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16 results for “within-host competition”

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zenodo40/100

Fig. 4 in Outcome of within-host competition demonstrates that parasite virulence doesn't equal success in a myxozoan model system

Fig. 4. Total number of a) genotype-I and b) genotype-II myxospores produced per actinospore, as a measure of parasite success, in fish from single and mixedgenotype treatments. Black bars denote genotype-I only, white denote genotype-II only, and grey denote mixed-genotype treatments. Letters indicate treatments that differed (Tukey's HSD tests, α = 0.05).

opencc-by-4.0Aug 2019View details →
zenodo40/100

Fig. 3 in Outcome of within-host competition demonstrates that parasite virulence doesn't equal success in a myxozoan model system

Fig. 3. Parasite copy number, as a measure of parasite competition in mixed-genotype treatments, in a) gill tissue sampled at 7d (t7), b) gill tissue sampled at 14d (t14) c) intestinal tissue sampled at 7d, and d) intestinal tissue sampled at 14d. Black bars denote genotype-I only, white denote genotype-II only, and grey denote mixedgenotype treatments. Inset striped grey bars represent total genotype I copy numbers, based on the proportion of genotype I in sequenced DNA samples (genotype II comprises the remainderthe solid grey bar). Letters indicate treatments that differed (Tukey's HSD tests, α = 0.05). Total number of genotype-I (black circles) and genotype-II (white circles) myxospores produced per actinospore, as a measure of parasite success in fish overlaid on parasite copy number in intestinal tissue sampled at 14d.

opencc-by-4.0Aug 2019View details →
zenodo40/100

Fig. 2 in Outcome of within-host competition demonstrates that parasite virulence doesn't equal success in a myxozoan model system

Fig. 2. Median day to death, as a measure of parasite virulence, in treatment groups. Black bars denote genotype-I only, white denote genotype-II only, and grey denote mixed-genotype treatments. Letters indicate treatments that differed (Tukey's HSD tests, α = 0.05).

opencc-by-4.0Aug 2019View details →
zenodo40/100

Fig. 1 in Outcome of within-host competition demonstrates that parasite virulence doesn't equal success in a myxozoan model system

Fig. 1. Experimental schematic and timeline. Timeline begins at t-3 when density of parasites in polychaete cultures (inset a) was estimated in replicate water samples to calculate dose administered on t0 and t6. Specific-pathogen-free (SPF) well water ("W") was used as a negative control and a mock exposure t0 and t6 in treatments that received no parasites on those exposure dates "W"- denotes water, "I: denotes genotype-I and "II" denotes genotype-II (inset b). * denote treatments used for cytokine and immunoglobulin assays (b).

opencc-by-4.0Aug 2019View details →
dryad32/100

Data from: Predators and patterns of within-host growth can mediate both among-host competition and the evolution of transmission potential of parasites

Parasite prevalence shows tremendous spatiotemporal variation. Theory indicates this variation might stem from life history characteristics of parasites and key ecological factors. Here, we illustrate how the interaction of an important predator and the schedule of 'transmission potential' of two parasites can explain parasite abundance. A field survey showed that a non-castrating fungus (Metschnikowia bicuspidata) commonly infected a dominant zooplankton host (Daphnia dentifera), while a castrating bacterial parasite (Pasteuria ramosa) was rare. This result seemed surprising given that the bacterium produces many more infectious propagules (spores) than the fungus upon host death. The fungus's dominance can be explained by the schedule of within host growth of parasites (i.e., how transmission potential changes over the course of infection) and spore release from 'sloppy predators' (Chaoborus spp., who consume Daphnia prey whole, then later regurgitate the carapace and parasite spores). In essence, sloppy predators create a niche that the faster-schedule fungus currently occupies. However, a selection experiment showed the slower-schedule bacterium can evolve into this faster-schedule, predator-mediated niche (but pays a cost in maximal spore yield to do so). Hence, our study shows how parasite life history can interact with predation to strongly influence the ecology, epidemiology, and evolution of infectious disease. 18 pages, 1 table, 5 figures; Appendix

opencc-zeroDec 2013View details →
dryad32/100

Data from: Predators and patterns of within-host growth can mediate both among-host competition and the evolution of transmission potential of parasites

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publicMar 2014View details →
dryad32/100

Data from: Alternative paths to success in a parasite community: within-host competition can favor higher virulence or direct interference

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publicSep 2012View details →
dryad32/100

Data from: Within-host competition between Borrelia afzelii ospC strains in wild hosts as revealed by massively parallel amplicon sequencing

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publicMay 2016View details →
dryad28/100

Data from: Within-host competition in genetically diverse malaria infections: parasite virulence and competitive success.

Humans and animals often become coinfected with pathogen strains that differ in virulence. The ensuing interaction between these strains can, in theory, be a major determinant of the direction of selection on virulence genes in pathogen populations. Many mathematical analyses of this assume that virulent pathogen lineages have a competitive advantage within coinfected hosts and thus predict that pathogens will evolve to become more virulent where genetically diverse infections are common. Although the implications of these studies are relevant to both fundamental biology and medical science, direct empirical tests for relationships between virulence and competitive ability are lacking. Here we use newly developed strain-specific real-time quantitative polymerase chain reaction protocols to determine the pairwise competitiveness of genetically divergent Plasmodium chabaudi clones that represent a wide range of innate virulences in their rodent host. We found that even against their background of widely varying genotypic and antigenic properties, virulent clones had a competitive advantage in the acute phase of mixed infections. The more virulent a clone was relative to its competitor, the less it suffered from competition. This result confirms our earlier work with parasite lines derived from a single clonal lineage by serial passage and supports the virulence-competitive ability assumption of many theoretical models. To the extent that our rodent model captures the essence of the natural history of malaria parasites, public health interventions which reduce the incidence of mixed malaria infections should have beneficial consequences by reducing the selection for high virulence.

opencc-zeroDec 2013View details →
dryad28/100

Data from: Resource limitation prevents the emergence of drug resistance by intensifying within-host competition

Slowing the evolution of antimicrobial resistance is essential if we are to continue to successfully treat infectious diseases. Whether a drug-resistant mutant grows to high densities, and so sickens the patient and spreads to new hosts, is determined by the competitive interactions it has with drug-susceptible pathogens within the host. Competitive interactions thus represent a good target for resistance management strategies. Using an in vivo model of malaria infection, we show that limiting a resource that is disproportionately required by resistant parasites retards the evolution of drug resistance by intensifying competitive interactions between susceptible and resistant parasites. Resource limitation prevented resistance emergence regardless of whether resistant mutants arose de novo or were experimentally added before drug treatment. Our work provides proof of principle that chemotherapy paired with an "ecological" intervention can slow the evolution of resistance to antimicrobial drugs, even when resistant pathogens are present at high frequencies. It also suggests that a broad range of previously untapped compounds could be used for treating infectious diseases.

opencc-zeroDec 2016View details →
zenodo28/100

Fig. 6 in Outcome of within-host competition demonstrates that parasite virulence doesn't equal success in a myxozoan model system

Fig. 6. Log fold change in immunogloblulin expression relative to controls on day 14 in intestine samples. Parasite copy numbers measured in intestine samples are overlaid on IgM intestine plot (parasite copy number data are the same for the IgT plot). Letters denote treatments that differed (Tukey's HSD tests, α = 0.05).

opencc-by-4.0Aug 2019View details →
zenodo28/100

Fig. 5 in Outcome of within-host competition demonstrates that parasite virulence doesn't equal success in a myxozoan model system

Fig. 5. Log-foldchange in cytokine expression relative to controls at day-14 in spleen and intestine samples. Parasite copy numbers measured in gill tissues is overlaid on IFN-gamma spleen plot and parasite copy numbers measured in intestine samples are overlaid on IFN-gamma intestine plot, but parasite copy number data are the same for, and apply to, all cytokine plots underneath. Letters denote treatments that differed (Tukey's HDS tests, α = 0.05).

opencc-by-4.0Aug 2019View details →
dryad28/100

Data from: Within-host competition in genetically diverse malaria infections: parasite virulence and competitive success.

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publicFeb 2014View details →
dryad28/100

Data from: Within-host competition and drug resistance in the human malaria parasite Plasmodium falciparum

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publicFeb 2016View details →
dryad28/100

Data from: Resource limitation prevents the emergence of drug resistance by intensifying within-host competition

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publicDec 2018View details →
dryad28/100

Data from: Host sexual dimorphism affects the outcome of within-host pathogen competition

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publicMay 2019View details →

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