolates were obtained from 46 patients (one isolate per patient; 30 males,16 females) with an age range of 1 day to 84 years, and were collected from different sample types, the majority from respiratory tract infections (17) and wounds (13). Resistance to imipenem was detected in 15 isolates collected from different hospitals of the city. These isolates grouped into the same genotype, named A, and were resistant to all antibiotics tested including imipenem, with susceptibility only to colistin. Experiments to detect carbapenemases revealed the presence of the OXA-58 carbapenemase. Further analysis revealed the location of the bla(OXA-58) gene on a 40 kb plasmid. To our knowledge, this is the first report of carbapenem resistance in A. baumannii isolates from Bolivia that is conferred by the OXA-58 carbapenemase. The presence of this gene in a multidrug-resistant clone and its location within a plasmid is of great concern with regard to the spread of carbapenem-resistant A. baumannii in the hospital environment in Bolivia.

Introduction: The aim of this study was to detect carbapenemases in imipenem-resistant Acinetobacter baumannii isolates obtained in the microbiology department of a Basque Country Public Health Service hospital over a period of 19 months, and to genetically characterize the resistant clones., Methods: Susceptibility tests to imipenem, meropenem, ticarcillin, ceftazidime, cefotaxime, cefepime and aztreonam were done by determining the minimum inhibitory concentration on agar plates. A tRNA technique was used for species identification and PCR with primers ERIC2, AP3 and M13 for genetic typing of resistant isolates. Carbapenemase production was detected by the Hodge test and metallo-beta-lactamase by the EDTA test and Etest MBL., Results: A total of 76 isolates were resistant to imipenem and 49 of these were resistant to all the betalactam antibiotics tested. Genetic typing showed three predominant clones, denominated I (9 isolates), II (48 isolates) and III (8 isolates). Hodge and EDTA tests were positive in 45 and 8 isolates belonging to clone II, 8 and 4 belonging to clone I and 7 and 3 belonging to clone III, respectively. The Etest confirmed 7 results (45% of the 17 positive EDTA test isolates)., Conclusion: Our results show that one factor contributing to the high level of imipenem resistance in the isolates analyzed is dissemination of a predominant, multiresistant clone able to produce OXA-type carbapenemases and metallo-beta-lactamases.

Introduction: Acinetobacter baumannii is opportunistic in debilitated hospitalised patients. Because information from some South American countries was previously lacking, this study examined the emergence of multi-resistant A. baumannii in three hospitals in Cochabamba, Bolivia, from 2008 to 2009. Methodology: Multiplex PCR was used to identify the main resistance genes in 15 multi-resistant A. baumannii isolates. RT-PCR was used to measure gene expression. The genetic environment of these genes was also analysed by PCR amplification and sequencing. Minimum inhibitory concentrations were determined for key antibiotics and some were determined in the presence of an efflux pump inhibitor, 1-(1-napthylmethyl) piperazine. Results: Fourteen strains were found to be multi-resistant. Each strain was found to have the blaOXA-58 gene with the ISAba3-like element upstream, responsible for over-expression of the latter and subsequent carbapenem resistance. Similarly, ISAba1, upstream of the blaADC gene caused over-expression of the latter and cephalosporin resistance; mutations in the gyrA(Ser83 to Leu) and parC (Ser-80 to Phe) genes were commensurate with fluoroquinolone resistance. In addition, the adeA, adeB efflux genes were over-expressed. All 15 isolates were positive for at least two aminoglycoside resistance genes. Conclusion: This is one of the first reports analyzing the multi-drug resistance profile of A. baumannii strains isolated in Bolivia and shows that the over-expression of theblaOXA-58, blaADC and efflux genes together with aminoglycoside modifying enzymes and mutations in DNA topoisomerases are responsible for the multi-resistance of the bacteria and the subsequent difficulty in treating infections caused by them. [ABSTRACT FROM AUTHOR]