Use of a Feeding Bundle Appears to Reduce Central Line Utilization in Neonates.

We investigated whether a standardized feeding bundle reduces central line utilization in very low birth weight neonates. A chart review of infants ≤1500 g requiring a central line was prepared for 2009 to 2012. Infants were stratified into 3 weight groups: ≤750 g, 751 to 1000 g, and 1001 to 1500 g. The number of central line-associated bloodstream infections (CLABSIs) was recorded. Central line utilization decreased in all of the groups: 0.45 to 0.28 in ≤750 g infants, 0.4 to 0.27 in 751 to 1000 g infants, and 0.39 to 0.3 in 1001 to 1500 g infants (all of the P < 0.001). The CLABSIs rate was unchanged. Implementation of a feeding bundle decreased central line utilization. A feeding bundle had no effect on the rate of CLABSIs.

Clinical epidemiology of carbapenem-intermediate or -resistant Enterobacteriaceae.

OBJECTIVES: Despite the increasing incidence of carbapenem-intermediate or -resistant Enterobacteriaceae (CIRE), risk factors associated with CIRE infections have not been well defined. This study characterizes factors associated with CIRE among two different source populations. METHODS: A case-control study was performed at a tertiary care medical centre between January 2005 and December 2009. Cases were adults with a culture-confirmed Enterobacteriaceae infection with reduced susceptibility to meropenem or ertapenem. The CIRE cases were matched 1:1 to patients from two different control series: (i) those with carbapenem-susceptible Enterobacteriaceae (CSE) infections; and (ii) inpatients residing on the same ward within 30 days of CIRE culture date. Logistic regression was used to identify variables independently associated with CIRE among each source population. Restricted multivariate analyses were performed to determine if covariates predictive of CIRE varied by infecting organism or presence of the bla(KPC) gene. RESULTS: There were 102 cases of CIRE during the study period. The only covariate independently associated with CIRE in all multivariate analyses was the cumulative number of prior antibiotic exposures. Compared with CSE controls, the odds ratios (95% confidence interval) were 1.43 (1.19-1.72), 2.05 (1.70-2.47) and 2.93 (2.43-3.53) for 1, 2 and ≥ 3 antibiotic exposures, respectively. The strength of this association was comparable for the hospitalized control group and analyses stratified by organism and presence of the bla(KPC) gene. CONCLUSIONS: A patient's cumulative antibiotic exposure history is likely to be more important than any one specific exposure when determining the likelihood of developing a CIRE infection.

Predictors of Adverse Outcomes in Children With Staphylococcus aureus Bacteremia.

OBJECTIVES: Staphylococcus aureus bacteremia is a common infection, associated with significant morbidity and mortality in children. Factors associated with adverse treatment outcomes are poorly understood in the pediatric population. METHODS: Our study compared clinical and microbiologic characteristics of children admitted during a 5-year period (2007-2012) to a large university-based hospital and found to have S aureus bacteremia with outcome measures, in order to identify risk factors associated with treatment failure (defined as 30-day mortality, delayed microbiologic resolution, or recurrence of S aureus bacteremia within 60 days of completing effective antibiotic therapy). RESULTS: In all, 71 patients were found to have S aureus bacteremia, and of these, 17 patients (24%) experienced treatment failure. Based on the logistic regression model, only high vancomycin minimum inhibitory concentration in combination with a high-risk source of infection (i.e., infected graft or device, intra-abdominal infection, or respiratory tract infection) was significantly associated with risk of treatment failure. CONCLUSIONS: Infection associated with a high-risk source may increase the chance of treatment failure in pediatric patients with S aureus bacteremia. Vancomycin minimum inhibitory concentration alone was not found to be a predictor of treatment outcomes.

Predictors of 30-day mortality among patients with Pseudomonas aeruginosa bloodstream infections: impact of delayed appropriate antibiotic selection.

Although a growing number of studies have found a relationship between delayed appropriate antibiotic therapy and mortality, few have attempted to quantify the temporal association between delayed appropriate antibiotic therapy and mortality. This study was designed to measure the elapsed time associated with an increased risk of 30-day mortality among patients with Pseudomonas aeruginosa bacteremia. The retrospective cohort study was conducted among immunocompetent, adult patients with P. aeruginosa bacteremia onset at least 2 days after hospital admission between 1 January 2001 and 30 September 2006. Classification and regression tree analysis (CART) was used to identify the delay in appropriate antibiotic therapy that was associated with an increased risk of 30-day mortality. During the study period, 100 patients met the inclusion criteria. The CART-derived breakpoint between early and delayed treatment was 52 h. The delayed treatment group experienced a >2-fold significant increase in 30-day mortality compared to the early treatment group (44 and 19%, respectively, P = 0.008). Delayed appropriate therapy of >52 h (odds ratio [OR] = 4.1; 95% confidence interval [CI] 1.2 to 13.9, P = 0.03) was independently associated with 30-day mortality in the multivariate analysis. Antibiotic resistance > or =3 classes (adjusted OR [AOR] = 4.6; 95% CI = 1.9 to 11.2, P = 0.001) and chronic obstructive pulmonary disease (AOR = 5.4; 95% CI = 1.5 to 19.7, P = 0.01) were independently associated with delayed appropriate therapy of >52 h. The data strongly suggest that delaying appropriate therapy for approximately 2 days significantly increases the risk of 30-day mortality in patients with P. aeruginosa bloodstream infections.

Clinical prediction tool to identify patients with Pseudomonas aeruginosa respiratory tract infections at greatest risk for multidrug resistance.

Despite the increasing prevalence of multiple-drug-resistant (MDR) Pseudomonas aeruginosa, the factors predictive of MDR have not been extensively explored. We sought to examine factors predictive of MDR among patients with P. aeruginosa respiratory tract infections and to develop a tool to estimate the probability of MDR among such high-risk patients. This was a single-site, case-control study of patients with P. aeruginosa respiratory tract infections. Multiple-drug resistance was defined as resistance to four or more antipseudomonal antimicrobial classes. Clinical data on demographics, antibiotic history, and microbiology were collected. Classification and regression tree analysis (CART) was used to identify the duration of antibiotic exposure associated with MDR P. aeruginosa. Log-binomial regression was used to model the probability of MDR P. aeruginosa. Among 351 P. aeruginosa-infected patients, the proportion of MDR P. aeruginosa was 35%. A significant relationship between prior antibiotic exposure and MDR P. aeruginosa was found for all of the antipseudomonal antibiotics studied, but the duration of prior exposure associated with MDR varied between antibiotic classes; the shortest prior exposure duration was observed for carbapenems and fluoroquinolones, and the longest duration was noted for cefepime and piperacillin-tazobactam. Within the final model, the predicted MDR P. aeruginosa likelihood was most dependent upon length of hospital stay, prior culture sample collection, and number of CART-derived prior antibiotic exposures. A history of a prolonged hospital stay and exposure to antipseudomonal antibiotics predicts multidrug resistance among patients with P. aeruginosa respiratory tract infections at our institution. Identifying these risk factors enabled us to develop a prediction tool to assess the risk of resistance and thus guide empirical antibiotic therapy.

Risk factors associated with extended-spectrum beta-lactamase-producing organisms at a tertiary care hospital.

BACKGROUND: In 1995, beta-lactam inhibitor combinations replaced third-generation cephalosporins as empirical therapy in an effort to manage extended-spectrum beta-lactamase (ESBL) resistance. This study investigated the relationship between antibiotic usage and ESBL organisms from 1994 through 2002 using epidemiological and molecular analysis. METHODS: A case-control study of 119 patients with ESBL organisms and 132 patients with non-ESBL organisms was conducted. Demographics, co-morbidities, device utilization and antibiotic use were analysed for all patients and infected patients only (cases = 75, controls = 83). Both exposure and degree of exposure (in grams) to antibiotics were included. A dot blot hybridization technique was used to identify genes in plasmid extracts from the ESBL organisms. RESULTS: Ventilator days OR 1.1 (1.06, 1.15) P < 0.001, adult respiratory distress syndrome (ARDS) OR 3.1 (1.0, 9.7) P = 0.05, prior aminoglycoside use OR 2.7 (1.2, 6.1) P = 0.02, prior third-generation cephalosporin use OR 7.2 (2.6, 20) P < 0.001, and prior trimethoprim/sulfamethoxazole use OR 8.8 (3.1, 26) P < 0.001 were significantly associated with ESBL organisms by multivariate analysis. All models were concordant with a significant association of ventilator days, third-generation cephalosporins and trimethoprim/sulfamethoxazole with ESBL organisms. beta-Lactamase inhibitor combinations were not associated with ESBL organisms. Hybridization of plasmid extracts demonstrated that 95% of the ESBL organisms carried intI1, a mobile DNA element with a sulphonamide-resistance (R) gene and a frequent carrier of other R factors. Genes for specific types of trimethoprim-R and aminoglycoside-R were present in 26% and 40% of the extracts, respectively. CONCLUSIONS: These data indicate that, besides patient risk factors and third-generation cephalosporins, other antibiotics may provide selective pressures in maintaining ESBL organisms due to multiple resistance genes on plasmids. beta-Lactamase inhibitor combinations appear to be an acceptable substitute to third-generation cephalosporins in strategies to control ESBL organisms.

Risk factors associated with nosocomial methicillin-resistant Staphylococcus aureus (MRSA) infection including previous use of antimicrobials.

Methicillin-resistant Staphylococcus aureus (MRSA) is a major nosocomial pathogen worldwide. To investigate an association between antimicrobial use and MRSA, a case control study of 121 patients infected with MRSA compared with 123 patients infected with methicillin-susceptible S. aureus (MSSA) was carried out. Antimicrobial use was analysed by three different logistic regression models: all beta-lactam antibiotics, beta-lactam antibiotics grouped in classes and antimicrobial use in grammes. Patients infected with MRSA tended to have more co-morbidities, longer lengths of stay (LOS) and greater exposure to antibiotics than MSSA-infected patients. Multivariate analysis identified levofloxacin [odds ratio (OR) 8.01], macrolides (OR 4.06), previous hospitalization (OR 1.95), enteral feedings (OR 2.55), surgery (OR 2.24) and LOS before culture (OR 1.03) as independently associated with MRSA infection. All models were concordant with the exception of macrolides, which were not significant based on the number of grammes administered. There were no significant differences in the types of infection or the attributed mortality in either group. MRSA-infected patients had a significantly longer LOS before infection [18.8 +/- 18.2 compared with 8.4 +/- 6.9 (P < 0.001)] and a significantly longer post-diagnosis LOS [27.8 +/- 32.9 compared with 18.6 +/- 21 (P = 0.01)] than MSSA-infected patients.

Survey of plasmid-associated genetic markers in enterobacteriaceae with reduced susceptibilities to cephalosporins.

Clinical isolates of Enterobacteriaceae with reduced susceptibilities to cephalosporins were collected from 1993 to 2000. The organisms were screened for the extended-spectrum beta-lactamase (ESBL) phenotype, and plasmid extracts were screened for genetic markers by hybridization. A bla(TEM) probe was derived from pUC19; other probes were derived from pACM1, the plasmid responsible for the first known appearance of an ESBL in our institution. These probes included bla(SHV), int, aac(3)-Ia, dfrA1, IS6100, tetA, IncM markers, and Anon 13, a marker for the Klebsiella pneumoniae chromosomal sequences that flank bla(SHV-5). There were 42 hybridization patterns among 237 isolates. Patterns designated pACM1-like occurred in 44% of the isolates (eight species) and were always associated with the clavulanic acid (CA)-susceptible ESBL phenotype. The TEM marker was not predictive of the ESBL phenotype. Mapping indicated the presence of an SHV marker and up to 7.5 kb of its flanking chromosomal sequences in three non-IncM plasmids obtained in transformation experiments. We theorize that this DNA segment spread to other plasmids from pACM1-like sources. CA insensitivity became more frequent with time and was usually associated with either the TEM marker or the absence of both bla markers. One plasmid-encoded enzyme with characteristics of an AmpC beta-lactamase was observed in a transformant lacking both TEM and SHV markers. Although SHV type ESBLs were a continuing source of reduced susceptibility to cephalosporins in our institution, organisms with different resistance mechanisms were added to the hospital microflora in later years. These changes might be related, in part, to ESBL control strategies implemented in 1995.