Communication Strategies to Improve Antibiotic Prescribing in Pediatric Urgent Care Centers

OBJECTIVE: Urgent care (UC) clinicians frequently prescribe inappropriate antibiotics for upper respiratory illnesses. In a national survey, pediatric UC clinicians reported family expectations as a primary driver for prescribing inappropriate antibiotics. Communication strategies effectively reduce unnecessary antibiotics while increasing family satisfaction. We aimed to reduce inappropriate prescribing practices in otitis media with effusion (OME), acute otitis media (AOM), and pharyngitis in pediatric UC clinics by a relative 20% within 6 months using evidence-based communication strategies. METHODS: We recruited participants via e-mails, newsletters, and Webinars from pediatric and UC national societies. We defined antibiotic-prescribing appropriateness based on consensus guidelines. Family advisors and UC pediatricians developed script templates based on an evidence-based strategy. Participants submitted data electronically. We reported data using line graphs and shared deidentified data during monthly Webinars. We used χ2 tests to evaluate change in appropriateness at the beginning and end of the study period. RESULTS: The 104 participants from 14 institutions submitted 1183 encounters for analysis in the intervention cycles. Using a strict definition of inappropriateness, overall inappropriate antibiotic prescriptions for all diagnoses trended downward from 26.4% to 16.6% (P = 0.13). Inappropriate prescriptions trended upward in OME from 30.8% to 46.7% (P = 0.34) with clinicians\u27 increased use of watch and wait for this diagnosis. Inappropriate prescribing for AOM and pharyngitis improved from 38.6% to 26.5% (P = 0.03) and 14.5% to 8.8% (P = 0.44), respectively. CONCLUSIONS: Using templates to standardize communication with caregivers, a national collaborative decreased inappropriate antibiotic prescriptions for AOM and had downward trend in inappropriate antibiotic prescriptions for pharyngitis. Clinicians increased the inappropriate use of watch and wait antibiotics for OME. Future studies should evaluate barriers to the appropriate use of delayed antibiotic prescriptions

Transcriptional coactivation by EHMT2 restricts glucocorticoid-induced insulin resistance in a study with male mice

The classical dogma of glucocorticoid-induced insulin resistance is that it is caused by the transcriptional activation of hepatic gluconeogenic and insulin resistance genes by the glucocorticoid receptor (GR). Here, we find that glucocorticoids also stimulate the expression of insulin-sensitizing genes, such as Irs2. The transcriptional coregulator EHMT2 can serve as a transcriptional coactivator or a corepressor. Using male mice that have a defective EHMT2 coactivation function specifically, we show that glucocorticoid-induced Irs2 transcription is dependent on liver EHMT2's coactivation function and that IRS2 play a key role in mediating the limitation of glucocorticoid-induced insulin resistance by EHMT2's coactivation. Overall, we propose a model in which glucocorticoid-regulated insulin sensitivity is determined by the balance between glucocorticoid-modulated insulin resistance and insulin sensitizing genes, in which EHMT2 coactivation is specifically involved in the latter process

Transcriptional coactivation by EHMT2 restricts glucocorticoid-induced insulin resistance in a study with male mice

Abstract The classical dogma of glucocorticoid-induced insulin resistance is that it is caused by the transcriptional activation of hepatic gluconeogenic and insulin resistance genes by the glucocorticoid receptor (GR). Here, we find that glucocorticoids also stimulate the expression of insulin-sensitizing genes, such as Irs2. The transcriptional coregulator EHMT2 can serve as a transcriptional coactivator or a corepressor. Using male mice that have a defective EHMT2 coactivation function specifically, we show that glucocorticoid-induced Irs2 transcription is dependent on liver EHMT2’s coactivation function and that IRS2 play a key role in mediating the limitation of glucocorticoid-induced insulin resistance by EHMT2’s coactivation. Overall, we propose a model in which glucocorticoid-regulated insulin sensitivity is determined by the balance between glucocorticoid-modulated insulin resistance and insulin sensitizing genes, in which EHMT2 coactivation is specifically involved in the latter process

Candida auris in Healthcare Facilities, New York, USA, 2013–2017

Candida auris is an emerging yeast that causes healthcare-associated infections. It can be misidentified by laboratories and often is resistant to antifungal medications. We describe an outbreak of C. auris infections in healthcare facilities in New York City, New York, USA. The investigation included laboratory surveillance, record reviews, site visits, contact tracing with cultures, and environmental sampling. We identified 51 clinical case-patients and 61 screening case-patients. Epidemiologic links indicated a large, interconnected web of affected healthcare facilities throughout New York City. Of the 51 clinical case-patients, 23 (45%) died within 90 days and isolates were resistant to fluconazole for 50 (98%). Of screening cultures performed for 572 persons (1,136 total cultures), results were C. auris positive for 61 (11%) persons. Environmental cultures were positive for samples from 15 of 20 facilities. Colonization was frequently identified during contact investigations; environmental contamination was also common