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Fig. 4 in Co-infection of Echinococcus equinus and Echinococcus canadensis (G6/7) in a gray wolf in Turkey: First report and genetic variability of the isolates
Fig. 4. The haplotype network for the mt-CO1 gene (815 bp) of E. canadensis (G6/7). The size of the circles is proportional to the frequency of each haplotype. The number of mutations separating haplotypes is indicated by dash marks. The host diversity of haplotypes is shown in different colors. Hap: Haplotype.
Fig. 2 in Co-infection of Echinococcus equinus and Echinococcus canadensis (G6/7) in a gray wolf in Turkey: First report and genetic variability of the isolates
Fig. 2. Phylogenetic tree of Echinococcus granulosus s.l. isolates generated using mt-CO1 gene sequences (815 bp). The phylogenetic tree was constructed using the Maximum Likelihood method and TN93 + G model. Evolutionary analyses were conducted in MEGA X. For each reference sequence, the GenBank accession number and species name are listed below: MN787562 (E. equinus), KY766905 (E. equinus), KP161210 (E. equinus) AB786665 (E. equinus) AF346403 (E. equinus), KX010854 (E. canadensis) MK321260 (E. canadensis) KX010856 (E. canadensis), AB893263 (E. canadensis), AB777923 (E. canadensis), MK165232 (E. ortleppi), MT072979 (E. granulosus s.s.), NC_044548 (E. granulosus s.s.), MG672293 (E. granulosus s.s.), KT001423 (E. multilocularis), AY684274 (T. saginata). ■: E. canadensis (G6/7) isolates; ▴: E. equinus isolates.
Fig. 3 in Co-infection of Echinococcus equinus and Echinococcus canadensis (G6/7) in a gray wolf in Turkey: First report and genetic variability of the isolates
Fig. 3. The haplotype network for the mt-CO1 gene (815 bp) of E. equinus. The size of the circles is proportional to the frequency of each haplotype. The number of mutations separating haplotypes is indicated by dash marks. The host diversity of haplotypes is shown in different colors. Hap: Haplotype.
Fig. 3 in Ranavirus and helminth parasite co-infection in invasive American bullfrogs in the Atlantic forest, Brazil
Fig. 3. (a) The negative relationship between log-transformed Nematoda abundance and Ranavirus load (copies-ng; P <0.05). Points represent individuals that tested positive for Ranavirus infection with viral load assay data (N = 12). The nematode abundances in Ranavirus-negative individuals are shown on the x-axis. (b) The relationship between log-transformed total macroparasite abundance and bullfrog snout-vent length (cm) and Ranavirus infection status with fitted regression lines (P <0.001). Data represent individuals from sites that had at least one Ranavirus infection (4 sites, N = 35).
Fig. 2 in Ranavirus and helminth parasite co-infection in invasive American bullfrogs in the Atlantic forest, Brazil
Fig. 2. (a) Observed occurrence matrix of presence (red cells) and absence (white cells) of Ranavirus and helminth taxa (6 rows) infection in individual bullfrogs (Aquarana catesbeiana; 65 columns). (b) Simulated occurrence matrix (65 columns, one null matrix out of 1000 simulations). (c) Distribution of simulated cooccurrence metric (blue histogram bars; 1000 null matrices). Vertical red line = observed co-occurrence metric. Dashed vertical lines = 95% and 99% confidence intervals. (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)
Fig. 1 in Ranavirus and helminth parasite co-infection in invasive American bullfrogs in the Atlantic forest, Brazil
Fig. 1. Distribution of helminth macroparasite taxa and Ranavirus infection status and prevalence across sampling locations. The thick gray outline shown in the inset map of Brazil highlights the states where American bullfrog (Aquarana catesbeiana) sampling took place (SP = S˜ao Paulo, PR = Paran´a, SC = Santa Catarina). Green shading represents tropical and subtropical forest biomes. Sample locations included Embu das Artes (Site 1, N = 13), Piedade (Site 2, N = 10), and Iporanga (Site 3, N = 4) in S˜ao Paulo; Quatro Barras (Site 4, N = 10), Piraquara (5, N = 2), and S˜ao Jose´dos Pinhais (Site 6, N = 4) in Paran´a; and Blumenau (Site 7, N = 9), Urubici (Site 8, N = 10), and Chapeco´(Site 9, N = 3) in Santa Catarina. Helminth pie chart size corresponds to average helminth abundance in bullfrogs. Differences in helminth taxa richness (P <0.001) and evenness (PIE; P <0.001) were detected; however, helminth abundance did not differ among sites between collection sites. Sites where Ranavirus was detected (N = 4) have a corresponding pie chart, in which the size corresponds to average viral load (copies-ng) per individual at a site. Estimated Ranavirus prevalence among the positive sites did not differ significantly (P = 0.06). Viral load of positive individuals differed among sites (P <0.05), but differences were driven by the high load found in the single Blumenau (Site 7) Ranavirus-positive bullfrog. (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)
Drug-Drug Interactions Between Rifapentine and Dolutegravir in HIV/LTBI Co-Infected Individuals
ClinicalTrials.gov study NCT04272242. IPD Sharing: YES. Countries: 7. Publications: 1.
Data from: Exogenous glucocorticoids amplify the costs of infection by reducing resistance and tolerance, but effects are mitigated by co-infection
Individual variation in parasite defenses, such as resistance and tolerance, can underlie heterogeneity in fitness and could influence disease transmission dynamics. Glucocorticoid hormone concentrations often change in response to fluctuating environmental conditions and mediate changes in immune function, resource allocation, and tissue repair. Thus, changes in glucocorticoid hormone concentrations might mediate individual variation in investment in resistance versus tolerance. In this study, we experimentally increased glucocorticoid concentrations in red-winged blackbirds (Agelaius phoeniceus) that were naturally infected with haemosporidian parasites and assessed changes in resistance and tolerance of infection. Glucocorticoid treatment increased burdens of Plasmodium, the parasite causing avian malaria, but only in the absence of co-infection with another Haemosporidian, Haemoproteus. Thus, glucocorticoids might reduce resistance to infection, but co-infection can mitigate the negative consequences of increased hormone concentrations. Glucocorticoid treatment also decreased tolerance of infection. We found no evidence that the inflammatory immune response or rate of red blood cell production underlie the effects of glucocorticoids on resistance and tolerance. Our findings suggest that exogenous glucocorticoids can increase the costs of haemosporidian infections by both increasing parasite numbers and reducing an individual's ability to cope with infection. These effects could scale up to impact populations of both host and parasite.
Pneumocystis spp. in pigs: a longitudinal quantitative study and co-infections assessment in Austrian farms
<p>The present upload represents the supplementary materials of the manuscript " <em>Pneumocystis</em> spp. in pigs: a longitudinal quantitative study and co-infections assessment in Austrian farms" which is under submission</p>
Cestode infection facilitates co-infection by other parasites in a metapopulation of threespine stickleback
<p><span><span><span><span><span><span><span><span><span><span><span>Parasitic infections are a global occurrence and impact the health of many species. Co-infections, where two or more species of parasite are present in a host, are a common phenomenon across species. Co-infecting parasites can interact directly or indirectly via their manipulation of (and susceptibility to) the immune system of their shared host. Helminths, such as the cestode <i>Schistocephalus solidus</i>, are well known to suppress immunity of their host (threespine stickleback), potentially facilitating other parasite species. Yet, hosts can evolve a more robust immune response (as seen in some stickleback populations), potentially turning facilitation into inhibition. Using wild-caught stickleback from 21 populations with non-zero <i>S. solidus</i> prevalence, we show there is an overall tendency towards facilitation: individuals with <i>S. solidus</i> infections have 28% higher diversity of other parasites, compared to <i>S. solidus</i>-uninfected individuals from the corresponding lakes. This facilitation effect, however, is stronger in lakes where <i>S. solidus</i> is particularly successful but tends towards inhibition in lakes with sparse and smaller cestodes (indicative of stronger host immune response). These results illustrate how even a single parasite species can vary geographically in their capacity for facilitation or inhibition of co-infections.</span></span></span></span></span></span></span></span></span></span></span></p>
Fig. 3 in . Study of Nosema spp. in the Tomsk region, Siberia: co-infection is widespread in honeybee colonies
Fig. 3. Distribution of Nosema in bee colonies (Apis mellifera) throughout the Tomsk
Fig. 1 in . Study of Nosema spp. in the Tomsk region, Siberia: co-infection is widespread in honeybee colonies
Fig. 1. Dynamics of infestation of bee colonies and apiaries with Nosema spp. in 2012–
Fig. 4 in . Study of Nosema spp. in the Tomsk region, Siberia: co-infection is widespread in honeybee colonies
Fig. 4. Long-term dynamics of infestation of apiaries with different Nosema species in
Fig. 1 in Co-infection of Echinococcus equinus and Echinococcus canadensis (G6/7) in a gray wolf in Turkey: First report and genetic variability of the isolates
Fig. 1. Stereomicroscopic view of adult parasites obtained from gray wolf's intestine.
Helminth-associated changes in host immune phenotype connect top-down and bottom-up interactions during co-infection
<p>Within-host parasite interactions can be mediated by the host and changes in host phenotypes often serve as indicators of the presence or intensity of parasite interactions.</p> <p>Parasites like helminths induce a range of physiological, morphological, and immunological changes in hosts that can drive bottom-up (resource-mediated) or top-down (immune-mediated) interactions with co-infecting parasites. Although top-down and bottom-up interactions are typically studied in isolation, the diverse phenotypic changes induced by parasite infection may serve as a useful tool for understanding if, and when, these processes act in concert.</p> <p>Using an anthelmintic treatment study of African buffalo (Syncerus caffer), we tracked changes in host immunological and morphological phenotypes during helminth-coccidia co-infection to investigate their role in driving independent and combinatorial bottom-up and top-down parasite interactions. We also examined repercussions for host fitness.</p> <p>Clearance of a blood-sucking helminth, Haemonchus, from the host gastrointestinal tract induced a systemic Th2 immune phenotype, while clearance of a tissue-feeding helminth, Cooperia, induced a systemic Th1 phenotype. Furthermore, the Haemonchus-associated systemic Th2 immune phenotype drove simultaneous top-down and bottom-up effects that increased coccidia shedding by changing the immunological and morphological landscapes of the intestine.</p> <p>Higher coccidia shedding was associated with lower host body condition, a lower chance of pregnancy, and older age at first pregnancy, suggesting that coccidia infection imposed significant condition and reproductive costs on the host.</p> <p>Our findings suggest that top-down and bottom-up interactions may commonly co-occur and that tracking key host phenotypes that change in response to infection can help uncover complex pathways by which parasites interact.</p>
Identity and density of parasite exposures alter the outcome of co-infections: Implications for management
<p>1) Although research has focused on density-dependent responses of hosts to single-parasite infections, hosts are exposed to numerous parasites simultaneously under natural conditions and if these exposures lead to infections, they can threaten host populations and ecosystem stability. Moreover, spatiotemporal variation in abundance of co-occurring parasites might influence host infection intensity. If interactions are consistent between different co-infecting parasites, then these patterns could give managers another tool to control disease spread and even predict problematic disease emergences.</p> <p>2) We investigated how parasite density and identity alter within-host co-infection dynamics. To test this, we simultaneously exposed Cuban treefrogs (Osteopilus septentrionalis) as a model amphibian species to all pairwise combinations of three problematic parasites that commonly co-infect amphibians: the fungus Batrachochytrium dendrobatidis (Bd), the nematode Aplectana hamatospicula, and Ranavirus. Hosts were exposed to one parasite at a fixed dose and another parasite at a range of five doses.</p> <p>3) Higher doses of Bd decreased Ranaviral and A. hamatospicula loads, but Bd load was not influenced by the dose of either parasite. Ranaviral load was negatively associated with A. hamatospicula dose, but A. hamatospicula load was not affected by Ranaviral dose. We found that all the pairwise co-infections were dependent on parasite density and that pairwise interactions were highly asymmetric – strong in one direction and weak in the other – consistent with interactions dominating food webs.</p> <p>4) Synthesis and applications: We also revealed that the exposure dose of A. hamatospicula was positively associated with host tolerance to Bd infection and negatively associated with Ranaviral load in hosts. Ranavirus and Bd cause mass die-offs in amphibians, but A. hamatospicula does not. Therefore, in systems where these parasites coexist, maintaining or increasing densities of A. hamatospicula could reduce the negative effects of Bd and Ranavirus infections. Additionally, if these asymmetric and density dependent patterns from community ecology are applicable to other amphibian co-infections or co-infections in other systems, this should allow conservation organizations and resource managers to predict outbreaks and manage host declines associated with deadly parasites by modifying the abundance of co-infecting parasites that might be easier to manage.</p>
Identification of microbial taxa present in Ctenocephalides felis (cat flea) reveals widespread co-infection and associations with vector phylogeny
<p><strong>Background </strong></p> <p><em>Ctenocephalides</em> <em>felis</em>, the cat flea, is the most common ectoparasite of cats and dogs worldwide. As a cause of flea allergy dermatitis and a vector for two genera of zoonotic pathogens (<em>Bartonella</em> and <em>Rickettsia</em> spp.), the effect of the <em>C</em>. felis <em>microbiome</em> on pathogen transmission and vector survival is of substantial medical importance to both human and veterinary medicine. The aim of this study was to assay the pathogenic and commensal eubacterial microbial communities of individual <em>C</em>. <em>felis</em> from multiple geographic locations and analyze these findings by location, qPCR pathogen prevalence, and flea genetic diversity.</p> <p><strong>Methods </strong></p> <p>16S Next Generation Sequencing (NGS) was utilized to sequence the microbiome of fleas collected from free-roaming cats, and the <em>cox1</em> gene was used for flea phylogenetic analysis. NGS data were analyzed for 168 individual fleas from seven locations within the US and UK. Given inconsistency in the genera historically reported to constitute the <em>C</em>. <em>felis</em> microbiome, we utilized the decontam prevalence method followed by literature review to separate contaminants from true microbiome members.</p> <p><strong> Results </strong></p> <p>NGS identified a single dominant and cosmopolitan amplicon sequence variant (ASV) from <em>Rickettsia</em> and <em>Wolbachia</em> while identifying one dominant <em>Bartonella</em> <em>clarridgeiae</em> and one dominant <em>Bartonella henselae/Bartonella</em> <em>koehlerae</em> ASV. Multiple less common ASVs from these genera were detected within restricted geographical ranges. Co-detection of two or more genera (<em>Bartonella</em>, <em>Rickettsia</em>, and/or <em>Wolbachia</em>) or multiple ASVs from a single genus in a single flea was common. <em>Achromobacter</em>, <em>Peptoniphilus</em>, and <em>Rhodococcus</em> were identified as additional candidate members of the <em>C</em>. <em>felis</em> microbiome on the basis of decontam analysis and literature review. <em>Ctenocephalides</em> <em>felis</em> phylogenetic diversity as assessed by the <em>cox1</em> gene fell within currently characterized clades while identifying seven novel haplotypes. NGS sensitivity and specificity for <em>Bartonella</em> and <em>Rickettsia</em> spp. DNA detection was compared to targeted qPCR.</p> <p><strong>Conclusions </strong></p> <p>Our findings confirm the widespread coinfection of fleas with multiple bacterial genera and strains, proposing three additional microbiome members. The presence of minor <em>Bartonella</em>, <em>Rickettsia</em>, and <em>Wolbachia</em> ASVs was found to vary by location and flea haplotype. These findings have important implications for flea-borne pathogen transmission and control. </p>
Ontogeny of immunity and potential implications for co-infection
<p>Immunity changes through ontogeny and can mediate facilitative and inhibitory interactions among co-infecting parasite species. In amphibians, most immune memory is not carried through metamorphosis, leading to variation in the complexity of immune responses across life stages. To test if the ontogeny of host immunity might drive interactions among co-infecting parasites, we simultaneously exposed Cuban treefrogs (<em>Osteopilus septentrionalis</em>) to a fungus (<em>Bactrachochytrium dendrobaditis</em>) and a nematode (<em>Aplectana hamatospicula</em>) at tadpole, metamorphic, and post-metamorphic life stages. We measured metrics of host immunity, host health, and parasite abundance. We predicted facilitative interactions between co-infecting parasites as the different immune responses hosts mount to combat these infectious are energetically challenging to mount simultaneously. We found ontogenetic differences in IgY levels and cellular immunity but no evidence that metamorphic frogs were more immunosuppressed than tadpoles. There was also little evidence that these parasites facilitated one another and no evidence that <em>A. hamatospicula </em>infection altered host immunity or health. However, Bd, which is known to be immunosuppressive, decreased immunity in metamorphic frogs. This made metamorphic frogs both less resistant and less tolerant of Bd infection than the other life stages. These findings indicate that changes in immunity altered host responses to parasite exposures throughout ontogeny.</p>
Data from: Widespread amphibian Perkinsea infections associated with Ranidae hosts, cooler months, and Ranavirus co-infection
<p>Amphibians suffer from large-scale population declines globally, and emerging infectious diseases contribute heavily to these declines. Amphibian Perkinsea (Pr) is a worldwide anuran pathogen associated with mass mortality events, yet little is known about its epidemiological patterns, especially in comparison to the body of literature on amphibian chytridiomycosis and ranavirosis. </p> <p>Here, we establish Pr infection patterns in natural anuran populations and identify important covariates including climate, host attributes, and co-infection with Ranavirus (Rv). </p> <p>We used quantitative (q)PCR to determine the presence and intensity of Pr and Rv across 1234 individuals sampled throughout central Florida in 2017-2019. We then implemented random forest ensemble learning models to predict infection with both pathogens based on physiological and environmental characteristics. </p> <p>Perkinsea infected 32% of all sampled anurans, and Pr prevalence was significantly elevated in Ranidae frogs, cooler months, metamorphosed individuals, and frogs co-infected with Rv, while Pr intensity was significantly higher in ranid frogs and individuals collected dead. Ranavirus prevalence was 17% overall and was significantly higher in Ranidae frogs, metamorphosed individuals, locations with higher average temperatures, and individuals co-infected with Pr. Perkinsea prevalence was significantly higher than Rv prevalence across months, regions, life stages, and species. Among locations, Pr prevalence was negatively associated with crayfish prevalence and positively associated with relative abundance of microhylids, but Rv prevalence did not associate with any tested co-variates. Co-infections were significantly more common than single infections for both pathogens, and we propose that Pr infections may propel Rv infections because seasonal Rv infection peaks followed Pr infection peaks and random forest models found Pr intensity was a leading factor explaining Rv infections. </p> <p>Our study elucidates epidemiological patterns of Pr in Florida and suggests that Pr may be under-recognized as a cause of anuran declines, especially in the context of pathogen co-infection.</p>
The Aedes aegypti RNA interference response against Zika virus in the context of co-infection with dengue and chikungunya viruses
<p>This is the corresponding data of the Publication in Plos Neglected tropical diseases.</p> <p>Zika virus (ZIKV) is a mosquito-borne human-pathogenic arbovirus of the <em>Flaviviridae</em> family, genus <em>Flavivirus</em>. Other arboviruses, including dengue (DENV) or chikungunya (CHIKV) virus, can occur in the same regions as ZIKV and are also transmitted by <em>Aedes aegypti</em>. Notably, it has been shown that these viruses can co-infect this mosquito, andco-transmission occurs. Such processes may add to the serious public health issues already linked to those pathogens. Arbovirus infections in mosquitoes are controlled through an immune response called RNA interference (RNAi). It is however unknown whether immune responses changs when a mosquito is exposed to a co-infection of ZIKV with either DENV or CHIKV. In this study, we provide evidence that ZIKV co-infections with CHIKV or DENV are similarly well controlled by RNAi as single infections. These findings give new insights into the dynamics of arboviral co-infections in mosquito vectors that increase our understanding of co-infection scenarios during arbovirus outbreaks.</p>
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Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
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DANDI Archive for NWB datasets
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The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.