Epizootic Of Beak Deformities In Alaska: Investigation Of An Emerging Avian Disease

Thesis (Ph.D.) University of Alaska Fairbanks, 2012The sudden appearance of morphological abnormalities in a wild population is often associated with underlying ecological disturbances, including those related to introduction of new pathogens or pollutants. An epizootic of beak deformities recently documented among Black-capped Chickadees (Poecile atricapillus) and other resident bird species in Alaska has raised concern about underlying causes. This dissertation describes results from several recent studies of what we have termed "avian keratin disorder." The primary objectives of the research were to characterize the physiology and pathology of beak deformities and to address specific ecological questions related to this emerging avian disease. In a study of beak growth rates in captive chickadees, I determined that accelerated epidermal growth is the primary physical mechanism by which beak deformities develop and are maintained. Affected birds also exhibited high rates of mortality and skin lesions, suggesting that this disorder significantly compromises individual health. I used radiography, histopathology, and electron microscopy to describe the pathology of avian keratin disorder. As part of this effort, I established baseline information about normal passerine beak and claw structure and developed methods for processing hard-cornified tissues. The suite of lesions that I observed in affected chickadees does not correspond with any known avian diseases, suggesting the presentation of a novel disorder in wild birds. In addition, the detailed characterization of gross and microscopic changes has allowed me to eliminate a number of likely etiologies, including nutritional problems, microbial pathogens, and select toxicants. As a complement to diagnostic pathology, I conducted field studies to investigate possible causes and patterns of occurrence of beak deformities. I used stable isotope analysis to investigate the association between diet and beak deformities. I found that winter dietary patterns differed between chickadees with normal beaks and those with beak deformities, but that such differences are more likely a result than a cause of avian keratin disorder. My field research on Northwestern Crows in Alaska confirmed high prevalence of a nearly identical condition to that observed in chickadees. These findings indicate that avian keratin disorder affects multiple, ecologically-distinct species across a large geographic area. Together, the studies presented in this dissertation provide new insights and identify priority research areas for a rapidly emerging disease in wild birds

A Natural Experiment on the Condition-Dependence of Achromatic Plumage Reflectance in Black-Capped Chickadees

Honest advertisement models posit that only individuals in good health can produce and/or maintain ornamental traits. Even though disease has profound effects on condition, few studies have experimentally tested its effects on trait expression and even fewer have identified a mechanistic basis for these effects. Recent evidence suggests that black and white, but not grey, plumage colors of black-capped chickadees (Poecile atricapillus) are sexually selected. We therefore hypothesized that birds afflicted with avian keratin disorder, a condition that affects the beak and other keratinized tissues, would show reduced expression of black and white, but not grey, color. UV-vis spectrometry of black-capped chickadees affected and unaffected by avian keratin disorder revealed spectral differences between them consistent with this hypothesis. To elucidate the mechanistic bases of these differences, we used scanning electron microscopy (SEM), electron-dispersive x-ray spectroscopy (EDX) and a feather cleaning experiment. SEM showed extreme feather soiling in affected birds, and EDX revealed that this was most likely from external sources. Experimentally cleaning the feathers increased color expression of ornamental feathers of affected, but not unaffected, birds. These data provide strong evidence that black and white color is an honest indicator in chickadees, and that variation in feather dirtiness, likely due to differences in preening behavior is a mechanism for this association

Harmful algal blooms in the Alaskan Arctic: an emerging threat as the ocean warms

© The Author(s), 2022. This article is distributed under the terms of the Creative Commons Attribution License. The definitive version was published in Anderson, D., Fachon, E., Hubbard, K., Lefebvre, K., Lin, P., Pickart, R., Richlen, M., Sheffield, G., & Van Hemert, C. Harmful algal blooms in the Alaskan Arctic: an emerging threat as the ocean warms. Oceanography, 35(2), (2022), https://doi.org/10.5670/oceanog.2022.121.Harmful algal blooms (HABs) present an emerging threat to human and ecosystem health in the Alaskan Arctic. Two HAB toxins are of concern in the region: saxitoxins (STXs), a family of compounds produced by the dinoflagellate Alexandrium catenella, and domoic acid (DA), produced by multiple species in the diatom genus Pseudo-nitzschia. These potent neurotoxins cause paralytic and amnesic shellfish poisoning, respectively, in humans, and can accumulate in marine organisms through food web transfer, causing illness and mortality among a suite of wildlife species. With pronounced warming in the Arctic, along with enhanced transport of cells from southern waters, there is significant potential for more frequent and larger HABs of both types. STXs and DA have been detected in the tissues of a range of marine organisms in the region, many of which are important food resources for local residents. The unique nature of the Alaskan Arctic, including difficult logistical access, lack of response infrastructure, and reliance of coastal populations on the noncommercial acquisition of marine resources for nutritional, cultural, and economic well-being, poses urgent and significant challenges as this region warms and the potential for impacts from HABs expands.The authors acknowledge that the Alaskan Arctic as described here includes the lands and waters of the Inupiaq, Saint Lawrence Island Yupik, and Central Yupik peoples. Funding for DMA, RSP, EF, PL, and MLR was provided by grants from NSF Office of Polar Programs (OPP-1823002 and OPP-1733564) and NOAA’s Arctic Research program (through the Cooperative Institute for the North Atlantic Region [CINAR]; NA14OAR4320158 and NA19OAR4320074), and for DMA, KH, and KAL through NOAA’s Center for Coastal and Ocean Studies ECOHAB Program (NA20NOS4780195). Additional support was provided for DMA, MLR, and EF by the US National Park Service Shared Beringian Heritage Program (P21AC12214-00). We also thank Natalie Renier (WHOI Graphic Services) and Emily Bowers (Northwest Fisheries Science Center) for creating figures. Any use of trade, firm, or product names is for descriptive purposes only and does not imply endorsement by the US Government. This is ECOHAB Contribution number 1007

Epizootic of beak deformities in wild birds: a review of avian keratin disorder worldwide

An epizootic of debilitating beak deformities in wild birds has been documented in recent decades. Avian keratin disorder (AKD) is characterized by overgrowth of beak keratin and was first observed in clusters among Black-capped Chickadees (Poecile atricapillus) in Alaska. The prevalence of beak deformities is higher among Black-capped Chickadees and American Crows (Corvus brachyrhynchos) in Alaska than in any other population ever recorded. Reports of birds with similar beak deformities have also been documented across North America, in South America, and in Europe. We compiled reports from community-science programs, bird monitoring studies, and scientific literature to summarize the current geographic scope and bird species affected by AKD-like beak deformities. From 1946 to 2021, >3,300 community-science observers reported 290 species with beak deformities, comprising >4,000 birds in Alaska, 1,900 elsewhere in North America, and >1,700 from outside of North America. We also examined the occurrence of beak deformities in populations of Red-tailed Hawks (Buteo jamaicensis) in the Pacific Northwest, Red-cockaded Woodpeckers (Dryobates borealis) in North Carolina, and Austral Thrushes (Turdus falcklandii) in Patagonia. Clinical signs of AKD in Black-capped Chickadees have been strongly associated with the occurrence of a novel picornavirus, which has now been detected in multiple species exhibiting morphologically similar beak deformities. Our detailed compilation, including geographic occurrence of individuals and species apparently affected, will help identify research and conservation actions required to evaluate and mitigate impacts of beak deformities on wild birds.Fil: Gerik, Daniel. United States Geological Survey; Estados UnidosFil: Van Hemert, Caroline. United States Geological Survey; Estados UnidosFil: Handel, Collen. United States Geological Survey; Estados UnidosFil: Lawson, Becki. Zoological Society of London. Institute of Zoology; Reino UnidoFil: Walters, Jeff. Virginia Tech University; Estados UnidosFil: Brust, Kerry. Sandhills Ecological Institute; Estados UnidosFil: Prinz, Anna. Sandhills Ecological Institute; Estados UnidosFil: Van Lanen, Andy. Sandhills Ecological Institute; Estados UnidosFil: Schillaci, Jessie. Directorate of Public Works; Estados UnidosFil: Cottrell, Susan. Falcon Research Group; Estados UnidosFil: Anderson, Clifford. Falcon Research Group; Estados UnidosFil: Gorosito, Cristian Andrés. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Patagonia Norte. Centro de Investigación Esquel de Montaña y Estepa Patagónica. Universidad Nacional de la Patagonia "San Juan Bosco". Centro de Investigación Esquel de Montaña y Estepa Patagónica; ArgentinaFil: Cueto, Víctor. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Patagonia Norte. Centro de Investigación Esquel de Montaña y Estepa Patagónica. Universidad Nacional de la Patagonia "San Juan Bosco". Centro de Investigación Esquel de Montaña y Estepa Patagónica; ArgentinaFil: Zylberberg, Maxine. University of California; Estados Unidos20th Alaska Bird ConferenceAnchorageEstados UnidosUS Fish and Wildlife Service's Migratory Bird Management Divisio

Genome-wide interaction study of a proxy for stress-sensitivity and its prediction of major depressive disorder

Individual response to stress is correlated with neuroticism and is an important predictor of both neuroticism and the onset of major depressive disorder (MDD). Identification of the genetics underpinning individual differences in response to negative events (stress-sensitivity) may improve our understanding of the molecular pathways involved, and its association with stress-related illnesses. We sought to generate a proxy for stress-sensitivity through modelling the interaction between SNP allele and MDD status on neuroticism score in order to identify genetic variants that contribute to the higher neuroticism seen in individuals with a lifetime diagnosis of depression compared to unaffected individuals. Meta-analysis of genome-wide interaction studies (GWIS) in UK Biobank (N = 23,092) and Generation Scotland: Scottish Family Health Study (N = 7,155) identified no genome-wide significance SNP interactions. However, gene-based tests identified a genome-wide significant gene, ZNF366, a negative regulator of glucocorticoid receptor function implicated in alcohol dependence (p = 1.48x10-7; Bonferroni-corrected significance threshold p < 2.79x10-6). Using summary statistics from the stress-sensitivity term of the GWIS, SNP heritability for stress-sensitivity was estimated at 5.0%. In models fitting polygenic risk scores of both MDD and neuroticism derived from independent GWAS, we show that polygenic risk scores derived from the UK Biobank stress-sensitivity GWIS significantly improved the prediction of MDD in Generation Scotland. This study may improve interpretation of larger genome-wide association studies of MDD and other stress-related illnesses, and the understanding of the etiological mechanisms underpinning stress-sensitivity

Hair Cortisol in Twins : Heritability and Genetic Overlap with Psychological Variables and Stress-System Genes

A. Palotie on työryhmän jäsen.Hair cortisol concentration (HCC) is a promising measure of long-term hypothalamus-pituitary-adrenal (HPA) axis activity. Previous research has suggested an association between HCC and psychological variables, and initial studies of inter-individual variance in HCC have implicated genetic factors. However, whether HCC and psychological variables share genetic risk factors remains unclear. The aims of the present twin study were to: (i) assess the heritability of HCC; (ii) estimate the phenotypic and genetic correlation between HPA axis activity and the psychological variables perceived stress, depressive symptoms, and neuroticism; using formal genetic twin models and molecular genetic methods, i.e. polygenic risk scores (PRS). HCC was measured in 671 adolescents and young adults. These included 115 monozygotic and 183 dizygotic twin-pairs. For 432 subjects PRS scores for plasma cortisol, major depression, and neuroticism were calculated using data from large genome wide association studies. The twin model revealed a heritability for HCC of 72%. No significant phenotypic or genetic correlation was found between HCC and the three psychological variables of interest. PRS did not explain variance in HCC. The present data suggest that HCC is highly heritable. However, the data do not support a strong biological link between HCC and any of the investigated psychological variables.Peer reviewe

Identification of common genetic risk variants for autism spectrum disorder

Autism spectrum disorder (ASD) is a highly heritable and heterogeneous group of neurodevelopmental phenotypes diagnosed in more than 1% of children. Common genetic variants contribute substantially to ASD susceptibility, but to date no individual variants have been robustly associated with ASD. With a marked sample-size increase from a unique Danish population resource, we report a genome-wide association meta-analysis of 18,381 individuals with ASD and 27,969 controls that identified five genome-wide-significant loci. Leveraging GWAS results from three phenotypes with significantly overlapping genetic architectures (schizophrenia, major depression, and educational attainment), we identified seven additional loci shared with other traits at equally strict significance levels. Dissecting the polygenic architecture, we found both quantitative and qualitative polygenic heterogeneity across ASD subtypes. These results highlight biological insights, particularly relating to neuronal function and corticogenesis, and establish that GWAS performed at scale will be much more productive in the near term in ASD

Dissecting the Shared Genetic Architecture of Suicide Attempt, Psychiatric Disorders, and Known Risk Factors

Background Suicide is a leading cause of death worldwide, and nonfatal suicide attempts, which occur far more frequently, are a major source of disability and social and economic burden. Both have substantial genetic etiology, which is partially shared and partially distinct from that of related psychiatric disorders. Methods We conducted a genome-wide association study (GWAS) of 29,782 suicide attempt (SA) cases and 519,961 controls in the International Suicide Genetics Consortium (ISGC). The GWAS of SA was conditioned on psychiatric disorders using GWAS summary statistics via multitrait-based conditional and joint analysis, to remove genetic effects on SA mediated by psychiatric disorders. We investigated the shared and divergent genetic architectures of SA, psychiatric disorders, and other known risk factors. Results Two loci reached genome-wide significance for SA: the major histocompatibility complex and an intergenic locus on chromosome 7, the latter of which remained associated with SA after conditioning on psychiatric disorders and replicated in an independent cohort from the Million Veteran Program. This locus has been implicated in risk-taking behavior, smoking, and insomnia. SA showed strong genetic correlation with psychiatric disorders, particularly major depression, and also with smoking, pain, risk-taking behavior, sleep disturbances, lower educational attainment, reproductive traits, lower socioeconomic status, and poorer general health. After conditioning on psychiatric disorders, the genetic correlations between SA and psychiatric disorders decreased, whereas those with nonpsychiatric traits remained largely unchanged. Conclusions Our results identify a risk locus that contributes more strongly to SA than other phenotypes and suggest a shared underlying biology between SA and known risk factors that is not mediated by psychiatric disorders.Peer reviewe

Evidence for Increased Genetic Risk Load for Major Depression in Patients Assigned to Electroconvulsive Therapy

Electroconvulsive therapy (ECT) is the treatment of choice for severe and treatment-resistant depression; disorder severity and unfavorable treatment outcomes are shown to be influenced by an increased genetic burden for major depression (MD). Here, we tested whether ECT assignment and response/nonresponse are associated with an increased genetic burden for major depression (MD) using polygenic risk score (PRS), which summarize the contribution of diseaserelated common risk variants. Fifty-one psychiatric inpatients suffering from a major depressive episode underwent ECT. MD-PRS were calculated for these inpatients and a separate population-based sample (n = 3,547 healthy; n = 426 self-reported depression) based on summary statistics from the Psychiatric Genomics Consortium MDD-working group (Cases: n = 59,851; Controls: n = 113,154). MD-PRS explained a significant proportion of disease status between ECT patients and healthy controls (p = .022, R2 = 1.173%); patients showed higher MD-PRS. MD-PRS in population-based depression self-reporters were intermediate between ECT patients and controls (n.s.). Significant associations between MD-PRS and ECT response (50% reduction in Hamilton depression rating scale scores) were not observed. Our findings indicate that ECT cohorts show an increased genetic burden for MD and are consistent with the hypothesis that treatment-resistant MD patients represent a subgroup with an increased genetic risk for MD. Larger samples are needed to better substantiate these findings