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43 results for “Schistosome”
Phenotypic data related to genetic architecture of transmission stage production and virulence in schistosome parasites
<p>These data were generated related to the study of the <strong>Genetic architecture of transmission stage production and virulence in schistosome parasites</strong>.</p> <p><strong>Abstract:</strong> Both theory and experimental data from multiple pathogens suggest that the production of transmission stages should be strongly associated with virulence, but the genetic bases of parasite transmission/virulence traits are poorly understood. In the blood fluke <em>Schistosoma mansoni</em>, parasite genotypes show extensive variation in numbers of cercariae larvae shed from infected snails. Furthermore, high shedding parasites cause high mortality to snails while low shedding parasites cause low mortality, consistent with expected trade-offs between parasite transmission and virulence. To understand the genetic basis of transmission stage production/virulence, we conducted reciprocal crosses between schistosomes from two laboratory populations that differ 8-fold in cercarial shedding and in their virulence to inbred snail hosts. Each parasite generation, we determined four-week cercarial shedding profiles in inbred <em>Biomphalaria glabrata</em> snails infected with single parasite larvae. We sequenced the whole genome of the F0 parents and the exome of the F1 progeny and 188 F2 progeny from each cross, and used linkage mapping to reveal quantitative trait loci (QTLs) underlying transmission stage production. Cercarial production is polygenic: we found three major QTLs on chromosome 1, 3 and 5 (Log-of-the-odds (LOD) = 5.61, 8.19, 6.25) and two minor QTLs on chromosome 2 and 4. These QTLs act additively and explained 28.56% of the phenotypic variation in cercarial shedding. Alleles inherited from the high and low shedding parents were co-dominant at all QTLs, except for chr. 1 and chr. 4 where the “high cercarial shedding” allele is recessive. These results demonstrate that the genetic architecture of key traits directly relevant to schistosome ecology can be dissected using classical linkage mapping approaches, and set the stage for fine mapping and functional validation of the genes involved using the growing armory of functional and cell biology tools available for this parasite.</p> <p> </p> <p>This dataset is made of 4 tables:</p> <ul> <li>F0_parental_populations.csv</li> <li>F1.csv</li> <li>F2.csv</li> <li>sex.tsv</li> </ul> <p> </p> <p><strong>F0_parental_populations.csv</strong></p> <p> </p> <p>This table contains the number of cercariae produced by each individual <em>Biomphalaria glabrata</em> Bg26 snails infected with single genotypes of <em>Schistosoma mansoni</em> parasite. We have compared the transmission stage production between two different populations of <em>S. mansoni</em> parasite. This dataset was originally published in Le Clec'h et al., 2019 (Striking differences in virulence, transmission and sporocyst growth dynamics between two schistosome populations. Parasites and Vectors. 2019 Oct 16;12(1):485. doi: 10.1186/s13071-019-3741-z).</p> <p> </p> <p>This table is made of 9 columns:</p> <ul> <li><strong>id</strong>: the unique identifier of each sample.</li> <li><strong>schistosoma_population</strong>: the population of schistosome used for the infection of the snail. Each snail was infected with a single parasite genotype. We have used SmLE (high shedder/highly virulent population) and SmBRE (low shedding/low virulent population).</li> <li><strong>Shed.1</strong>: the number of cercariae produced by each parasite genotype at the first shedding week (4 weeks after exposure to parasite).</li> <li><strong>Shed.2</strong>: the number of cercariae produced by each parasite genotype at the second shedding week (5 weeks after exposure to parasite).</li> <li><strong>Shed.3</strong>: the number of cercariae produced by each parasite genotype at the third shedding week (6 weeks after exposure to parasite).</li> <li><strong>Shed.4</strong>: the number of cercariae produced by each parasite genotype at the fourth shedding week (7 weeks after exposure to parasite).</li> <li><strong>sum</strong>: the sum of the cercariae produced by each parasite genotype over the 4 weeks of shedding (Shed.1 + Shed.2 + Shed.3 + Shed.4).</li> <li><strong>average</strong>: the average number of cercariae produced by each parasite genotype over the 4 weeks of shedding.</li> <li><strong>sex</strong>: the sex of each parasite genotype determined by PCR <sup>1</sup>.</li> </ul> <p> </p> <p><strong>F1.csv</strong></p> <p> </p> <p>This table contains the number of cercariae produced by each individual <em>Biomphalaria glabrata</em> Bg26 snails infected with single genotypes of F1 progeny from the cross SmLE x SmBRE (see the manuscript for details).</p> <p> </p> <p>This table is made of 11 columns:</p> <ul> <li><strong>id</strong>: the unique identifier of each sample.</li> <li><strong>cross</strong>: F1A or F1B cross. Each snail was infected with a single parasite genotype from either F1A or F1B progeny.</li> <li><strong>Shed.1</strong>: the number of cercariae produced by each parasite genotype at the first shedding week (4 weeks after exposure to parasite).</li> <li><strong>Shed.2</strong>: the number of cercariae produced by each parasite genotype at the second shedding week (5 weeks after exposure to parasite).</li> <li><strong>Shed.3</strong>: the number of cercariae produced by each parasite genotype at the third shedding week (6 weeks after exposure to parasite).</li> <li><strong>Shed.4</strong>: the number of cercariae produced by each parasite genotype at the fourth shedding week (7 weeks after exposure to parasite).</li> <li><strong>sum</strong>: the sum of the cercariae produced by each parasite genotype over the 4 weeks of shedding (Shed.1 + Shed.2 + Shed.3 + Shed.4).</li> <li><strong>average</strong>: the average number of cercariae produced by each parasite genotype over the 4 weeks of shedding.</li> <li><strong>PO</strong>: the total phenoloxidase activity in infected snail hemolymph, measured at 7.5 weeks post-exposure <sup>2</sup>.</li> <li><strong>Hb</strong>: the hemoglobin rate in infected snail hemolymph, measured at 7.5 weeks post-exposure <sup>3</sup>.</li> <li><strong>sex</strong>: the sex of each parasite genotype determined by PCR <sup>1</sup>.</li> </ul> <p> </p> <p><strong>F2.csv</strong></p> <p>This table contains the number of cercariae produced by each individual <em>Biomphalaria glabrata</em> Bg26 snails infected with single genotypes of F2 progeny from the cross SmLE x SmBRE (see the manuscript for details).</p> <p> </p> <p>This table is made of 10 columns:</p> <ul> <li><strong>id</strong>: the unique identifier of each sample.</li> <li><strong>cross</strong>: F2A or F2B cross. Each snail was infected with a single parasite genotype from either F2A or F2B progeny.</li> <li><strong>Shed.1</strong>: the number of cercariae produced by each parasite genotype at the first shedding week (4 weeks after exposure to parasite).</li> <li><strong>Shed.2</strong>: the number of cercariae produced by each parasite genotype at the second shedding week (5 weeks after exposure to parasite).</li> <li><strong>Shed.3</strong>: the number of cercariae produced by each parasite genotype at the third shedding week (6 weeks after exposure to parasite).</li> <li><strong>Shed.4</strong>: the number of cercariae produced by each parasite genotype at the fourth shedding week (7 weeks after exposure to parasite).</li> <li><strong>sum</strong>: the sum of the cercariae produced by each parasite genotype over the 4 weeks of shedding (Shed.1 + Shed.2 + Shed.3 + Shed.4)</li> <li><strong>average</strong>: the average number of cercariae produced by each parasite genotype over the 4 weeks of shedding.</li> <li><strong>PO</strong>: the total phenoloxidase activity in infected snail hemolymph, measured at 7.5 weeks post-exposure <sup>2</sup>.</li> <li><strong>Hb</strong>: the hemoglobin rate in infected snail hemolymph, measured at 7.5 weeks post-exposure <sup>3</sup>.</li> </ul> <p> </p> <p><strong>sex.csv</strong></p> <p> </p> <p>This table contains the <em>in silico</em> sexing of F0 parents, F1 parents and F2 progeny of <em>S. mansoni</em> parasites.</p> <p>This table is made of 4 columns:</p> <ul> <li><strong>id</strong>: the unique identifier of each sample</li> <li><strong>read_depth</strong>: the read depth ratio between the Z-linked and pseudo-autosomal regions.</li> <li><strong>ratio</strong>: computed ratio between the Z-linked and pseudo-autosomal regions.</li> <li><strong>sex</strong>: the sex of each parasite genotype determined <em>in silico</em>: a ratio around 1 corresponds to a male carrying two Z chromosomes while a ratio around 0.5 corresponds to a female carrying only one Z chromosome.</li> </ul> <p><strong>Notes:</strong></p> <p><sup>1</sup>. Le Clec’h W, Chevalier F et al. Real-time PCR for sexing Schistosoma mansoni cercariae. Mol Biochem Parasitol. Jan-Feb 2016; 205(1-2):35-8.doi: 10.1016/j.molbiopara.2016.03.010. Epub 2016 Mar 26.</p> <p><sup>2</sup>. Le Clec’h W et al. Characterization of hemolymph phenoloxidase activity in two Biomphalaria snail species and impact of Schistosoma mansoni infection. Parasit Vectors. 2016 Jan 22; 9:32.doi: 10.1186/s13071-016-1319-6.</p> <p><sup>3</sup>. Le Clec'h et al. Striking differences in virulence, transmission and sporocyst growth dynamics between two schistosome populations. Parasit Vectors. 2019 Oct 16; 12(1):485. doi: 10.1186/s13071-019-3741-z.</p>
Technique of microsurgical transplantation of schistosomes sporocysts
<p>Video instructions on the technique of microsurgical transplantation of schistosome sporocysts from a donor snail to a recipient snail (in English).</p> <p>Produced at IHPE (http://ihpe.univ-perp.fr/)</p>
Technique de transplantation microchirurgicale de sporocystes de schistosomes.
<p>Video instructions on the technique of microsurgical transplantation of schistosome sporocysts from a donor snail to a recipient snail (in French).</p> <p>Produced at IHPE (http://ihpe.univ-perp.fr/)</p>
Fig. 1 in Species-specific qPCR assays allow for high-resolution population assessment of four species avian schistosome that cause swimmer's itch in recreational lakes
Fig. 1. Abundance of cercariae by sampling site. Water samples were obtained in mid-June and cercariae abundance was determined using the pan-avian schistosomes qPCR.
Fig. 2 in Species-specific qPCR assays allow for high-resolution population assessment of four species avian schistosome that cause swimmer's itch in recreational lakes
Fig. 2. Percent contribution of T. stagnicolae, T. szidati, T. physellae and A. brantae species to each lake. Water samples from different locations and dates were tested using the species-specific qPCR assay and results were pooled by lake to understand the relative contribution overall of each species to each lake. The percent contribution (based on gene copy number) of each species was calculated.
Fig. 3 in Species-specific qPCR assays allow for high-resolution population assessment of four species avian schistosome that cause swimmer's itch in recreational lakes
Fig. 3. Lifecycles of T. stagnicolae, A. brantae, T. szidati, and T. physellae. life cycle summary of the avian schistosome species targeted for species-specific qPCR tests designed in this study.
Phenotype, genotype and fitness data related to genetic analysis of praziquantel response in schistosome parasites.
<p>These data are related to the study of the Genetic analysis of praziquantel response in schistosome parasites implicates a Transient Receptor Potential channel.</p> <p>Mass treatment with praziquantel (PZQ) monotherapy is the mainstay for schistosomiasis treatment. This drug shows imperfect cure rates in the field and parasites showing reduced PZQ response can be selected in the laboratory, but the extent of resistance in <em>Schistosoma mansoni</em> populations is unknown. We examined the genetic basis of variation in PZQ response in a <em>S. mansoni</em> population (SmLE-PZQ-R) selected with PZQ in the laboratory: 35% of these worms survive high dose (73 µg/mL) PZQ treatment. We used genome wide association to map loci underlying PZQ response. The major chr. 3 peak contains a transient receptor potential (Sm.TRPM_PZQ) channel (Smp_246790), activated by nanomolar concentrations of PZQ. PZQ response shows recessive inheritance and marker-assisted selection of parasites at a single Sm.TRPM_PZQ SNP enriched populations of PZQ-resistant (PZQ-ER) and sensitive (PZQ-ES) parasites showing >377 fold difference in PZQ response. The PZQ-ER parasites survived treatment in rodents better than PZQ-ES. Resistant parasites show 2.25-fold lower expression of Sm.TRPM_PZQ than sensitive parasites. Specific chemical blockers of Sm.TRPM_PZQ enhanced PZQ resistance, while Sm.TRPM_PZQ activators increased sensitivity. A single SNP in Sm.TRPM_PZQ differentiated PZQ-ER and PZQ-ES lines, but mutagenesis showed this was not involved in PZQ response, suggesting linked regulatory changes. We surveyed Sm.TRPM_PZQ sequence variation in 259 parasites from the New and Old World revealing one nonsense mutation that results in a truncated protein with no PZQ-binding site. Our results demonstrate that Sm.TRPM_PZQ underlies variation in PZQ response in <em>S. mansoni</em> and provides an approach for monitoring emerging PZQ-resistance alleles in schistosome elimination programs.</p> <p>This dataset is divided in 3 folders. Each folder has a readme detailing its content.</p> <p><strong>1-Phenotyping_data</strong></p> <p>This folder includes the data tables related to the phenotyping of the worms performed during this study. The phenotype measured was the viability of worms following PZQ treatment (i.e., PZQ response). This viability was assessed microscopically or using worm lactate production released in culture media.</p> <p>The data correspond to the following experiments:</p> <ul> <li>PZQ response of single adult male worms from SmLE and SmLE-PZQ-R populations to different doses of PZQ. This data was used to determine the PZQ IC50 of each population.</li> <li>Lactate production from single SmLE-PZQ-R adult male worms and correlation with visual observation. This was a proof-of-principle that lactate production can be used to efficiently and unbiasedly phenotype schistosome adult male worms in response to PZQ drug.</li> <li>PZQ response of single SmLE-PZQ-R adult male worms. These worms were then divided in low and high producer in response to PZQ and used to perform a genome-wide association study.</li> <li>PZQ response of single adult male worms from SmLE-PZQ-ER and SmLE-PZQ-ES populations to different doses of PZQ. This data was used to determine the PZQ IC50 of each population.</li> <li>PZQ response of single adult male worms from SmLE-PZQ-ER and SmLE-PZQ-ES populations in presence of Sm.TRPM_PZQ blocker (MB2) and activator (MV1) with and without PZQ drug.</li> <li>In vivo PZQ response of schistosome worms from SmLE-PZQ-ER and SmLE-PZQ-ES populations.</li> </ul> <p><strong>2-Genotyping_data</strong></p> <p>This folder includes the data tables related to the genotyping of the worms performed during this study. Worms were genotyping using PCR-RFLP (genotyping of single nucleotide polymorphisms (SNPs) on chr2 and chr3 QTLs) or using qPCR (genotyping of a copy number variation (CNV) on chr3 QTL).</p> <p>The data correspond to the following experiment:</p> <ul> <li>Association between PZQ response of single adult male worms from SmLE-PZQ-R population and their respective genotype on chromosome 2 (SNP) and chromosome 3 (SNP and CNV) loci.</li> </ul> <p><strong>3-Fitness_data</strong></p> <p>This folder includes the data tables related to the fitness of the parasite populations. We collected data regarding:</p> <ul> <li>The number of surviving and infected snails after exposure to SmLE-PZQ-ER or SmLE-PZQ-ES miracidia.</li> <li>The number of adult worms recovered from golden Syrian female hamsters exposed to SmLE-PZQ-ER or SmLE-PZQ-ES cercariae.</li> </ul> <p>All the data were collected during 12 generations of parasites and are used to evaluate a potential impact of PZQ resistance on the parasite fitness.</p>
Sanger sequencing traces of specific exons of the Sm.TRPM_PZQ gene from schistosome field samples
<p>Praziquantel (PZQ) is the only drug available to treat schistosomiasis, which is caused by schistosome blood flukes. In <em>Schistosoma mansononi</em>, the transient receptor potential (TRP) channel Sm.TRPM<sub>PZQ</sub> is strongly suspected to be the target of PZQ. Our <a href="https://doi.org/10.1101/2021.06.09.447779">genetic analysis of <em>S. mansoni</em> response to PZQ</a> revealed a QTL on its chromosome 3 which contains the <em>Sm.TRPM<sub>PZQ</sub></em> gene, strongly suggesting that <em>Sm.TRPM<sub>PZQ</sub></em> could be responsible for PZQ resistance. Therefore, understanding the natural variation in this gene and identifying potential resistance alleles will be a valuable tool for monitoring mass treatment programs aimed at schistosomiasis elimination.</p> <p>We investigated our schistosome collection to examine mutations present in <em>Sm.TRPM<sub>PZQ</sub></em> in natural schistosome populations. We analyzed exome sequencing data from 259 miracidia, cercariae or adult parasites from 3 African countries (Senegal, Niger, Tanzania), the Middle East (Oman) and South America (Brazil). We were able to sequence 36/41 exons of <em>Sm.TRPM<sub>PZQ</sub></em> from 122/259 parasites on average (s.e. = 18.65). We identified several mutations in critical areas of the channel. However, these mutations were supported by a limited number of reads only and required confirmation by Sanger sequencing.</p> <p>The present dataset corresponds to the sequencing effort done on specific exons which carried the mutations to be confirmed. We generated PCR products which were sequenced on on ABI sequencer using Eurofins Genomics services. The SCF files were then analyzed using PolyPhred (see manuscript for details about PCR conditions and data analysis). The trace files are available in the traces folder. Each filename carries a barcode which corresponds to a combination of sample, exon, and primer. All the combinations and corresponding barcodes are listed in the barcode_list.tsv file.</p> <p>Table header details of the barcode list:</p> <ul> <li><em>Sample</em>: the name of sample. The sample coding is as follows: species.country_patientID. BR: Brazil, SN: Senegal, NE: Niger, TZ: Tanzania, OM: Oman.</li> <li><em>Exon</em>: the exon targeted. The exon number corresponds to the exon number of isoform 5 and not the exon number of the gene.</li> <li><em>Barcode</em>: the barcode provided by Eurofins Genomics.</li> <li><em>Primer</em>: the primer used for sequencing. F: forward, R: reverse.</li> </ul>
A self-purifying microfluidic system for identifying drugs acting against adult schistosomes
<p><span>The discovery of novel antihelmintic molecules to combat the development and spread of schistosomiasis, a disease caused by several <em>Schistosoma</em> flatworm species, mobilizes significant research efforts worldwide. With a limited number of biochemical assays for measuring the viability of adult worms, the anti-schistosomicidal activity of molecules is usually evaluated by microscopic observation of worm mobility and/or integrity upon drug exposure. Even if these phenotypical assays enable multiple parameters analysis, they are often conducted during several days and need to be associated with image-based analysis to minimized subjectivity. We describe here a self-purifying microfluidic system enabling the selection of healthy adult worms and the identification of molecules acting instantly on the parasite. The worms are assayed in a dynamic environment that eliminates unhealthy worms that cannot attach firmly to the chip walls prior to being exposed to the drug. The detachment of the worms is also used as a second step readout for identifying active compounds. We have validated this new fluidic screening approach using the two major antihelmintic drugs, Praziquantel and Artemisinin. The reported dynamic system is simple to produce and to parallelize. Importantly, it enables quick and sensitive detection of antischistosomal compounds in no more than one hour. </span></p>
Temperature affects predation of schistosome-competent snails by a novel invader, the marbled crayfish Procambarus virginalis
<p><span>The human burden of environmentally transmitted infectious diseases can depend strongly on ecological factors, including the presence or absence of natural enemies. The marbled crayfish (<em>Procambarus</em> <em>virginalis</em>) is a novel invasive species that can tolerate a wide range of ecological conditions and colonize diverse habitats. Marbled crayfish first appeared in Madagascar in 2005 and quickly spread across the country, overlapping with the distribution of freshwater snails that serve as the intermediate host of schistosomiasis–a parasitic disease of poverty with human prevalence ranging up to 94% in Madagascar. It has been hypothesized that the marbled crayfish may serve as a predator of schistosome-competent snails in areas where native predators cannot and yet no systematic study to date has been conducted to estimate its predation rate on snails. Here, we experimentally assessed marbled crayfish consumption of uninfected and infected schistosome-competent snails (<em>Biomphalaria</em> <em>glabrata</em> and <em>Bulinus</em> <em>truncatus</em>) across a range of temperatures, reflective of the habitat range of the marbled crayfish in Madagascar. We found that the relationship between crayfish consumption and temperature is unimodal with a peak at ~27.5°C. Per-capita consumption increased with body size and was not affected either by snail species or their infectious status. We detected a possible satiation effect, i.e., a small but significant reduction in per-capita consumption rate over the 72-hour duration of the predation experiment. Our results suggest that ecological parameters, such as temperature and crayfish weight, influence rates of consumption and, in turn, the potential impact of the marbled crayfish invasion on snail host populations. </span></p>
Data from: First evidence of a genetic basis for thermal adaptation in a schistosome host snail
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Temperature affects predation of schistosome-competent snails by a novel invader, the marbled crayfish Procambarus virginalis
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A self-purifying microfluidic system for identifying drugs acting against adult schistosomes
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Striking differences in virulence, transmission, and sporocyst growth dynamics between two schistosome populations
<p>Dataset (v2) associated with the accepted publication in Parasites & Vectors - Striking differences in virulence, transmission, and sporocyst growth dynamics between two schistosome populations.</p>
No evidence for schistosome parasite fitness trade-offs in the intermediate and definitive host - Phenotype dataset
<p>The present dataset contains all the phenotype data (.csv files) and R scripts used for data analysis, and to generated the figures (Figures 2 to 5) present in the manuscript entitled "No evidence for schistosome parasite fitness trade-offs in the intermediate and definitive host".</p> <p>The uploaded archive (.zip) contains 4 folders corresponding to the 4 Figures present in the manuscript (Figure 2, Figure 3, Figure 4 and Figure 5). Each folder contains the phenotype data tables (.csv files), a R script used to analyze the data and to generate the Figures and a readme file, explaining how the phenotype data tables are organized.</p>
Data from: Host immunity, nutrition and coinfection alter longitudinal infection patterns of schistosomes in a free ranging African buffalo population
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Contribution of parasite and host genotype to immunopathology of schistosome infections
<p>The present dataset contains all the phenotype data (.csv files) and R scripts used for data analysis and generation of figures (Fig. 2-6) present in the manuscript entitled "Contribution of parasite and host genotype to immunopathology of schistosome infections."</p>
Figure 2. The cytochrome c oxidase 1 in Evidence Of A Putative Novel Species Of Avian Schistosome Infecting Planorbella Trivolvis
Figure 2. The cytochrome c oxidase 1 (COI) phylogenetic tree including members of the avian Schistosomatidae. Nodal support indicated by Bayesian posterior probabilities. GenBank accession numbers precede taxon names. The representative sample from this study is in bold.
Figure 1. The 28S in Evidence Of A Putative Novel Species Of Avian Schistosome Infecting Planorbella Trivolvis
Figure 1. The 28S phylogenetic tree of Schistosomatidae. Nodal sup- port indicated by Bayesian posterior probabilities. GenBank accession numbers precede taxon names. The representative sample from this study is in bold.
Antioxidant Supplements in the Reversal of Schistosomal Peri-portal Fibrosis
ClinicalTrials.gov study NCT01260012. IPD Sharing: Not stated. Countries: 1. Publications: 8.
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