共查询到20条相似文献,搜索用时 31 毫秒
1.
Day T 《Proceedings. Biological sciences / The Royal Society》2002,269(1498):1317-1323
Smallpox causes roughly 20% mortality whereas chickenpox causes less than 0.1%. Most 'verbal' (i.e. non-mathematical) discussions using a mortality definition of virulence would therefore label smallpox as more virulent. Indeed, the virulence of many diseases is measured using such case mortalities, chi, or related measures such as expected host lifespan, T, or lethal dose, LD(x). But chi, T and LD(x) are only indirectly related to parasite-induced instantaneous mortality rate, alpha, which is the mortality measure used in much of the theory developed to explain virulence evolution. Here I point out that relatively deadly pathogens can actually have lower values of alpha than benign pathogens, demonstrating that alpha does not, by itself, reflect the extent to which a parasite causes host mortality. I present mathematical relationships between alpha and chi, T and LD(x), and use these to demonstrate that predictions about virulence evolution can be qualitatively altered depending upon which measure is used as the definition of virulence. Two simple examples are presented to illustrate this point, one of which demonstrates that the well-cited prediction that virulence should evolve to be higher when disease-independent host mortality increases need not hold. This prediction has been made in terms of parasite-induced instantaneous mortality, alpha, but if virulence is measured using case mortality (or T or LD(x)) then this prediction can easily be reversed. Theoretical and empirical researchers must use compatible mortality measures before a productive exchange between the two can take place, and it is suggested that case mortality (or lethal dose) is best suited as a single (mortality) measure of parasite virulence. 相似文献
2.
A. P. Møller E. Arriero E. Lobato S. Merino 《Biological reviews of the Cambridge Philosophical Society》2009,84(4):567-588
Parasitism is a common cause of host mortality, but little is known about the ecological factors affecting parasite virulence (the rate of mortality among infected hosts). We reviewed 117 field estimates of parasite-induced nestling mortality in birds, showing that there was significant consistency in mortality among host and parasite taxa. Virulence increased towards the tropics in analyses of both species-specific data and phylogenetic analyses. We found evidence of greater parasite prevalence being associated with reduced virulence. Furthermore, bird species breeding in open nest sites suffered from greater parasite-induced mortality than hole-nesting species. By contrast, parasite specialization and generation time of parasites relative to that of hosts explained little variation in virulence. Likewise, there were little or no significant effects of host genetic variability, host sociality, host migration, host insular distribution or host survival on parasite virulence. These findings suggest that parasite-induced nestling mortality in birds is mainly determined by geographical location and to a smaller extent nest site and prevalence. 相似文献
3.
Stéphane Cornet Nathalie Franceschi Lo?c Bollache Thierry Rigaud Gabriele Sorci 《Proceedings. Biological sciences / The Royal Society》2009,276(1676):4229-4236
Parasites often manipulate host immunity for their own benefit, either by exacerbating or suppressing the immune response and this may directly affect the expression of parasite virulence. However, genetic variation in immunodepression, which is a prerequisite to its evolution, and the relationship between immunodepression and virulence, have rarely been studied. Here, we investigated the variation among sibships of the acanthocephalan parasite, Pomphorhynchus laevis, in infecting and in immunodepressing its amphipod host, Gammarus pulex. We also assessed the covariation between infectivity, parasite-induced immune depression and host mortality (parasite virulence). We found that infectivity, the intensity of immunodepression and virulence were variable among parasite sibships. Infectivity and the level of immunodepression were not correlated across parasite sibships. Whereas infectivity was unrelated to host mortality, we found that gammarids that were exposed to the parasite sibships that immunodepressed their hosts the most survived better. This positive covariation between host survival and immunodepression suggests that gammarids exposed to the less immunodepressive parasites could suffer from damage imposed by a higher activity of the phenoloxidase. 相似文献
4.
Evolution of virulence in a heterogeneous host population 总被引:1,自引:0,他引:1
Regoes RR Nowak MA Bonhoeffer S 《Evolution; international journal of organic evolution》2000,54(1):64-71
Abstract.— There is a large body of theoretical studies that investigate factors that affect the evolution of virulence, that is parasite-induced host mortality. In these studies the host population is assumed to be genetically homogeneous. However, many parasites have a broad range of host types they infect, and trade-offs between the parasite virulence in different host types may exist. The aim of this paper is to study the effect of host heterogeneity on the evolution of parasite virulence. By analyzing a simple model that describes the replication of different parasite strains in a population of two different host types, we determine the optimal level of virulence in both host types and find the conditions under which strains that specialize in one host type dominate the parasite population. Furthermore, we show that intrahost evolution of the parasite during an infection may lead to stable polymorphisms and could introduce evolutionary branching in the parasite population. 相似文献
5.
Garamszegi LZ 《Ecology letters》2006,9(8):933-940
Parasite virulence, i.e. the damage done to the host, may be a by-product of the parasite's effort to maximize its fitness. Accordingly, several life-history trade-offs may explain interspecific differences in virulence, but such constraints remain little tested in an evolutionary context. In this phylogenetic study of primate malarias, I investigated the relationship between virulence and other parasite life-history traits. I used peak parasitaemia as a proxy for virulence, because it reflected parasite reproductive success and parasite-induced mortality. Peak parasitaemia was higher in specialist than in generalist species, even when confounding life-history traits were controlled. While there was a significant phylogenetic relationship between the number of competitors per host and host specialization, peak parasitaemia was unrelated to within-host competition. Therefore, the key evolutionary factor that favours virulence is host specialization, and the evolutionary success of virulent parasites, such as Plasmodium falciparum , may be better understood when the trade-off in virulence between different hosts is considered. Such phylogenetic results may help us design better protection programmes against malaria. 相似文献
6.
Dieter Ebert Katrina L. Mangin 《Evolution; international journal of organic evolution》1997,51(6):1828-1837
It is predicted that host exploitation should evolve to maximize parasite fitness and that virulence (= parasite-induced host mortality) evolves along with the rate of host exploitation. If the life expectancy of a parasite is short, it is expected to evolve a higher rate of host exploitation and therefore higher virulence because the penalty to the parasite for killing the host is reduced. We tested this hypothesis by keeping for 14 months the horizontally transmitted microsporidian parasite Glugoides intestinalis in mono-clonal host cultures (Daphnia magna) under conditions of high and low host background mortality. High host mortality, and thus parasite mortality, was achieved by replacing weekly 70–80% of all hosts in a culture with uninfected hosts from stock cultures (Replacement lines). In the low-mortality treatment no replacement took place. Contrary to our expectation, parasites from the Replacement lines evolved a lower within-host growth rate and virulence than parasites from the Nonreplacement lines. Across lines we found a strong positive correlation between within-host growth rate and virulence. We did further experiments to answer the question why our data did not support the predictions. Sporophorous vesicles (SVs, spore clusters) were smaller in doubly infected than in singly infected host-gut cells, indicating that competition within cells bears costs for the parasite. Due to our experimental protocol, the average life span of infections had been much higher in the Nonreplacement lines. Since the number of parasites inside a host increases with the time since infection, long-lasting infections led to high frequencies of multiply infected host-gut cells. Therefore, we speculated that within-cell competition was more severe in the Nonreplacement lines and may have led to selection for accelerated within-host growth. SVs in the Nonreplacement lines were indeed significantly larger. Our results point out that single-factor explanations for the evolution of virulence can lead to wrong predictions and that multiple infections are an important factor in virulence evolution. 相似文献
7.
Spatial variation in parasite-induced mortality in an amphipod: shore height versus exposure history 总被引:1,自引:0,他引:1
Characterizing the causes of spatial and temporal variation in parasite-induced mortality under natural conditions is crucial to better understanding the factors driving host population dynamics. Our goal was to quantify this variation in the amphipod Paracalliope novizealandiae, a second intermediate host of the trematode, Maritrema novaezealandensis. If infection and development of trematode metacercariae are benign, we expected mature metacercariae to accumulate within amphipods inhabiting high infestation areas. In field samples, intensity levels of mature metacercariae decreased linearly when amphipods harbored >5 immature metacercariae. This finding is consistent with the hypothesis that the parasite can be detrimental at high intensities of infection. Short-term field experiments showed that host survival also declines with the intensity of new infections and drops below 80% when early stage metacercariae reach 10 amphipod?1. However, parasite effects varied over space and time. High-shore amphipods suffered an increased risk of infection in the summer and a lower likelihood of survival: there was a 10–30% decrease in survivorship for any given infection intensity at high- versus low-shore locations. We also tested for differences in the susceptibility of naive and exposed populations using transplant experiments, and found that naive amphipods acquired greater parasite loads (on average, 4.7 vs. 2.8 metacercariae amphipod?1). Because survival decreases rapidly with infection intensity of both early- and late-stage metacercariae, naive populations would suffer considerably if the parasite were to increase its range. Our results indicate that trematode infections cause high mortality in amphipods during summer months under natural conditions, and emphasize that the effects of parasitism vary at local spatial scales and with exposure history. 相似文献
8.
Mosquito mortality and the evolution of malaria virulence 总被引:1,自引:0,他引:1
Ferguson HM Mackinnon MJ Chan BH Read AF 《Evolution; international journal of organic evolution》2003,57(12):2792-2804
Abstract Several laboratory studies of malaria parasites (Plasmodium sp.) and some field observations suggest that parasite virulence, defined as the harm a parasite causes to its vertebrate host, is positively correlated with transmission. Given this advantage, what limits the continual evolution of higher parasite virulence? One possibility is that while more virulent strains are more infectious, they are also more lethal to mosquitoes. In this study, we tested whether the virulence of the rodent malaria parasite P. chabaudi in the laboratory mouse was correlated with the fitness of mosquitoes it subsequently infected. Mice were infected with one of seven genetically distinct clones of P. chabaudi that differ in virulence. Weight loss and anemia in infected mice were monitored for 16–17 days before Anopheles stephensi mosquitoes were allowed to take a blood meal from them. Infection virulence in mice was positively correlated with transmission to mosquitoes (infection rate) and weakly associated with parasite burden (number of oocysts). Mosquito survival fell with increasing oocyst burden, but there was no overall statistically significant relationship between virulence in mice and mosquito mortality. Thus, there was no evidence that more virulent strains are more lethal to mosquitoes. Both vector survival and fecundity depended on parasite clone, and contrary to expectations, mosquitoes fed on infections more virulent to mice were more fecund. The strong parasite genetic effects associated with both fecundity and survival suggests that vector fitness could be an important selective agent shaping malaria population genetics and the evolution of phenotypes such as virulence in the vector. 相似文献
9.
In this article we explore how host survival and fecundity are affected by host-parasite coevolution. We examine a situation in which hosts upon being infected can mount a defensive response to clear the infection, but in which there is a fecundity cost to such immunological up-regulation. We also suppose that the parasite exploits the host and thereby causes an elevated host mortality rate. We determine the coevolutionary stable strategies of the parasite's level of exploitation and the host's level of up-regulation, and illustrate the patterns of reduced host fitness (i.e., virulence) that these produce. We find that counterintuitive patterns of virulence are often expected to arise as a result of the interaction between coevolved host and parasite strategies. In particular, despite the fact that the parasite imposes only a mortality cost on the host, coevolution by the host results in a pattern whereby infected hosts always have the same probability of death from infection, but they vary in the extent to which their fecundity is reduced. This contrasts with previous results and arises from our inclusion of two important factors absent from previous theory: costs of immunological up-regulation and a more suitable measure of parasite-induced mortality. 相似文献
10.
Regoes RR Ebert D Bonhoeffer S 《Proceedings. Biological sciences / The Royal Society》2002,269(1488):271-279
In many epidemiological models of microparasitic infections it is assumed that the infection process is governed by the mass-action principle, i.e. that the infection rate per host and per parasite is a constant. Furthermore, the parasite-induced host mortality (parasite virulence) and the reproduction rate of the parasite are often assumed to be independent of the infecting parasite dose. However, there is empirical evidence against those three assumptions: the infection rate per host is often found to be a sigmoidal rather than a linear function of the parasite dose to which it is exposed; and the lifespan of infected hosts as well as the reproduction rate of the parasite are often negatively correlated with the parasite dose. Here, we incorporate dose dependences into the standard modelling framework for microparasitic infections, and draw conclusions on the resulting dynamics. Our model displays an Allee effect that is characterized by an invasion threshold for the parasite. Furthermore, in contrast to standard epidemiological models a parasite strain needs to have a basic reproductive rate that is substantially greater than 1 to establish an infection. Thus, the conditions for successful invasion of the parasite are more restrictive than in mass-action infection models. The analysis further suggests that negative correlations of the parasite dose with host lifespan and the parasite reproduction rate helps the parasite to overcome the invasion constraints of the Allee-type dynamics. 相似文献
11.
Jacobus C. de Roode Sonia Altizer 《Evolution; international journal of organic evolution》2010,64(2):502-514
Evolutionary models predict that parasite virulence (parasite-induced host mortality) can evolve as a consequence of natural selection operating on between-host parasite transmission. Two major assumptions are that virulence and transmission are genetically related and that the relative virulence and transmission of parasite genotypes remain similar across host genotypes. We conducted a cross-infection experiment using monarch butterflies and their protozoan parasites from two populations in eastern and western North America. We tested each of 10 host family lines against each of 18 parasite genotypes and measured virulence (host life span) and parasite transmission potential (spore load). Consistent with virulence evolution theory, we found a positive relationship between virulence and transmission across parasite genotypes. However, the absolute values of virulence and transmission differed among host family lines, as did the rank order of parasite clones along the virulence-transmission relationship. Population-level analyses showed that parasites from western North America caused higher infection levels and virulence, but there was no evidence of local adaptation of parasites on sympatric hosts. Collectively, our results suggest that host genotypes can affect the strength and direction of selection on virulence in natural populations, and that predicting virulence evolution may require building genotype-specific interactions into simpler trade-off models. 相似文献
12.
13.
Mennerat A Hamre L Ebert D Nilsen F Dávidová M Skorping A 《Journal of evolutionary biology》2012,25(5):856-861
Models of virulence evolution for horizontally transmitted parasites often assume that transmission rate (the probability that an infected host infects a susceptible host) and virulence (the increase in host mortality due to infection) are positively correlated, because higher rates of production of propagules may cause more damages to the host. However, empirical support for this assumption is scant and limited to microparasites. To fill this gap, we explored the relationships between parasite life history and virulence in the salmon louse, Lepeophtheirus salmonis, a horizontally transmitted copepod ectoparasite on Atlantic salmon Salmo salar. In the laboratory, we infected juvenile salmon hosts with equal doses of infective L. salmonis larvae and monitored parasite age at first reproduction, parasite fecundity, area of damage caused on the skin of the host, and host weight and length gain. We found that earlier onset of parasite reproduction was associated with higher parasite fecundity. Moreover, higher parasite fecundity (a proxy for transmission rate, as infection probability increases with higher numbers of parasite larvae released to the water) was associated with lower host weight gain (correlated with lower survival in juvenile salmon), supporting the presence of a virulence–transmission trade‐off. Our results are relevant in the context of increasing intensive farming, where frequent anti‐parasite drug use and increased host density may have selected for faster production of parasite transmission stages, via earlier reproduction and increased early fecundity. Our study highlights that salmon lice, therefore, are a good model for studying how human activity may affect the evolution of parasite virulence. 相似文献
14.
Host-parasite coevolution can lead to a variety of outcomes, but whereas experimental studies on clonal populations have taken prominence over the last years, experimental studies on obligately out-crossing organisms are virtually absent so far. Therefore, we set up a coevolution experiment using four genetically distinct lines of Tribolium castaneum and its natural obligately killing microsporidian parasite, Nosema whitei. After 13 generations of experimental coevolution, we employed a time-shift experiment infecting hosts from the current generation with parasites from nine different time points in coevolutionary history. Although initially parasite-induced mortality showed synchronized fluctuations across lines, a general decrease over time was observed, potentially reflecting evolution towards optimal levels of virulence or a failure to adapt to coevolving sexual hosts. 相似文献
15.
One of the most accepted views in the theoretical literature on virulence evolution is that a parasite's virulence will evolve to higher levels when its host's background mortality rate increases. Surprisingly, however, although many sources of background mortality involve predation, there has not yet been any theoretical research that explicitly considers how the dynamics of this important ecological interaction affects virulence evolution. Here, we consider how predation affects virulence evolution by explicitly introducing a predator into a classical susceptible–infected–susceptible epidemiological model. We find that, contrary to previous predictions, different sources of host mortality affect virulence evolution in different ways. Moreover, the way in which virulence evolution is affected depends on how tightly coupled the predator's dynamics are to the host population, and this can result in somewhat counterintuitive results. For example, indirect ecological effects can cause elevated host mortality to result in the evolution of lower parasite virulence, even if this elevated mortality arises from factors unrelated to predation. 相似文献
16.
We demonstrate a correlated response of the virulence and the mode of transmission of the microsporidian parasite Edhazardia aedis to selection on the age at pupation of its host, the mosquito Aedes aegypti. We selected three lines of mosquitoes each for early or late pupation and exposed the larvae after zero, two and four generations of selection to a low and a high concentration of the parasite’s spores. Before selection the parasites induced a similar level of mortality in the six lines; after four generations of selection mortality was higher in the mosquitoes selected for late pupation than in those selected for early pupation. Overall, parasite-induced mortality was positively correlated with the mean age at pupation of the matching uninfected line. When they died, mosquitoes selected for early pupation harboured mostly binucleate spores, which are responsible for vertical transmission. Mosquitoes selected for late pupation were more likely to harbour uninucleate spores, which are responsible for horizontal transmission. The parasite enhanced this tendency for horizontal transmission by prolonging the larval period in the lines selected for late pupation, but not in the ones selected for early pupation. These results suggest that the genetic basis of the mosquito’s age at pupation helps to determine the parasite’s mode of transmission: parasites in rapidly developing mosquitoes are benign and transmit vertically, while parasites in slowly developing mosquitoes are virulent and transmit horizontally. Thus, as the host’s life history evolves, the parasite’s performance changes, because the host’s evolution changes the environment in which the parasite develops. 相似文献
17.
Empirical studies often reveal deleterious effects of parasites on host survival, but the ecological and environmental processes modulating parasite‐associated host mortality are not well understood. We conducted meta‐analysis of experimental studies assessing parasite‐associated mortality (n = 52) to evaluate broad‐scale patterns in host mortality risk relative to host or parasite taxon, parasite life cycle, or local environmental conditions. Overall, likelihood of host mortality was ~2.6 times higher among infected individuals when compared with hosts that either lacked parasites or had experimentally‐reduced parasite burdens. Parasites with complex life cycles reliant on predation‐mediated transmission generally were associated with higher mortality risk than those exploiting other transmission strategies. We also detected a negative relationship between parasite‐associated host mortality and latitude; host mortality risk declined by ~2.6% with each degree increase in latitude. This result indicated the likely importance of abiotic factors in determining parasite effects. Host taxonomy further influenced parasite‐associated mortality risk, with amphibian, fish, and mollusc hosts generally having higher hazard than arthropod, mammal, and bird hosts. Our results suggest patterns that conform to the predicted link between host mortality and parasite transmissibility, and pathogenicity. The relationship between host mortality and latitude in particular may portend marked shifts in host–parasite relationships pursuant to ongoing and projected global climate change. 相似文献
18.
Blastocystis is an extracellular, enteric pathogen that induces intestinal disorders in a range of hosts including humans. Recent studies have identified potential parasite virulence factors in and host responses to this parasite; however, little is known about Blastocystis-host attachment, which is crucial for colonization and virulence of luminal stages. By utilizing 7 different strains of the parasite belonging to two clinically relevant subtypes ST-4 and ST-7, we investigated Blastocystis-enterocyte adhesion and its association with parasite-induced epithelial barrier disruption. We also suggest that drug resistance in ST-7 strains might result in fitness cost that manifested as impairment of parasite adhesion and, consequently, virulence. ST-7 parasites were generally highly adhesive to Caco-2 cells and preferred binding to intercellular junctions. These strains also induced disruption of ZO-1 and occludin tight junction proteins as well as increased dextran-FITC flux across epithelial monolayers. Interestingly, their adhesion was correlated with metronidazole (Mz) susceptibility. Mz resistant (Mzr) strains were found to be less pathogenic, owing to compromised adhesion. Moreover, tolerance of nitrosative stress was also reduced in the Mzr strains. In conclusion, the findings indicate that Blastocystis attaches to intestinal epithelium and leads to epithelial barrier dysfunction and that drug resistance might entail a fitness cost in parasite virulence by limiting entero-adhesiveness. This is the first study of the cellular basis for strain-to-strain variation in parasite pathogenicity. Intra- and inter-subtype variability in cytopathogenicity provides a possible explanation for the diverse clinical outcomes of Blastocystis infections. 相似文献
19.
Summary. We report that the social parasite Polistes atrimandibularis (Zimmermann) can exploit at least three more host species than previously described. One of these, P. associus, has never been reported as host of a social parasite. Our data show no constraints in host choice, indicating P. atrimandibularis is a generalist social parasite. 相似文献
20.
Cameron R. Currie 《Oecologia》2001,128(1):99-106
The prevalence and impact of a specialized microfungal parasite (Escovopsis) that infects the fungus gardens of leaf-cutting ants was examined in the laboratory and in the field in Panama. Escovopsis is a common parasite of leaf-cutting ant colonies and is apparently more frequent in Acromyrmex spp. gardens than in gardens of the more phylogenetically derived genus Atta spp. In addition, larger colonies of Atta spp. appear to be less frequently infected with the parasite. In this study, the parasite Escovopsis had a major impact on the success of this mutualism among ants, fungi, and bacteria. Infected colonies had a significantly lower rate of fungus garden accumulation and produced substantially fewer workers. In addition, the extent of the reduction in colony growth rate depended on the isolate, with one isolate having a significantly larger impact than two others, suggesting that Escovopsis has different levels of virulence. Escovopsis is also spatially concentrated within parts of ant fungus gardens, with the younger regions having significantly lower rates of infection as compared to the older regions. The discovery that gardens of fungus-growing ants are host to a virulent pathogen that is not related to any of the three mutualists suggests that unrelated organisms may be important but primarily overlooked components of other mutualistic associations. 相似文献