Introduction: Vancomycin-associated acute kidney injury (V-AKI) is a common adverse reaction; however, there is currently no method to systematically monitor its incidence. We previously developed and internally validated an electronic algorithm to identify cases of V-AKI using structured electronic health record data at the Johns Hopkins Hospital, which demonstrated excellent agreement with chart review (percent agreement 92.5%; weighted kappa coefficient 0.95), as well as excellent sensitivity (89.7%) and specificity (98.2%) in detecting at least possible V-AKI events. The objective of this study was to evaluate the generalizability of the V-AKI electronic algorithm. Methods: We identified a retrospective cohort of adult and pediatric patients who received ≥1 dose of intravenous vancomycin while admitted to University of Virginia (UVA) Medical Center from 1/2021-1/2023. An increase in creatinine (Cr) of ≥0.3 mg/dL within 48 hours or ≥50% increase in baseline Cr within 7 days, occurring after the first dose and up to 72 hours after the last dose of IV vancomycin, was considered a potential V-AKI event. The electronic algorithm was executed at UVA with only limited contextualization of hospital specific variables (e.g., procedure names). Patients were categorized as excluded/not meeting criteria, or as having an unlikely, possible or probable V-AKI event using a causality framework. A random subset of the cohort underwent chart review by a blinded reviewer for external validation. Percent agreement and a weighted kappa coefficient were calculated. The sensitivity and specificity in identifying at least possible V-AKI events was determined. Results: The electronic algorithm was validated using 200 cases and demonstrated 60.0% percent agreement with chart review (Figure). The weighted kappa coefficient was 0.75. The algorithm was 83.8% sensitive and 71.4% specific in detecting at least possible V-AKI events. Among the 80 discrepant cases, there was only a 1-category difference in 62.5% of cases. The most common reasons for discrepant assessments, which were partly due to inconsistencies in chart review, included disagreement regarding timing of AKI onset (18.6%) and whether renal function returned to baseline (16.3%). Conclusions: An electronic algorithm to identify V-AKI events was successfully implemented at another institution. Although agreement with chart review was only fair, sensitivity in detecting at least possible V-AKI events remained excellent. The electronic algorithm may be useful for systematically and reproducibly identifying V-AKI events across institutions in a scalable manner to inform stewardship interventions. However, further refinement of the algorithm and improvement in consistency of chart review assessments is needed.

Disclosure: Lindsay Donohue: Advisor – Abbvie

Background: Burkholderia multivorans are gram-negative bacteria typically found in water and soil. B. multivorans outbreaks among patients without cystic fibrosis have been associated with exposure to contaminated medical devices or nonsterile aqueous products. Acquisition can also occur from exposure to environmental reservoirs like sinks or other hospital water sources. We describe an outbreak of B. multivorans among hospitalized patients without cystic fibrosis at 2 hospitals within the same healthcare system in California (hospitals A and B) between August 2021 and July 2022. Methods: We defined confirmed case patients as patients without cystic fibrosis hospitalized at hospital A or hospital B between January 2020 to July 2022 with B. multivorans isolated from any body site matching the outbreak strain. We reviewed medical records to describe case patients and to identify common exposures. We evaluated infection control practices and interviewed staff to detect exposures to nonsterile water. Select samples from water, ice, drains, and sink splash zone surfaces were collected and cultured for B. multivorans in March 2022 and July 2022 from both hospitals. Common aqueous products used among case patients were tested for B. multivorans. Genetic relatedness between clinical and environmental samples was determined using random amplified polymorphic DNA (RAPD) and repetitive extragenic palindromic polymerase chain reaction (Rep-PCR). Results: We identified 23 confirmed case patients; 20 (87%) of these were identified at an intensive care unit (ICU) in hospital A. B. multivorans was isolated from respiratory sources in 18 cases (78%). We observed medication preparation items, gloves, and patient care items stored within sink splash zones in ICU medication preparation rooms and patient rooms. Nonsterile water and ice were used for bed baths, swallow evaluations, and ice packs. B. multivorans was cultured from ice and water dispensed from an 11-year-old ice machine in the ICU at hospital A in March 2022 but no other water sources. Additional testing in July 2022 yielded B. multivorans from ice and a drain pan from a new ice machine in the same ICU location at hospital A. All products were negative. Clinical and environmental isolates were the same strain by RAPD and Rep-PCR. Conclusions: The use of nonsterile water and ice from a contaminated ice machine contributed to this outbreak. Water-related fixtures can serve as reservoirs for Burkholderia, posing infection risk to hospitalized and immunocompromised patients. During outbreaks of water-related organisms, such as B. multivorans , nonsterile water and ice use should be investigated as potential sources of transmission and other options should be considered, especially for critically ill patients.

Disclosures: None

Background: Candida auris is a frequently drug-resistant yeast that can cause invasive disease and is easily transmitted in healthcare settings. Pediatric cases are rare in the United States, with <10 reported before 2022. In August 2021, the first C. auris case in Las Vegas was identified in an adult. By May 2022, 117 cases were identified across 16 healthcare facilities, including 3 pediatric cases at an acute-care hospital (ACH) with adult cases, representing the first pediatric cluster in the United States. The CDC and Nevada Division of Public and Behavioral Health (NVDPBH) sought to describe these cases and risk factors for C. auris acquisition. Methods: We defined a case as a patient’s first positive C. auris specimen. We reviewed medical records and infection prevention and control (IPC) practices. Environmental sampling was conducted on high-touch surfaces throughout affected adult and pediatric units. Isolate relatedness was assessed using whole-genome sequencing (WGS). Results: All 3 pediatric patients were born at the facility and had congenital heart defects. All were aged <6 months when they developed C. auris bloodstream infections; 2 developed C. auris endocarditis. One patient died. Patients overlapped in the pediatric cardiac intensive care unit; 2 did not leave between birth and C. auris infection. Mobile medical equipment was shared between adult and pediatric patients; lapses in cleaning and disinfection of shared mobile medical equipment and environmental surfaces were observed, presenting opportunities for transmission. Overall, 32 environmental samples were collected, and C. auris was isolated from 2 specimens from an adult unit without current cases. One was a composite sample from an adult patient’s bed handles, railings, tray table and call buttons, and the second was from an adult lift-assistance device. WGS of specimens from adult and pediatric cases and environmental isolates were in the same genetic cluster, with 2–10 single-nucleotide polymorphisms (SNPs) different, supporting within-hospital transmission. The pediatric cases varied by 0–3 SNPs; at least 2 were highly related. Conclusions: C. auris was likely introduced to the pediatric population from adults via inadequately cleaned and disinfected mobile medical equipment. We made recommendations to ensure adequate cleaning and disinfection and implement monitoring and audits. No pediatric cases have been identified since. This investigation demonstrates transmission can occur between unrelated units and populations and that robust infection prevention and control practices throughout the facility are critical for reducing C. auris environmental burden and limiting transmission, including to previously unaffected vulnerable populations, like children.

Disclosures: None

OBJECTIVES/GOALS: Nearly all thoracic aortic aneurysm patients suffer from hypertension leading to elevated wall tension and abnormal extracellular matrix remodeling. PTSD patients have higher blood pressure both at rest and in response to stimuli. Although stress is associated with cardiovascular disease, the exact mechanism linking the two is still unknown. METHODS/STUDY POPULATION: Adult C57BL/6 mice underwent a PTSD induction protocol consisting of inescapable foot shock followed by single prolonged stress. The mice were assessed incrementally for their PTSD-like phenotype using specific behavioral tests chosen to assess for each of the human criteria of PTSD according to the DSM-V. Tail cuff blood pressure measurements were taken serially throughout the 16-week protocol. At terminal study, thoracic aortic diameter measurements were obtained through digital microscopy and plasma was harvested for cytokine analysis. Thoracic aortic aneurysms (TAA) were induced through periadventitial application of a calcium chloride solution on the descending thoracic aorta in BPH/2J and BPN/3J adult mice. The thoracic aortic diameter was measured at terminal study through digital microscopy. RESULTS/ANTICIPATED RESULTS: Using our PTSD-like mouse model we have demonstrated that PTSD-like mice have significantly higher systolic blood pressure following a reminder of the traumatic event than control mice recapitulating the human phenotype. They also had increased plasma proinflammatory cytokines and larger thoracic aortic diameters than control mice. Although the increased thoracic aortic diameter is not an aneurysm, it suggests ECM remodeling is occurring predisposing the aorta to aneurysm formation. Finally, we have shown that in neurogenic hypertensive mice, TAA formation was accelerated by 12 weeks with roughly 70% dilation at 4 weeks post-TAA induction surgery as compared to roughly a 20% dilation in control mice. DISCUSSION/SIGNIFICANCE: Altogether, these studies reinforce the link between stress and TAA development, and our mouse model will allow for the underlying mechanism to be elucidated. Better understanding of the mechanism linking PTSD and TAA will allow for the creation of novel therapeutics to treat PTSD symptoms while also delaying TAA progression.