Climate exerts complex influences on leptospirosis transmission, affecting human behavior, zoonotic host population dynamics, and survival of the pathogen in the environment. Here, we describe the spatiotemporal distribution of leptospirosis incidence reported to China's National Infectious Disease Surveillance System from 2004-2014 in an endemic region in western China, and employ distributed lag models at annual and sub-annual scales to analyze its association with hydroclimatic risk factors and explore evidence for the potential role of a soil reservoir in the transmission of Leptospira spp. More than 97% of the 2,934 reported leptospirosis cases occurred during the harvest season between August and October, and most commonly affected farmers (83%). Using a distributed lag Poisson regression framework, we characterized incidence rate ratios (IRRs) associated with interquartile range increases in precipitation of 3.45 (95% confidence interval 2.57-4.64) over 0-1-year lags, and 1.90 (1.18-3.06) over 0-15-week lags. Adjusting for soil moisture decreased IRRs for precipitation at both timescales (yearly adjusted IRR: 1.05, 0.74-1.49; weekly adjusted IRR: 1.36, 0.72-2.57), suggesting precipitation effects may be mediated through soil moisture. Increased soil moisture was positively associated with leptospirosis at both timescales, suggesting that the survival of pathogenic Leptospira spp. in moist soils may be a critical control on harvest-associated leptospirosis transmission in the study region. These results support the hypothesis that soils may serve as an environmental reservoir and may play a significant yet underrecognized role in leptospirosis transmission.

Individuals with coronavirus disease 2019 (COVID-19) frequently develop neurological symptoms, but the biological underpinnings of these phenomena are unknown. Through single-cell RNA sequencing (scRNA-seq) and cytokine analyses of cerebrospinal fluid (CSF) and blood from individuals with COVID-19 with neurological symptoms, we find compartmentalized, CNS-specific T cell activation and B cell responses. All affected individuals had CSF anti-severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) antibodies whose target epitopes diverged from serum antibodies. In an animal model, we find that intrathecal SARS-CoV-2 antibodies are present only during brain infection and not elicited by pulmonary infection. We produced CSF-derived monoclonal antibodies from an individual with COVID-19 and found that these monoclonal antibodies (mAbs) target antiviral and antineural antigens, including one mAb that reacted to spike protein and neural tissue. CSF immunoglobulin G (IgG) from 5 of 7 patients showed antineural reactivity. This immune survey reveals evidence of a compartmentalized immune response in the CNS of individuals with COVID-19 and suggests a role of autoimmunity in neurologic sequelae of COVID-19.