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Parasite Transmission (parasite + transmission)
Selected AbstractsThe role of host sex in parasite dynamics: field experiments on the yellow-necked mouse Apodemus flavicollisECOLOGY LETTERS, Issue 2 2004Nicola Ferrari Abstract We investigated the role of host sex in parasite transmission and questioned: ,Is host sex important in influencing the dynamics of infection in free living animal populations?' We experimentally reduced the helminth community of either males or females in a yellow-necked mice (Apodemus flavicollis) population using an anthelmintic, in replicated trapping areas, and subsequently monitored the prevalence and intensity of macroparasites in the untreated sex. We focussed on the dominant parasite Heligmosomoides polygyrus and found that reducing parasites in males caused a consistent reduction of parasitic intensity in females, estimated through faecal egg counts, but the removal of parasites in females had no significant influence on the parasites in males. This finding suggests that males are responsible for driving the parasite infection in the host population and females may play a relatively trivial role. The possible mechanisms promoting such patterns are discussed. [source] VACCINATION, WITHIN-HOST DYNAMICS, AND VIRULENCE EVOLUTIONEVOLUTION, Issue 1 2006Jean-Baptiste André Abstract We explore the potential consequences of vaccination on parasite epidemiology and evolution. Our model combines a microscopic (within-host dynamics) and a macroscopic (epidemiological dynamics) description of the interaction between the parasite and its host. This approach allows relevant epidemiological traits such as parasite transmission, parasite virulence, and host recovery to emerge from a mechanistic model of acute infection describing the interaction between the parasite and the host immune system. We model the effect of a vaccine as an activator of immunity enhancing the replication rate of lymphocytes, their initial density at infection's initiation, their efficacy to kill the parasite, or their activation delay after infection. We analyze the evolution of the replication rate of parasites and show that vaccination may promote the evolution of faster replicating and, consequently, more virulent strains. We also show that intermediate vaccination coverage may lead to the coexistence of two different parasite strategies (a low-virulence strain adapted to naive hosts, and a high-virulence strain, more generalist, adapted to both naive and vaccinated hosts). We discuss the consequences of various vaccination strategies under different epidemiological situations using several distinct measures to evaluate the cost induced by the parasite on individuals and entire host populations. [source] Isolation of cDNA clones encoding putative odourant binding proteins from the antennae of the malaria-transmitting mosquito, Anopheles gambiaeINSECT MOLECULAR BIOLOGY, Issue 2 2002Harald Biessmann Abstract One way of controlling disease transmission by blood-feeding mosquitoes is to reduce the frequency of insect,host interaction, thus reducing the probability of parasite transmission and re-infection. A better understanding of the olfactory processes responsible for allowing mosquitoes to identify human hosts is required in order to develop methods that will interfere with host seeking. We have therefore initiated a molecular approach to isolate and characterize the genes and their products that are involved in the olfactory recognition pathway of the mosquito Anopheles gambiae, which is the main malaria vector in sub-Saharan Africa. We report here the isolation and preliminary characterization of several cDNAs from male and female A. gambiae antennal libraries that encode putative odourant binding proteins. Their conceptual translation products show extensive sequence similarity to known insect odourant binding proteins (OBPs)/pheromone binding proteins (PBPs), especially to those of D. melanogaster. The A. gambiae OBPs described here are expressed in the antennae of both genders, and some of the A. gambiae OBP genes are well conserved in other disease-transmitting mosquito species, such as Aedes aegypti and Culex quinquefasciatus. [source] Does infectious disease influence the efficacy of marine protected areas?JOURNAL OF APPLIED ECOLOGY, Issue 4 2005A theoretical framework Summary 1Marine protected areas are increasingly being recommended as an essential component of the management of exploited marine species, but virtually no attention has been given to the influence of parasites. This may be substantial, as a primary effect of marine reserves is to increase the density of an exploited population within the reserve relative to outside the reserve, which may facilitate parasite transmission. 2We used a simple deterministic model of microparasitic infection in a fishery with a reserve to investigate equilibrium yield and parasite prevalence inside and outside the reserve as a function of three control variables: the proportion of habitat inside the reserve, fishing mortality and the rate of interchange between the stock and the reserve. 3While our model is generic, we parameterized it with values that may be appropriate to the interaction between abalone and Rickettsia. 4The presence of a pathogen does not necessarily decrease yield when a reserve is present, particularly if the rate of movement of adult hosts between stock and reserve is low. 5Synthesis and applications. Pathogens have important implications for the design of marine reserves. Our modelling identifies two key considerations. First, ,fishing out' a pathogen by reducing the host population density to a level below the threshold for disease maintenance is a potential management strategy that is made more difficult by establishing a reserve. Secondly, the effect of a highly transmissible pathogen without a reserve is to cause a rapid decline in equilibrium yield for efforts beyond those that produce maximum sustainable yield, making the fishery prone to collapse. Introducing a reserve decreases yield in this case, but makes the fishery much more resistant to collapse. [source] Virulence evolution and the trade-off hypothesis: history, current state of affairs and the futureJOURNAL OF EVOLUTIONARY BIOLOGY, Issue 2 2009S. ALIZON Abstract It has been more than two decades since the formulation of the so-called ,trade-off' hypothesis as an alternative to the then commonly accepted idea that parasites should always evolve towards avirulence (the ,avirulence hypothesis'). The trade-off hypothesis states that virulence is an unavoidable consequence of parasite transmission; however, since the 1990s, this hypothesis has been increasingly challenged. We discuss the history of the study of virulence evolution and the development of theories towards the trade-off hypothesis in order to illustrate the context of the debate. We investigate the arguments raised against the trade-off hypothesis and argue that trade-offs exist, but may not be of the simple form that is usually assumed, involving other mechanisms (and life-history traits) than those originally considered. Many processes such as pathogen adaptation to within-host competition, interactions with the immune system and shifting transmission routes, will all be interrelated making sweeping evolutionary predictions harder to obtain. We argue that this is the heart of the current debate in the field and while species-specific models may be better predictive tools, the trade-off hypothesis and its basic extensions are necessary to assess the qualitative impacts of virulence management strategies. [source] Mechanisms of pathogenesis and the evolution of parasite virulenceJOURNAL OF EVOLUTIONARY BIOLOGY, Issue 2 2008S. A. FRANK Abstract When studying how much a parasite harms its host, evolutionary biologists turn to the evolutionary theory of virulence. That theory has been successful in predicting how parasite virulence evolves in response to changes in epidemiological conditions of parasite transmission or to perturbations induced by drug treatments. The evolutionary theory of virulence is, however, nearly silent about the expected differences in virulence between different species of parasite. Why, for example, is anthrax so virulent, whereas closely related bacterial species cause little harm? The evolutionary theory might address such comparisons by analysing differences in tradeoffs between parasite fitness components: transmission as a measure of parasite fecundity, clearance as a measure of parasite lifespan and virulence as another measure that delimits parasite survival within a host. However, even crude quantitative estimates of such tradeoffs remain beyond reach in all but the most controlled of experimental conditions. Here, we argue that the great recent advances in the molecular study of pathogenesis provide a way forward. In light of those mechanistic studies, we analyse the relative sensitivity of tradeoffs between components of parasite fitness. We argue that pathogenic mechanisms that manipulate host immunity or escape from host defences have particularly high sensitivity to parasite fitness and thus dominate as causes of parasite virulence. The high sensitivity of immunomodulation and immune escape arise because those mechanisms affect parasite survival within the host, the most sensitive of fitness components. In our view, relating the sensitivity of pathogenic mechanisms to fitness components will provide a way to build a much richer and more general theory of parasite virulence. [source] Relatedness affects competitive performance of a parasitic plant (Cuscuta europaea) in multiple infectionsJOURNAL OF EVOLUTIONARY BIOLOGY, Issue 4 2004S. Puustinen Abstract Theoretical models predict that parasite relatedness affects the outcome of competition between parasites, and the evolution of parasite virulence. We examined whether parasite relatedness affects competition between parasitic plants (Cuscuta europaea) that share common host plants (Urtica dioica). We infected hosts with two parasitic plants that were either half-siblings or nonrelated. Relative size asymmetry between the competing parasites was significantly higher in the nonrelated infections compared to infections with siblings. This higher asymmetry was caused by the fact that the performance of some parasite genotypes decreased and that of others increased when grown in multiple infections with nonrelated parasites. This result agrees with the predictions of theories on the evolution of parasite virulence: to enhance parasite transmission, selection may favour reduced competition with genetically related parasites in hosts infected by several genotypes. However, in contrast to the most common predictions, nonrelated infections were not more virulent than the sibling infections. [source] Possible mechanisms underlying age-related resistance to bovine babesiosisPARASITE IMMUNOLOGY, Issue 4 2005Annetta Zintl SUMMARY Calves infected with the tick-borne parasites Babesia spp. do not develop severe clinical babesiosis. Instead they display persistent low parasitaemias without any apparent ill-effects. This age-related resistance not only benefits the host, but also furthers parasite transmission. Both calves and adult animals respond with a Th I immune response to primary infection. Here we hypothesize that the difference in the outcome of infection may at least partly be explained by the localization and timing of the inflammatory response: in calves NO production occurs early and appears to be concentrated in the spleen. On the other hand, there is evidence that a delayed and systemic inflammatory response occurs in adult animals that is ineffectual and probably contributes to the pathogenesis. An improved understanding of the possible mechanisms that underlie this phenomenon may lead to new approaches for the treatment and immune prophylaxis of the disease. [source] Does environmental stress affect insect-vectored parasite transmission?PHYSIOLOGICAL ENTOMOLOGY, Issue 3 2004J. G. Vontas First page of article [source] | ||||||||||