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17 results for “rodent malaria”
The effect of parasite dose on disease severity in the rodent malaria Plasmodium chabaudi
<p>Experiments were designed to look at the relationship between infective dose and disease severity using two clones of <em>Plasmodium chabaudi</em> that differ in virulence. We asked whether there were dose–severity relationships, whether clone differences in virulence were maintained over a range of doses, and whether disease severity could be accounted for by parasite dynamics. Groups of mice were infected with parasite doses differing by an order of magnitude, ranging from 100 to 1×10<sup><sup>8</sup></sup> parasites. Infective dose affected the probability of death, but only with the more virulent clone. Dose also affected morbidity. For both clones, higher doses induced greater anaemia. Larger doses caused greater weight loss, but only for infections with the more virulent clone. Here, for a given dose, mice lost a fixed amount of weight, irrespective of their initial weight. Larger doses induced earlier mortality and morbidity than did lower dose treatments. Finally, dose affected parasite dynamics, with earlier and higher peak parasite densities in larger dose infections. All these effects were small relative to clone differences in disease severity, which were apparent across the range of doses. Dose effects were manifested through the timing and/or magnitude of peak parasite densities, broadly supporting the idea that dose affects disease severity by altering the time the host has to control parasite densities and ameliorate the effects of parasites. We discuss the possible efficacy of intervention strategies aimed at reducing human disease severity by reducing infective parasite dose.</p>
The effect of parasite dose on disease severity in the rodent malaria Plasmodium chabaudi
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Data from: A nutrient mediates intraspecific competition between rodent malaria parasites in vivo
Hosts are often infected with multiple strains of a single parasite species. Within-host competition between parasite strains can be intense and has implications for the evolution of traits that impact patient health, such as drug resistance and virulence. Yet the mechanistic basis of within-host competition is poorly understood. Here, we demonstrate that a parasite nutrient, para-aminobenzoic acid (pABA), mediates competition between a drug resistant and drug susceptible strain of the malaria parasite, Plasmodium chabaudi. We further show that increasing pABA supply to hosts infected with the resistant strain worsens disease and changes the relationship between parasite burden and pathology. Our experiments demonstrate that, even when there is profound top-down regulation (immunity), bottom-up regulation of pathogen populations can occur and that its importance may vary during an infection. The identification of resources that can be experimentally controlled opens up the opportunity to manipulate competitive interactions between parasites and hence their evolution.
Data from: The fitness of drug-resistant malaria parasites in a rodent model: multiplicity of infection
Malaria infections normally consist of more than one clonally-replicating lineage. Within-host interactions between sensitive and resistant parasites can have profound effects on the evolution of drug resistance. Here, using the Plasmodium chabaudi mouse malaria model, we ask whether the costs and benefits of resistance are affected by the number of co-infecting strains competing with a resistant clone. We found strong competitive suppression of resistant parasites in untreated infections and marked competitive release following treatment. The magnitude of competitive suppression depended on competitor identity. However, there was no overall effect of the diversity of susceptible parasites on the extent of competitive suppression or release. If these findings generalize, then transmission intensity will impact on resistance evolution because of its effect on the frequency of mixed infections, not because of its effect on the distribution of clones per host. This would greatly simplify the computational problems of adequately capturing within-host ecology in models of drug resistance evolution in malaria.
Fig. 1 in Rodent malaria in Gabon: Diversity and host range
Fig. 1. Location of the provinces of Gabon where rodent samples were collected. The map shows the sites where rodents were captured (in red) and the site where some Anopheles infected with rodent malaria parasites were found in a previous study (in green) (Makanga et al., 2016). The number of individuals collected in each province is indicated between brackets. (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)
Fig. 4 in Rodent malaria in Gabon: Diversity and host range
Fig. 4. Map showing the distribution of rodent malaria parasite species in Central Africa. This map is based on the data provided in Landau and Chabau (1994) (blue) and the data obtained in our study (red). P. v.: Plasmodium vinckei; P. y.: Plasmodium yoelii; P. c: Plasmodium chabaudi; P. v: Plasmodium vinckei; P. berghei: Plasmodium berghei and P. sp. GAB: Plasmodium sp GAB. (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)
Fig. 2 in Rodent malaria in Gabon: Diversity and host range
Fig. 2. Phylogenetic relationships between the CYTB sequences of Plasmodium parasites obtained in our study (in colour) and the sequences obtained from existing databases (in black). The tree was built using partial CYTB sequences (700 bp-long). The names of our isolates (for instance, n14GB-Ron48_Mus musculus-DJM) include: 1) the year and country of collection (n14GB: n14: 2014 and GB: Gabon); 2) the sample number (Ron48: Rodent number 48); 3) the rodent species and 4) the abbreviation of the sample site (FCV: Franceville; MIM: Mimongo, LEK: Lekoni, DJM: Djoumou; MKK: Makokou; KLM: Koulamoutou). The name of isolates clustering with Plasmodium yoelii is in green, and of isolates clustering with Plasmodium vinckei is in blue. CAM: Cameroon and CAR: Central African Republic. In our study we called P. sp. GAB the new Plasmodium lineage found in some Gabonese rodents. (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)
Fig. 3 in Rodent malaria in Gabon: Diversity and host range
Fig. 3. Map of malaria parasite distribution for each host species and infection rate for each Plasmodium species or lineage (Plasmodium yoelii spp, Plasmodium vinckei lentum, and Plasmodium sp GAB). a) for Mus musculus; b) for Lemniscomys striatus; c) for Mastomys natalensis; d) for Praomys sp. and e) for Grammomys poensis. Plasmodium sp GAB (P. sp. GAB) corresponds to the new phylogenetic lineage of rodent Plasmodium described in our study.
Data from: The fitness of drug-resistant malaria parasites in a rodent model: multiplicity of infection
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Data from: A nutrient mediates intraspecific competition between rodent malaria parasites in vivo
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Data from: The evolutionary consequences of blood-stage vaccination on the rodent malaria Plasmodium chabaudi
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The dynamic change of immune responses between acute and recrudescence stages of rodent malaria infection
GEO Series GSE192930. Mus musculus. 3 samples. Type: Expression profiling by high throughput sequencing.
Impact of dietary restriction (DR) on the transcriptome of the rodent malaria parasite Plasmodium berghei [microarray]
GEO Series GSE69628. Plasmodium berghei. 24 samples. Type: Expression profiling by array.
Rodent malaria parasite RNA does not affect mouse BeadChip results
GEO Series GSE145634. Plasmodium chabaudi; Mus musculus. 10 samples. Type: Expression profiling by array.
Global gene expression of the rodent malaria parasites Plasmodium yoelii, Plasmodium berghei and Plasmodium chabaudi blood-stage parasites
GEO Series GSE80015. Plasmodium yoelii; Plasmodium berghei; Plasmodium chabaudi. 36 samples. Type: Expression profiling by array.
Comprehensive immune profiling reveals IFN-γ signaling in T cells mediates parasite phagocytosis in a rodent malaria model : Spatial transcriptomics data
GEO Series GSE283333. Mus musculus. 2 samples. Type: Other.
Comprehensive immune profiling reveals IFN-γ signaling in T cells mediates parasite phagocytosis in a rodent malaria model : Bulk RNA-seq
GEO Series GSE279789. Mus musculus. 28 samples. Type: Expression profiling by high throughput sequencing.
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Allen Brain Atlas
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International Brain Laboratory public data
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
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