aztreonam, and amikacin were recommended as first-line antibiotics agents for non-MDR GNB infections; piperacillin/tazobactam and carbapenems for MDR GNB in community-acquired and healthcare-related or nosocomial infections, respectively; and vancomycin or linezolid for GPB infections, regardless of drug-resistance status. Multivariate analysis revealed days of hospital stay before SAI, upper gastrointestinal bleeding, white blood cell count, alanine aminotransferase, serum creatinine concentration, total bilirubin, and international normalized ratio as key independent predictors of 28-day mortality.CONCLUSION: MDR pathogens and antibiotic strategies were identified in patients with acute decompensated cirrhosis with culture-positive SAI, which may help optimize therapy and improve clinical outcomes.]]>
Alanine Transaminase ; Amikacin ; Anti-Bacterial Agents ; Aztreonam ; Bilirubin ; Carbapenems ; Ceftazidime ; China ; Creatinine ; Cross Infection ; Escherichia coli ; Fibrosis ; Fungi ; Gram-Negative Bacteria ; Gram-Positive Bacteria ; Hemorrhage ; Hospitals, Teaching ; Humans ; International Normalized Ratio ; Klebsiella pneumoniae ; Length of Stay ; Leukocyte Count ; Linezolid ; Methicillin-Resistant Staphylococcus aureus ; Mortality ; Multivariate Analysis ; Prevalence ; Proportional Hazards Models ; Retrospective Studies ; Risk Factors ; Vancomycin

BACKGROUND: Escherichia coli and Klebsiella pneumoniae clinical isolates producing CTX-M extendedspectrum β-lactamases (ESBLs) were assessed for antimicrobial resistance phenotypes varied by group of enzymes. METHODS: A total of 1,338 blood isolates, including 959 E. coli and 379 K. pneumoniae, were studied. All the strains were collected between January and July 2017 from eight general hospitals in South Korea. The species were identified by matrix-assisted laser desorption ionization-time of flight mass spectrometry. Antimicrobial susceptibilities were determined by disk diffusion methods and ESBL phenotypes by double-disk synergy tests using disks containing cefotaxime, ceftazidime, cefepime, aztreonam, and clavulanic acid (CA). The genes for β-lactamases were identified by PCR and sequencing. RESULTS: Of total microbes, 31.6% (303/959) E. coli and 24.0% (91/379) K. pneumoniae were resistant to cefotaxime and 28.1% (269/959) E. coli and 20.1% (76/379) K. pneumoniae were CTX-M-type ESBL producers. Among the detected CTX-M ESBLs, 58.0% (156/269) in E. coli and 86.8% (66/76) in K. pneumoniae belonged to group 1, 46.8% (126/269) in E. coli and 14.5% (11/76) in K. pneumoniae were group 9. Ten E. coli and one K. pneumoniae isolates co-produced both groups of CTX-M ESBL. The group 1 CTX-M producers had a higher level of resistance to cefotaxime, ceftazidime, cefepime, and aztreonam and exhibited stronger synergistic activities when combined with CA compared to group 9. CONCLUSION: ESBL phenotypes differ by CTX-M ESBL group and phenotype testing with drugs including 4th generation cephalosporins and monobactams is critical for screening CTX-M-producers with better sensitivity.
Aztreonam ; Cefotaxime ; Ceftazidime ; Cephalosporins ; Clavulanic Acid ; Diffusion ; Escherichia coli ; Hospitals, General ; Klebsiella pneumoniae ; Korea ; Mass Screening ; Mass Spectrometry ; Monobactams ; Phenotype ; Pneumonia ; Polymerase Chain Reaction

BACKGROUND/AIMS: Klebsiella pneumoniae is second most common organism of gram-negative bacteremia in Korea and one of the most common cause of urinary tract infection, and intra-abdominal infection. METHODS: We compared clinical and microbiological characteristics about K. pneumoniae bacteremia in a tertiary hospital between 10 years. Group A is who had K. pneumoniae bacteremia at least one time from January 2004 to December 2005. Group B is from January 2012 to December 2013. We also analyzed antibiotic resistance, clinical manifestation of the K. pneumoniae bacteremia divided into community-acquired infections, healthcare associated infections, and nosocomial infections. RESULTS: The resistance for ampicillin, aztreonam, cefazolin, and cefotaxime significantly increased compared to 10 years ago. Extended spectrum β-lactamase positivity surged from 4.3% to 19.6%. Ten years ago, 1st, 2nd cephalosporin, and aminoglycoside were used more as empirical antibiotics. But these days, empirical antibiotics were broad spectrum such as 3rd and 4th cephalosporin. In treatment outcome, acute kidney injury decreased from 47.5% to 28.7%, and mortality decreased from 48.9% to 33.2%. In community-acquired infections, there was similar in antimicrobial resistance and mortality. In healthcare-associated and nosocomial infections, there was significantly increasing in antibiotic resistance, decreasing in mortality, and acute kidney injury. CONCLUSIONS: In community-acquired infections, broader antibiotics were more used than 10 years ago despite of similar antimicrobial resistance. When K. pneumoniae bacteremia is suspected, we recommend to use the narrow spectrum antibiotics as initial therapy if there are no healthcare-associated risk factors, because the antibiotic resistance is similar to 10 years ago in community-acquired infections.
Acute Kidney Injury ; Ampicillin ; Anti-Bacterial Agents ; Aztreonam ; Bacteremia* ; Cefazolin ; Cefotaxime ; Community-Acquired Infections ; Cross Infection ; Drug Resistance ; Drug Resistance, Microbial ; Intraabdominal Infections ; Klebsiella pneumoniae* ; Klebsiella* ; Korea ; Mortality ; Pneumonia ; Risk Factors ; Tertiary Care Centers ; Treatment Outcome ; Urinary Tract Infections

BACKGROUND: From January 2014 to December 2015, 69 clones of Enterobacter cloacae showing multidrug resistance to six classes of antimicrobial agents were collected from two medical centers in Korea. METHODS: Minimum inhibitory concentrations were determined using the E-test method, and 17 genes were detected using polymerase chain reaction (PCR). The epidemiological relatedness of the strains was identified using repetitive element sequence-based PCR and multilocus sequence typing. RESULTS: The 69 E. cloacae clones produced extended spectrum β lactamase (ESBL) and AmpC and showed multidrug resistance to cefotaxime, ceftazidime, and aztreonam. We identified the following sequence types: ST56 of type VI for ESBL SHV (N=12, 17.4%); ST53, ST114, ST113, and ST550 of types I, IV, VI, and VII, respectively, for CTX-M (N=11, 15.9%); and ST668 of type III for the carbapenemase NDM gene (N=1, 1.5%). The AmpC DHA gene (N=2, 2.89%) was confirmed as ST134, although its type was not identified, whereas EBC (MIR/ACT; N=18, 26.1%) was identified as ST53, ST24, ST41, ST114, ST442, ST446, ST484, and ST550 of types V, I, III, IV, VII, and VI, respectively. The formed subclasses were bla CTX-M-3 and bla CTX-M-22 by CTX-M-1, bla CTX-M-9 and bla CTX-M-125 by CTX-M-9, bla DHA-1 by DHA, and bla MIR-7 and bla ACT-15,17,18,25,27,28 by EBC (MIR/ACT). CONCLUSIONS: There were no epidemiological relationships between the gene products and the occurrence of resistance among the strains.
Anti-Infective Agents ; Aztreonam ; Cefotaxime ; Ceftazidime ; Cloaca ; Clone Cells ; Drug Resistance, Multiple* ; Enterobacter cloacae* ; Enterobacter* ; Korea ; Methods ; Microbial Sensitivity Tests ; Multilocus Sequence Typing ; Polymerase Chain Reaction

OBJECTIVES: The purpose of this study was to determine the presence of IMP and OXA genes in clinical strains of Pseudomonas aeruginosa (P. aeruginosa) that are carriers of the ampC gene. METHODS: In this study, 105 clinical isolates of P. aeruginosa were collected. Antibiotic resistance patterns were determined using the disk diffusion method. The strains carrying AmpC enzymes were characterized by a combination disk method. Multiplex-PCR was used to identify resistance and virulence genes, chi-square test was used to determine the relationship between variables. RESULTS: Among 105 isolates of P. aeruginosa, the highest antibiotic resistance was to cefotaxime and aztreonam, and the least resistance was to colictin and ceftazidime. There were 49 isolates (46.66%) that showed an AmpC phenotype. In addition, the frequencies of the resistance genes were; OXA48 gene 85.2%, OXA199, 139 3.8%, OXA23 3.8%, OXA2 66.6%, OXA10 3.8%, OXA51 85.2% and OXA58 3.8%. The IMP27 gene was detected in 9 isolates (8.57%) and the IMP3.34 was detected in 11 isolates (10.47%). Other genes detected included; lasR (17.1%), lasB (18%) and lasA (26.6%). There was a significant relationship between virulence factors and the OX and IMP genes (p ≤ 0.05). CONCLUSION: The relationship between antibiotic resistance and virulence factors observed in this study could play an important role in outbreaks associated with P. aeruginosa infections.
Aztreonam ; beta-Lactamases ; Cefotaxime ; Ceftazidime ; Diffusion ; Disease Outbreaks ; Drug Resistance, Microbial* ; Methods ; Phenotype ; Pseudomonas aeruginosa ; Virulence Factors* ; Virulence*

An increasing prevalence of infections caused by multidrug-resistant (MDR) Pseudomonas aeruginosa (P. aeruginosa) causes a serious therapeutic problem in clinical setting. This study investigated the antimicrobial susceptibility, resistance mechanisms against aminoglycosides, and molecular epidemiology of 76 blood isolates of P. aeruginosa from two Korean hospitals. Thirty-four isolates were susceptible to all 13 antimicrobial agents tested, whereas 28 isolates showed a MDR or extensively drug-resistant phenotype. There was a significant difference in resistance rates of P. aeruginosa isolates against aztreonam, piperacillin-tazobactam, imipenem, meropenem, ciprofloxacin, and norfloxacin between two hospitals. Genes for aminoglycoside-modifying enzymes (AMEs), including aphA6 (n = 14), aadB (n = 11), aacA4 (n = 8), and aphA1 (n = 1), and 16S rRNA methylase armA (n = 6) were detected in 26 P. aeruginosa isolates resistant to aminoglycosides. There was no significant difference in carriage of genes for AME and 16S rRNA methylase between two hospitals, but aacA4 and aphA1 were specifically detected in P. aeruginosa isolates from one hospital. Seventy-six P. aeruginosa isolates were classified into 55 pulsotypes at similarity value of 0.85, and 31 and 24 pulsotypes were specifically detected in each hospital. This study demonstrates that differences in antimicrobial susceptibility of P. aeruginosa isolates between two hospitals are possibly due to the presence of diverse clones specific in each hospital.
Aminoglycosides ; Anti-Infective Agents ; Aztreonam ; Ciprofloxacin ; Clone Cells ; Imipenem ; Molecular Epidemiology ; Norfloxacin ; Phenotype ; Prevalence ; Pseudomonas aeruginosa* ; Pseudomonas*

BACKGROUND: In 2010, the Clinical and Laboratory Standards Institute (CLSI) revised the minimum inhibitory concentration (MIC) breakpoints of cephalosporins and aztreonam to exempt extended-spectrum beta-lactamase (ESBL) confirmatory tests for Enterobacteriaceae. However, the CLSI did not change the MIC breakpoint of cefepime. Here, a proficiency survey of a strain of ESBL-producing Klebsiella pneumoniae was analyzed for MIC distribution and interpretation of cephalosporins and aztreonam. METHODS: The survey strain, K. pneumoniae, which produced SHV-18, was distributed to 170 clinical laboratories as 1 of 5 presumptive clinical specimens through the proficiency survey of the clinical microbiology division of the Korean Association of Quality Assurance for Clinical Laboratories (KAQACL). MIC, zone diameter of inhibition (ZDI), and interpretation of tested antimicrobials, methods of antimicrobial susceptibility testing (AST), and ESBL confirmatory results were collected. RESULTS: According to the revised breakpoints of the 2010 CLSI guidelines, MIC results indicated resistance to aztreonam in 100%, cefepime in 5.5%, cefotaxime in 20%, ceftazidime in 100%, and ceftriaxone in 100% of samples by broth microdilution methods. ZDI results also indicated resistance to aztreonam in 75%, cefepime in 0%, cefotaxime in 66.7%, ceftazidime in 100%, and ceftriaxone in 80% of samples by disk diffusion method. Ninety (75.6%) participants performed an ESBL confirmatory test, and 89 (98.9%) reported ESBL-positive tests. Of the 55 laboratories that tested the susceptibility of cefepime, 50 (90.9%) self-reported to be "resistant" because of ESBL-positive results. CONCLUSIONS: In conclusion, susceptibility testing of ESBL producers against certain cephalosporins is not reliable enough to apply the revised breakpoints presented in the 2010 CLSI guidelines. It is therefore necessary to reach a consensus for interpretation of ASTs of ESBL producers in Korea. Ideally, clinicians should be provided two interpretations based on both the revised breakpoints and ESBL confirmatory testing.
Aztreonam ; beta-Lactamases ; Cefotaxime ; Ceftazidime ; Ceftriaxone ; Cephalosporins ; Consensus ; Diffusion ; Enterobacteriaceae ; Klebsiella ; Klebsiella pneumoniae ; Korea ; Microbial Sensitivity Tests ; Pneumonia ; Sprains and Strains

PURPOSE: We studied the differences in the antibiotic susceptibilities of the microorganisms that causeing urinary tract infections (UTI) in children to obtain useful information on appropriate drug selection for childhood UTI. METHODS: We retrospectively analyzed the antibiotic susceptibilities of 429 microorganisms isolated from 900 patients diagnosed with UTI in the Department of Pediatrics, Chungbuk National University Hospital, from 2003 to 2008. RESULTS: The most common causative microorganisms for UTI were Escherichia coli (81.4%), Klebsiella pneumoniae (8.4%), Enterobacter spp. (1.7%), and Proteus spp. (0.4%). E. coli showed relatively high susceptibility as compared to imipenem (100%), amikacin (97.7%), aztreonam (97.9%), cefepime (97.7%), and ceftriaxone (97.1%), while it showed relatively low susceptibility to gentamicin (GM) (79.0%), trimethoprim/sulfamethoxazole (TMP/SMX) (68.7%), ampicillin/sulbactam (33.0%), and ampicillin (AMP) (28.6%). There were no significant differences in the image findings for causative microorganisms. CONCLUSION: Gram-negative organisms showed high susceptibility to amikacin and third-generation cephalosporins, and low susceptibility to AMP, GM, and TMP/SMX. Therefore, the use of AMP or TMP/SMX as the first choice in empirical and prophylactic treatment of childhood UTI in Korea should be reconsidered and investigated further.
Amikacin ; Ampicillin ; Aztreonam ; Ceftriaxone ; Cephalosporins ; Child ; Enterobacter ; Escherichia coli ; Gentamicins ; Humans ; Imipenem ; Klebsiella pneumoniae ; Korea ; Pediatrics ; Proteus ; Retrospective Studies ; Urinary Tract ; Urinary Tract Infections

BACKGROUND: In the present study, the resistance mechanisms against carbapenems and aminoglycosides for 23 strains of multi-drug-resistant Acinetobacter baumannii isolated at a university hospital were investigated. METHODS: The minimal inhibitory concentrations (MICs) were determined via broth microdilution or Etest. The genes encoding OXA-type carbapenemases and 16S rRNA methylase were identified using multiplex PCR, and the amplified products were sequenced. Conjugation experiments were conducted, and an epidemiologic study was performed using enterobacterial repetitive intergenic consensus (ERIC)-PCR. RESULTS: In the isolates, the MICs of the tested aminoglycosides, including arbekacin, were >1024 microg/mL; the MICs of aztreonam, cefepime, ceftazidime, and ciprofloxacin ranged from 64 to 128 microg/mL; and the MICs of carbapenem ranged from 32 to 64 microg/mL, as determined through the broth microdilution test. According to the E-test, the MICs of ampicillin/sulbactam and colistin were 8 and 0.25 to 0.38 microg/mL, respectively. Sequence analysis confirmed that all of the isolates expressed carbapenemases OXA-23 and OXA-66, as well as armA 16S rRNA methylase. In addition, ISAba1 was identified upstream of the gene encoding OXA-23. OXA-23 and armA were not transferred to Escherichia coli J53 cells in the transconjugation experiments. ERIC-PCR molecular fingerprinting produced a single pattern in all cases. CONCLUSION: The co-production of OXA-23 and armA 16S rRNA methylase may be attributed to the multidrug resistance of the A. baumannii isolates in the present study. Stricter surveillance and more rapid detection are necessary to prevent the spread of this type of resistance in the future.
Acinetobacter ; Acinetobacter baumannii ; Aminoglycosides ; Aztreonam ; Carbapenems ; Ceftazidime ; Cephalosporins ; Ciprofloxacin ; Colistin ; Consensus ; Dermatoglyphics ; Dibekacin ; Drug Resistance, Multiple ; Epidemiologic Studies ; Escherichia coli ; Methyltransferases ; Multiplex Polymerase Chain Reaction ; Republic of Korea ; RNA, Ribosomal, 16S ; Sequence Analysis

BACKGROUND: In 2010, the Clinical and Laboratory Standards Institute (CLSI) revised breakpoints for cephalosporins and carbapenems and indicated that extended-spectrum beta-lactamase (ESBL) testing is no longer necessary for Enterobacteriaceae. We compared the results of the CLSI 2010 and the European Committee on Antimicrobial Susceptibility Testing (EUCAST) MIC breakpoints for Enterobacteriaceae producing ESBL and/or plasmid-mediated AmpC beta-lactamase (PABL). METHODS: A total of 94 well-characterized clinical isolates of Escherichia coli, Klebsiella oxytoca, Klebsiella pneumoniae, Proteus mirabilis, Salmonella spp., Shigella spp., Citrobacter freundii, Enterobacter aerogenes, Enterobacter cloacae, and Serratia marcescens were analyzed. Of them, 57 were ESBL producers, 24 were PABL producers, and 13 were ESBL plus PABL co-producers. Broth microdilution MIC tests were performed for cefotaxime, ceftazidime, aztreonam, cefepime, and imipenem. RESULTS: Among the 94 isolates containing ESBL and/or PABL, the number of isolates that were susceptible to cefotaxime, ceftazidime, aztreonam, cefepime, and imipenem according to the CLSI 2010 vs. the EUCAST breakpoints were 4 (4.3%) vs. 4 (4.3%); 26 (27.7%) vs. 8 (8.5%); 37 (39.4%) vs. 14 (14.9%); 71 (75.5%) vs. 31 (33.0%); and 76 (80.9%) vs. 90 (95.7%), respectively. Of the 18 isolates that were not susceptible to imipenem according to the CLSI 2010 breakpoints, 13 isolates (72.2%) were P. mirabilis. CONCLUSION: The CLSI 2010 MIC breakpoints without tests to detect ESBL and/or PABL for Enterobacteriaceae could be unreliable. Thus, special tests for ESBLs and AmpC beta-lactamases are required to detect the resistance mechanisms involved.
Aztreonam ; Bacterial Proteins ; beta-Lactamases ; beta-Lactams ; Carbapenems ; Cefotaxime ; Ceftazidime ; Cephalosporins ; Citrobacter freundii ; Enterobacter aerogenes ; Enterobacter cloacae ; Enterobacteriaceae ; Escherichia coli ; Imipenem ; Klebsiella oxytoca ; Klebsiella pneumoniae ; Proteus mirabilis ; Salmonella ; Serratia marcescens ; Shigella