An Approach to Improving Compliance of Treatment in Asymptomatic Bacteriuria.

INTRODUCTION: Asymptomatic bacteriuria (ASB) is the presence of bacteria in the urine without attributable signs or symptoms of a urinary tract infection (UTI). This condition is often inappropriately treated per the 2019 Infectious Disease Society of America guidelines. This quality improvement project aimed to reduce improper treatment of ASB via a three-phase spaced repetition approach over a 12-month 2021-2022 period within a Michigan emergency department (ED), targeting 43 ED clinicians. METHODS: During Phase I, a 20-minute teleconference educational intervention was delivered by an Infectious Disease physician and pharmacist. During Phase II, a "hard stop" was implemented within the electronic health record preventing reflex urinalysis culture without indication. During Phase III, a latent period of no intervention took place. The authors' goal was to achieve > 80% compliance to ASB treatment guidelines. RESULTS: Overall compliance after the project initiative was 66.7%, an absolute increase of 16.7% from baseline compliance. Using data from 54 patients, this represented a statistically significant (p = 0.01) increase from baseline but fell short of the target of > 80%. DISCUSSION: Although the authors fell short of their goal of a 30% increase, data from the project suggests a spaced repetition approach to education and workflow changes could be an effective method to increasing medical provider compliance with treatment of ASB. CONCLUSION: Identifying the ideal strategy to change treatment patterns of ED clinicians for ASB to align with guidelines remains key. There is still a need for ongoing efforts in this realm for progress to be made. Keywords: asymptomatic bacteriuria, urinary tract infection, compliance, spaced repetition, antibiotics.

Loss of TRPC2 function in mice alters sex differences in brain regions regulating social behaviors.

The transient receptor potential cation channel 2 (TRPC2) conveys pheromonal information from the vomeronasal organ (VNO) to the brain. Both male and female mice lacking this gene show altered sex-typical behavior as adults. We asked whether TRPC2, highly expressed in the VNO, normally participates in the development of VNO-recipient brain regions controlling mounting and aggression, two behaviors affected by TRPC2 loss. We now report significant effects of TRPC2 loss in both the posterodorsal aspect of the medial amygdala (MePD) and ventromedial nucleus of the hypothalamus (VMH) of male and female mice. In the MePD, a sex difference in neuron number was eliminated by the TRPC2 knockout (KO), but the effect was complex, with fewer neurons in the right MePD of females, and fewer neurons in the left MePD of males. In contrast, MePD astrocytes were unaffected by the KO. In the ventrolateral (vl) aspect of the VMH, KO females were like wildtype (WT) females, but TRPC2 loss had a dramatic effect in males, with fewer neurons than WT males and a smaller VMHvl overall. We also discovered a glial sex difference in VMHvl of WTs, with females having more astrocytes than males. Interestingly, TRPC2 loss increased astrocyte number in males in this region. We conclude that TRPC2 normally participates in the sexual differentiation of the mouse MePD and VMHvl. These changes in two key VNO-recipient regions may underlie the effects of the TRPC2 KO on behavior.