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The last moves: the effect of hunting and culling on the risk of disease spread from a population of reindeer

1. Hunting and culling are frequently used to combat infectious wildlife diseases. The aim is to markedly lower population density in order to limit disease transmission or to eradicate the host. Massive host culling can yield a trade-off when combating wildlife disease; it follows that intrusive actions may have unintended behavioural side-effects, leading to the geographic spread of disease. The manner in which such excessive hunting and culling of hosts can affect the movement and dispersion of cervids has not been studied. 2. In this study, we quantified the behaviour (daily movements and habitat use) and dispersion of GPS-marked reindeer (n = 24) before and during the eradication of an entire population (>2000 reindeer) infected with chronic wasting disease (CWD) in Norway. We compared behaviour and dispersion during 10 ordinary hunting seasons (2007-16), an extended hunt in 2017 and marksmen culling (2017/18). 3. Seasonality had a major impact on movements. Reindeer movements during the early hunting season (20 August–20 September) did not increase the overall movements compared to that in the pre-hunt season (20 July–19 August), while extended hunting into October (as in 2017) and marksmen culling from November to February markedly increased daytime movements relative to that normally observed in this time of the year. Towards the end of the eradication, the remaining reindeer sought refuge at restricted high-elevation areas with limited forage production. Reindeer used novel areas towards the perimeter of the range, but active herding during culling stopped one herd from leaving the CWD zone. 4. Synthesis and applications: With emerging wildlife diseases, host culling is becoming a more frequently used tool for managers in Europe. Our study highlights the potential trade-off between combating disease transmission within a population and the risk of geographic spread. Such insight is important to design mitigation measures, such as perimeter fencing or herding, to avoid the risk of the geographic spread of disease in cases of severe and economically important wildlife diseases.

Inbreeding and disease avoidance in a free‐ranging koala population

Habitat destruction and fragmentation are increasing globally, forcing surviving species into small, isolated populations. Isolated populations typically experience heightened inbreeding risk, and associated inbreeding depression and population decline; although individuals in these populations may mitigate these risks through inbreeding avoidance strategies. For koalas, as dietary specialists already under threat in the northern parts of their range, increased habitat fragmentation and associated inbreeding costs are of great conservation concern. Koalas are known to display passive inbreeding avoidance through sex-biased dispersal, although population isolation will reduce dispersal pathways. We tested whether free-ranging koalas display active inbreeding avoidance behaviours. We used VHF tracking data, parentage reconstruction, and veterinary examination results to test whether female koalas make mate choices based on [1] relatedness, and [2] chlamydial disease in available mates. We found no evidence that female koalas based their mate choice on the relative relatedness of available mates. In fact, as the relatedness of potential mates increases, so did inbreeding events. We also found no evidence that female koalas based their mate choice on the chlamydial disease status of available mates. The absence of active inbreeding avoidance mechanisms in koalas is concerning from a conservation perspective, as small, isolated populations may be at even higher risk of inbreeding depression than expected. At-risk koala populations may require urgent conservation interventions to augment gene flow and reduce inbreeding risks. Similarly, if koalas are not avoiding mating with individuals with chlamydial disease, populations may be at higher risk from disease than anticipated, further impacting population viability.

Data and code from: Vector demography, dispersal, and the spread of disease: Experimental epidemics under elevated resource supply

1. The spread of many diseases depends on the demography and dispersal of arthropod vectors. Classic epidemiological theory typically ignores vector dynamics and instead makes the simplifying assumption of frequency-dependent transmission. Yet vector ecology may be critical for understanding the spread of disease over space and time and how disease dynamics respond to environmental change. 2. Here, we ask how environmental change shapes vector demography and dispersal, and how these traits of vectors govern the spatiotemporal spread of disease. 3. We developed disease models parameterized by traits of vectors and fit them to experimental epidemics. The experiment featured a viral pathogen (CYDV-RPV) vectored by aphids (Rhopalosiphum padi) among populations of grass hosts (Avena sativa) under two rates of environmental resource supply (i.e., fertilization of the host). We compared a non-spatial model that ignores vector movement, a lagged dispersal model that emphasizes the delay between vector reproduction and dispersal, and a travelling wave model that generates waves of infections across space and time. 4. Resource supply altered both vector demography and dispersal. The lagged dispersal model fit best, indicating that vectors first reproduced and then dispersed among hosts in the experiment. Elevated resources decreased vector population growth rates, nearly doubled their carrying capacity per host, increased dispersal rates when vectors carried the virus, and homogenized disease risk across space. 5. Together, the models and experiment show how environmental eutrophication can shape spatial disease dynamics – for example, homogenizing disease risk across space – by altering the demography and behavior of vectors.

Quantifying species traits related to oviposition behavior and offspring survival in two important disease vectors

Animals with complex life cycles have traits related to oviposition and juvenile survival that can respond to environmental factors in similar or dissimilar ways. We examined the preference-performance hypothesis (PPH), which states that females lacking parental care select juvenile habitats that maximize fitness, for two ubiquitous mosquito species, Aedes albopictus and Culex quinquefasciatus. Specifically, we examined if environmental factors known to affect larval abundance patterns in the field played a role in the PPH for these species. We first identified important environmental factors from a field survey that predicted larvae across different spatial scales. We then performed two experiments, the first testing the independent responses of oviposition and larval survival to these environmental factors, followed by a combined experiment where initial oviposition decisions were allowed to affect larval life history measures. We used path analysis for this last experiment to determine important links among factors in explaining egg numbers, larval mass, development time, and survival. For separate trials, Aedes albopictus displayed congruence between oviposition and larval survival, however C. quinquefasciatus did not. For the combined experiment path analysis suggested neither species completely fit predictions of the PPH, with density dependent effects of initial egg number on juvenile performance in A. albopictus. For these species the consequences of female oviposition choices on larval performance do not appear to fit expectations of the PPH.

opencc-zeroDec 2019View details →

Bayesian diagnostic meta-analysis dataset of pelvic examination in pelvic inflammatory disease

Pelvic inflammatory disease (PID) is not merely a transient sexually transmitted disease. It can lead to chronic pain, ectopic pregnancy, and infertility. Although the Centers for Disease Control and Prevention have established minimum diagnostic criteria, including pelvic examination, the diagnostic value of pelvic tenderness has recently garnered controversy. Our meta-analysis aimed to confirm whether pelvic examination can help diagnose PID among at-risk women. Design A Bayesian meta-analysis of studies reporting diagnostic data of patients at risk for PID. Setting We searched MEDLINE, EMBASE, CENTRAL, CINAHL, Google, and Google Scholar for eligible articles. Participants Female patients at risk for PID. Main results The literature search produced 5,395 articles. After quality assessment, 16 studies and their 4,083 participants were eligible for synthesis on pelvic tenderness.

opencc-by-4.0Oct 2020View details →

Apresentação para Sessão Oral - CBEB2020: Evaluation of the Motor Performance of People with Parkinson's Disease through the Autocorrelation Function Estimated from Sinusoidal Drawings

The objective of this work was to use the autocorrelation function to assess the fine motor performance of a healthy control group (CG) and people with Parkinson's disease (PD), whose fluctuations caused by the disease compromise motor skills, performed mainly by the hands and fingers essential for daily activities such as dressing, carrying objects and taking care of personal hygiene. For this, accelerometer signals were collected while the volunteers drew a sinusoidal pattern. The correlogram was estimated and two features were calculated from it: (i) the normalized area under the curve (𝑨𝒖𝑪); (ii) the difference between matching peaks and valleys from the reference and estimated correlograms (𝒗𝒎𝒎). These features allowed for the discrimination between drawing patterns of CG (𝒗𝒎𝒎= 0.154±0.063, 𝑨𝒖𝑪 = 0.204±0.040) and PD (𝒗𝒎𝒎 = 0.239±0.085, 𝑨𝒖𝑪 = 0.179±0.033) groups. Following the verification of normality (Shapiro-Wilk, p > 0.05), the t-test was applied to confirm the significant differences between groups (p < 0.05). The Cohen’s d effect size (p < 0.05) was medium (0.730) for 𝑨𝒖𝑪 and large (1.252) for 𝒗𝒎𝒎. This further confirms the differences between the features extracted from the groups. Therefore, the features 𝑨𝒖𝑪 and 𝒗𝒎𝒎 estimated from the autocorrelation function are effective for the assessment of the motor performance of healthy individuals and people with PD.

opencc-by-4.0Oct 2020View details →

Apresentação para o Prêmio Iniciação Científica - CBEB2020: Evaluation of the Motor Performance of People with Parkinson's Disease through the Autocorrelation Function Estimated from Sinusoidal Drawings

opencc-by-4.0Sep 2020View details →

Data for "Elephant Genomes Reveal Insights into Differences in Disease Defense Mechanisms between Species".

Data for "Elephant Genomes Reveal Insights into Differences in Disease Defense Mechanisms between Species".

opencc-zeroNov 2020View details →

Risk factors for non-communicable diseases in Bangladesh: Findings of the population-based cross-sectional national survey 2018

Objectives: To determine the national prevalence of risk factors of non-communicable diseases (NCD) in the adult population of Bangladesh. Design: The study was a population-based national cross-sectional study. Setting: This study used 496 primary sampling units (PSUs) developed by the Bangladesh Bureau of Statistics. The PSUs were equally allocated to each division and urban and rural stratum within each division. Participants: The participants were adults aged 18-69 years, who were usual residents of the households for at least six months, and stayed the night before the survey. Out of 9900 participants, 8185 (82.7%) completed STEP-1 and STEP-2, and 7208 took part in STEP-3. Primary and secondary outcome: The prevalence of behavioral, physical, and biochemical risk factors of NCD. Data were weighted to generate national estimates. Results: Tobacco use was significantly (p<0.05) higher in the rural (45.2%) than the urban (38.8%) population. Inadequate fruit/vegetable intake was significantly (P<0.05) higher in the urban (92.1%) than in the rural (88.9%) population. The mean salt intake per day was higher in the rural (9.0 gm) than urban (8.9 gm) population. Among all, 3.0% had no, 70.9% had 1-2, and 26.2% had ≥3 NCD risk factors. The urban population was more likely to have insufficient physical activity (AOR: 1.2, 95% CI: 1.2–1.2), obesity (AOR: 1.5, 95% CI: 1.5–1.5), hypertension (AOR: 1.3, 95% CI: 1.3–1.3), diabetes (AOR: 1.6, 95% CI: 1.6–1.6), and hyperglycemia (AOR: 1.1, 95% CI: 1.1–1.1). Conclusions: Considering the high prevalence of the behavioral, physical, and biochemical risk factors, diverse population and high-risk group targeted interventions are essential to combat the rising burden of NCDs.

opencc-zeroNov 2020View details →

Genome-wide association results from: Transcriptomic stratification of late-onset Alzheimer's cases reveals novel genetic modifiers of disease pathology

Late-Onset Alzheimer's disease (LOAD) is a common, complex genetic disorder well-known for its heterogeneous pathology. The genetic heterogeneity underlying common, complex diseases poses a major challenge for targeted therapies and the identification of novel disease-associated variants. Case-control approaches are often limited to examining a specific outcome in a group of heterogenous patients with different clinical characteristics. Here, we developed a novel approach to define relevant transcriptomic endophenotypes and stratify decedents based on molecular profiles in three independent human LOAD cohorts. By integrating post-mortem brain gene co-expression data from 2114 human samples with LOAD, we developed a novel quantitative, composite phenotype that can better account for the heterogeneity in genetic architecture underlying the disease. We used iterative weighted gene co-expression network analysis (WGCNA) to reduce data dimensionality and to isolate gene sets that are highly co-expressed within disease subtypes and represent specific molecular pathways. We then performed single variant association testing using whole genome-sequencing data for the novel composite phenotype in order to identify genetic loci that contribute to disease heterogeneity. Distinct LOAD subtypes were identified for all three study cohorts (two in ROSMAP, three in Mayo Clinic, and two in Mount Sinai Brain Bank). Single variant association analysis identified a genome-wide significant variant in TMEM106B (p-value < 5´10-8, rs1990620G) in the ROSMAP cohort that confers protection from the inflammatory LOAD subtype. Taken together, our novel approach can be used to stratify LOAD into distinct molecular subtypes based on affected disease pathways.

opencc-zeroNov 2020View details →

Longitudinal proteomic profiling of high-risk patients with COVID-19 reveals markers of severity and predictors of fatal disease

End-stage kidney disease (ESKD) patients are at high risk of severe COVID-19. We performed dense serial blood sampling in hospitalised and non-hospitalised ESKD patients with COVID-19 (n=256 samples from 55 patients) and used Olink immunoassays to measure 436 circulating proteins. Comparison to 51 non-infected ESKD patients revealed 221 proteins differentially expressed in COVID-19, of which 69.7% replicated in an independent cohort of 46 COVID-19 patients. 203 proteins were associated with clinical severity scores, including IL6, markers of monocyte recruitment (e.g. CCL2, CCL7), neutrophil activation (e.g proteinase-3) and epithelial injury (e.g. KRT19). Random Forests machine learning identified predictors of current or future severity such as KRT19, PARP1, PADI2, CCL7, and IL1RL1 (ST2). Survival analysis with joint models revealed 69 predictors of death including IL22RA1, CCL28, and the neutrophil-derived chemotaxin AZU1 (Azurocidin). Finally, longitudinal modelling with linear mixed models uncovered 32 proteins that display different temporal profiles in severe versus non-severe disease, including integrins and adhesion molecules. Our findings point to aberrant innate immune activation and leucocyte-endothelial interactions as central to the pathology of severe COVID-19. The data from this unique cohort of high-risk individuals provide a valuable resource for identifying drug targets in COVID-19.

opencc-zeroDec 2020View details →

Data from: Sleep, inflammation, and cognitive behavior of aged wild-type mice subjected to diffuse brain injury and aged 3xTg-AD mice as a model of Alzheimer's disease

Identifying differential responses between sexes following traumatic brain injury (TBI) can elucidate the mechanisms behind disease pathology. Peripheral and central inflammation in the pathophysiology of TBI can increase sleep in male rodents, but this remains untested in females. We hypothesized that diffuse TBI would increase inflammation and sleep in males more so than in females. Diffuse TBI was induced in C57BL/6J mice and serial blood samples were collected (baseline, 1, 5, 7 days post‐injury [DPI]) to quantify peripheral immune cell populations and sleep regulatory cytokines. Brains and spleens were harvested at 7DPI to quantify central and peripheral immune cells, respectively. Mixed‐effects regression models were used for data analysis. Female TBI mice had 77%–124% higher IL‐6 levels than male TBI mice at 1 and 5DPI, whereas IL‐1β and TNF‐α levels were similar between sexes at all timepoints. Despite baseline sex differences in blood‐measured Ly6Chigh monocytes (females had 40% more than males), TBI reduced monocytes by 67% in TBI mice at 1DPI. Male TBI mice had 31%–33% more blood‐measured and 31% more spleen‐measured Ly6G+ neutrophils than female TBI mice at 1 and 5DPI, and 7DPI, respectively. Compared with sham, TBI increased sleep in both sexes during the first light and dark cycles. Male TBI mice slept 11%–17% more than female TBI mice, depending on the cycle. Thus, sex and TBI interactions may alter the peripheral inflammation profile and sleep patterns, which might explain discrepancies in disease progression based on sex.

opencc-zeroDec 2020View details →

Wikidata Dump Rare diseases

RDF dump of wikidata produced with <a href="https://tools.wmflabs.org/wdumps/">wdumps</a>. <a href="https://tools.wmflabs.org/wdumps/dump/1005">View on wdumper</a> entity count: 0, statement count: 0, triple count: 0

opencc-by-4.0Jun 2020View details →

m6A-TWAS weights for "Genetic Analyses Support the Contribution of mRNA N6-methyladenosine (m6A) Modification to Human Diseases Heritability"

We included the m6A-TWAS weights (trained using FUSION) for our manuscript "Genetic Analyses Support the Contribution of mRNA N6-methyladenosine (m6A) Modification to Human Diseases Heritability".  This dataset is a supplement to the m6A QTL summary statistics data and imputed genotype data at https:// doi.org/10.5281/zenodo.3870952.

opencc-zeroJan 2021View details →

A specific IL6 polymorphic genotype modulates the risk of T. cruzi parasitemia while IL18, IL17A and IL1B variant profiles and HIV infection protect against cardiomyopathy in Chagas disease

Background: Chagas disease caused by Trypanosoma cruzi (T. cruzi) affects approximately six million individuals worldwide. Clinical manifestations are expected to occur due to the parasite persistence and host immune response. Herein we investigated potential associations between IL1B, IL6, IL17A or IL18 polymorphism profiles and cardiomyopathy or T. cruzi parasitemia, as well as the impact of HIV infection on cardiopathy. Methods: 206 patients and 90 control individuals were analyzed. IL1B rs1143627 T>C, IL6 rs1800795 C>G, IL17A rs2275913 G>A, IL18 rs187238 C>G, and IL18 rs1946518 C>A SNVs were analyzed by real-time PCR and T. cruzi parasitemia by PCR. Results: Our data revealed association between a cytokine gene polymorphism and parasitemia never previously reported. The IL6 rs1800795 CG genotype lowered the risk of positive parasitemia (OR=0.45, 95% CI 0.24–0.86, P=0.015). Original findings included associations between IL17A rs2275913 AA and IL18 s1946518 AA genotypes with decreased risk of developing cardiomyopathy (OR=0.27, 95% CI 0.07-0.97, P=0.044; and OR=0.35, 95% CI 0.14-0.87, P=0.023, respectively). IL18 rs1946518 AA and IL1B rs1143627 TC were associated with reduced risk for cardiomyopathy severity, including NYHA (New York Heart Association) class≥ 2 (OR=0.21, 95% CI 0.06-0.68, P=0.009; and OR=0.48, 95% CI 0.24-0.95, P=0.036, respectively) and LVEF (Left Ventricular Ejection Fraction) <45% for IL18 rs1946518 AA (OR=0.22, 95% CI 0.05-0.89, P=0.034). A novel, unexpected protective effect of HIV infection against development/progression of cardiomyopathy was identified, based on a lower risk of developing cardiopathy (OR=0.48, 95% CI 0.23‐0.96, P=0.039), NYHA class≥2 (OR=0.15, 95% CI 0.06‐0.39, P<0.001) and LVEF<45% (OR=0.03, 95% CI 0.00‐0.25, P=0.001). Digestive involvement was negatively associated with NYHA ≥2 and LVEF<45% (OR=0.20, 95% CI 0.09‐0.47, P<0.001; and OR=0.24, 95% CI 0.09-0.62, P=0.004, respectively). Conclusions: Our data support a protective role of IL17A AA, IL18 AA and IL1B TC genotypes against development/progression of cardiomyopathy and a modulatory effect of the IL6 CG genotype on the risk of parasitemia in Chagas disease. Notably, HIV infection was shown to protect against development/progression of cardiopathy, potentially associated with a synergistic effect of HIV and HAART, attenuating a Th1-mediated response in the myocardium. This proposed hypothesis requires confirmation, however, in larger and more comprehensive future studies.

opencc-zeroSep 2019View details →

Data from: Increases and decreases in marine disease reports in an era of global change

Outbreaks of marine infectious diseases have caused widespread mass mortalities, but the lack of baseline data has precluded evaluating whether disease is increasing or decreasing in the ocean. We use an established literature proxy method from Ward and Lafferty (2004) to analyze a 44-year global record of normalized disease reports from 1970 to 2013. Major marine hosts are combined into nine taxonomic groups, from seagrasses to marine mammals, to assess disease swings, defined as positive or negative multi-decadal shifts in disease reports across related hosts. Normalized disease reports increased significantly between 1970 and 2013 in corals and urchins, indicating positive disease swings in these environmentally sensitive ectotherms. Coral disease reports in the Caribbean correlated with increasing temperature anomalies, supporting the hypothesis that warming oceans drive infectious coral diseases. Meanwhile, disease risk may also decrease in a changing ocean. Disease reports decreased significantly in fish and elasmobranchs, which have experienced steep human-induced population declines and diminishing population density that, while concerning, may reduce disease. The increases and decreases in disease reports across the 44-year record transcend short-term fluctuations and regional variation. Our results show that long-term changes in disease reports coincide with recent decades of widespread environmental change in the ocean.

opencc-zeroDec 2016View details →

Data from: Transmission and temporal dynamics of anther-smut disease (Microbotryum) on alpine carnation (Dianthus pavonius)

1. Theory has shown that sterilizing diseases with frequency-dependent transmission (characteristics shared by many sexually transmitted diseases) can drive host populations to extinction. 2. Anther-smut disease (caused by Microbotryum sp.) has become a model plant pathogen system for studying the dynamics of vector and sexually transmitted diseases: infected individuals are sterilized, producing spores instead of pollen, and the disease is spread between reproductive individuals by insect pollinators. We investigated anther-smut disease in a heavily infected population of Dianthus pavonius (alpine carnation) over an eight-year period to determine disease impacts on host population dynamics. 3. Over the eight years, disease prevalence remained consistently high (>40%) while the host population numbers declined by over 50%. 4. The observed rate of vector transmission to reproductive, adult hosts was inadequate to explain the high disease prevalence. Additional density-dependent aerial transmission to highly susceptible juveniles, indicated from experimental field and greenhouse studies, is likely to play a key role in maintaining the high disease prevalence. 5. Epidemiological models that accounted for the mixed transmission mode predicted an eventual decline in disease. 6. Synthesis: Our results demonstrate that high prevalence of a sterilizing disease does not necessarily drive host populations towards extinction and also highlights the importance of demographic studies for establishing the presence of alternative transmission modes.

opencc-zeroMay 2020View details →

Data from: Disentangling the steps of the infection process responsible for juvenile disease susceptibility

1. Juveniles of diverse host taxa, including vertebrates, invertebrates and plants, are more susceptible to parasitic infections than adults, a phenomenon still poorly understood. 2. To shed light on the mechanisms underlying this host age effect, we investigated its expression during different steps of the infection process of a bacterial parasite of the planktonic crustacean Daphnia. To do so, we infected juvenile and adult Daphnia magna with the bacterium Pasteuria ramosa and monitored parasite development in experiments specific to different steps of the infection process. 3. We did not find an effect of host age on parasite attachment, but found a strong increase in the penetration time of the parasite into hosts with increasing age. Host age at exposure also affected within-host parasite development, which was delayed in old adult D. magna in comparison to young adults and juveniles. Furthermore, parasite clearance was observed only in old adults, suggesting that old hosts have a better immune response than young adults and juveniles. 4. Our results reveal a step-specific effect of host age on disease progression, giving support for different hypotheses explaining high juvenile disease susceptibility. While these mechanisms are likely to work independently from each other, earlier steps of the infection process influence later steps, and thus may respond more readily to selection than later steps. 5. Our results also highlight that clearance can occur both during early parasite establishment and surprisingly at progressed infection phases, an undocumented phenomenon in invertebrates, where late infections are often considered chronic, lasting until host death.

opencc-zeroDec 2018View details →

Data from: Developmental Dieldrin exposure alters DNA methylation at genes related to dopaminergic neuron development and Parkinson's disease in mouse midbrain

Human and animal studies have shown that exposure to the organochlorine pesticide dieldrin is associated with increased risk of Parkinson's disease (PD). Despite previous work showing a link between developmental dieldrin exposure and increased neuronal susceptibility to MPTP toxicity in male C57BL/6 mice, the mechanism mediating this effect has not been identified. Here, we tested the hypothesis that developmental exposure to dieldrin increases neuronal susceptibility via genome-wide changes in DNA methylation. Starting at 8 weeks of age and prior to mating, female C57BL/6 mice were exposed to 0.3 mg/kg dieldrin by feeding (every 3 days) throughout breeding, gestation, and lactation. At 12 weeks of age, pups were sacrificed and ventral mesencephalon, containing primarily substantia nigra, were microdissected. DNA was isolated and dieldrin-related changes in DNA methylation were assessed via reduced representation bisulfite sequencing (RRBS). We identified significant, sex-specific differentially methylated CpGs (DMCs) and regions (DMRs) by developmental dieldrin exposure (FDRNr4a2 and Lmx1b genes, which are involved in dopaminergic neuron development and maintenance. Developmental dieldrin exposure had distinct effects on the male and female epigenome. Together, our data suggest that developmental dieldrin exposure establishes sex-specific poised epigenetic states early in life. These poised epigenomes may mediate sensitivity to subsequent toxic stimuli and contribute to the development of late-life neurodegenerative disease, including PD.