Experimental studies on parasitization by Apanteles glomeratus.

ABSTRACT. The host-finding sequence of Apanteles glomeratus females and the factors involved in it were analysed. A female wasp is attracted by the leaf odour of the food plant of the host ( Pieris rapae crucivord ). She then walks slowly with the tips of her antennae rubbing the leaf surface. When she comes across damage produced by the host's feeding, her antennae are raised and she turns towards the damage. She often then erects her wings and/or bends her abdomen forward in response to a chemical produced from the leaf by the host's saliva. Long-lasting searching elicited by this odour normally leads to an encounter with a host caterpillar, whereupon odour from the host itself releases opposition. Host saliva, faeces and silk are also involved in these responses, but the response to fresh leaf damage has the most specific function in the overall strategy of host-finding.     

Stimuli inducing detachment of larvalArrenurus danbyensis (Hydrachnidia: Arrenuridae) from adultCoquillettidia perturbans (Diptera: Culicidae)

In this study, potential cues for detachment of parasitic larvalArrenurus danbyensis Mullen mites fromCoquillettidia perturbans (Walker) mosquitoes were investigated. Contact with water did not induce a dramatic rate of dissociation. Crushing the host's abdomen was not as effective as crushing the head or thorax; although general body trauma has an effect, it is not sufficient to explain these results. Crushing the host's head following application of a ligature slowed the rate of mite detachment. We infer that haemolymph-borne cues, possibly hormones, are released by crushing the head or thorax of the host and induce rapid mite detachment. External application of Ringers solution or body fluids from mosquitoes significantly increased rate of mite detachment. It is possible that two separate mechanisms stimulate detachment of mites: external haemolymph reception signifying damage to the host and internal reception of haemolymph-borne cues associated with oviposition behavior.     

Dynamic optimization of host defense, immune memory, and post-infection pathogen levels in mammals

When attacked by pathogens, higher vertebrates produce specific immune cells that fight against them. We here studied the host's optimal schedule of specific immune cell production. The damage caused by the pathogen increases with the pathogen amount in the host integrated over time. On the other hand, there is also a cost incurred by the production of specific immune cells, not only in terms of the energy needed to produce and maintain the cells, but also with respect to damages sustained by the host's body as a result of immune activity. The optimal strategy of the host is the one that minimizes the total cost, defined as a weighted sum of the damage caused by pathogens and the costs caused by the specific immune cells. The problem is solved by using Pontryagin's maximum principle and dynamic programming. The optimal defense schedule is typically as follows: In the initial phase after infection, immune cells are produced at the fastest possible rate. The amount of pathogen increases temporarily but is eventually suppressed. When the pathogen amount is suppressed to a sufficiently low level, the immune cell number decreases and converges to a low steady level, which is maintained by alternately switching between fastest production and no production. We examine the effect of time delay required to have fully active immune cells by comparing cases with different number of rate limiting steps before producing immune cells. We examine the effect of the duration of time (time delay) required before full-scale production of active immune cells by comparing cases with different numbers of rate-limiting steps before immune-cell production. We also discuss the role of immune memory based on the results of the optimal immune reaction.     

DNA double-strand break repair functions defend against parvovirus infection.

We measured parvovirus replication and sensitivity to X-ray damage in nine CHO cell lines representing a variety of DNA repair deficiencies. We found that parvovirus replication efficiency increases with radiosensitivity. Parvovirus replication is disrupted at an early stage of infection in DNA repair-proficient cells, before conversion of the single-stranded viral DNA genome into the double-stranded replicative form. Thus, status of the DNA repair machinery inversely correlates with parvovirus replication and is proportional to the host's ability to repair X-ray-induced damage.     

Coevolution of parasite virulence and host life history

Most models about the evolutionary interactions between a parasite's virulence and its host's life history neglect two potentially important aspects: epidemiological and coevolutionary feedback. We emphasize their importance by presenting models that describe the coevolution of a semelparous host's age at reproduction and a parasite's virulence in different environmental conditions. In particular, we first show that an epidemiological feedback will lead to a nonmonotonic response of the host's age at reproduction as virulence increases. We then show that the coevolutionary pressure on virulence can lead to complex associations between the host's life history and the parasite's virulence, which would not be expected with more traditional models of host or parasite evolution. Thus, for example, a high mortality rate of the host favours avirulent parasites and late reproduction of the host when the environmental conditions allow the host to grow rapidly, but early reproduction and high virulence when growth is slow.     

The anti-parasitic effects of nitric oxide

Endogenous and exogenous nitric oxide (NO) possesses antiparasitic effects on both Protozoa and Metazoa. However, NO production requires a tight control to limit cytotoxic damage to the host's own cells. The best known parasitic macromolecular targets for NO(-donors) are cysteine proteases, which are relevant in several aspects of the parasite life cycle and parasite-host relationships, and appear as promising targets for anti-parasitic chemotherapy.     

Ectoparasites: direct impact on host fitness

Despite being restricted to the host's first line of defence (the integument, away from vital organs), ectoparasite damage has a pronounced impact on host fitness. This generalization can be explained by the reduced dependence of most ectoparasites on their individual host, which minimizes the fitness loss linked to host death. This explanation implies that permanent ectoparasites evolve less 'aggressively' than do either nest or field ectoparasites. This, and other determinants of ectoparasitic virulence are discussed here by Tovi Lehmann.     

The effect of evolution on host-parasitoid systems

It is well known that a simple first-order difference equation can exhibit complex population dynamics, such as sustained oscillations and chaos. An interesting problem is whether such oscillatory dynamics are expected to occur in real populations. This paper assumes that the resident system is composed of 1-host and 1-parasitoid and that only the host is allowed to evolve, but not the parasitoid. Based on the invasibility of a host to host-parasitoid systems, we investigate the dynamics of the host-parasitoid system favored by natural selection. We consider two cases. In the first case, the host's evolution involving both the intrinsic growth rate and the sensitivity to density is considered. In the second case, the host's evolution involving both the intrinsic growth rate and the vulnerability to the parasitoid is considered. In both cases, we see that the dynamics with a stable equilibrium will not be favored by natural selection without the trade-off between the host's traits which are allowed to evolve. The host-parasitoid system with a stable equilibrium will be eventually invaded by a host type that develops an unstable equilibrium with the parasitoid. If there is a trade-off between the host's traits which are allowed to evolve, a host-parasitoid system with a stable equilibrium can be favored by natural selection.     

Inducible defense against pathogens and parasites: optimal choice among multiple options

Defense against pathogen, parasites and herbivores is often enhanced after their invasion into the host's body. Sometimes different options are adopted depending on the identity and the quantity of the pathogen, exemplified by the switch between Th1 and Th2 systems in mammalian immunity. In this paper, we study the optimal defense of the host when two alternative responses are available, which differ in the effectiveness of suppressing the growth of pathogen (parasite, or herbivore), the damage to the host caused by the defense response, and the magnitude of time delay before the defense response becomes fully effective. The optimal defense is the one that minimizes the sum of the damages caused by the pathogen and the cost due to defense activities. The damage by pathogens increases in proportion to the time integral of the pathogen abundance, and the cost is proportional to the defense activity. We can prove that a single globally optimal combination of defense options always exists and there is no other local optimum. Depending on the parameters, the optimal is to adopt only the early response, only the late response, or both responses. The defense response with a shorter time delay is more heavily used when the pathogen grows fast, the initial pathogen abundance is large, and the difference in time delay is long. We also study the host's optimal choice between constitutive and inducible defenses. In the constitutive defense, the response to pathogen attack works without delay, but it causes the cost even when the pathogen attack does not occur. We discuss mammalian immunity and the plant chemical defense from the model's viewpoint.     

Attachment and Feeding Devices of Water-Mite Larvae [Arrenurus spp.) Parasitic on Damselflies (Odonata, Zygoptera)

Water-mite larvae of the subgenus Arrenurus (Acari, Hydrachnellae) act as habitual ectoparasites on zygopteran imagines, mostly attached to the soft membranous cuticle. The powerful larval pedipalp claws grasp the cuticle and the distal sabre-like cheliceral segments tear it, thus obtaining the host's tissue fluids. The chelicerae and palps co-operate to anchor the larva. The attached larva soon produces—in the host's subcuticular epidermis layer, and separated from the haemocoele by the thin sheet of subepidermal connective tissue—an elongated pouch, the stylostome, consisting of an acellular gelatinous substance, apparently secreted by the larva. Presumably, interaction with components in the host's tissue fluids solidifies the stylostome, which becomes firmly fixed to the host's body wall. The stylostome is thought to lengthen by repeated alternation between the suction of tissue fluids from the host and secretion of fresh soft substance forming additional stylostome segments. The resilient stylostome develops in a cleft between the host's cuticle and the subepidermal connective tissue in connection with partial decomposition of the host's epidermis, probably caused by cytotoxins leaking from the stylostome. In attempts to wall off the wound and thus to avoid influx of foreign substances, the host lays down a melanin sleeve around the stylostome at the perforation site. Lodgement of the functional stylostome separated from the haemocoele within the host's tissues might explain why the newly-formed stylostome seems immune from cellular host reactions. However, cellular encapsulation and melanization appear to happen to outworn, non-active stylostomes.     

Racing against host's immunity defenses: a likely strategy for passive evasion of encapsulation in Asobara tabida parasitoids

The hymenopteran Asobara tabida Nees (Braconidae, Alysiinae) develops as a solitary endophagous parasite in larvae of several Drosophila species. Most A. tabida eggs possess a sticky chorion which attaches to the tissue of the host organs within a few hours following oviposition. A. tabida sticky eggs usually avoid encapsulation, though the probability of survival decreases in hosts carrying a larger number of circulating hemocytes. Here, we hypothesized that the elicitation of the encapsulation reaction may result from a race between two phenomena: the host's hemocytic reaction and the embedment of the parasitic egg within the host tissues. In order to test this hypothesis, we measured the speed of capsule formation in D. melanogaster larvae of different ages, knowing that the number of circulating hemocytes increases with the age of the larvae. Using a non-virulent A. tabida strain, the eggs of which do not attach to the host tissue, we found that the speed of capsule formation increased correlatively with the age of the D. melanogaster larva. Therefore, the hypothesis of a physiological race between host's immunity defenses and parasite's avoidance of host's defenses is strongly supported by our results. Also, A. tabida eggs which attach to the host's tissue before the attack by the hemocytes has taken place may be considered as a strategy of passive evasion from encapsulation.     

Shared control of epidemiological traits in a coevolutionary model of host-parasite interactions

Most models concerning the evolution of a parasite's virulence and its host's resistance assume that each component of the relationship (transmission, virulence, recovery, etc.) is controlled by either the host or the parasite but not by both. We present a model that describes the coevolution of host and parasite, assuming that the rate of transmission or the virulence depends on both genotypes. The evolution of these traits is constrained by trade-offs that account for costs of defense and attack strategies, in line with previous studies on the separate evolution of the host and the parasite. Considering shared control by the host and the parasite in determining the traits of the relationship leads to several novel predictions. First, the host should evolve maximal investment in defense against parasites with an intermediate replication rate. Second, the evolution of the parasite strongly depends on the way the host's defense is described. Third, the coevolutionary process may lead to decreasing the parasite's virulence as a response to a rise in the host's background mortality, contrary to classical predictions.     

Augmentation of therapeutic effect of adoptive immunotherapy through a synergy between transferred killer cells and host's fresh lymphocytes]

Among several approaches to augment the therapeutic effect of adoptive immunotherapy, we focused the antitumor synergy between transferred killer cells and host's fresh lymphocytes. Immunotherapy models using murine tumors or clinical experiments revealed that preadministration of immunostimulator such as OK-432, followed by chemotherapeutic agents such as cyclophosphamide, can induce host's non-cytotoxic fresh lymphocytes that act synergistically with cultured killer cells against autologous tumor cells. Immuno-chemo-lymphocytotherapy (a sequential treatment with OK-432, chemotherapy and adoptive immunotherapy) is useful to treat the patients with advanced cancer even if the number of transferred lymphocytes is limited.     

Polymorphus minutus affects antitoxic responses of gammarus roeseli exposed to cadmium

The acanthocephalan parasite Polymorphus minutus is a manipulator of its intermediate host Gammarus roeseli, which favours its transmission to the final host, a water bird. In contaminated environments, G. roeseli have to cope with two stresses, i.e. P. minutus infection and pollutants. As P. minutus survival relies on its host's survival, we investigated the influence of P. minutus on the antitoxic defence capacities and the energy reserves of G. roeseli females after cadmium exposure. In parallel, malondialdehyde, a toxic effect biomarker, was measured in G. roeseli females and in P. minutus. The results revealed that infected females displayed higher cell damage than uninfected ones, despite an apparent increase in reduced glutathione and metallothionein production. In fact, the increase of these antitoxic systems could be counterbalanced by carotenoid intake by the parasite, so that the overall defence system seemed less efficient in infected females than in uninfected ones. In addition, we demonstrated that cadmium induced cell damage in P. minutus, probably linked with cadmium accumulation in the parasite. Altogether, we observed a paradoxical pattern of responses suggesting that P. minutus increases cadmium toxicity in G. roeseli females although (i) it tends to increase several host antitoxic defence capacities and (ii) it bears part of the pollutant, as reflected by cell damage in the parasite.     

The penetration of Sporozoa into host cells]

The analysis of morphological and functional peculiarities of sporo- and merozoites as disseminative stages of the sporozoan life-cycle is given. Penetration of parasites into the host's cells is a complex multistepped process very similar to the induced but not completed phagocytosis. As a result of that process the formation of the integrated cell system, which consists of the host's cell and the unicellular parasite takes place.     

Caterpillars on the run – induced defences create spatial patterns in host plant damage

Herbivores usually consume a mere fraction of available plant biomass. Spatial patterns in feeding damage may be attributable to induced defences by the host plant; a damaged plant reacts by lowering its nutritional value, thereby forcing herbivores to move on before food gets worse. In this study, we test this general hypothesis on a specific model system: caterpillars of the alpine butterfly Parnassius smintheus feeding on lance-leaved stonecrop Sedum lanceolatum. We first describe spatial patterns in host distribution and feeding damage within alpine meadows. We then use laboratory experiments to test a key assumption behind the proposed mechanisms: that the host plant exhibits an induced response with a negative impact on larval performance, and that this response is activated with a delay. Finally, we relate the patterns observed to the actual behaviour of Parnassius larvae.
Overall, we found the level of feeding damage to be low (on damaged plants, only 5% of all leaves were fed upon). Within meadows, both host plants and feeding damage were clumped at a small spatial scale. This pattern seemed directly explicable by the timing of the host's induced defence. Laboratory experiments revealed a delay of 1–2 d before the defence reached a level affecting larval performance, and wild larvae switch plants more quickly than this. A simulation model demonstrated that the spatial distribution of host plant damage can be generated by a simple random walk, based on the empirically observed step frequency, length and turning angles. Hence, as the most parsimonious explanation for the observed level and pattern of host plant damage, we offer a scenario where induced changes in host-plant quality limits the time spent per plant, but the herbivore moves throughout the landscape without any particular directionality.     

Symbiont-mediated changes in Lolium arundinaceum inducible defenses: evidence from changes in gene expression and leaf composition

Plants have multiple strategies to deal with herbivory, ranging from chemical or physical defenses to tolerating damage and allocating resources for regrowth. Grasses usually tolerate herbivory, but for some cool-season grasses, their strategy may depend upon their interactions with intracellular symbionts. Neotyphodium endophytes are common symbionts in pooid grasses, and, for some host species, they provide chemical defenses against both vertebrate and invertebrate herbivores. Here, it was tested whether defenses provided by Neotyphodium coenophialum in Lolium arundinaceum (tall fescue) are inducible by both mechanical damage and herbivory from an invertebrate herbivore, Spodoptera frugiperda (fall armyworm), via a bioassay and by quantifying mRNA expression for lolC, a gene required for loline biosysnthesis. Both mechanical and herbivore damage had a negative effect on the reproduction of a subsequent herbivore, Rhopalosiphum padi (bird cherry-oat aphid), and herbivore damage caused an up-regulation of lolC. Uninfected grass hosts also had significantly higher foliar N% and lower C:N ratio compared with infected hosts, suggesting greater allocation to growth rather than defense. For L. arundinaceum, N. coenophialum appears to switch its host's defensive strategy from tolerance via compensation to resistance.     

Passive evasion of encapsulation in Macrocentrus cingulum Brischke (Hymenoptera: Braconidae), a polyembryonic parasitoid of Ostrinia furnacalis Guenée (Lepidoptera: Pyralidae)

The hymenopteran Macrocentrus cingulum usually deposits one egg into the larval body cavity of lepidopteran Ostrinia furnacalis, and the egg subsequently splits into several dozens of embryos during its development. How the parasitoid eggs and embryos avoid encapsulation by the host's immune response remains unknown. We compared hemocyte counts, morphologies and behaviors between unparasitized O. furnacalis larvae, and larvae parasitized by M. cingulum. No distinct differences were observed. Sephadex A-25 beads elicited a strong encapsulation response when injected into the parasitized host larvae, which indicates that parasitism by M. cingulum does not affect host's cellular immunity. However, there were significant differences in the host's encapsulation reactions towards injected eggs from different sources. Injected M. cingulum mature eggs excised from the lateral oviducts of the female wasps were not encapsulated, while immature eggs or driselase treated mature ones provoked an encapsulation response within 2 h after injection. Inspection of eggs by transmission electron microscopy revealed that the driselase collapsed the surface fibrous layer of the eggs, indicating that surface fibrous layer may play a role in protecting eggs from host's immune attack.     

Anti-inflammatory pathways as a host evasion mechanism for pathogens

Lipoxins play a key role in controlling potent pro-inflammatory responses triggered by infection with pathogens, such as Toxoplasma gondii and Mycobacterium tuberculosis. In order to contain microbial dissemination, infected hosts must mount a powerful immune response to prevent mortality. The onset of the chronic phase of infection is characterized by continuous cell-mediated immunity. Such potent responses are kept under tight control by a class of anti-inflammatory eicosanoids, the lipoxins. Here, we review such immune-containment strategies from the host's perspective, to keep pro-inflammatory responses under control during chronic disease, as well as from the perspective of the pathogen, which pirates the host's lipoxygenase machinery to its own advantage as a probable immune-escape mechanism.