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      Bacteremia Caused by Extended-Spectrum Beta-Lactamase–Producing Enterobacteriaceae in Vientiane, Lao PDR: A 5-Year Study

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          Abstract.

          Although there has been an increasing incidence of bacteremia caused by extended-spectrum beta-lactamase (ESBL)–producing Enterobacteriaceae (ESBL-E) across South East Asia, there are sparse data from the Lao PDR, where laboratory capacity for antimicrobial resistance surveillance is limited. We, therefore, retrospectively reviewed bacteremia caused by ESBL-producing Escherichia coli and Klebsiella pneumoniae between 2010 and 2014 at Mahosot Hospital, Vientiane, Lao PDR. Clinical and laboratory data relating to all episodes of ESBL-E bacteremia were reviewed over the 5-year period and compared with non–ESBL-E bacteremia. Blood cultures positive for E. coli or K. pneumoniae were identified retrospectively from laboratory records. Clinical and laboratory data were extracted from research databases and case notes and analyzed using STATA. Between 2010 and 2014, we identified 360 patients with E. coli ( n = 249) or K. pneumoniae ( n = 111) bacteremia, representing 34.8% of all patients with clinically significant bacteremia . Seventy-two (20%) isolates produced ESBL; E. coli accounted for 15.3% (55/360) and K. pneumoniae for 4.7% (17/360), respectively. The incidence of ESBL-producing E. coli bacteremia rose during the study period. By multiple logistic analysis, reported antibiotic use in the previous week was significantly associated with ESBL positivity ( P < 0.001, odds ratio 3.89). Although multiresistant, most ESBL-producing E. coli and K. pneumoniae remained susceptible to meropenem (65/65; 100%) and amikacin (64/65; 98.5%). We demonstrated an alarming increase in the incidence of ESBL-E as a cause of bacteremia in Vientiane during the study period. This has implications for empiric therapy of sepsis in Laos, and ongoing surveillance is essential.

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          Most cited references 38

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          Resistance in gram-negative bacteria: Enterobacteriaceae.

          The emergence and spread of resistance in Enterobacteriaceae are complicating the treatment of serious nosocomial infections and threatening to create species resistant to all currently available agents. Approximately 20% of Klebsiella pneumoniae infections and 31% of Enterobacter spp infections in intensive care units in the United States now involve strains not susceptible to third-generation cephalosporins. Such resistance in K pneumoniae to third-generation cephalosporins is typically caused by the acquisition of plasmids containing genes that encode for extended-spectrum beta-lactamases (ESBLs), and these plasmids often carry other resistance genes as well. ESBL-producing K pneumoniae and Escherichia coli are now relatively common in healthcare settings and often exhibit multidrug resistance. ESBL-producing Enterobacteriaceae have now emerged in the community as well. Salmonella and other Enterobacteriaceae that cause gastroenteritis may also be ESBL producers, which is of relevance when children require treatment for invasive infections. Resistance of Enterobacter spp to third-generation cephalosporins is most typically caused by overproduction of AmpC beta-lactamases, and treatment with third-generation cephalosporins may select for AmpC-overproducing mutants. Some Enterobacter cloacae strains are now ESBL and AmpC producers, conferring resistance to both third- and fourth-generation cephalosporins. Quinolone resistance in Enterobacteriaceae is usually the result of chromosomal mutations leading to alterations in target enzymes or drug accumulation. More recently, however, plasmid-mediated quinolone resistance has been reported in K pneumoniae and E coli, associated with acquisition of the qnr gene. The vast majority of Enterobacteriaceae, including ESBL producers, remain susceptible to carbapenems, and these agents are considered preferred empiric therapy for serious Enterobacteriaceae infections. Carbapenem resistance, although rare, appears to be increasing. Particularly troublesome is the emergence of KPC-type carbapenemases in New York City. Better antibiotic stewardship and infection control are needed to prevent further spread of ESBLs and other forms of resistance in Enterobacteriaceae throughout the world.
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            Predictors of mortality in patients with bloodstream infections caused by extended-spectrum-beta-lactamase-producing Enterobacteriaceae: importance of inadequate initial antimicrobial treatment.

            Bloodstream infections (BSI) caused by extended-spectrum beta-lactamase (ESBL)-producing organisms markedly increase the rates of treatment failure and death. We conducted a retrospective cohort analysis to identify risk factors for mortality in adult in-patients with BSI caused by ESBL-producing Enterobacteriaceae (ESBL-BSI). Particular attention was focused on defining the impact on the mortality of inadequate initial antimicrobial therapy (defined as the initiation of treatment with active antimicrobial agents >72 h after collection of the first positive blood culture). A total of 186 patients with ESBL-BSI caused by Escherichia coli (n = 104), Klebsiella pneumoniae (n = 58), or Proteus mirabilis (n = 24) were identified by our microbiology laboratory from 1 January 1999 through 31 December 2004. The overall 21-day mortality rate was 38.2% (71 of 186). In multivariate analysis, significant predictors of mortality were inadequate initial antimicrobial therapy (odds ratio [OR] = 6.28; 95% confidence interval [CI] = 3.18 to 12.42; P < 0.001) and unidentified primary infection site (OR = 2.69; 95% CI = 1.38 to 5.27; P = 0.004). The inadequately treated patients (89 of 186 [47.8%]) had a threefold increase in mortality compared to the adequately treated group (59.5% versus 18.5%; OR = 2.38; 95% CI = 1.76 to 3.22; P < 0.001). The regimens most commonly classified as inadequate were based on oxyimino cephalosporin or fluoroquinolone therapy. Prompt initiation of effective antimicrobial treatment is essential in patients with ESBL-BSI, and empirical decisions must be based on a sound knowledge of the local distribution of pathogens and their susceptibility patterns.
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              Clinical and economic impact of bacteremia with extended- spectrum-beta-lactamase-producing Enterobacteriaceae.

              We studied outcomes of extended-spectrum beta-lactamase (ESBL) production in Enterobacteriaceae bacteremia. Inpatients with bacteremia caused by ESBL-producing Escherichia coli, Klebsiella spp., or Proteus spp. (cases) were compared with patients with bacteremia caused by non-ESBL producers (controls). Outcomes included mortality, mortality due to infection, length of stay (LOS), delay in appropriate therapy (DAT), discharge to a chronic care facility, and hospital cost. Ninety-nine cases and 99 controls were enrolled. Thirty-five percent of cases died, versus 18% of controls (odds ratio [OR], 2.5; 95% confidence interval [CI], 1.3 to 4.7; P=0.01). Thirty percent of cases died due to infection, versus 16% of controls (OR, 2.3; 95% CI, 1.1 to 4.5; P=0.03). The median LOS after bacteremia for cases was 11 days (interquartile range, 5 to 21), versus 5 days for controls (interquartile range, 3 to 9) (P<0.001). DAT occurred in 66% of cases, versus 7% of controls (OR, 25.1; 95% CI, 10.5 to 60.2; P<0.001). Cases were more likely than controls to be discharged to chronic care (52% versus 21%; OR, 4.0; 95% CI, 1.9 to 8.3; P<0.001). The average hospital cost for cases was 65,509 Israeli shekels, versus 23,538 shekels for controls (P<0.001). After adjusting for differences between groups by using multivariable analysis, ESBL production remained a significant predictor of mortality (OR, 3.6; 95% CI, 1.4 to 9.5; P=0.008), increased LOS (1.56-fold; P=0.001), DAT (OR, 25.1; 95% CI, 10.5 to 60.2; P<0.001), and increased cost (1.57-fold; P=0.003). The mean increase in equivalent cost attributable to ESBL production was $9,620. ESBL production was associated with severe adverse outcomes, including higher overall and infection-related mortality, increased LOS, DAT, discharge to chronic care, and higher costs.
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                Author and article information

                Journal
                Am J Trop Med Hyg
                Am. J. Trop. Med. Hyg
                tpmd
                tropmed
                The American Journal of Tropical Medicine and Hygiene
                The American Society of Tropical Medicine and Hygiene
                0002-9637
                1476-1645
                May 2020
                09 March 2020
                09 March 2020
                : 102
                : 5
                : 1137-1143
                Affiliations
                [1 ]Adult Infectious Diseases Ward, Mahosot Hospital, Vientiane, Laos;
                [2 ]Lao-Oxford-Mahosot Hospital-Wellcome Trust Research Unit (LOMWRU), Microbiology Laboratory, Mahosot Hospital, Vientiane, Laos;
                [3 ]Centre for Tropical Medicine and Global Health, University of Oxford, Oxford, United Kingdom;
                [4 ]Institute of Research and Education Development (IRED), University of Health Sciences, Vientiane, Laos;
                [5 ]Faculty of Infectious and Tropical Diseases, London School of Hygiene and Tropical Medicine, London, United Kingdom
                Author notes
                [* ]Address correspondence to Andrew J. H. Simpson, Lao-Oxford-Mahosot Hospital-Wellcome Trust Research Unit (LOMWRU), Microbiology Laboratory, Mahosot Hospital, Vientiane, Laos. E-mail: andrew.s@ 123456tropmedres.ac

                Disclosure: Ethical approval for the study was granted by the Oxford Tropical Research Ethics Committee and the Lao National Ethics Committee for Health Research.

                Financial support: This work was supported by the Wellcome Trust, United Kingdom, through funding for the Lao-Oxford-Mahosot Hospital-Wellcome Trust Research Unit.

                Authors’ addresses: Ko Chang and Valy Keoluangkhot, Adult Infectious Diseases Ward, Mahosot Hospital, Vientiane, Laos, E-mails: me.chang2009@ 123456gmail.com and valy.keoluangkhot@ 123456gmail.com . Sayaphet Rattanavong, Viengmon Davong, Manivanh Vongsouvath, and Manophab Luangraj, Lao-Oxford-Mahosot Hospital-Wellcome Trust Research Unit (LOMWRU), Microbiology Laboratory, Mahosot Hospital, Vientiane, Laos, E-mails: sayaphet@ 123456tropmedres.ac , viengmon@ 123456tropmedres.ac , manivanh@ 123456tropmedres.ac , and manophab.l@ 123456tropmedres.ac . Mayfong Mayxay, Lao-Oxford-Mahosot Hospital-Wellcome Trust Research Unit (LOMWRU), Microbiology Laboratory, Mahosot Hospital, Vientiane, Laos, Centre for Tropical Medicine and Global Health, University of Oxford, Oxford, United Kingdom, and Institute of Research and Education Development (IRED), University of Health Sciences, Vientiane, Laos, E-mail: mayfong@ 123456tropmedres.ac . Andrew J. H. Simpson, Lao-Oxford-Mahosot Hospital-Wellcome Trust Research Unit (LOMWRU), Microbiology Laboratory, Mahosot Hospital, Vientiane, Laos, and Centre for Tropical Medicine and Global Health, University of Oxford, Oxford, United Kingdom, E-mail: andrew.s@ 123456tropmedres.ac . Paul N. Newton and David A. B. Dance, Lao-Oxford-Mahosot Hospital-Wellcome Trust Research Unit (LOMWRU), Microbiology Laboratory, Mahosot Hospital, Vientiane, Laos, Centre for Tropical Medicine and Global Health, University of Oxford, Oxford, United Kingdom, and Faculty of Infectious and Tropical Diseases, London School of Hygiene and Tropical Medicine, London, United Kingdom, E-mails: paul.newton@ 123456tropmedres.ac and david.d@ 123456tropmedres.ac .

                Article
                tpmd190304
                10.4269/ajtmh.19-0304
                7204562
                32157990
                © The American Society of Tropical Medicine and Hygiene

                This is an open-access article distributed under the terms of the Creative Commons Attribution (CC-BY) License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

                Page count
                Pages: 7
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                Infectious disease & Microbiology

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