Jails and prisons are exceptionally susceptible to viral outbreaks, such as severe acute respiratory syndrome coronavirus 2. The USA has extremely high rates of incarceration and COVID-19 is causing an urgent health crisis in correctional facilities and detention centres. Epidemics happening in prisons are compounding the elevated risks that COVID-19 poses to people of colour, older people, and those with comorbidities. Intersectoral community re-entry efforts in the USA and other countries have shown that releasing people from correctional facilities as a pandemic-era public health intervention is safe and can support both public safety and community rebuilding. Therefore, substantial decarceration in the USA should be initiated. A point of focus for such efforts is that many people in prison are serving excessively long sentences and pose acceptable safety risks for release. Properly managed, correctional depopulation will prevent considerable COVID-19 morbidity and mortality and reduce prevailing socioeconomic and health inequities.

A rapidly emerging global outbreak of monkeypox virus infection (MPXV) in over 50 non-endemic countries was identified in May 2022. We report the case and images of a patient with MPXV presenting with genital lesions later complicated by superimposed cellulitis in Colorado, USA. MPXV lesions are susceptible to bacterial superinfection, and with the advent of new cases, the early identification of skin lesions and their evolution during MPXV are imperative for treating clinicians. Clinicians should consider MPXV in differential diagnoses of sexually transmitted diseases presenting with genital lesions.

It is unclear if there is an association between COVID‐19 and cryptococcosis. Therefore, this study aimed to describe the clinical features, risk factors, and outcomes associated with cryptococcosis in hospitalised patients with COVID‐19. The objectives of this study were to determine the incidence of and examine factors associated with cryptococcosis after a diagnosis of COVID‐19. We used TriNetX to identify and sort patients 18 years and older hospitalised with COVID‐19 into two cohorts based on the presence or absence of a diagnosis of cryptococcosis following diagnosis of COVID‐19. Outcomes of interest included the incidence of cryptococcosis following the diagnosis of COVID‐19 as well as the proportion of patients in each group who had underlying comorbidities, received immunomodulatory therapy, required ICU admission or mechanical ventilation (MV), or died. Propensity score matching was used to adjust for confounding. Among 212,479 hospitalised patients with COVID‐19, 65 developed cryptococcosis. The incidence of cryptococcosis following COVID‐19 was 0.022%. Patients with cryptococcosis were more likely to be male and have underlying comorbidities. Among cases, 32% were people with HIV. Patients with cryptococcosis were more likely to have received tocilizumab (p < .0001) or baricitinib (p < .0001), but not dexamethasone (p = .0840). ICU admission (38% vs 29%), MV (23% vs 11%), and mortality (36% vs 14%) were significantly higher among patients with cryptococcosis. Mortality remained elevated after adjusted propensity score matching. Cryptococcosis occurred most often in hospitalised patients with COVID‐19 who had traditional risk factors, comparable to findings in patients without COVID‐19. Cryptococcosis was associated with increased ICU admission, MV, and mortality.

Aims This study aimed to estimate the annual mortality risk and its determinants in chronic Chagas cardiomyopathy. Methods and results We conducted a systematic search in MEDLINE, Web of Science Core Collection, Embase, Cochrane Library, and LILACS. Longitudinal studies published between 1 January 1946 and 24 October 2018 were included. A random‐effects meta‐analysis using the death rate over the mean follow‐up period in years was used to obtain pooled estimated annual mortality rates. Main outcomes were defined as all‐cause mortality, including cardiovascular, non‐cardiovascular, heart failure, stroke, and sudden cardiac deaths. A total of 5005 studies were screened for eligibility. A total of 52 longitudinal studies for chronic Chagas cardiomyopathy including 9569 patients and 2250 deaths were selected. The meta‐analysis revealed an annual all‐cause mortality rate of 7.9% [95% confidence interval (CI): 6.3–10.1; I2 = 97.74%; T2 = 0.70] among patients with chronic Chagas cardiomyopathy. The pooled estimated annual cardiovascular death rate was 6.3% (95% CI: 4.9–8.0; I2 = 96.32%; T2 = 0.52). The annual mortality rates for heart failure, sudden death, and stroke were 3.5%, 2.6%, and 0.4%, respectively. Meta‐regression showed that low left ventricular ejection fraction (coefficient = −0.04; 95% CI: −0.07, −0.02; P = 0.001) was associated with an increased mortality risk. Subgroup analysis based on American Heart Association (AHA) classification revealed pooled estimate rates of 4.8%, 8.7%, 13.9%, and 22.4% (P < 0.001) for B1/B2, B2/C, C, and C/D stages of cardiomyopathy, respectively. Conclusions The annual mortality risk in chronic Chagas cardiomyopathy is substantial and primarily attributable to cardiovascular causes. This risk significantly increases in patients with low left ventricular ejection fraction and those classified as AHA stages C and C/D.

Background: HIV-negative patients have substantial mortality from Pneumocystis jirovecii pneumonia (PJP). We lack predictors of HIV-negative PJP-associated mortality. Objective: We aim to characterize the role of prior corticosteroid exposure in PJP-related mortality. Methods: We queried a global research network to identify adult HIV-negative patients with PJP with or without corticosteroid exposure in the preceding year before diagnosis ( n = 8,021). We performed a propensity score-matched analysis to adjust baseline patient characteristics and analyzed outcomes. We follow-up the results with a multicenter ten years retrospective case-control cohort of HIV-negative patients tested for PJP by PCP Direct Fluorescent Antigen. We used a Cox proportional hazards model for survival analysis. Results: 1822 HIV-negative propensity-scored matched patients with prior corticosteroid exposure had significantly increased 10 weeks (16% versus 9%, p < 0.0001) and one-year mortality after PJP diagnosis (23% versus 14%, p < 0.0001). (1→3)-β-D-glucan (197.6 ± 155.8 versus 63 ± 0 pg/ml, p = 0.014), ferritin levels (1227 ± 2486 versus 768 ± 1060 mcg/l, p = 0.047), lymphopenia (1.5 ± 1.5 versus 2.0 ± 1.6 103 cells/µl, p < 0.0001) and hypoxia (SatO2: 86.7% versus 91.6%, p < 0.0001) were higher or worse in those with prior steroid use. Patients who died were more likely to have previously received dexamethasone (35% versus 16%, p < 0.001) or prednisone (49% versus 29%, p < 0.001). Adjusted Cox proportional-hazard model validation showed an independently increased mortality at 10 weeks (HR: 3.7, CI: 1.5–9.2, p = 0.004) and 1 year (HR: 4.5, CI: 2.0–10.4, p < 0.0001) among HIV-negative patients with previous corticosteroid exposure. Conclusion: Preceding corticosteroids in HIV-negative patients with PJP are associated with higher mortality. A higher fungal burden may influence corticosteroid-mediated mortality. Assessment of PJP prophylaxis must become a standard clinical best practice when instituting corticosteroid therapy courses.