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North Carolina (NC) has been experiencing a recent surge in human Lyme disease (LD) cases. Understanding the distribution of tick-borne diseases necessitates understanding the distribution of the ticks that transmit their causative pathogens. Unfortunately, in NC, knowledge on tick distribution is outdated. In this manuscript, we report the results of a state-wide entomologic survey conducted in 42 NC counties by flagging/dragging from spring 2018 to summer 2023.Ixodes scapularisnymphs and adults were screened forBorrelia burgdorferi(the causative agent of LD) and four other tick-borne bacterial pathogens (Anaplasma phagocytophilum,B. mayonii,B. miyamotoi, and Babesia microti) by the Centers for Disease Control and Prevention (CDC). Consistent with current data on human LD cases incidence and distribution, results of this study indicated a range expansion ofI. scapulariswith higher tick densities andB. burgdorferiinfection prevalence now occurring in the Blue Ridge Mountains province of western NC. Temporal analysis ofI. scapularispresence data indicated that this shift is fairly recent (about 10 years). Finally, in the Blue Ridge Mountains we detected a northeast-to-southwest gradient inI. scapularistick andB. burgdorferiinfection prevalence suggesting that this trend is driven by a spread of the northern cladeI. scapularisticks into NC from southwestern Virginia, along the Appalachian Mountains. Other pathogenic bacteria detected inI. scapularisticks includedB. miyamotoiandA. phagocytophilum, that were limited to the Blue Ridge Mountains.These results have important public health implications, including the need for enhanced tick surveillance, updated clinical awareness, and targeted public education in newly affected areas. 

The PEG addition into aqueous electrolytes has an opposite effect on an Fe metal anode compared to a Zn metal anode. 

ABSTRACT Dispersal can affect individual‐level fitness and population‐level ecological and evolutionary processes. Factors that affect dispersal could therefore have important eco‐evolutionary implications. Here, we investigated the extent to which an inflammation and tissue repair response—peritoneal fibrosis—which is known to restrict movement, could influence dispersal by conducting a mark‐recapture experiment in a lake in Alaska with threespine stickleback (Gasterosteus aculatus). A subset of captured stickleback were injected with aluminium phosphate to experimentally induce fibrosis (‘treatment group’), and another subset were injected with saline or received no injection—both of which do not induce fibrosis (‘control group’). We released all fish at one introduction point and re‐sampled stickleback throughout the lake for 8 days. We recaptured 123 individuals (n = 47 fibrosis treatment;n = 76 control) and dissected them to determine fibrosis levels. Overall, fibrosis did not affect dispersal. Some compelling (but not statistically significant) trends suggest that early‐stage inflammation may affect dispersal, providing opportunities for future work. By showing that effects on dispersal are not important side effects of fibrosis, these findings improve our understanding of the ecological implications of immune responses. 

Emerging infectious diseases, biodiversity loss, and anthropogenic environmental change are interconnected crises with massive social and ecological costs. In this Review, we discuss how pathogens and parasites are responding to global change, and the implications for pandemic prevention and biodiversity conservation. Ecological and evolutionary principles help to explain why both pandemics and wildlife die-offs are becoming more common; why land-use change and biodiversity loss are often followed by an increase in zoonotic and vector-borne diseases; and why some species, such as bats, host so many emerging pathogens. To prevent the next pandemic, scientists should focus on monitoring and limiting the spread of a handful of high-risk viruses, especially at key interfaces such as farms and live-animal markets. But to address the much broader set of infectious disease risks associated with the Anthropocene, decision-makers will need to develop comprehensive strategies that include pathogen surveillance across species and ecosystems; conservation-based interventions to reduce human–animal contact and protect wildlife health; health system strengthening; and global improvements in epidemic preparedness and response. Scientists can contribute to these efforts by filling global gaps in disease data, and by expanding the evidence base for disease–driver relationships and ecological interventions. 

Habitat degradation can increase zoonotic disease risks by altering infection dynamics in wildlife and increasing wildlife–human interactions. Bats are an important taxonomic group to consider these effects, because they harbour many relevant zoonotic viruses and have species‐ and context‐dependent responses to degradation that could affect zoonotic virus dynamics. Yet our understanding of the associations between habitat degradation and bat virus prevalence and seroprevalence are limited to a small number of studies, which often differ in the bats or viruses sampled, the study region, and methodology. To develop a broad understanding of the associations between bat viruses and habitat degradation, we conducted an initial phylogenetic meta‐analysis that combines published prevalence and seroprevalence (‘(sero)prevalence') with remote‐sensing habitat degradation data. Our dataset includes 588 unique records of (sero)prevalence across 16 studies, 64 bat species, and five virus families. We quantified the overall strength and direction of the relationship between habitat degradation and bat virus outcomes and tested how this relationship is moderated by the time between habitat degradation and bat sampling and by ecological traits of bat hosts while controlling for phylogenetic non‐independence among bat species. We found no effect of degradation on prevalence overall, although a weak effect may exist when forest loss occurs the year prior to bat sampling. In contrast, we detected a negative but weak association between degradation and seroprevalence overall that was strengthened when forest loss occurred the year prior to bat sampling. No bat traits that we investigated interacted with habitat degradation to impact virus outcomes, suggesting observed trends are independent of these traits. Biases in our initial dataset highlight opportunities for future work; prevalence was highly zero‐inflated, and seroprevalence was dominated byDesmodus rotundusand rabies virus. These findings and subsequent analyses will improve our understanding of how global change affects host–pathogen dynamics. 

The accelerating pace of emerging zoonotic diseases in the twenty-first century has motivated cross-disciplinary collaboration on One Health approaches, combining microbiology, veterinary and environmental sciences, and epidemiology for outbreak prevention and mitigation. Such outbreaks are often caused by spillovers attributed to human activities that encroach on wildlife habitats and ecosystems, such as land use change, industrialized food production, urbanization and animal trade. While the origin of anthropogenic effects on animal ecology and biogeography can be traced to the Late Pleistocene, the archaeological record—a long-term archive of human–animal–environmental interactions—has largely been untapped in these One Health approaches, thus limiting our understanding of these dynamics over time. In this review, we examine how humans, as niche constructors, have facilitated new host species and ‘disease-scapes’ from the Late Pleistocene to the Anthropocene, by viewing zooarchaeological, bioarchaeological and palaeoecological data with a One Health perspective. We also highlight how new biomolecular tools and advances in the ‘-omics’ can be holistically coupled with archaeological and palaeoecological reconstructions in the service of studying zoonotic disease emergence and re-emergence. 

Large carnivores (order Carnivora) are among the world's most threatened mammals due to a confluence of ecological and social forces that have unfolded over centuries. Combining specimens from natural history collections with documents from archival records, we reconstructed the factors surrounding the extinction of the California grizzly bear (Ursus arctos californicus), a once-abundant brown bear subspecies last seen in 1924. Historical documents portrayed California grizzlies as massive hypercarnivores that endangered public safety. Yet, morphological measurements on skulls and teeth generate smaller body size estimates in alignment with extant North American grizzly populations (approx. 200 kg). Stable isotope analysis (δ¹³C,δ¹⁵N) of pelts and bones (n= 57) revealed that grizzlies derived less than 10% of their nutrition from terrestrial animal sources and were therefore largely herbivorous for millennia prior to the first European arrival in this region in 1542. Later colonial land uses, beginning in 1769 with the Mission era, led grizzlies to moderately increase animal protein consumption (up to 26% of diet), but grizzlies still consumed far less livestock than otherwise claimed by contemporary accounts. We show how human activities can provoke short-term behavioural shifts, such as heightened levels of carnivory, that in turn can lead to exaggerated predation narratives and incentivize persecution, triggering rapid loss of an otherwise widespread and ecologically flexible animal. 

ABSTRACT We present the complete chloroplast genome of the eelgrassZostera pacificafrom Monterey, California. The genome is circular and 144,675  bp in length. It consists of 82 protein-coding, 31 transfer RNA, and 8 ribosomal RNA genes and is 99.44%–99.42% similar in nucleotide pairwise identity to the closely related speciesZostera marina.