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AbstractBackground:Approximately 10% of patients report allergies to penicillin, yet >90% of these allergies are not clinically significant. Patients reporting penicillin allergies are often treated with second-line, non–β-lactam antibiotics that are typically broader spectrum and more toxic. Orders for β-lactam antibiotics for these patients trigger interruptive alerts, even when there is electronic health record (EHR) data indicating prior β-lactam exposure.Objective:To describe the rate that interruptive penicillin allergy alerts display for patients who have previously had a β-lactam exposure.Design:Retrospective EHR review from January 2013 through June 2018.Setting:A nonprofit health system including 1 large tertiary-care medical center, a smaller associated hospital, 2 emergency departments, and ˜250 outpatient clinics.Participants:All patients with EHR-documented of penicillin allergies.Methods:We examined interruptive penicillin allergy alerts and identified the number and percentage of alerts that display for patients with a prior administration of a penicillin class or other β-lactam antibiotic.Results:Of 115,081 allergy alerts that displayed during the study period, 8% were displayed for patients who had an inpatient administration of a penicillin antibiotic after the allergy was noted, and 49% were displayed for patients with a prior inpatient administration of any β-lactam.Conclusions:Many interruptive penicillin allergy alerts display for patients who would likely tolerate a penicillin, and half of all alerts display for patients who would likely tolerate another β-lactam.

AbstractIn patients with β-lactam allergies, administration of non–β-lactam surgical prophylaxis is associated with increased risk of infection. Although many patients self-report β-lactam allergies, most are unconfirmed or mislabeled. A quality improvement process, utilizing a structured β-lactam allergy tool, was implemented to improve the utilization of preferred β-lactam surgical prophylaxis.

ABSTRACTFrancisella tularensisis a Gram-negative bacterium and the causative agent of the disease tularemia. Escape of F. tularensisfrom the phagosome into the cytosol of the macrophage triggers the activation of the AIM2 inflammasome through a mechanism that is not well understood. Activation of the AIM2 inflammasome results in autocatalytic cleavage of caspase-1, resulting in the processing and secretion of interleukin-1ß (IL-1ß) and IL-18, which play a crucial role in innate immune responses to F. tularensis. We have identified the 5-formyltetrahydrofolate cycloligasegene (FTL_0724) as being important for F. tularensislive vaccine strain (LVS) virulence. Infection of mice in vivowith a F. tularensisLVS FTL_0724mutant resulted in diminished mortality compared to infection of mice with wild-type LVS. The FTL_0724mutant also induced increased inflammasome-dependent IL-1ß and IL-18 secretion and cytotoxicity in macrophages in vitro. In contrast, infection of macrophages with a F. tularensisLVS rluD pseudouridine synthase(FTL_0699) mutant resulted in diminished IL-1ß and IL-18 secretion from macrophages in vitrocompared to infection of macrophages with wild-type LVS. In addition, the FTL_0699mutant was not attenuated in vivo. These findings further illustrate that F. tularensisLVS possesses numerous genes that influence its ability to activate the inflammasome, which is a key host strategy to control infection with this pathogen in vivo.