Parasite-induced Reduction Research Articles

Photosynthesis, chlorophyll content and water potential of a mistletoe-host pair in a semi-arid savanna

Mistletoes can have detrimental effects on host trees. Mistletoe-infected trees may suffer from reduced growth and loss of vigor thereby contributing to low productivity of host trees. However, hosts may tolerate low levels of infection. This study aimed to determine photosynthetic rate, chlorophyll content and transpiration rate of a mistletoe-host pair (Viscum rotundifolium-Boscia albitrunca) and the water potential of two mistletoe host pairs (V. rotundifolium-B. albitrunca and Tapinanthus oleifolius-Senegalia mellifera) in a semi-arid savanna at Windhoek, Namibia. Photosynthetic rates were measured using a LI-6400XT photosynthesis system, while photosynthetic pigments were extracted in acetone and quantified spectrophotometrically. Plant water potential was measured using a Scholander pressure chamber. Results revealed greater photosynthetic rates and amounts of photosynthetic pigments in B. albitrunca than in V. rotundifolium while transpiration rates showed opposite trends to photosynthetic rates. Non-host B. albitrunca trees recorded significantly higher photosynthetic rates than the hosts, which suggests a parasite-induced reduction of photosynthetic rate in host plants. Water potential was greater in host trees than in mistletoes. These findings show negative effects of mistletoes on host trees, which may ultimately affect their reproduction and survival. Further research may be required to determine effects of parasite density on host trees.

A Sterility-Mortality Tolerance Trade-Off Leads to Within-Population Variation in Host Tolerance.

While experimental studies have demonstrated within-population variation in host tolerance to parasitism, theoretical studies rarely predict for polymorphism to arise. However, most theoretical models do not consider the crucial distinction between tolerance to the effects of infection-induced deaths (mortality tolerance) and tolerance to the parasite-induced reduction in the reproduction of infected hosts (sterility tolerance). While some studies have examined trade-offs between host tolerance and resistance mechanisms, none has considered a correlation within different tolerance mechanisms. We assume that sterility tolerance and mortality tolerance are directly traded-off in a host population subjected to a pathogen and use adaptive dynamics to study their evolutionary behaviour. We find that such a trade-off between the two tolerance strategies can drive the host population to branch into dimorphic strains, leading to coexistence of strains with sterile hosts that have low mortality and fully fertile with high mortality rates. Further, we find that a wider range of trade-off shapes allows branching at intermediate- or high-infected population size. Our other significant finding is that sterility tolerance is maximised (and mortality tolerance minimised) at an intermediate disease-induced mortality rate. Additionally, evolution entirely reverses the disease prevalence pattern corresponding to the recovery rate, compared to when no strategies evolve. We provide novel predictions on the evolutionary behaviour of two tolerance strategies concerning such a trade-off.

Plasmodium infection inhibits tumor angiogenesis through effects on tumor-associated macrophages in a murine implanted hepatoma model

BackgroundHepatocellular carcinoma (HCC) is one of the leading causes of cancer-related death in China. The lack of an effective treatment for this disease results in a high recurrence rate in patients who undergo radical tumor resection, and the 5-year survival rate of these patients remains low. Our previous studies demonstrated that Plasmodium infection provides a potent antitumor effect by inducing innate and adaptive immunity in a murine Lewis lung carcinoma (LLC) model.MethodsThis study aimed to investigate the inhibitory effect of Plasmodium infection on hepatocellular carcinoma in mice, and various techniques for gene expression analysis were used to identify possible signal regulation mechanisms.ResultsWe found that Plasmodium infection efficiently inhibited tumor progression and prolonged survival in tumor-bearing mice, which served as a murine implanted hepatoma model. The inhibition of tumor progression by Plasmodium infection was related to suppression of tumor angiogenesis within the tumor tissue and decreased infiltration of tumor-associated macrophages (TAMs). Further study demonstrated that matrix metalloprotease 9 (MMP-9) produced by TAMs contributed to tumor angiogenesis in the tumor tissue and that the parasite-induced reduction in MMP-9 expression in TAMs resulted in the suppression of tumor angiogenesis. A mechanistic study revealed that the Plasmodium-derived hemozoin (HZ) that accumulated in TAMs inhibited IGF-1 signaling through the PI3-K and MAPK signaling pathways and thereby decreased the expression of MMP-9 in TAMs.ConclusionsOur study suggests that this novel approach of inhibiting tumor angiogenesis by Plasmodium infection is of high importance for the development of new therapies for cancer patients.DcTAkd_JguhWjRG6hMrBFrVideo abstract

High dilutions of antimony modulate cytokines production and macrophage – Leishmania (L.) amazonensis interaction in vitro

BackgroundIn previous results mice treated with high dilutions of antimony presented reduction of monocyte migration to the site of infection with increase in B lymphocytes population in the local lymph node. AimsTo know the mechanisms involved, a series of in vitro studies was done, using co-cultures of macrophages (RAW 264.7) and Leishmania (L.) amazonensis treated with different dilutions of antimony (Antimonium crudum or AC), in different times. MethodologySpreading, phagocytosis, the oxidative activity of macrophages, the viability of free promastigotes and the cytokines/chemokines concentration in the supernatant were evaluated. The assays were performed in quadruplicate. ResultsCells treated with AC 30cH (10−58M) and AC 200cH (10−398M) presented a temporary reduction of the spreading after 02h of incubation, followed by increase after 48h, being the most significant increase observed after the AC 200cH treatment. However, the percentage of internalized parasites at 48, 96 and 120h of incubation was also higher in cells treated with AC 200cH. It is suggested that the AC 200cH improves the ability of phagocytes to internalize the parasites, but not to digest them. The cytokines-chemokines panel corroborated these results. Both dilutions potentiated the parasite-induced reduction of cytokines production, especially IL-6, IL 12 p40 and γ-IFN, after 48h of incubation. In addition, the production of MIP-1 beta (CCL4), a chemokine involved in chronic inflammation, was also reduced after 120h. A specific effect of AC 30cH was seen by the inhibition of two peaks of CCL2 (MCP-1) observed in infected macrophages, at 24 and 120h. Since this cytokine is an important chemokine for monocytes, it explains the results obtained formerly in vivo. The morphology of macrophages after acridine orange staining revealed that the treatment with AC 30cH reduced substantially the acid vacuoles in the cytoplasm, indicating a certain inability of these cells to digest the parasites. On the other hand, a large peak of VEGF-A, associated with increase of internalized parasites was observed after 120h of treatment with AC 200cH, which could be associated to the regulation of the chronic inflammation events by M1-M2 polarization. There was no statistical difference among groups regarding the production of TNF, NO and H2O2, showing that the drugs do not alter macrophage cytotoxic activity. A clear quantitative and qualitative variation of the modulatory effects of AC 30cH and 200cH was seen, in function of time. ConclusionsBoth dilutions were able to potentiate the decrease of most of cytokines and chemokines induced by the parasite infection in vitro, which explains the clinical improvement seen previously in vivo, however, the mechanisms involved and the epidemiological significance of these findings are still under discussion.

Exploited and excreting: parasite type affects host nutrient recycling.

Parasite-induced changes in the nutrient balance of hosts could alter the availability of nutrients in ecosystems by changing consumer-driven nutrient recycling. While these effects on host nutrient use are mediated by host physiology, they likely depend on characteristics of the parasite and host diet quality. We examined this possibility by measuring nutrient release rates of uninfected Daphnia and conspecifics infected by two microparasites (the bacterium Pasteuria ramosa and the microsporidium Hamiltosporidium tvaerminnensis) from daphnid hosts fed food that varied in phosphorus content. We found that infection type and diet affected host nutrient release rates, but the strength of these effects varied among parasite treatments. To improve our understanding of these effects, we examined whether two separate aspects of host exploitation (parasite-induced reductions in host fecundity and parasite load) could account for variation in Daphnia nutrient release, ingestion, and elemental ratios caused by our infection and diet treatments. Regardless of whether we compared individuals across infection type or diet treatment, Daphnia fecundity described variation in multiple aspects of host nutrient use better than infection, diet, or spore load. Our results suggest that parasite-induced changes in host nutrient use are both parasite and diet specific, and that host fecundity could be a useful parameter for predicting the magnitude and direction of these changes.

Brown-headed cowbirds exploit a host's compensatory behavioral response to fecundity reduction

Host manipulation by parasites is generally regarded as a classic example of the extended phenotype, where selection favors parasite genes that adaptively alter their host’s phenotype. However, selection would simultaneously favor both hosts that recoup some fitness lost to infection (i.e., compensation) and the parasites that enhance transmission by exploiting the host’s compensatory responses. Using a long-term study (19 years) of an avian brood parasite system, we demonstrate that female prothonotary warblers Protonotaria citrea compensate for partial fecundity reduction during their first brood by initiating a second breeding attempt (i.e., double-brooding). Similarly, in successful nests with naturally reduced fecundity as a result of brood parasitism, we show that being parasitized also stimulates a compensatory double-brooding response, where female warblers raising at least 1 brown-headed cowbird Molothrus ater offspring are more likely to initiate a second brood when compared with successful nonparasitized first broods. In support of the exploitation of compensatory responses hypothesis, parasitized females are often parasitized again in their second brood, thereby providing additional fitness benefits to cowbirds while enabling parasitized warblers that double-brood to recoup some fitness lost in the first brood. Experimentally parasitized female warblers exhibited a similar increase in double-brooding behavior, and the double-brooding frequency of parasitized female warblers was not attributable to reduced post-fledgling survival of cowbirds, thereby supplying further support for the role of parasite-induced fecundity reduction in the compensatory double-brooding behavior of a host.

The expression of virulence for a mixed-mode transmitted parasite in a diapausing host.

Many parasites survive harsh periods together with their hosts. Without the possibility of horizontal transmission during host diapause, parasite persistence depends entirely on host survival. We therefore hypothesize that a parasite should be avirulent during its host's diapausing stage. In contrast, the parasite may express higher virulence, i.e. parasite-induced fitness reduction of the host, during host life stages with good opportunities for horizontal transmission. Here we study the effects of a vertically and horizontally transmitted microsporidium parasite, Hamiltosporidium tvaerminnensis, on the quantity and survival of resting eggs of its host Daphnia magna. We find that the parasite did not affect egg volume, hatching success and time to hatching of the Daphnia's resting eggs, although it did strongly reduce the number of resting eggs produced by infected females, revealing high virulence during the non-diapause phase of the host's life cycle. These results also explain another aspect of this system - namely the strong decline in natural population prevalence across diapause. This decline is not caused by mortality in infected resting stages, as was previously hypothesized, but because infected female hosts produce lower rates of resting eggs. Together, these results help explain the epidemiological dynamics of a microsporidian disease and highlight the adaptive nature of life stage-dependent parasite virulence.

Growth but not photosynthesis response of a host plant to infection by a holoparasitic plant depends on nitrogen supply.

Parasitic plants can adversely influence the growth of their hosts by removing resources and by affecting photosynthesis. Such negative effects depend on resource availability. However, at varied resource levels, to what extent the negative effects on growth are attributed to the effects on photosynthesis has not been well elucidated. Here, we examined the influence of nitrogen supply on the growth and photosynthesis responses of the host plant Mikania micrantha to infection by the holoparasite Cuscuta campestris by focusing on the interaction of nitrogen and infection. Mikania micrantha plants fertilized at 0.2, 1 and 5 mM nitrate were grown with and without C. campestris infection. We observed that the infection significantly reduced M. micrantha growth at each nitrate fertilization and more severely at low than at high nitrate. Such alleviation at high nitrate was largely attributed to a stronger influence of infection on root biomass at low than at high nitrate fertilization. However, although C. campestris altered allometry and inhibited host photosynthesis, the magnitude of the effects was independent of nitrate fertilizations. The infection reduced light saturation point, net photosynthesis at saturating irradiances, apparent quantum yield, CO2 saturated rate of photosynthesis, carboxylation efficiency, the maximum carboxylation rate of Rubisco, and maximum light-saturated rate of electron transport, and increased light compensation point in host leaves similarly across nitrate levels, corresponding to a similar magnitude of negative effects of the parasite on host leaf soluble protein and Rubisco concentrations, photosynthetic nitrogen use efficiency and stomatal conductance across nitrate concentrations. Thus, the more severe inhibition in host growth at low than at high nitrate supplies cannot be attributed to a greater parasite-induced reduction in host photosynthesis, but the result of a higher proportion of host resources transferred to the parasite at low than at high nitrate levels.

An experimental study on the causal relationships between (ecto-)parasites, testosterone and sexual signalling

Bird song is considered to have evolved via sexual selection and should as such honestly signal aspects of the quality of its bearer. To ensure honesty, the immunocompetence handicap hypothesis proposed a dual role of testosterone, having positive effects on sexual signalling but suppressive effects on immune function. However, recent studies showed that it is rather an immune activation that suppresses the androgen production. This reversed chain of causation may significantly alter the pathways, which translate the effects of parasites and pathogens into changes in the expression of male sexual traits. We infested male canaries with Ixodes ricinus tick nymphs to investigate the causal relationships between (ecto-)parasites, testosterone and sexual signalling, here singing behaviour. We focused on flexible song traits, which may quickly reflect changes in the infestation status, and tested whether these effects relate to changes in the plasma testosterone levels or health state. The experimental tick infestation altered the males’ song performance by reducing song consistency, a trait that had previously been identified to reflect male quality. The tick infestation lowered the plasma testosterone levels and had a negative effect on the health status in terms of a reduced hematocrit. Our pathway analysis then revealed that it is the parasite-induced reduction of the plasma testosterone levels but not of the health state that caused the changes in song consistency. Thus, our study supports the view that it is the effect of parasites and immune activation on plasma testosterone levels that generates the trade-off between immunocompetence and sexual signalling.

Patterns of a novel association between the scyphomedusaChrysaora plocamiaand the parasitic anemonePeachia chilensis

Jellyfish display strong population variability. Competitive interactions between fish and jellyfish have been depicted as a major mechanism controlling this variability. Biological associations involving jellyfish are, however, more diverse than predation–prey interactions and remain poorly understood. Parasitic associations in particular may have relevant effects on jellyfish host populations. We studied basic patterns (temporal patterns of parasite intensity–biomass and the distribution pattern of parasites among hosts) of the association between the parasitic anemonePeachia chilensisand its scyphozoan host,Chrysaora plocamia. The mean number of parasites per host (MI) was high (average = 465) and showed significant differences during the pelagic life phase of the medusa. The mean biomass of parasites per host was also significantly different among months but showed a different temporal pattern to that of MI, which may reflect recruitment pulses of parasitic larvae. The mean biomass ofP. chilensisper host averaged 56.3 mg ash-free dry mass, which represents a trophic flow of energy probably linking pelagic and benthic food webs. The distribution of parasites among hosts was best fitted to the negative binomial distribution model, as typical for host–parasite systems. We concluded that the parasite-induced host mortality and reduction of fecundity, represented by parasitic castration, is restricted to a few hosts and is therefore under the expected levels that characterize the dynamic equilibrium of host–parasite systems.

Stocking methods and parasite-induced reductions in capture: Modelling Argulus foliaceus in trout fisheries

Argulus foliaceus is a macroparasite which can have a significant impact on yield in recreational trout fisheries, partly by increasing fish mortalities but also by reducing the appetite of infected fish, making them less likely to respond to bait. The aim of this paper is to determine the impact of four commonly used fish stocking methods both on the parasite dynamics, and on fisheries' yields. The wider consequences of the resultant reduction in host feeding are also of interest. To this end four different stocking methods were incorporated into Anderson and May's macroparasite model, which comprises three differential equations representing the host, attached parasite and free-living parasite populations. To each of these a reduction in the fish capture rate, inversely linked to the mean parasite burden, is added and the effects interpreted. Results show that (1) the common practise of increasing the stocking rate as catches drop may be counterproductive; (2) in the absence of any wild population of reservoir hosts, the parasite will be unable to survive if the stocking rate does not exceed the rate of capture; (3) compensatory stocking to account for fish mortalities can have disastrous consequences on yield; and (4) the parasite can, under certain circumstances, maintain the host population by preventing their capture.

Hosts use altered macronutrient intake to circumvent parasite-induced reduction in fecundity

Explanations for the evolution of pathogen-induced fecundity reduction usually rely on a common principle: the trade-off between host longevity and reproduction. Recent advances in nutritional research have, however, challenged this assumption and shown that longevity and reproduction are not inextricably linked. In this study, we showed that beetles infected by cysticercoids of the tapeworm Hymenolepis diminuta increased their total food intake and, more particularly, their carbohydrate consumption compared with uninfected insects. This increased intake was only pronounced during the first 12 days p.i., when the parasite grows and develops into a mature metacestode. Despite consuming more nutrients, infected individuals sustained lower levels of body lipid and were less efficient at converting ingested protein to body protein. However they demonstrated a capacity to compose a diet that sustained high levels of reproductive output unless confined to foods that were nutritionally dilute. We did not find any indication that macronutrient intakes had an effect on host pro-phenoloxidase activity; however, phenoloxidase activity was significantly affected by protein intake. Our results showed that when offered nutritionally complementary diets, infected hosts do not systematically suffer a reduction in fecundity. Thus, in our view, the assumption that a reduction in host reproduction represents an adaptive response by the host or the parasite to divert resources away from reproduction toward other traits should be reassessed.

Trypanosoma brucei Modifies the Tsetse Salivary Composition, Altering the Fly Feeding Behavior That Favors Parasite Transmission

Tsetse flies are the notorious transmitters of African trypanosomiasis, a disease caused by the Trypanosoma parasite that affects humans and livestock on the African continent. Metacyclic infection rates in natural tsetse populations with Trypanosoma brucei, including the two human-pathogenic subspecies, are very low, even in epidemic situations. Therefore, the infected fly/host contact frequency is a key determinant of the transmission dynamics. As an obligate blood feeder, tsetse flies rely on their complex salivary potion to inhibit host haemostatic reactions ensuring an efficient feeding. The results of this experimental study suggest that the parasite might promote its transmission through manipulation of the tsetse feeding behavior by modifying the saliva composition. Indeed, salivary gland Trypanosoma brucei-infected flies display a significantly prolonged feeding time, thereby enhancing the likelihood of infecting multiple hosts during the process of a single blood meal cycle. Comparison of the two major anti-haemostatic activities i.e. anti-platelet aggregation and anti-coagulation activity in these flies versus non-infected tsetse flies demonstrates a significant suppression of these activities as a result of the trypanosome-infection status. This effect was mainly related to the parasite-induced reduction in salivary gland gene transcription, resulting in a strong decrease in protein content and related biological activities. Additionally, the anti-thrombin activity and inhibition of thrombin-induced coagulation was even more severely hampered as a result of the trypanosome infection. Indeed, while naive tsetse saliva strongly inhibited human thrombin activity and thrombin-induced blood coagulation, saliva from T. brucei-infected flies showed a significantly enhanced thrombinase activity resulting in a far less potent anti-coagulation activity. These data clearly provide evidence for a trypanosome-mediated modification of the tsetse salivary composition that results in a drastically reduced anti-haemostatic potential and a hampered feeding performance which could lead to an increase of the vector/host contact and parasite transmission in field conditions.

Flea infestation reduces the life span of the common vole

Parasitism is often a source of variation in host's fitness components. Understanding and estimating its relative importance for fitness components of hosts is fundamental from physiological, ecological and evolutionary perspectives. Host-parasite studies have often reported parasite-induced reduction of host fecundity, whereas the effect of parasitism on host survival has been largely neglected. Here, we experimentally investigated the effect of infestation by rat fleas (Nosopsyllus fasciatus) on the life span of wild-derived male common voles (Microtus arvalis) bred in captivity. We found that the mean life span of parasitized voles was reduced by 36% compared to control voles. Parasitized voles had a smaller body size, but a relatively larger heart and spleen than control voles. These results indicate an effect of flea infestation on host life span and our findings strongly suggest that ectoparasites should be taken into account in the studies of host population dynamics.

Expression of parasite virulence at different host population densities under natural conditions

It has recently been suggested that the expression of parasite virulence depends on host population density, such that infected hosts have a higher sensitivity to density, and thus reach their carrying capacity earlier than uninfected hosts. In this scenario, parasite-induced reduction in fitness (i.e., virulence) increases with host density. We tested this hypothesis experimentally, using outdoor mesocosm populations of Daphnia magna infected by the microsporidian Octosporea bayeri. Contrary to the prediction, virulence was independent of host density. In a competition experiment with initial prevalence of 50%, O. bayeri reduced the competitive ability of infected Daphnia within the asexual growth phase independent of initial host population density. In an additional experiment we set up populations with 100% and 0% prevalence and followed their population dynamics over the whole season. Consistent with the competition experiment, we found no difference in population dynamics within the asexual growth phase of the host, suggesting that infected hosts are not more sensitive to density than uninfected hosts. The additional experiment, however, included more than the initial growth phase as did the competition experiment. Eventually, after 100 days, 100% infected populations assumed a reduced carrying capacity compared to uninfected populations. We identify and discuss three reasons for the discrepancy between our experiment and the predictions.

Virulence-transmission trade-offs and population divergence in virulence in a naturally occurring butterfly parasite

Why do parasites harm their hosts? Conventional wisdom holds that because parasites depend on their hosts for survival and transmission, they should evolve to become benign, yet many parasites cause harm. Theory predicts that parasites could evolve virulence (i.e., parasite-induced reductions in host fitness) by balancing the transmission benefits of parasite replication with the costs of host death. This idea has led researchers to predict how human interventions-such as vaccines-may alter virulence evolution, yet empirical support is critically lacking. We studied a protozoan parasite of monarch butterflies and found that higher levels of within-host replication resulted in both higher virulence and greater transmission, thus lending support to the idea that selection for parasite transmission can favor parasite genotypes that cause substantial harm. Parasite fitness was maximized at an intermediate level of parasite replication, beyond which the cost of increased host mortality outweighed the benefit of increased transmission. A separate experiment confirmed genetic relationships between parasite replication and virulence, and showed that parasite genotypes from two monarch populations caused different virulence. These results show that selection on parasite transmission can explain why parasites harm their hosts, and suggest that constraints imposed by host ecology can lead to population divergence in parasite virulence.

Chronology of parasite-induced alteration of fish behaviour: effects of parasite maturation and host experience

We monitored temporal changes in the magnitude of altered host behaviour in minnows (Pimephales promelas) experimentally infected with metacercariae of a brain-encysting trematode (Ornithodiplostomum ptychocheilus). This parasite develops and then encysts in a region of the brain that mediates the optomotor response (OMR), an innate behaviour that links visual stimuli with motor performance. The OMR of infected and uninfected minnows was evaluated between 0 and 10 weeks post-infection (p.i.), an interval spanning the development period of metacercariae to infectivity in birds. Trials involved monitoring the time an individual minnow spent following a spinning drum that had been painted with alternating black and white stripes. At 2 and 4 weeks p.i., infected minnows followed the drum 40% less often than controls. Differences between controls and infected fish declined thereafter, and were undetectable by 10 weeks p.i. Both control and infected fish habituated equally rapidly to the spinning drum. However, the difference in performance between controls and infected fish was 29% for experienced fish and 48% for fish that had never experienced the drum. Because maximum parasite-induced reduction in OMR coincided with the period of maximum parasite development, the behavioural effects are most likely due to unavoidable pathology in the brain associated with developing larvae.

Vector survival and parasite infection: the effect of Wuchereria bancrofti on its vector Culex quinquefasciatus.

This paper investigates a cohort of 2187 laboratory reared Culex quinquefasciatus fed on 69 human volunteers, including 59 persons with different levels of Wuchereria bancrofti microfilariae and 10 without microfilaria. Mosquitoes were followed until death. Mosquito survival was analysed in relation to the level of microfilaria in the human and larval count in the dead mosquito. Vector mortality during the extrinsic incubation period (12 days post-engorgement) was significantly higher in mosquitoes fed on microfilaraemic volunteers (50%) than in those fed on amicrofilaraemics (29%). Both the percentage infected and the geometric mean parasite density was significantly higher among mosquitoes which died before 13 days (45% infected and 10 larvae per infected mosquito) than those surviving beyond 13 days (39% and 2.2), suggesting a parasite loss of more than 80% during the extrinsic incubation period. A large proportion (62%) of the mosquitoes that died during the early of phase of parasite development were infected (36% in low, 26% in medium and 90% in high human Mf-density). Survival analysis showed that the parasite load in mosquitoes and the human Mf-density for a given parasite load are independent risk factors of vector survival. Overall, the hazard of dying was found to be 11-15 times higher among mosquitoes fed on microfilaraemic volunteers than those fed on amicrofilaraemics. The hazard doubles for every increase of about 60-70 parasites in the vector. As a consequence of the parasite-induced reduction in vector survival, the transmission success of the parasite is reduced. The implication of the results on control/elimination of lymphatic filariasis using mass-drug administration is discussed.

Water flows in the parasitic association Rhinanthus minor/Hordeum vulgare

Using the facultative root hemiparasite Rhinanthus minor and its host Hordeum vulgare several aspects of water relations have been measured in this parasitic association. Extraction of xylem sap by the parasite from the host's roots is facilitated by con siderably higher transpiration per leaf area in the parasite than in the host and by the fact that stomata of attached Rhinanthus were open all day and night despite extremely high ABA concentrations in the leaves. By comparison, another root hemiparasite, Melampyrum arvense, parasitizing various grasses in the field, showed normal diurnal stomatal behaviour. The abnormal behaviour of Rhinanthus stomata was not due to anatomical reasons as closure could be induced by applying high external ABA concentrations. Remarkable differences have been detected between the hydraulic conductance of barley seminal roots showing relatively low values and that of Rhinanthus seminal roots showing very high values. The latter could be related to the observed high ABA concentrations in these roots. Whole plant water uptake, transpirational losses, growth-dependent deposition, and the flows of water within the plants have been measured in singly growing Rhinanthus and Hordeum plants and in the parasitic association between the two. Water uptake, deposition and transpiration in Rhinanthus were dramatically increased after attachment to the barley host; most of the water used by the parasite was extracted as xylem sap from the host, thereby scavenging 20% of the total water taken up by the host's roots. This water uptake by the parasitized host, however, due to a parasite-induced reduction in the host's growth, was decreased by 22% as compared to non-parasitized barley. The overall changes in growth-related water deposition in the host and parasite pointed to decreased shoot growth and relatively favoured root growth in the host and to strongly favoured shoot growth in the parasite. These changes in the host became more severe, when more than one Rhinanthus was parasitizing one barley plant.

The energetic budget of Anopheles stephensi infected with Plasmodium chabaudi: is energy depletion a mechanism for virulence?

Evidence continues to accumulate showing that the malaria parasites (Plasmodium spp.) reduce the survival and fecundity of their mosquito vectors (Anopheles spp.). Our ability to identify the possible epidemiological and evolutionary consequences of these parasite-induced fitness reductions has been hampered by a poor understanding of the physiological basis of these shifts. Here, we explore whether the reductions in fecundity and longevity are the result of a parasite-mediated depletion or reallocation of the energetic resources of the mosquito. Mosquitoes infected with Plasmodium chabaudi were expected to have less energetic resources than uninfected mosquitoes, and energy levels were predicted to be lowest in mosquitoes infected with the most virulent parasite genotypes. Not only was there no evidence of a parasite-mediated reduction in the overall energetic budget of mosquitoes, but Plasmodium was actually associated with increased levels of glucose, a key insect nutritional and energetic resource. The data strongly suggest the existence of an increase in sugar feeding in mosquitoes infected with Plasmodium. We suggest different adaptive explanations for an enhanced sugar uptake in infected mosquitoes and call for more studies to investigate the physiological role of glucose in the Plasmodium-mosquito interaction.