397 research outputs found

    Impact of Anguillicolides crassus on American eels (Anguilla rostrata)

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    American eels Anguilla rostrata are infected by an introduced parasitic nematode Anguillicoloides crassus, which can cause extreme necrosis of their swimbladders, yet effects on the eel population are currently unknown. We collected 3 eel life stages (glass, elver, and yellow) and the presence of A. crassus and swimbladder damage in each eel was quantified. The preliminary data show over 60% prevalence and an even higher prevalence of damaged swimbladders

    Temporal, spatial, and biological variation of nematode epidemiology in American eels

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    This is the accepted manuscript version of the article. American eels (Anguilla rostrata) are infected by the non-native parasitic nematode Anguillicoloides crassus, which can cause severe swim bladder damage. We investigated epidemiology of A. crassus to better understand its population-level effects on American eels. Nematode prevalence, abundance, and intensity and swim bladder damage were quantified in glass eels, elvers, and yellow eels from the lower Chesapeake Bay and related to season of capture, river system, and total length. Age-variant force-of-infection and disease-associated mortality were estimated using a three-state irreversible disease model, which assumes recovery is not possible. Results showed glass eels have very low infection prevalence and severity compared with elvers and yellow eels. Nematode abundance varied by season, river, and eel length, whereas swim bladder damage varied by season and eel length. Nematode abundance and swim bladder damage were weakly positively correlated. Force-of-infection, based on swim bladder damage, peaked at age 2, and disease-positive eels had an estimated lower annual survival probability of 0.76 compared with disease-negative eels. Full understanding of American eel population dynamics will require broader knowledge of cryptic disease-associated mortality throughout North America

    Banner News

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    https://openspace.dmacc.edu/banner_news/1107/thumbnail.jp

    The role of different microbiota in metastatic brain tumors

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    View full abstracthttps://openworks.mdanderson.org/leading-edge/1005/thumbnail.jp

    Limited available evidence supports theoretical predictions of reduced vaccine efficacy at higher exposure dose

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    Understanding the causes of vaccine failure is important for predicting disease dynamics in vaccinated populations and planning disease interventions. Pathogen exposure dose and heterogeneity in host susceptibility have both been implicated as important factors that may reduce overall vaccine efficacy and cause vaccine failure. Here, we explore the effect of pathogen dose and heterogeneity in host susceptibility in reducing efficacy of vaccines. Using simulation-based methods, we find that increases in pathogen exposure dose decrease vaccine efficacy, but this effect is modified by heterogeneity in host susceptibility. In populations where the mode of vaccine action is highly polarized, vaccine efficacy decreases more slowly with exposure dose than in populations with less variable protection. We compared these theoretical results to empirical estimates from a systematic literature review of vaccines tested over multiple exposure doses. We found that few studies (nine of 5,389) tested vaccine protection against infection over multiple pathogen challenge doses, with seven studies demonstrating a decrease in vaccine efficacy with increasing exposure dose. Our research demonstrates that pathogen dose has potential to be an important determinant of vaccine failure, although the limited empirical data highlight a need for additional studies to test theoretical predictions on the plausibility of reduced host susceptibility and high pathogen dose as mechanisms responsible for reduced vaccine efficacy in high transmission settings

    Aquaculture Reuse Water, Genetic Line, and Vaccination Affect Rainbow Trout (Oncorhynchus mykiss) Disease Susceptibility and Infection Dynamics

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    Infectious hematopoietic necrosis virus (IHNV) and Flavobacterium psychrophilum are major pathogens of farmed rainbow trout. Improved control strategies are desired but the influence of on-farm environmental factors that lead to disease outbreaks remain poorly understood. Water reuse is an important environmental factor affecting disease. Prior studies have established a replicated outdoor-tank system capable of varying the exposure to reuse water by controlling water flow from commercial trout production raceways. The goal of this research was to evaluate the effect of constant or pulsed reuse water exposure on survival, pathogen prevalence, and pathogen load. Herein, we compared two commercial lines of rainbow trout, Clear Springs Food (CSF) and Troutex (Tx) that were either vaccinated against IHNV with a DNA vaccine or sham vaccinated. Over a 27-day experimental period in constant reuse water, all fish from both lines and treatments, died while mortality in control fish in spring water was PPP ≤ 0.001), while risk of death did not differ in spring water (P=0.98). Sham-vaccinated fish had 2.1-fold greater risk of death compared to vaccinated fish (P=0.02). Both IHNV prevalence and load were lower in vaccinated fish compared to sham-vaccinated fish, and unexpectedly, F. psychrophilum load associated with fin/gill tissues from live-sampled fish was lower in vaccinated fish compared to sham-vaccinated fish. As a result, up to forty-five percent of unvaccinated fish were naturally co-infected with F. psychrophilum and IHNV and the coinfected fish exhibited the highest IHNV loads. Under laboratory challenge conditions, co-infection with F. psychrophilum and IHNV overwhelmed IHNV vaccine-induced protection. In summary, we demonstrate that exposure to reuse water or multi-pathogen challenge can initiate complex disease dynamics that can overwhelm both vaccination and host genetic resistance

    Elucidating the Role of Microbiome in Low- and High-Grade Glioma

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    https://openworks.mdanderson.org/sumexp22/1117/thumbnail.jp

    Immune-mediated competition in rodent malaria is most likely caused by induced changes in innate immune clearance of merozoites

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    Malarial infections are often genetically diverse, leading to competitive interactions between parasites. A quantitative understanding of the competition between strains is essential to understand a wide range of issues, including the evolution of virulence and drug resistance. In this study, we use dynamical-model based Bayesian inference to investigate the cause of competitive suppression of an avirulent clone of Plasmodium chabaudi (AS) by a virulent clone (AJ) in immuno-deficient and competent mice. We test whether competitive suppression is caused by clone-specific differences in one or more of the following processes: adaptive immune clearance of merozoites and parasitised red blood cells (RBCs), background loss of merozoites and parasitised RBCs, RBC age preference, RBC infection rate, burst size, and within-RBC interference. These processes were parameterised in dynamical mathematical models and fitted to experimental data. We found that just one parameter μ, the ratio of background loss rate of merozoites to invasion rate of mature RBCs, needed to be clone-specific to predict the data. Interestingly, μ was found to be the same for both clones in single-clone infections, but different between the clones in mixed infections. The size of this difference was largest in immuno-competent mice and smallest in immuno-deficient mice. This explains why competitive suppression was alleviated in immuno-deficient mice. We found that competitive suppression acts early in infection, even before the day of peak parasitaemia. These results lead us to argue that the innate immune response clearing merozoites is the most likely, but not necessarily the only, mediator of competitive interactions between virulent and avirulent clones. Moreover, in mixed infections we predict there to be an interaction between the clones and the innate immune response which induces changes in the strength of its clearance of merozoites. What this interaction is unknown, but future refinement of the model, challenged with other datasets, may lead to its discovery
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