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Uncovering the genetic and evolutionary basis of local adaptation is a major focus of evolutionary biology. The recent development of cost-effective methods for obtaining high-quality genome-scale data makes it possible to identify some of the loci responsible for adaptive differences among populations. Two basic approaches for identifying putatively locally adaptive loci have been developed and are broadly used: one that identifies loci with unusually high genetic differentiation among populations (differentiation outlier methods) and one that searches for correlations between local population allele frequencies and local environments (genetic-environment association methods). Here, we review the promises and challenges of these genome scan methods, including correcting for the confounding influence of a species’ demographic history, biases caused by missing aspects of the genome, matching scales of environmental data with population structure, and other statistical considerations. In each case, we make suggestions for best practices for maximizing the accuracy and efficiency of genome scans to detect the underlying genetic basis of local adaptation. With attention to their current limitations, genome scan methods can be an important tool in finding the genetic basis of adaptive evolutionary change.

Plague is a highly virulent disease believed to have killed millions during three historic human pandemics. Worldwide, it remains a threat to humans and is a potential agent of bioterrorism. Dissemination of Yersinia pestis, the etiological agent of plague, by blocked fleas has been the accepted paradigm for flea-borne transmission. However, this mechanism, which requires a lengthy extrinsic incubation period before a short infectious window often followed by death of the flea, cannot sufficiently explain the rapid rate of spread that typifies plague epidemics and epizootics. Inconsistencies between the expected rate of spread by blocked rat fleas and that observed during the Black Death has even caused speculation that plague was not the cause of this medieval pandemic. We used the primary vector to humans in North America, Oropsylla montana, which rarely becomes blocked, as a model for studying alternative flea-borne transmission mechanisms. Our data revealed that, in contrast to the classical blocked flea model, O. montana is immediately infectious, transmits efficiently for at least 4 d postinfection (early phase) and may remain infectious for a long time because the fleas do not suffer block-induced mortality. These factors match the criteria required to drive plague epizootics as defined by recently published mathematical models. The scenario of efficient early-phase transmission by unblocked fleas described in our study calls for a paradigm shift in concepts of how Y. pestis is transmitted during rapidly spreading epizootics and epidemics, including, perhaps, the Black Death.

Epidemics of chronic wasting disease (CWD) of North American Cervidae have potential to harm ecosystems and economies. We studied a migratory population of mule deer (Odocoileus hemionus) affected by CWD for at least three decades using a Bayesian framework to integrate matrix population and disease models with long-term monitoring data and detailed process-level studies. We hypothesized CWD prevalence would be stable or increase between two observation periods during the late 1990s and after 2010, with higher CWD prevalence making deer population decline more likely. The weight of evidence suggested a reduction in the CWD outbreak over time, perhaps in response to intervening harvest-mediated population reductions. Disease effects on deer population growth under current conditions were subtle with a 72% chance that CWD depressed population growth. With CWD, we forecasted a growth rate near one and largely stable deer population. Disease effects appear to be moderated by timing of infection, prolonged disease course, and locally variable infection. Long-term outcomes will depend heavily on whether current conditions hold and high prevalence remains a localized phenomenon.

We lack a clear understanding of the enzootic maintenance of the bacterium (Yersinia pestis) that causes plague and the sporadic epizootics that occur in its natural rodent hosts. A key to elucidating these epidemiological dynamics is determining the dominant transmission routes of plague. Plague can be acquired from the bites of infectious fleas (which is generally considered to occur via a blocked flea vector), inhalation of infectious respiratory droplets, or contact with a short-term infectious reservoir. We present results from a plague modeling approach that includes transmission from all three sources of infection simultaneously and uses sensitivity analysis to determine their relative importance. Our model is completely parameterized by using data from the literature and our own field studies of plague in the black-tailed prairie dog (Cynomys ludovicianus). Results of the model are qualitatively and quantitatively consistent with independent data from our field sites. Although infectious fleas might be an important source of infection and transmission via blocked fleas is a dominant paradigm in the literature, our model clearly predicts that this form of transmission cannot drive epizootics in prairie dogs. Rather, a short-term reservoir is required for epizootic dynamics. Several short-term reservoirs have the potential to affect the prairie dog system. Our model predictions of the residence time of the shortterm reservoir suggest that other small mammals, infectious prairie dog carcasses, fleas that transmit plague without blockage of the digestive tract, or some combination of these three are the most likely of the candidate infectious reservoirs.

Host populations for the plague bacterium, Yersinia pestis, are highly variable in their response to plague ranging from near deterministic extinction (i.e., epizootic dynamics) to a low probability of extinction despite persistent infection (i.e., enzootic dynamics). Much of the work to understand this variability has focused on specific host characteristics, such as population size and resistance, and their role in determining plague dynamics. Here, however, we advance the idea that the relative importance of alternative transmission routes may vary causing shifts from epizootic to enzootic dynamics. We present a model that incorporates host and flea ecology with multiple transmission hypotheses to study how transmission shifts determine population responses to plague. Our results suggest enzootic persistence relies on infection of an off-host flea reservoir and epizootics rely on transiently maintained flea infection loads through repeated infectious feeds by fleas. In either case, early-phase transmission by fleas (i.e., transmission immediately following an infected blood meal) has been observed in laboratory studies, and we show that it is capable of driving plague dynamics at the population level. Sensitivity analysis of model parameters revealed that host characteristics (e.g., population size and resistance) vary in importance depending on transmission dynamics, suggesting that host ecology may scale differently through different transmission routes enabling prediction of population responses in a more robust way than using either host characteristics or transmission shifts alone.

Interdisciplinary approaches are merited when attempting to understand the complex and idiosyncratic processes driving the spillover of pathogens from wildlife and vector species to human populations. Public health data are often available for zoonotic pathogens but can lead to erroneous conclusions if the data have been spatially or temporally aggregated. As an illustration, we use human Lyme disease incidence data as a case study to examine correlations between mammalian biodiversity, fried chicken restaurants and obesity rates on human disease incidence. We demonstrate that Lyme disease incidence is negatively correlated with mammalian biodiversity, the abundance of fried chicken restaurants and obesity rates. We argue, however, that these correlations are spurious, representing both an ‘ecologic fallacy’ and Simpson’s paradox, and are generated by the use of aggregated data. We argue that correlations based on aggregated data across large spatial scales must be rigorously examined before being invoked as proof of disease ecology theory or as a rationale for public health policy.

Modern population genetics underwent a major paradigm shift during the last decade of the 20th century with the discovery that thousands of genes of known function and position in a genome can be analyzed simultaneously in a single individual. The impact of this technology on insect population genetics is potentially profound. Sampling distributions of genetic statistics can now be derived from many individual loci or among many segregating sites within a gene. Inferences regarding random mating, gene flow, effective population sizes, disequilibrium, and relatedness among populations can now be based on patterns of variation at many loci. More importantly, genome-wide sampling enables population geneticists to distinguish effects that act on the whole genome from those that act on individual loci or nucleotides. We introduce the term \"population genomics\" to describe the process of simultaneous sampling of numerous variable loci within a genome and the inference of locus-specific effects from the sample distributions. The four critical assumptions implicit in the population genomics approach are explained in detail. Studies adopting this paradigm are reviewed, and the steps necessary to complete a population genomics study are outlined.

Climate cycling during the Quaternary played a critical role in the diversification of avian lineages in North America, greatly influencing the genetic characteristics of contemporary populations. To test the hypothesis that North American Northern Goshawks (Accipitergentilis) were historically isolated within multiple Late Pleistocene refugia, we assessed diversity and population genetic structure as well as migration rates and signatures of historical demography using mitochondrial control-region data. On the basis of sampling from 24 locales, we found that Northern Goshawks were genetically structured across a large portion of their North American range. Long-term population stability, combined with strong genetic differentiation, suggests that Northern Goshawks were historically isolated within at least three refugial populations representing two regions: the Pacific (CascadesSierra-Vancouver Island) and the Southwest (Colorado Plateau and Jemez Mountains). By contrast, populations experiencing significant growth were located in the Southeast Alaska-British Columbia, Arizona Sky Islands, Rocky Mountains, Great Lakes, and Appalachian bioregions. In the case of Southeast Alaska-British Columbia, Arizona Sky Islands, and Rocky Mountains, Northern Goshawks likely colonized these regions from surrounding refugia. The near fixation for several endemic haplotypes in the Arizona Sky Island Northern Goshawks (A. g apache) suggests long-term isolation subsequent to colonization. Likewise, Great Lakes and Appalachian Northern Goshawks differed significantly in haplotype frequencies from most Western Northern Goshawks, which suggests that they, too, experienced long-term isolation prior to a more recent recolonization of eastern U.S. forests.

Plague is a reemerging, rodent-associated zoonosis caused by the flea-borne bacterium Yersinia pestis. As a vector-borne disease, rates of plague transmission may increase when fleas are abundant. Fleas are highly susceptible to desiccation under hot-dry conditions; we posited that their densities decline during droughts. We evaluated this hypothesis with black-tailed prairie dogs (Cynomys ludovicianus) in New Mexico, June–August 2010–2012. Precipitation was relatively plentiful during 2010 and 2012 but scarce during 2011, the driest spring–summer on record for the northeastern grasslands of New Mexico. Unexpectedly, fleas were 200% more abundant in 2011 than in 2010 and 2012. Prairie dogs were in 27% better condition during 2010 and 2012, and they devoted 287% more time to grooming in 2012 than in 2011. During 2012, prairie dogs provided with supplemental food and water were in 23% better condition and carried 40% fewer fleas. Collectively, these results suggest that during dry years, prairie dogs are limited by food and water, and they exhibit weakened defenses against fleas. Long-term data are needed to evaluate the generality of whether droughts increase flea densities and how changes in flea abundance during sequences of dry and wet years might affect plague cycles in mammalian hosts.