Main text Land use change (e.g. agriculture, urbanization) is widely recognised to influence zoonotic disease risk and emergence in humans 1,2 , but whether this is underpinned by predictable ecological changes remains unclear 3. In particular, it has been hypothesised that systematic differences in species resilience to human impacts, linked to traits, life histories and phylogeny, might result in habitat disturbance causing predictable changes in potential reservoir host diversity and species composition 4,5. Here, we analyse 6801 ecological assemblages and 376 host species worldwide, controlling for research effort, and show that land use has global and systematic effects on local zoonotic host communities. Known wildlife hosts of human-shared pathogens and parasites overall comprise a significantly greater proportion of local species richness (18%-72% increase) and total abundance (21%-144% increase) in sites under substantial human use (secondary, agricultural and urban ecosystems) than in nearby undisturbed habitats. The magnitude of this effect varies taxonomically and is strongest for rodent, bat and passerine bird zoonotic host species, which may be one factor underpinning the global importance of these taxa as zoonotic reservoirs. Crucially, we further show that mammal species that harbor more pathogens overall (either humanshared or non human-shared) are more likely to occur in human-managed ecosystems, suggesting that these trends may be mediated by ecological or life-history traits that influence both host status and human-tolerance 6,7. Our results suggest that global changes in mode and intensity of land use are creating growing hazardous interfaces between people, livestock and wildlife reservoirs of zoonotic disease. Anthropogenic environmental change impacts many dimensions of human health and wellbeing, including the incidence and emergence of zoonotic and vector-borne diseases 1. Although large-scale research into environmental drivers of disease has mostly focused on climate, there is growing consensus that land use change (conversion of natural habitats to agricultural, urban or otherwise anthropogenic ecosystems) is a globally-significant mediator of human infection risk and disease emergence 2,4. Land use change directly and indirectly drives biodiversity loss, turnover and homogenisation (including through invasions and rare species losses) 8,9 , modifies landscape structure in ways that modulate epidemiological processes (e.g. fragmentation 10 , resource provisioning 11) and can increase human-wildlife

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Background Environmental trade-offs associated with land use-for example, between food security and biodiversity conservation-are crucial dimensions of planetary health. Land use-driven biodiversity change might predictably affect disease risk if reservoir host species are consistently more likely to persist under human disturbance (ie, if ecological communities in modified habitats generally have a higher zoonotic potential than those in unmodified habitats). Such a phenomenon has been observed in specific disease systems, but with substantial change in global land use projected for this century, assessing its global and taxonomic generality would shed light on an important hypothesised driver of environmental synergies or trade-offs between conservation and public health.Methods We collated data on hosts of human parasites and pathogens from the published literature, and combined these with the Projecting Responses of Ecological Diversity in Changing Terrestrial Systems (PREDICTS) global database of local ecological communities and associated land use data. We analysed the effects of land use on host richness and abundance across 7330 sites globally, controlling for disease-related research effort and differences in survey methods.

Improved taxonomic methods are needed to quantify declining populations of insect pollinators. This study devises a high-throughput DNA barcoding protocol for a regional fauna (United Kingdom) of bees (Apiformes), consisting of reference library construction, a proof-of-concept monitoring scheme, and the deep barcoding of individuals to assess potential artefacts and organismal associations. A reference database of Cytochrome Oxidase subunit 1 (cox1) sequences including 92.4% of 278 bee species known from the UK showed high congruence with morphological taxon concepts, but molecular species delimitations resulted in numerous split and (fewer) lumped entities within the Linnaean species. Double tagging permitted deep illumina sequencing of 762 separate individuals of bees from a UK-wide survey. Extracting the target barcode from the amplicon mix required a new protocol employing read abundance and phylogenetic position, which revealed 180 molecular entities of Apiformes identifiable to species. An additional 72 entities were ascribed to mitochondrial pseudogenes based on patterns of read abundance and phylogenetic relatedness to the reference set. Clustering of reads revealed a range of secondary Operational Taxonomic Units (OTUs) in almost all samples, resulting from traces of insect species caught in the same traps, organisms associated with the insects including a known mite parasite of bees, and the common detection of human DNA, besides evidence for low-level cross-contamination in pan traps and laboratory steps. Custom scripts were generated to conduct critical steps of the bioinformatics protocol. The resources built here will greatly aid DNA-based monitoring to inform management and conservation policies for the protection of pollinators.