COVID-19 Outbreaks in Correctional Facilities with Work-Release Programs - Idaho, July-November 2020.

As of April 16, 2021, U.S. correctional and detention facilities reported 399,631 cases of COVID-19 in incarcerated persons, resulting in 2,574 deaths (1). During July 14-November 30, 2020, COVID-19 was diagnosed in 382 persons incarcerated in Idaho correctional facilities with work-release programs. Work-release programs (which place incarcerated persons in community businesses) have social and economic benefits, but might put participants at increased risk for bidirectional transmission of SARS-CoV-2, the virus that causes COVID-19. The Idaho Department of Correction (IDOC) operates 13 state-run correctional facilities, including six low-security facilities dedicated to work-release programs. This report describes COVID-19 outbreaks in five IDOC facilities with work-release programs,* provides the mitigation strategies that IDOC implemented, and describes the collaborative public health response. As of November 30, 2020, 382 outbreak-related COVID-19 cases were identified among incarcerated persons in five Idaho correctional facilities with work-release programs; two outbreaks were linked to food processing plants. Mitigation strategies that helped to control outbreaks in IDOC facilities with work-release programs included isolation of persons with COVID-19, identification and quarantine of close contacts, mass testing of incarcerated persons and staff members, and temporary suspension of work-release programs. Implementation of public health recommendations for correctional and detention facilities with work-release programs, including mass testing and identification of high-risk work sites, can help mitigate SARS-CoV-2 outbreaks. Incarcerated persons participating in work-release should be included in COVID-19 vaccination plans.

An observational study of haemostatic changes, leptin and soluble endoglin during pregnancy in women with different BMIs.

Obesity increases the risk of venous thromboembolism (VTE) in pregnancy. The pathogenesis is hypothesized to be because of multiple factors including prothrombotic changes, but there has been minimal haemostatic research looking at the combined state of obesity and pregnancy. We aimed to determine whether variation in BMI in the third trimester of pregnancy was associated with prothrombotic changes. We recruited 110 women into four groups depending on their BMI at first antenatal appointment: normal, overweight, obese and morbidly obese. Women with increased risk of VTE, and/or receiving thromboprophylaxis, and/or more than 35 years and those in labour were excluded. Thromboelastography, platelet count, prothrombin time, activated partial thromboplastin time, fibrinogen, prothrombin fragment 1 + 2, free and total protein S, plasminogen activator inhibitor type 1, tissue plasminogen activator antigen, D-dimers, soluble endoglin and leptin levels were measured. There were no significant differences in haemostatic measures with changing BMI. There was a positive correlation between BMI and both platelet count (correlation coefficient r = 0.214, P = 0.036) and leptin (r = 0.435, P < 0.001), but only leptin had a significant association with BMI once adjusted for age, gestation and parity. Despite recruitment into the morbidly obese group being suboptimal, these findings suggest that in pregnancy, the increased risk of VTE seen in obese mothers is not mediated through increased prothrombotic changes, and thus the increased risk of VTE in obese pregnant women may be because of other mechanisms, for example endothelial dysfunction, inflammation and venous stasis.