Host Mortality (host + mortality)

Distribution by Scientific Domains


Selected Abstracts


Contrasting frequencies of parasitism and host mortality among phorid and conopid parasitoids of bumble-bees

ECOLOGICAL ENTOMOLOGY, Issue 2 2002
Michael C. Otterstatter
Abstract 1. Phorid (Diptera, Phoridae) and conopid (Diptera, Conopidae) parasitism among four North American bumble-bee (Hymenoptera, Apidae) species was investigated. Male bumble-bees experienced a significantly higher incidence of parasitism by the phorid, Apocephalus borealis Brues, and a significantly lower incidence of parasitism by the conopid, Physocephala texana Williston, than did workers. 2. The incidence of parasitism by A. borealis and P. texana varied between bumble-bee sexes and species in patterns that did not reflect differences in relative host abundance. Differences in foraging behaviour between bumble-bee workers and males, as well as between species, may explain these results. 3. Bumble-bee workers and males parasitised by A. borealis had significantly shorter lifespans than unparasitised bees. Based on previous estimates of bumble-bee mortality, A. borealis parasitism may reduce worker lifespans by up to 70%. In contrast, the mortality rate of bees parasitised by P. texana was not significantly different from that of unparasitised bees. 4. These results contrast with previous work highlighting the importance of conopid parasitism to bumble-bee populations, and suggest that phorid parasitism may impose greater costs to bumble-bees than does conopid parasitism in local populations. [source]


Interspecific competition between the ichneumonid Campoletis chlorideae and the braconid Microplitis mediator in their host Helicoverpa armigera

ENTOMOLOGIA EXPERIMENTALIS ET APPLICATA, Issue 1 2008
Shen-Peng Tian
Abstract We investigated interspecific competition between Campoletis chlorideae Uchida (Hymenoptera: Ichneumonidae) and Microplitis mediator (Haliday) (Hymenoptera: Braconidae) in their host, the cotton bollworm, Helicoverpa armigera (Hübner) (Lepidoptera: Noctuidae) under laboratory conditions. Cotton bollworm larvae were allowed to be parasitized by both wasp species simultaneously or sequentially at different time intervals. When host larvae were parasitized simultaneously by both parasitoids, the majority of the cocoons produced were of M. mediator. When host larvae were parasitized initially by M. mediator followed by C. chlorideae at 12 or 24 h, parasitoids emerging from the multiparasitized hosts were mainly M. mediator. In contrast, when host larvae were parasitized initially by C. chlorideae, followed by M. mediator 12 or 24 h later, parasitoids emerging from the multiparasitized hosts were mainly C. chlorideae. Dissections of host larvae at various time intervals after parasitization by the two parasitoids showed that first instars of M. mediator could physically attack the larvae of C. chlorideae, but not the eggs of C. chlorideae. When a host was parasitized by both wasp species sequentially, more host larvae died and the number of wasp offspring was significantly reduced compared to a host parasitized by only one wasp. Conversely, in simultaneous multiparasitism, the host mortality and wasp offspring production were not significantly different from those parasitized by single wasp species. [source]


WHEN SHOULD A TROPHICALLY TRANSMITTED PARASITE MANIPULATE ITS HOST?

EVOLUTION, Issue 2 2009
Geoffrey A. Parker
We investigate evolution of two categories of adaptive host manipulation by trophically transmitted helminths: (1) predation suppression decreases the host's mortality before the helminth is capable of establishing in its next host; (2) predation enhancement increases the existing host's mortality after it can establish in its next host. If all parasite mortality is purely random (time-independent), enhancement must increase predation by the next host sufficiently more (depending on manipulative costs) than it increases the average for all forms of host mortality; thus if host and parasite die only through random predation, manipulation must increase the "right" predation more than the "wrong" predation. But if almost all parasites die in their intermediate host through reaching the end of a fixed life span, enhancement can evolve if it increases the right predation, regardless of how much it attracts wrong predators. Although enhancement is always most favorable when it targets the right host, suppression aids survival to the time when establishment in the next host is possible: it is most favorable if it reduces all aspects of host (and hence parasite) mortality. If constrained to have selective effects, suppression should reduce the commonest form of mortality. [source]


WITHIN-HOST POPULATION DYNAMICS AND THE EVOLUTION OF MICROPARASITES IN A HETEROGENEOUS HOST POPULATION

EVOLUTION, Issue 2 2002
Vitaly V. Ganusov
Abstract Why do parasites harm their hosts? The general understanding is that if the transmission rate and virulence of a parasite are linked, then the parasite must harm its host to maximize its transmission. The exact nature of such trade-offs remains largely unclear, but for vertebrate hosts it probably involves interactions between a microparasite and the host immune system. Previous results have suggested that in a homogeneous host population in the absence of super- or coinfection, within-host dynamics lead to selection of the parasite with an intermediate growth rate that is just being controlled by the immune system before it kills the host (Antia et al. 1994). In this paper, we examine how this result changes when heterogeneity is introduced to the host population. We incorporate the simplest form of heterogeneity,random heterogeneity in the parameters describing the size of the initial parasite inoculum, the immune response of the host, and the lethal density at which the parasite kills the host. We find that the general conclusion of the previous model holds: parasites evolve some intermediate growth rate. However, in contrast with the generally accepted view, we find that virulence (measured by the case mortality or the rate of parasite-induced host mortality) increases with heterogeneity. Finally, we link the within-host and between-host dynamics of parasites. We show how the parameters for epidemiological spread of the disease can be estimated from the within-host dynamics, and in doing so examine the way in which trade-offs between these epidemiological parameters arise as a consequence of the interaction of the parasite and the immune response of the host. [source]


Dispersion patterns of parasites in 0+ year three-spined sticklebacks: a cross population comparison

JOURNAL OF FISH BIOLOGY, Issue 6 2002
M. Kalbe
Two ciliates and 16 metazoan parasites were identified in 434 0+ year three-spined sticklebacks Gasterosteus aculeatus collected from two small rivers and four lakes located in Schleswig-Holstein, Germany. By repeated sampling and analysis of dispersion patterns of six frequently occurring parasites no consistent evidence was found for mortality induced by a single parasite species. Linear log-variance to log-mean abundance ratios with slopes of c. 2 indicated negative binomial distributions for five of the six parasites. The numbers of these six parasites were combined as multiples of S.D. of each parasite species over all samples to form an ,individual parasitation index' (IPI), which showed that only in one locality a slight decrease in parasite burden occurred between September and April. In two of the lake populations, however, there was a distinct decline in the degree of dispersion in spring samples. This indicates that a combination of different species might cause parasite-induced host mortality, undetectable by patterns obtained from single species. There were differences in parasite diversity and intensity of infection among river compared to lake populations suggesting a role for parasites as selective agents in the ecological divergence of three-spined sticklebacks. [source]


A meta-analysis of parasite virulence in nestling birds

BIOLOGICAL REVIEWS, Issue 4 2009
A. P. Mĝller
Abstract 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. [source]


WHEN SHOULD A TROPHICALLY TRANSMITTED PARASITE MANIPULATE ITS HOST?

EVOLUTION, Issue 2 2009
Geoffrey A. Parker
We investigate evolution of two categories of adaptive host manipulation by trophically transmitted helminths: (1) predation suppression decreases the host's mortality before the helminth is capable of establishing in its next host; (2) predation enhancement increases the existing host's mortality after it can establish in its next host. If all parasite mortality is purely random (time-independent), enhancement must increase predation by the next host sufficiently more (depending on manipulative costs) than it increases the average for all forms of host mortality; thus if host and parasite die only through random predation, manipulation must increase the "right" predation more than the "wrong" predation. But if almost all parasites die in their intermediate host through reaching the end of a fixed life span, enhancement can evolve if it increases the right predation, regardless of how much it attracts wrong predators. Although enhancement is always most favorable when it targets the right host, suppression aids survival to the time when establishment in the next host is possible: it is most favorable if it reduces all aspects of host (and hence parasite) mortality. If constrained to have selective effects, suppression should reduce the commonest form of mortality. [source]