Te-Li Chen

Association Between Recent Use of Fluoroquinolones and Rhegmatogenous Retinal Detachment: A Population-Based Cohort Study

BACKGROUNDnAn association between use of oral fluoroquinolones (FQs) and retinal detachment remains controversial. This study was to determine the association of recent use of oral FQs and rhegmatogenous retinal detachment (RRD) after adjustment for confounding factors known to be associated with RRD.nnnMETHODSnThis retrospective population-based cohort study with parallel groups included adults treated with an oral FQ (FQ cohort = 178 179 prescriptions) and propensity score-matched adults treated with oral amoxicillin (amoxicillin cohort = 178 179 prescriptions). The data were extracted from the Taiwan National Health Insurance Research Database from 1998 to 2010. Interaction terms were used to identify populations at risk. RRD was defined according to the International Classification of Diseases, Ninth Revision, Clinical Modification.nnnRESULTSnDuring the 90-day follow-up period, 96 patients (0.054%) in the FQ cohort developed RRD compared to 46 (0.026%) among the matched amoxicillin cohort. The overall adjusted hazard ratio (HR) for FQ use and RRD was 2.07 (95% confidence interval [CI], 1.45-2.96). The interval between use of oral FQs and onset of RRD was 35.5 days (interquartile range, 14-57 days). Interaction terms were not significant for age, sex, diabetes, indications for antimicrobials, or underlying ophthalmic conditions. The adjusted HRs differed for specific FQs. These were 10.68 (95% CI, 3.28-34.82) for ciprofloxacin, 2.41 (95% CI, .76-7.68) for levofloxacin, 2.00 (95% CI, 1.06-3.79) for norfloxacin, and 1.17 (95% CI, .59-2.31) for ofloxacin.nnnCONCLUSIONSnThe use of oral FQs was associated with the subsequent occurrence of RRD. The FQ risk was independent of age, sex, diabetes, indications for antimicrobials, and underlying ophthalmic conditions. Certain FQs carried higher risk of RRD.

Bacteremic nosocomial pneumonia caused by Acinetobacter baumannii and Acinetobacter nosocomialis: a single or two distinct clinical entities?

The phenotypically indistinguishable Acinetobacter baumannii and Acinetobacter nosocomialis have become leading pathogens causing nosocomial pneumonia in critically ill patients. A.xa0baumannii and A.xa0nosocomialis nosocomial pneumonias were grouped as a single clinical entity previously. This study aimed to determine whether they are the same or a different clinical entity. A total of 121 patients with A.xa0baumannii and 131 with A.xa0nosocomialis bacteremic nosocomial pneumonia were included during an 8-year period. Despite the similar Charlson co-morbidity scores at admission, patients with A.xa0baumannii pneumonia were more likely to have abnormal haematological findings, lobar pneumonia, significantly higher Acute Physiology and Chronic Health Evaluation II scores and higher frequency of shock at the onset of bacteraemia than those with A.xa0nosocomialis pneumoni. A.xa0baumannii isolates were resistant to more classes of antimicrobials, except colistin, and therefore the patients with A.xa0baumannii pneumonia were more likely to receive inappropriate antimicrobial therapy. The 14-day mortality was significantly higher in patients with A.xa0baumannii pneumonia (34.7% vs. 15.3%, p 0.001). A.xa0baumannii was an independent risk factor for mortality (OR, 2.03; 95% CI, 1.05-3.90; p 0.035) in the overall cohort after adjustment for other risk factors for death, including inappropriate antimicrobial therapy. The results demonstrated the difference in clinical presentation, microbial characteristics and outcomes between A.xa0baumannii and A.xa0nosocomialis nosocomial pneumonia, and supported that they are two distinct clinical entities.

Association Between Recent Use of Proton Pump Inhibitors and Nontyphoid Salmonellosis: A Nested Case-Control Study

BACKGROUNDnThe association between proton pump inhibitors (PPIs) and nontyphoid salmonellosis (NTS) continues to be debated. The current study was designed to determine the association between use of oral PPIs and the diagnosis of NTS.nnnMETHODSnThe Taiwan National Health Insurance Research Database from 2000 to 2010 was searched for cases of NTS, defined by the International Classification of Disease, Ninth revision, Clinical Modification. A nested case-control study in hospitalized population was conducted using 4 controls for each case patient (14 736 case patients and 58 944 controls), matched for age, month and year of entry, Charlson comorbidity index score, and well-known predisposing factors for NTS, including autoimmune diseases, acquired immunodeficiency syndrome, diabetes, cirrhosis, transplantation, gastrointestinal operations or diseases, and malignancies.nnnRESULTSnPersons with NTS had a higher rate of using oral PPIs within the prior year (adjusted odds ratio [OR], 2.09; 95% confidence interval [CI], 1.95-2.24; P < .001). The association was greatest for current PPI use (adjusted OR, 5.39; 95% CI, 4.79-6.06; P < .001). Although use of H2-receptor antagonists (adjusted OR, 1.84; 95% CI, 1.71-1.98), antibiotics (5.21; 4.81-5.64), steroids (3.18; 2.99-3.39), and nonsteroidal anti-inflammatory drugs (2.37; 2.26-2.48) within the 30 days were also associated with NTS, the linkage between PPI use and NTS remained significant in the subgroup without these medications.nnnCONCLUSIONSnThe use of oral PPIs was associated with the occurrence of NTS. The risk waned with time after discontinuation.

Comparison between bacteremia caused by carbapenem resistant Acinetobacter baumannii and Acinetobacter nosocomialis

BackgroundIt is unknown whether there are differences between bacteremia caused by carbapenem resistant Acinetobacter baumannii (CRAB) and carbapenem resistant Acinetobacter nosocomialis (CRAN). This study aims to investigate the differences, especially in clinical outcomes, between patients with bacteremia caused by CRAB or CRAN.MethodsThis is a 9-year retrospective study comparing the clinical manifestations, antimicrobial susceptibilities, and clinical outcomes of 71 patients with CRAB bacteremia and 64 patients with CRAN bacteremia.ResultsPatients with CRAB were more likely to have hematologic malignancies and presented with more shock episodes than those with CRAN. CRAB isolates were more resistant to various classes of antimicrobials except colistin, and therefore the patients with CRAB bacteremia were more likely to receive inappropriate antimicrobial therapies. The 14-day mortality was significantly higher in patients with CRAB (40.8% vs. 14.1%; p = 0.001), and in this study, acquisition of CRAB was identified as an independent risk factor for mortality (odds ratio = 4.003; 95% confidence interval = 1.566-10.231; p = 0.004).ConclusionsCRAB and CRAN bacteremia are different in clinical characteristics, antimicrobial susceptibilities, and mortality rates. Genomic species identification should be performed in the study of carbapenem resistant Acinetobacters to better delineate the role of different species.

Risk factors of community-onset urinary tract infections caused by plasmid-mediated AmpC β-lactamase-producing Enterobacteriaceae

BACKGROUNDnThe AmpC β-lactamase (AmpC)-producing Enterobacteriaceae emerged worldwide. This study was conducted to determine the risk factors of community-onset urinary tract infections (UTIs) caused by plasmid-mediated AmpC-producing Enterobacteriaceae.nnnMETHODSnPatients who were diagnosed as community-onset UTIs caused by Enterobacteriaceae in a tertiary-care teaching hospital from December 2010 to January 2012 were included. Extended-spectrum β-lactamase (ESBL)-producing isolates were excluded. We identified plasmid-mediated AmpC-producing Enterobacteriaceae both phenotypically (by disk potentiation test and double-disk synergy test) and genotypically (by Multiplex polymerase chain reaction (PCR) assay). The demographic data, clinical characteristics, and risk factors of acquisition were described.nnnRESULTSnAmong the 323 non-ESBL-producing Enterobacteriaceae identified in community-onset UTIs, 50 isolates were phenotypically positive for AmpC. Escherichia coli was the most common AmpC-producing organism (60%), followed by Klebsiella pneumonia (8%), and Enterobacter cloacae and Proteus mirabilis (6% for each species). The independent risk factors for acquisition of AmpC-producing Enterobacteriaceae included prior history of cerebral vascular accident [odds ratio (OR) = 2.014; 95% confidence interval (CI) = 1.007-4.031; p = 0.0048], and prior use of fluoroquinolones (OR = 4.049; 95% CI = 1.759-9.319; p = 0.001) and cephamycin (OR = 9.683; 95% CI = 2.007-45.135; p = 0.004). AmpC-producing isolates were multidrug resistant. Carbapenems, cefepime, and piperacillin/tazobactam had the best in vitro efficacy. The most commonly identified plasmid-mediated AmpC gene was bla(CIT), followed by bla(DHA)/bla(EBC), and bla(MOx).nnnCONCLUSIONnFor community-onset UTIs, AmpC-producing Enterobacteriaceae should be suspected in those with prior history of cerebral vascular accident and prior use of antimicrobials. To treat these multiple-resistant isolates, carbapenems, cefepime, and piperacillin/tazobactam may be considered.

Evolution of carbapenem resistance in Acinetobacter baumannii: An 18-year longitudinal study from a medical center in northern Taiwan

BACKGROUNDnCarbapenem-resistant Acinetobacter baumannii has emerged as an important cause of nosocomial infections with high morbidity and mortality. The carbapenemases, especially class D carbapenem-hydrolyzing oxacillinases (CHDLs), play an important role, but the relationship between their prevalence trend and carbapenem resistance remains unclear.nnnMATERIALS AND METHODSnBetween 1995 and 2012, we collected 667 isolates of A. baumannii from a single medical center in northern Taiwan. Pulsed-field gel electrophoresis (PFGE) was used to determine clonality. Antimicrobial susceptibility was determined. Carbapenemase genes and associated genetic structures were detected by polymerase chain reaction.nnnRESULTSnIsolates were heterogeneous on PFGE. Susceptibility to carbapenem decreased steadily over the study period from 88.1% (2001-2003) to <25% (2010-2012), whereas the isolates remained susceptible to colistin (nearly 100%) and partially susceptible to tigecycline (80%). Starting in 2001, isolates carrying the ISAba1-blaOXA-51-like allele were consistently identified. Isolates containing the transposons Tn2006 or Tn2008 first appeared in 2007 with increasing carriage rates from 17.5% (2007-2009) to 50.0% (2010-2012). The IS1008-ΔISAba3-blaOXA-58-like, blaOXA-72 and metallo-β-lactamase genes were detected only sporadically. Isolates carrying CHDL genes were resistant to multiple drugs, including carbapenem, but remained susceptible to colistin (100.0%).nnnCONCLUSIONnIncreased carbapenem resistance in A. baumannii may be caused by the increased prevalence of isolates containing the ISAba1-blaOXA-51-like allele and the transposons Tn2006 and Tn2008.

Predictors of mortality in surgical patients with Acinetobacter baumannii bacteremia

BACKGROUNDnAcinetobacter baumannii has emerged as an important pathogen of nosocomial infection. The aim of this study was to evaluate the predictors of poor outcome in surgical patients with A baumannii bacteremia.nnnMETHODSnWe retrospectively recruited a total of 50 patients who developed A baumannii bacteremia within 2 weeks after surgery during a 113-month period. The primary outcome for this study was all-cause 14-day mortality. Clinical and laboratory data, antimicrobial susceptibility, treatment, and Sequential Organ Failure Assessment (SOFA) score were evaluated as possible predictors of outcome.nnnRESULTSnThe 14-day mortality was 20% and there was no association between type of surgery and mortality. The SOFA score was the only independent predictor of 14-day mortality after adjustment for other variables. The calibration was acceptable (Hosmer-Lemeshow χ(2) = 3.65, p = 0.72) and the discrimination was good (area under the receiver operating characteristic curve: 0.80 ± 0.07, 95% confidence interval, 0.67-0.94). We found that a SOFA score ≥ 7 was a significant predictor of 14-day mortality in surgical patients with A baumannii bacteremia.nnnCONCLUSIONSnThe SOFA score assessed at the onset of bacteremia is a reliable tool for predicting 14-day mortality in surgical patients with A baumannii bacteremia.

Acinetobacter baumannii nosocomial pneumonia: is the outcome more favorable in non-ventilated than ventilated patients?

BackgroundAcinetobacter baumannii hospital-acquired pneumonia (HAP) is associated with a high mortality worldwide. Non-ventilated patients with HAP (NVHAP) caused by nosocomial pathogens are reported to have a more favorable outcome than those with ventilator-associated pneumonia (VAP). The current study was designed to determine whether bacteremic patients with A. baumannii NVHAP also have a lower mortality than those receiving assisted ventilation.MethodsThis retrospective 10-year study was conducted at a 2900-bed teaching hospital located in Northern Taiwan. The population consisted of 144 patients with A. baumannii bacteremia and HAP. Of these 96 had VAP and 48 had NVHAP. Charts were reviewed for demographic characteristics, comorbidities, clinical manifestations, antimicrobial susceptibility, and 14-day mortality. Clonal relationships were determined by molecular typing.ResultsThere were no significant differences between the two groups in comorbidities (Charlson scores). Patients with NVHAP were more likely to have developed bacteremia earlier, outside the ICU and undergone fewer invasive procedures. They had significantly lower APACHE II scores, fewer bilateral pneumonias and lower rates of antimicrobial resistance. No specific clones were identified in either group. The unadjusted (crude) 14-day mortality rates were not significantly different between the groups (NVHAP 43.8% vs. VAP 31.3%, p = 0.196). The adjusted 14-day mortality risk was significantly lower in ventilator-assisted patients (odds ratio = 0.201; 95% confidence interval = 0.075-0.538; p = 0.001).ConclusionsPatients with bacteremic NVHAP and VAP caused by A. baumannii had similar crude mortality rates, but on logistic regression analysis those receiving ventilator assistance had a significantly lower mortality. This may have been due to better airway protection, more intensive monitoring with earlier diagnosis and treatment in patients with VAP, greater innate susceptibility to infection in those with NVHAP and differences in the virulence of A. baumannii.

Molecular epidemiology of carbapenem non-susceptible Acinetobacter nosocomialis in a medical center in Taiwan

The mechanism by which carbapenem non-susceptible Acinetobacter nosocomialis (CNSAN) is disseminated is rarely described in the literature. In this study, we delineated the molecular epidemiology of CNSAN isolated from patients in a medical center in Taiwan. Fifty-four non-duplicate bloodstream isolates of CNSAN were collected at the Taipei Veterans General Hospital between 2001 and 2007. Pulsed-field gel electrophoresis (PFGE) was performed to determine their clonal relationship. Carbapenem-resistance genes and associated genetic structures were detected by polymerase chain reaction (PCR) mapping. Southern hybridization was performed to determine the plasmid location of carbapenem-resistance genes. Transmissibility of these genes to Acinetobacterbaumannii was demonstrated by conjugation tests. The overall carbapenem non-susceptibility rate among A. nosocomialis isolates during the study period was 21.6% (54/250). PFGE revealed three major pulsotypes: H (n=23), I (n=10), and K (n=8). The most common carbapenem-resistance gene was blaOXA-58 (43/54, 79.6%), containing an upstream insertion sequence IS1006 and a truncated ISAba3 (IS1006-ΔISAba3-like-blaOXA-58). All isolates belonging to the pulsotypes H, I, and K carried plasmid located IS1006-ΔISAba3-like-blaOXA-58. A common plasmid carrying ISAba1-blaOXA-82 was found in six isolates, which belonged to five pulsotypes. A type 1 integron that carried blaIMP-1 was detected in different plasmids of seven isolates, which belonged to five pulsotypes. Plasmids carrying these carbapenem-resistant determinants were transmissible from A. nosocomialis to A. baumannii via conjugation. In this medical center, CNSAN mainly emerged through clonal dissemination; propagation of plasmids and integrons carrying carbapenem-resistant determinants played a minor role. This study showed that plasmids carrying carbapenem-resistant determinants are transmissible from A. nosocomialis to A. baumannii.

A retrospective study of the incidence, clinical characteristics, identification, and antimicrobial susceptibility of bacteremic isolates of Acinetobacter ursingii

BackgroundAcinetobacter ursingii bacteremia is rarely reported. We investigated the incidence and clinical features of A. ursingii bacteremia, performance of the identification system, and antimicrobial susceptibility of the isolates. Acinetobacter ursingii bacteremia patients were compared with A. baumannii bacteremia patients.MethodsIn this 9-year retrospective study, A. ursingii was identified using 16S rRNA and 16S–23S rRNA internal transcribed spacer sequence analysis. The performances of the Vitek 2, Phoenix, and matrix-assisted laser desorption ionization time-of-flight (MALDI-TOF) mass spectrometer systems for identifying isolates were tested. Pulsed-field gel electrophoresis (PFGE) was used to determine the clonality of the isolates. The minimal inhibitory concentrations of the antimicrobials were determined using the Vitek 2 system.ResultsNineteen patients were identified. Acinetobacter ursingii was noted in 1.5–5.2xa0% of all Acinetobacter bacteremia cases. For the PFGE analysis, two isolates had smeared DNA, two had 93xa0% similarity, and 15 had similarity <80xa0%. Among 16 patients with complete medical records, 10 (62.5xa0%) had no identifiable source of A. ursingii bacteremia. Most patients (nu2009=u200912) had underlying malignant disease. Patients with A. ursingii bacteremia had lower Acute Physiology and Chronic Health Evaluation II scores than those with A. baumannii bacteremia (median [interquartile range], 17.1 [10.0–24.7] vs. 24.9 [14.6–35.1]). Patients with A. ursingii bacteremia were also less likely admitted to the intensive care unit than patients with A. baumannii bacteremia (18.8xa0% vs 63.5xa0%, p valueu2009<u20090.01). About half of the patients with A. ursingii (50.8xa0%) and A. baumannii bacteremia (62.5xa0%) had received inappropriate antimicrobial therapy within 48xa0h after bacteremia onset. However, patients with A. ursingii bacteremia had significantly lower 14-day (6.25xa0% vs 29.8xa0%, p valueu2009=u20090.04) and 28-day mortality rates (6.25xa0% vs 37.3xa0%, p valueu2009=u20090.02) than patients with A. baumannii bacteremia. Nine isolates (47.4xa0%) were correctly identified as A. ursingii and the other 10 isolates (52.6xa0%) were incorrectly identified as A. lwoffii by the Vitek 2 system. The Phoenix system incorrectly identified all 19 isolates. The MALDI-TOF mass spectrometer system correctly identified all 19 isolates. All the A. ursingii isolates were resistant or showed intermediate susceptibility to ceftriaxone and ceftazidime, but were susceptible to levofloxacin and imipenem.ConclusionsAcinetobacter ursingii is a rare pathogen that mostly caused primary bacteremia in patients with malignancies. Patients with A. ursingii bacteremia had significantly lower disease severity and mortality ratesxa0than patients with A. baumannii bacteremia.