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Background and Aims Coronavirus disease 2019 (COVID‐19) has been associated with acute liver injury (ALI) manifested by increased liver enzymes in reports worldwide. Prevalence of liver injury and associated clinical characteristics are not well defined. We aim to identify the prevalence of and risk factors for development of COVID‐19‐associated ALI in a large cohort in the United States. Approach and Results In this retrospective cohort study, all patients who underwent SARS‐CoV‐2 testing at three hospitals in the NewYork‐Presbyterian network were assessed. Of 3,381 patients, 2,273 tested positive and had higher initial and peak alanine aminotransferase (ALT) than those who tested negative. ALI was categorized as mild if ALT was greater than the upper limit of normal (ULN) but <2 times ULN, moderate if ALT was between 2 and 5 times the ULN, and severe if ALT was >5 times the ULN. Among patients who tested positive, 45% had mild, 21% moderate, and 6.4% severe liver injury (SLI). In multivariable analysis, severe ALI was significantly associated with elevated inflammatory markers, including ferritin (odds ratio [OR], 2.40; P < 0.001) and interleukin‐6 (OR, 1.45; P = 0.009). Patients with SLI had a more severe clinical course, including higher rates of intensive care unit admission (69%), intubation (65%), renal replacement therapy (RRT; 33%), and mortality (42%). In multivariable analysis, peak ALT was significantly associated with death or discharge to hospice (OR, 1.14; P = 0.044), controlling for age, body mass index, diabetes, hypertension, intubation, and RRT. Conclusions ALI is common in patients who test positive for SARS‐CoV‐2, but is most often mild. However, among the 6.4% of patients with SLI, a severe disease course should be anticipated.

In this multicenter, dose-ranging study of maribavir for the treatment of cytomegalovirus (CMV) infections deemed refractory or resistant to current antivirals, 67% of patients achieved clearance of CMV viremia within 6 weeks, with responses maintained for up to 24 weeks.

New Jersey polyomavirus (NJPyV-2013) is a novel polyomavirus that may have tropism for vascular endothelial cells.

Carbapenem-resistant Klebsiella pneumoniae (CRKP) infection is increasing in incidence and is associated with increased mortality in liver transplantation (LT) recipients. We performed a retrospective cohort study of all patients transplanted between January 2010 and January 2013 to identify the incidence and risk factors for post-LT CRKP infection and evaluate the impact of this infection on outcomes in a CRKP-endemic area. We studied 304 recipients, of whom 20 (6.6%) developed CRKP and 36 (11.8%) carbapenem-susceptible Klebsiella pneumoniae (CSKP) infections in the year following LT. Among the 20 recipients with post-LT CRKP infection, 8 (40%) were infected in ≥ 2 sites; 13 (65%) had surgical site–intra-abdominal infections; 12 (60%) had pneumonia; and 3 (15%) had a urinary tract infection. There were 6 patients with a CRKP infection before LT, 5 of whom developed a CRKP infection after LT. Significant risk factors for post-LT CRKP infection in multivariate analysis included laboratory Model for End-Stage Liver Disease at LT (odds ratio [OR], 1.07; P = 0.001), hepatocellular carcinoma (OR, 3.19; P = 0.02), Roux-en-Y biliary choledochojejunostomy (OR, 3.15; P = 0.04), and bile leak (OR, 5.89; P = 0.001). One-year estimated patient survival was 55% (95% confidence interval, 31%–73%), 72% (55%–84%), and 93% (89%–96%), for patients with CRKP, CSKP, and no Klebsiella pneumoniae infection, respectively. In multivariate analysis, CRKP (hazard ratio [HR], 6.92; P < 0.001) and CSKP infections (CSKP, HR, 3.84; P < 0.001), as well as bile leak (HR, 2.10; P = 0.03) were the strongest predictors of post-LT mortality. In an endemic area, post-LT CRKP infection is common, occurring in 6.6% of recipients, and is strongly associated with post-LT mortality. Improved strategies for screening and prevention of CRKP infection are urgently needed.

Background Little is known about the epidemiology of carbapenem-resistant Klebsiella pneumoniae (CRKP) bacteriuria following kidney transplantation. We determined the incidence of post-transplant CRKP bacteriuria in adults who underwent kidney transplant from 2007 to 2010 at two New York City centers. Methods We conducted a case-control study to identify factors associated with CRKP bacteriuria compared to of carbapenem-susceptible K. pneumoniae (CSKP) bacteriuria, assessed whether CRKP bacteriuria was associated with mortality or graft failure, and compared outcomes of treated episodes of CRKP and CSKP bacteriuria. Results Of 1852 transplants, 20 (1.1%) patients developed CRKP bacteriuria. Factors associated with CRKP bacteriuria included receipt of multiple organs (odds ratio [OR] 4.7, 95% confidence interval [CI] = 1.1–20.4), deceased donor allograft (OR 5.9, 95% CI 1.3–26.8), transplant admission length of stay (OR 1.1 per day, 95% CI 1.0–1.1), pre-transplant CRKP infection or colonization (OR 18.3, 95% CI 2.0–170.5), diabetes mellitus (OR 2.8, 95% CI 1.0–7.8), and receipt of antimicrobials other than trimethoprim-sulfamethoxazole (OR 4.3, 95% CI 1.6–11.2). Conclusion Compared to CSKP bacteriuria, CRKP bacteriuria was associated with increased mortality (30% vs. 10%, P = 0.03) but not graft failure. Treated episodes of CRKP bacteriuria were less likely to achieve microbiologic clearance (83% vs. 97%; P = 0.05) and more likely to recur within 3 months (50% vs. 22%, P = 0.02) than CSKP episodes. CRKP bacteriuria after kidney transplant is associated with mortality and antimicrobial failure after treatment.

Objective: To assess the clinical utilization and performance of the FilmArray® Meningitis/Encephalitis (ME) multiplex polymerase chain reaction (PCR) panel in a hospital setting. Background: Rapid diagnosis and treatment of central nervous system (CNS) infections are critical to reduce morbidity and mortality. The ME panel is a Food and Drug Administration (FDA) approved rapid multiplex PCR assay that targets 14 bacteria, viruses, and fungi. Previous studies show an overall agreement of 93–99% between the ME panel and conventional diagnostic testing. However, few studies have evaluated the clinical implementation of the ME assay, which is available for routine use at our institution. Methods: We performed a single center retrospective chart review of inpatients who underwent ME panel testing from August 2016 to May 2017. Clinical, radiologic, and laboratory data were reviewed to determine the clinical significance of results. Indication for lumbar puncture (LP), time to results of the ME panel, and duration of antimicrobial therapy were evaluated. Results: Seven hundred and five inpatients underwent ME testing, of whom 480 (68.1%) had clinical suspicion for CNS infection with 416 (59.0%) receiving empiric antimicrobial treatment for CNS infection. The median time-to-result of the ME panel was 1.5 h (IQR, 1.4–1.7). Overall agreement between the ME panel results and clinico-laboratory assessment was 98.2%. Forty-five patients tested positive by ME, of which 12 (26.6%) were determined likely to be clinically insignificant. Conclusions: Routine availability of the ME panel led to overutilization of diagnostic test ordering, as demonstrated by the fact that over one-third of ME panel tests performed were ordered for patients with little or no suspicion for CNS infection. The median time from LP to ME panel result was 1.5 h (IQR, 1.4–1.7). The ME panel's rapid turn-around time contributed to the overuse of the test. Approximately one-quarter of positive ME results were deemed clinically insignificant, though the impact of these positive results requires additional evaluation. Twenty-four and forty-eight hours after the ME panel resulted, 68 and 25% of patients started on empiric therapy remained on antibiotics, respectively. The median time from diagnosis to discontinuation and/or narrowing of antibiotic coverage was 25.6 h (IQR, 3.6–42.5). Further consideration of the appropriate indications for use of the ME panel in clinical settings is required.

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