IMPORTANCE Risks for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection among health care personnel (HCP) are unclear. OBJECTIVE To evaluate the risk factors associated with SARS-CoV-2 seropositivity among HCP with the a priori hypothesis that community exposure but not health care exposure was associated with seropositivity. DESIGN, SETTING, AND PARTICIPANTS This cross-sectional study was conducted among volunteer HCP at 4 large health care systems in 3 US states. Sites shared deidentified data sets, including previously collected serology results, questionnaire results on community and workplace exposures at the time of serology, and 3-digit residential zip code prefix of HCP. Site-specific responses were mapped to a common metadata set. Residential weekly coronavirus disease 2019 (COVID-19) cumulative incidence was calculated from state-based COVID-19 case and census data. EXPOSURES Model variables included demographic (age, race, sex, ethnicity), community (known COVID-19 contact, COVID-19 cumulative incidence by 3-digit zip code prefix), and health care (workplace, job role, COVID-19 patient contact) factors. MAIN OUTCOME AND MEASURES The main outcome was SARS-CoV-2 seropositivity. Risk factors for seropositivity were estimated using a mixed-effects logistic regression model with a random intercept to account for clustering by site. RESULTS Among 24 749 HCP, most were younger than 50 years (17 233 [69.6%]), were women (19 361 [78.2%]), were White individuals (15 157 [61.2%]), and reported workplace contact with patients with COVID-19 (12 413 [50.2%]). Many HCP worked in the inpatient setting (8893 [35.9%]) and were nurses (7830 [31.6%]). Cumulative incidence of COVID-19 per 10 000 in the community up to 1 week prior to serology testing ranged from 8.2 to 275.6; 20 072 HCP (81.1%) reported no COVID-19 contact in the community. Seropositivity was 4.4% (95% CI, 4.1%-4.6%; 1080 HCP) overall. In multivariable analysis, community COVID-19 contact and community COVID-19 cumulative incidence were associated with seropositivity

Background Bacteremia is a significant cause of morbidity and mortality in critically ill children. Our objective was to assess whether daily chlorhexidine gluconate (CHG) bathing compared with standard bathing practices would reduce bacteremia in critically ill children. Methods In an unmasked, cluster-randomized, two-period crossover trial (Pediatric SCRUB), 10 pediatric intensive care units (ICUs) at 5 hospitals in the United States were randomly assigned to bathe patients > 2 months of age daily with a 2% CHG-impregnated cloth or with standard bathing practices for a six-month period. Units switched to the alternative bathing method during the second six-month period. Among 6,482 eligible patient admissions, 1521 were excluded due to a length of stay less than 2 days and 14 refused to participate. The primary outcome was an episode of bacteremia. This study is registered with ClinicalTrials.gov (Identifier: NCT00549393). Findings 4·947 patient admissions were eligible for analysis. In the intent to treat population, there was a non-statistically significant reduction in incidence of bacteremia among patients receiving daily CHG bathing (3·52 per 1,000 days, 95%CI 2·64–4·61) compared with patients receiving standard bathing practices (4·93 per 1,000 days, 95%CI 3·91–6·15) [adjusted incidence rate ratio (aIRR) 0·71, 95% CI 0·42–1·20]. In the per protocol population, the incidence of bacteremia was 36% lower among patients receiving daily CHG bathing (3·28 per 1,000 days, 95%CI 2·27–4·58)) compared with patients receiving standard bathing practices (4·93 per 1,000 days, 95%CI 3·91–6·15) [aIRR 0·64, 95% CI 0·42–0·98]. There were no serious study related adverse events, and the incidence of CHG-associated skin reactions was 1·2 per 1,000 days (95% CI 0·60–2·02). Interpretation Critically ill children receiving daily CHG bathing had a lower incidence of bacteremia, and the treatment was well tolerated. Funding Primarily by Sage Products, Inc.. Additional funding from U.S. National Institutes of Health.

Coevolution of intracellular bacterial pathogens and their host cells resulted in the appearance of effector molecules that when translocated into the host cell modulate its function, facilitating bacterial survival within the hostile host environment. Some of these effectors interact with host chromatin and other nuclear components. In this report, we show that the AnkA protein of Anaplasma phagocytophilum, which is translocated into the host cell nucleus, interacts with gene regulatory regions of host chromatin and is involved in downregulating expression of CYBB (gp91 phox ) and other key host defense genes. AnkA effector protein rapidly accumulated in nuclei of infected cells coincident with changes in CYBB transcription. AnkA interacted with transcriptional regulatory regions of the CYBB locus at sites where transcriptional regulators bind. AnkA binding to DNA occurred at regions with high AT contents. Mutation of AT stretches at these sites abrogated AnkA binding. Histone H3 acetylation decreased dramatically at the CYBB locus during A. phagocytophilum infection, particularly around AnkA binding sites. Transcription of CYBB and other defense genes was significantly decreased in AnkA-transfected HL-60 cells. These data suggest a mechanism by which intracellular pathogens directly regulate host cell gene expression mediated by nuclear effectors and changes in host chromatin structure.Intracellular pathogens, through longstanding associations with host cells, evolved mechanisms that promote survival within the often-hostile environment of their hosts (13). Global analysis of mammalian gene expression in response to intracellular bacteria identified major pathways affected during infection (4). However, previous studies largely focused on interactions of bacteria and/or bacterial effectors with the host cell surface and cytoplasmic signaling pathways (19). Transfer of bacterial effector proteins into the eukaryotic host cell cytoplasm is also a recognized mechanism of bacterial control over host cells for organisms such as Yersinia (29), Shigella (1), and Listeria (27). In contrast, mechanisms by which bacterial proteins enter the host cell and directly alter gene transcription are underinvestigated, and only a few bacterial molecules that enter the eukaryotic host nucleus are reported. Cytolethal distending toxin, a tripartite toxin produced by a number of bacteria, is translocated into the host cell nucleus and by exerting DNA damage leads to G 2 /M cell cycle arrest, cellular distention, and nuclear enlargement in intoxicated cells (17). Similarly, some proteins of the Amoeba proteus X-bacterium symbiont translocate into the nucleus and induce S-adenosylmethionine synthetase expression (22), whereas T-DNA from Agrobacterium tumefaciens is transported into the nucleus and induces plant cell transformation (20). Additionally, Shigella flexneri OspF is injected into host cells and alters host gene transcription by targeting chromatin access for the transcription factor NF-B (2). Using Anaplasma phagocytophilum...

Objective(s) To characterize the epidemiology and identify risk factors for complications necessitating removal of peripherally inserted central venous catheters (PICCs) in children. Design Cohort study Setting The Johns Hopkins Children’s Center, Baltimore, Maryland. Participants Hospitalized children who had a PICC inserted outside of the neonatal ICU between January 1, 2003 and December 1, 2009. Main Exposures Age, PICC dwell time, PICC insertion site, PICC tip location, pediatric ICU exposure, indication for PICC insertion Outcome Measures Complications necessitating PICC removal as recorded by the PICC Team. Results During the study period, 2574 PICCs were placed in 1807 children. Complications necessitating catheter removal occurred in 20.8% of PICCs during 46,021 catheter days (11.6 complications per 1,000 catheter days). These included accidental dislodgement (4.6%), infection (4.3%), occlusion (3.6%), local infiltration (3.0%), leakage (1.5%), breaks (1.4%), phlebitis (1.2%) and thrombosis (0.5%). From 2003 to 2009 complications decreased by 15% per year (IRR 0.85; 95%CI 0.81-0.89). In adjusted analysis, all non-central PICC tip locations - midline (IRR 4.59, 95% CI 3.69-5.69), mid-clavicular (IRR 2.15, 95% CI 1.54-2.98), and other (IRR 3.26 95% CI 1.72-6.15) - compared to central tip location were associated with an increased risk of complications. Pediatric ICU exposure and age less than one year old were independently associated with complications necessitating PICC removal. Conclusion(s) Non-central PICC tip locations, younger age, and pediatric ICU exposure were independent risk factors for complications necessitating PICC removal. Despite reductions in PICC complications, further efforts are needed to prevent PICC-associated complications in children.

The data suggest that hospitals have a financial incentive to reduce SSIs, but hospitals should expect to see an increase in both cost and revenue when SSIs are reduced.

A best-practice central line maintenance care bundle can be implemented in hospitalized pediatric oncology patients, although long ramp-up times may be necessary to reap maximal benefits. Further research is needed to determine if this CLABSI rate reduction can be sustained and spread.

Prolonged catheter dwell time, pediatric ICU exposure, and administration of parenteral nutrition as the indication for PICC insertion are important predictors of PICC-associated CLABSI in hospitalized children. A careful assessment of these risk factors may be important for future success in preventing CLABSIs in hospitalized children with PICCs.

OBJECTIVETo describe pathogen distribution and antimicrobial resistance patterns for healthcare-associated infections (HAIs) reported to the National Healthcare Safety Network (NHSN) from pediatric locations during 2011–2014.METHODSDevice-associated infection data were analyzed for central line-associated bloodstream infection (CLABSI), catheter-associated urinary tract infections (CAUTI), ventilator-associated pneumonia (VAP), and surgical site infection (SSI). Pooled mean percentage resistance was calculated for a variety of pathogen-antimicrobial resistance pattern combinations and was stratified by location for device-associated infections (neonatal intensive care units [NICUs], pediatric intensive care units [PICUs], pediatric oncology and pediatric wards) and by surgery type for SSIs.RESULTSFrom 2011 to 2014, 1,003 hospitals reported 20,390 pediatric HAIs and 22,323 associated pathogens to the NHSN. Among all HAIs, the following pathogens accounted for more than 60% of those reported: Staphylococcus aureus (17%), coagulase-negative staphylococci (17%), Escherichia coli (11%), Klebsiella pneumoniae and/or oxytoca (9%), and Enterococcus faecalis (8%). Among device-associated infections, resistance was generally lower in NICUs than in other locations. For several pathogens, resistance was greater in pediatric wards than in PICUs. The proportion of organisms resistant to carbapenems was low overall but reached approximately 20% for Pseudomonas aeruginosa from CLABSIs and CAUTIs in some locations. Among SSIs, antimicrobial resistance patterns were similar across surgical procedure types for most pathogens.CONCLUSIONThis report is the first pediatric-specific description of antimicrobial resistance data reported to the NHSN. Reporting of pediatric-specific HAIs and antimicrobial resistance data will help identify priority targets for infection control and antimicrobial stewardship activities in facilities that provide care for children.Infect Control Hosp Epidemiol 2018;39:1–11