The first report of infection with Klebsiella pneumoniae carrying the bla kpc gene in State of Mato Grosso do Sul, Brazil
Marilene Rodrigues ChangCamila Arguelo BibergFernando Aguilar LopesAndyane Freitas TetilaAntônio Carlos Campos Pignatari
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Abstract:
The increased frequency and dissemination of enterobacteria resistant to various antimicrobials is currently worldwide concern. In January 2010, a 94-year-old patient with chronic lymphocytic leukemia was admitted to the University Hospital. This patient died 21 days after hospitalization due to the clinical worsening. Klebsiella pneumoniae producing of extended-spectrum β-lactamases (ESBLs) was isolated of urine culture. This bacterium demonstrated resistance to ceftazidime, ciprofloxacin, levofloxacin, ertapenem and imipenem. Susceptibility to cefoxitin, cefepime, meropenem, colistin and tigecycline. This study reports the first case of infection by Klebsiella pneumoniae carrying the bla kpc gene in the State of Mato Grosso do Sul, Brazil.Keywords:
Ertapenem
Tigecycline
Colistin
Cefepime
Objective: This study aimed to determine outcome and cost of colistin and tigecycline for treatment of gram-negative infections. Methods: Data were retrospectively collected from electronic database of patients who hospitalized in Mahasarakham Hospital between January and June of 2012. Patient characteristics, treatment outcome and cost were analyzed with appropriate statistics. Results: There were 70 patients: 40 patients receiving colistin and 30 patients receiving tigecycline. Most of them had infection with Acinebacter baumannii (100% vs. 90%). Proportion of patients with clinical improvement was higher in patients with colistin treatment than tigecycline treatment (47.5% vs. 33.3%, p=0.234). When controlling for sex, age, sepsis, ICU treatment and receiving other antibiotics, clinical improvement in patients with colistin treatment was not different from that in patients with tigecycline treatment (adjusted OR = 1.390, 95%CI 0.313 - 6.173, p=0.665). Median medication cost per patient in patients receiving colistin was lower than patients receiving tigecycline (2,640 baht vs. 37,437 baht, p<0.001). Conclusion: The findings of this study indicate that colistin and tigecycline treatment for gram-negative infections have no different outcome but treatment with colistin will reduce medication cost rather than treatment with tigecycline.
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Carbapenemase-producing Enterobacterales have become a severe public health concern because of their rapidly transmissible resistance elements and limited treatment options. The most effective antimicrobial combinations against carbapenemase-producing Enterobacterales are currently unclear. Here, we aimed to assess the therapeutic effects of seven antimicrobial combinations (colistin-meropenem, colistin-tigecycline, colistin-rifampicin, colistin-erythromycin, meropenem-tigecycline, meropenem-rifampicin, and meropenem-tigecycline-colistin) against twenty-four carbapenem-producing Enterobacterales (producing blaKPC, blaNDM, coexisting blaNDM and blaIMP, and coexisting mcr-1/8/9 and blaNDM genes) and one carbapenem-susceptible Enterobacterales using the checkerboard assay, time-kill curves, and scanning electron microscopy. None of the combinations were antagonistic. The combination of colistin-rifampicin showed the highest synergistic effect of 76% (19/25), followed by colistin-erythromycin at 60% (15/25), meropenem-rifampicin at 24% (6/25), colistin-meropenem at 20% (5/25), colistin-tigecycline at 20% (5/25), and meropenem-tigecycline at 4% (1/25). The triple antimicrobial combinations of meropenem-tigecycline-colistin had a synergistic effect of 100%. Most double antimicrobial combinations were ineffective on isolates with coexisting blaNDM and blaIMP genes. Meropenem with tigecycline showed no synergistic effect on isolates that produced different carbapenemase genes and were highly resistant to meropenem (92% meropenem MIC ≥ 16 mg/mL). Colistin-tigecycline showed no synergistic effect on Escherichia coli producing blaNDM-1 and Serratia marcescens. Time-kill curves showed that antimicrobial combinations achieved an eradication effect (≥ 3 log10 decreases in colony counts) within 24 h without regrowth, based on 1 × MIC of each drug. The synergistic mechanism of colistin-rifampicin may involve the colistin-mediated disruption of bacterial membranes, leading to severe alterations in their permeability, then causes more rifampicin to enter the cell and induces cell death. In conclusion, the antimicrobial combinations evaluated in this study may facilitate the successful treatment of patients infected with carbapenemase-producing pathogens.
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An alarming increase in the resistance rates of tigecycline and colistin among carbapenemase-producing Acinetobacter baumannii recovered from a Greek hospital over a 3-year period (2011-2013) was investigated. The antimicrobial resistance profiles and carbapenemase gene content were determined for a collection of colistin- and/or tigecycline-resistant carbapenemase-producing A. baumannii isolates (n = 42), which were recovered consecutively during the study period. A gradual increase in the incidence of blaOXA-23 producers was observed from 2011 to 2013. A cluster of 21 isolates comprised tigecycline-resistant blaOXA-23 producers displayed a single antimicrobial resistance pattern. The emergence of two blaOXA-23 producers resistant to both tigecycline and colistin was documented. Furthermore, determination of the mechanisms of colistin and tigecycline resistance and molecular typing by the tri-locus sequence typing (3LST) scheme for nine isolates recovered from bloodstream infections were performed. Out of nine isolates, five tigecycline- and two colistin-resistant isolates were blaOXA-23 producers of 3LST ST101 corresponding to the international clone II recovered during 2012-2013. All nine isolates were positive for the presence of the adeB gene of the AdeABC efflux pump. Three colistin-resistant isolates possessed novel substitutions in PmrB, which may be implicated in colistin resistance. To the best of our knowledge, this is the first report of the acquisition of tigecycline and colistin resistance among blaOXA-23-producing A. baumannii of 3LST ST101 in Greece; thus, continuous surveillance and molecular characterization, prudent use of antibiotics and implementation of infection control measures for A. baumannii are urgent.
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OBJECTIVES: To determine in vitro antimicrobial susceptibility and synergistic activity of colistin in combination with tigecycline against clinical strains of carbapenem- resistant Acinetobacter baumannii (CRAB).MATERIAL AND METHODS: Colistin and tigecycline minimum inhibitory concentrations (MICs) of 12-clinical CRAB isolates were determined by broth microdilution. Checkerboard testing was performed to assess the interaction of the colistin-tigecycline combination. Fractional inhibitory concentration indexes (ΣFIC) in the range of 0.5 to 1.0, > 1.0 to < 4.0 and ≥ 4.0 are considered as additive, indifferent, and antagonistic effects, respectively.RESULTS: All CRAB isolates were susceptible to colistin. Three out of 12 CRABs were susceptible to tigecycline based on a pharmacokinetic-pharmacodynamics (PK-PD) breakpoint (MICs ≤ 0.25 μg/mL). The MIC of both antimicrobials was decreased in most of the CRAB isolates in the checkerboard synergy testing. The interaction of colistin and tigecycline combination revealed both additive and indifferent effects in five and seven of the 12-CRAB isolates, respectively. Neither synergism nor antagonism of colistin and tigecycline combination was demonstrated.CONCLUSION: No synergistic effect between colistin and tigecycline against CRAB isolates was detected. However, the combination of these two drugs is likely to result in a decrease in the MIC of both drugs. Further studies with a larger sample to determine the in vitro synergistic activity of colistin and tigecycline combination are required.
Tigecycline
Colistin
Acinetobacter baumannii
Broth microdilution
Checkerboard
Carbapenem
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Abstract Background Treatment of pandrug-resistant isolates often necessitates combination therapy. Checkerboard synergy and time-killing assay tests were performed to evaluate the benefits of a triple combination with meropenem, ertapenem, and colistin against 10 colistin-resistant K. pneumoniae clinical isolates harboring different β-lactamases. (bla OXA-48 , bla NDM ). Materials and methods In this study, ertapenem and meropenem (ERT/MEM), meropenem and colistin (MEM/COL), ertapenem, meropenem and colistin (ERT/MEM/COL) combinations were tested using checkerboard techniques and time-kill assays of each antibiotic alone and in combination against 10 colistin-resistant clinical K. pneumoniae isolates. An analysis of K. pneumoniae isolate B6 using a scanning electron microscope revealed morphologic changes in the cell surface after treatment with each antibiotic both alone and in combination. The whole genome of K. pneumoniae KPNB1 was sequenced using an Ion Torrent PGM sequencer. Results According to the checkboard results, synergistic combinations were observed with ertapenem/meropenem (5/10 isolates), meropenem/colistin (7/10) and ertapenem/meropenem/colistin (9/10); no antagonism was observed for all combinations. For the time-kill assay results; synergism and bactericidal effects were observed with meropenem/colistin (10/10) and with ertapenem/meropenem/colistin (10/10) combinations, and an indifference effect was observed with the ertapenem and meropenem (10/10) combination. Strain number 1 was found 100% identical to Klebsiella pneumoniae subsp. pneumoniae HS11286 according to the outcomes of complete genome sequence analysis, and the strain carried the genes bla OXA-181 , bla CTXM-15 , blaNDM, arr-3, aac (6′)-Ib-cr, rmtF , and catB1. Conclusion Using double carbapenem antibiotics with colistin could be a potential alternative to treat colistin and carbapenem-resistant K. pneumoniae . The present study is the first Turkish report of OXA–181-type carbapenemase causing colistin resistance.
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Acinetobacter baumannii species cause nosocomial infections and can subsequently develop multidrug resistance (MDR). The objective of this study was to evaluate the susceptibility of A. baumannii to a novel combination of colistin and tigecycline, which may provide a faster and more efficacious treatment via a synergistic effect.We included 50 MDR A. baumannii samples that were isolated in our clinics between 2009 and 2014. We used broth microdilution (BMD) and the E-test to evaluate the effects of colistin and tigecycline, and the E-test to assess the interaction of the colistin-tigecycline combination. The interaction between the two antibiotics was evaluated using the fractional inhibition concentration (FIC) index and was classified as follows: FIC≤0.5, synergistic; 0.5
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To analyse the in vitro activity of colistin, fosfomycin and tigecycline alone or in combination against enterobacterial NDM-1 producers. MIC values of colistin, fosfomycin and tigecycline were determined for 28 NDM-1-producing enterobacterial isolates. In vitro synergy combination testing was performed for eight clinical isolates and one Escherichia coli transconjugant (six being susceptible to the three antibiotics) using microdilution and chequerboard techniques. MICs of colistin, fosfomycin and tigecycline were determined, showing that one-third of NDM-1-producing isolates were resistant or intermediate to at least one of the three drugs. Nevertheless, in vitro synergistic activity was observed for colistin plus fosfomycin and colistin plus tigecycline in very rare cases. Synergistic activity was observed for colistin and fosfomycin, and colistin and tigecycline in rare cases, most of the interactions being indifferent.
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AbstractThe development of resistance is a compelling reason for reviewing administration of antibiotics. Recently, most Acinetobacter infections are caused by multidrug-resistant (MDR) strains which have necessitated the use of tigecycline or colistin. This study was undertaken to determine the susceptibility of Acinetobacter spp. To these and other drugs. A total of 250 Acinetobacter isolates were collected from the 8 government hospitals over a period of 6 months. Susceptibility to 18 antibiotics, including tigecycline and colistin, was investigated by determining their minimum inhibitory concentrations using e test. Of the 250 isolates, 13.6% and 12% were resistant to tigecycline and colistin. A total of 25.2% and 37.2% were resistant to imipenem and meropenem, respectively. Of the 250 isolates 88.4% were MDR. This relatively high prevalence of tigecycline and colistin-resistant isolates indicates an emerging therapeutic problem which may severely compromise the treatment of MDR Acinetobacter spp. infections in Kuwait.Keywords: Acinetobacter sppresistancetigecyclinecolistinKuwait
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There are no comparative data evaluating outcomes of ertapenem treatment for infections with AmpC-producing Enterobacteriaceae. This retrospective matched case-control study was conducted between 2009 and 2012. Sixteen cases treated with ertapenem were matched 1:2 with 32 control cases treated with cefepime based on age, culture source, and hospital service. There were more cefepime-resistant organisms in the ertapenem group (cefepime resistance present in 44% of patients treated with ertapenem compared with 0% of control patients, p < 0.001). Ertapenem was used empirically in 25% of patients compared with 88% who received cefepime empirically (p < 0.001). Consequently, 56% of patients on ertapenem received inappropriate initial therapy compared with 9% of patients on cefepime (p < 0.001). No differences in clinical success were identified (69% for ertapenem vs 88% for cefepime, p = 0.138). Although a trend favoring cefepime could be suspected, it should be noted that no statistically significant difference in clinical success was detected despite the presence of more resistant organisms and delays in initiation of appropriate therapy among patients receiving ertapenem.
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The aim of the study is to determine in-vitro effects of imipenem–tigecycline, imipenem–colistin and tigecycline–colistin against carbapenem-resistant Enterobacteriaceae (CRE) isolates. A total of 25 CRE isolates were included to the study. The minimum inhibition concentrations of imipenem, colistin-sulphate and tigecycline were determined with broth dilution method. Synergistic effects of imipenem–tigecycline, imipenem–colistin and tigecycline–colistin were investigated by microdilution checkerboard technique. All of the isolates were resistant to imipenem, whereas 25% of the isolates were resistant to colistin and tigecycline. Imipenem–colistin, imipenem–tigecycline and tigecycline–colistin combinations were synergistic against 40% (10/25), 24% (6/25), and 36% (9/25) of the isolates, respectively. Antagonism was observed in 8% (2/25) of the isolates in tigecycline–colistin combination. Tigecycline–colistin was the most effective (70% synergy) combination in Klebsiella spp. strains; whereas imipenem–colistin was the most effective (75% synergy) combination in Escherichia coli strains. Synergistic effect was variable and strain-depended against CRE isolates that have been tested.
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