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As of March 2021, coronavirus disease (COVID-19) had led to >500,000 deaths in the United States, and the state of Tennessee had the fifth highest number of cases per capita. We reviewed the Tennessee Department of Health COVID-19 surveillance and chart-abstraction data during March 15‒August 15, 2020. Patients who died from COVID-19 were more likely to be older, male, and Black and to have underlying conditions (hereafter comorbidities) than case-patients who survived. We found 30.4% of surviving case-patients and 20.3% of deceased patients had no comorbidity information recorded. Chart-abstraction captured a higher proportion of deceased case-patients with >1 comorbidity (96.3%) compared with standard surveillance deaths (79.0%). Chart-abstraction detected higher rates of each comorbidity except for diabetes, which had similar rates among standard surveillance and chart-abstraction. Investing in public health data collection infrastructure will be beneficial for the COVID-19 pandemic and future disease outbreaks.

BackgroundCarbapenem-resistant Enterobacterales (CRE) are among the most concerning antibiotic resistance threats due to high rates of multidrug resistance, transmissibility in healthcare settings, and high mortality rates. We evaluated the potential for regional genomic surveillance to trackblaKPC-carrying CRE (KPC-CRE) transmission across healthcare facilities in three U.S. states.MethodsClinical isolates were collected from Connecticut (CT; 2017-2018), Minnesota (MN; 2012-2018), and Tennessee (TN; 2016-2017) through the U.S. Centers for Disease Control and Prevention’s Multi-site Gram-negative Surveillance Initiative and additional surveillance. KPC-CRE isolates were whole-genome sequenced, and case report data on patient comorbidities, healthcare utilization, and interfacility patient transfer were extracted.FindingsIn CT, most KPC-CRE isolates showed evidence of importation from outside the state, with limited local transmission. In MN, cases were mainly from sporadic importation and transmission ofblaKPC-carryingKlebsiella pneumoniae(KPC-Kp) ST258, and clonal expansion of an imported epidemic lineage ofblaKPC-carryingEnterobacter hormaechei(KPC-Ec) ST171 primarily at a single focal facility and its satellite facilities. In TN, KPC-Kp ST258, and more recently emerged KPC-Kp ST307 and KPC-Eh ST114 were most common, with largely non-overlapping facility networks mediating the spread of ST258 versus ST307 and ST114.ConclusionsThe underlying processes driving KPC-CRE burden can differ substantially across regions, and different STs can spread via distinct pathways within a region. Integrating genomic and epidemiological data from regional surveillance, and information on interfacility patient transfers, can provide insights to target interventions.

Background: Carbapenem-resistant Enterobacteriaceae (CRE) are an urgent public health threat associated with poor patient outcomes. CRE that produce carbapenemase (CP-CRE) are of particular concern because the mechanism-conferring genes in plasmids can be transferred to other bacteria. CRE are reportable in Tennessee (TN); isolate submission is required for CP production and resistance mechanism testing. We aimed to compare patient characteristics and outcomes between CP-CRE and non–CP-CRE patients to guide potential public health interventions. Methods: A retrospective cohort study to compare 30-day mortality, and clinical characteristics of CP-CRE to non–CP-CRE patients was conducted. Laboratory data were gathered from CRE isolates of Tennessee residents from July 1, 2015, to June 30, 2018. The most recent Council of State and Territorial Epidemiologists CRE and CP-CRE case definition was used to confirm and classify cases. Healthcare exposures within 1 year prior to onset, demographic characteristics, and clinical characteristics were obtained by linking surveillance data with the inpatient and outpatient Tennessee hospital discharge data. Cases were also matched with Tennessee vital statistics data to determine all-cause 30-day mortality from the event date. We evaluated risk ratios of 30-day mortality with a multivariable regression model. Results: Among 1,034 CRE cases that had at least 1 isolate submitted to public health, 445 (43.0%) were CP-CRE and 589 (57.0%) were non–CP-CRE. Among CP-CRE isolates, the blaKPC gene was found in 434 (98.9%). CP-CRE cases were more likely to have isolates from normally sterile sites, to have an organism with elevated resistance to meropenem (minimum inhibitory concentration, >16 µg/mL), to have prior admission to a long-term acute-care hospital, and to live in a nursing home (all P < .001). Also, 77 CP-CRE cases (17.3%) and 56 non–CP-CRE cases (9.6%) died within 30 days of infection onset. The risk of 30-day mortality was 57% higher for CP-CRE (adjusted risk ratio, 1.57; 95% CI:, 1.10–2.23) compared to non–CP-CRE patients after adjusting for comorbidities, nursing home residence, and prior healthcare exposures. Conclusions: CP-CRE cases had poorer outcomes than non–CP-CRE cases. This may be related in part to a higher proportion of sterile site infections among CP-CRE cases; our study was underpowered to analyze this subpopulation of sterile site cases. We plan to continue monitoring and performing analyses as mortality and hospital discharge data from more recent years become available and as more cases accumulate.Funding: NoneDisclosures: None

Leukopenia is a serious, frequent side effect associated with azathioprine use. Currently, we use thiopurine methyltransferase (TPMT) testing to predict leukopenia in patients taking azathioprine. We hypothesized that a risk score incorporating additional clinical and genetic variables would improve the prediction of azathioprine-associated leukopenia. In the discovery phase, we developed four risk score models: (1) age, sex, and TPMT metabolizer status; (2) model 1 plus additional clinical variables; (3) sixty candidate single nucleotide polymorphisms; and (4) model 2 plus model 3. The area under the receiver-operating-characteristic curve (AUC) of the risk scores was 0.59 (95%CI: 0.54-0.64), 0.75 (0.71-0.80), 0.66 (0.61-0.71), and 0.78 (0.74-0.82) for models one, two, three and four, respectively. During the replication phase, models two and four (AUC=0.64, 95%CI: 0.59-0.70 and AUC=0.63, 95%CI: 0.58-0.69, respectively) were significant in an independent group. Compared to TPMT testing alone, additional genetic and clinical variables improve the prediction of azathioprine-associated leukopenia.

Background: The Tennessee (TN) Department of Health (TDH) has been identifying clusters of reportable conditions using the Electronic Surveillance System for Early Notification of Community-Based Epidemics (ESSENCE), a cluster detection method using space-time scan permutation statistics based on patient ZIP code. CRE are reportable in Tennessee; isolate submission is required for carbapenemase (CP) production and resistance mechanism (eg, KPC gene) testing. The Council for Outbreak Response: Healthcare-Associated Infections (HAI) and Antimicrobial-Resistant (AR) Pathogens (CORHA) released proposed thresholds of reporting CRE to public health. Thresholds vary by healthcare facility type and regional epidemiology. The TDH HAI/AR program currently runs a daily automated SAS code using the CORHA reporting threshold to help public health identify suspect KPC clusters. We evaluated our rule-based CORHA method against 2 space-time statistic-based methods for KPC cluster detection in Tennessee. Methods: Simulations for each cluster detection method were performed using retrospective CP-CRE surveillance data for 2018. Simulations were conducted using (1) CORHA reporting thresholds by facility case count to flag clusters of 2 or more cases within 28 days, (2) ESSENCE using patient residence ZIP code and the earliest of collection date or symptom onset date as is used for other reportable conditions in Tennessee, and (3) a modified space-time statistical method using SaTScan in which reporting facility, rather than a geographic location, was used as space variable to detect within-facility clusters within 1–28 days. We compared the number and overlap of cases and clusters identified with each method. Univariate logistic regression with CORHA flagging as predictor and flagging by each ESSENCE or CORHA method as outcome variables, were used to compare cases tagged by each method pair, respectively. Results: Of 183 KPC CP-CRE cases, 54 (30.6%) were flagged as part of suspect clusters by at least 1 method. Simulations generated 16 alerts (36 cases) using CORHA, 10 clusters (25 cases) using modified SaTScan, and 10 clusters (20 cases) using standard ESSENCE protocol. Among KPC CP-CRE cases flagged by CORHA, 12 (33.3%) were also flagged by modified SaTScan and 2 (5%) by ESSENCE. A case flagged using CORHA method has 5.15 (95% CI, 2.10–12.64) times higher odds of also being flagged by the modified SaTScan method compared to cases not flagged by CORHA. Conclusions: An algorithm based on CORHA thresholds for reporting CRE to public health had strong agreement with modified SaTScan, a space-time method. We intend to explore the extension of the time interval for ESSENCE.Funding: NoneDisclosures: None

OBJECTIVE: Hypertension is highly prevalent in patients with rheumatoid arthritis (RA). In other populations, high sodium (Na(+)) and low potassium (K(+)) intake are associated with an increased risk of hypertension, and in animal models a high salt intake exacerbated arthritis. Patients with RA have many comorbidities associated with salt-sensitivity, but their salt intake and its relationship to blood pressure and inflammation is unknown. METHODS: Using the Kawasaki formula, Na(+) and K(+) urinary excretion (reflecting intake) was estimated in 166 patients with RA and 92 controls, frequency matched for age, sex, and race. Inflammatory markers and disease activity were measured in RA patients. We tested the associations between blood pressure and Na(+) and K(+) excretion. RESULTS: Estimated 24 hour Na(+) excretion was similarly high in both RA (median [IQR] 5.1 g, [3.9 g–6.6 g]) and controls (4.9 g, [4.0 g–6.5 g]), p=0.9; despite higher rates of hypertension in RA (54% vs. 39%, p=0.03). The Na(+):K(+) excretion ratio was significantly higher in RA (2.0 [1.6–2.4]) vs. 1.7 [1.5–2.1]), p=0.02] compared to controls. In RA, a lower K(+) excretion was inversely correlated with diastolic blood pressure (adjusted-β= -1.79, p=0.04). There was no significant association between Na(+) or K(+) excretion and inflammatory markers. CONCLUSIONS: Despite a similar Na(+) excretion, patients with RA had higher rates of hypertension than controls, a finding compatible with increased salt sensitivity. Patients with RA had a lower Na(+):K(+) excretion ratio than controls, and lower K(+) excretion was associated with higher diastolic blood pressure in RA.