Parasite-induced Changes Research Articles

Intestinal injury and the gut microbiota in patients with Plasmodium falciparum malaria.

The pathophysiology of severe falciparum malaria involves a complex interaction between the host, parasite, and gut microbes. In this review, we focus on understanding parasite-induced intestinal injury and changes in the human intestinal microbiota composition in patients with Plasmodium falciparum malaria. During the blood stage of P. falciparum infection, infected red blood cells adhere to the vascular endothelium, leading to widespread microcirculatory obstruction in critical tissues, including the splanchnic vasculature. This process may cause intestinal injury and gut leakage. Epidemiological studies indicate higher rates of concurrent bacteraemia in severe malaria cases. Furthermore, severe malaria patients exhibit alterations in the composition and diversity of the intestinal microbiota, although the exact contribution to pathophysiology remains unclear. Mouse studies have demonstrated that the gut microbiota composition can impact susceptibility to Plasmodium infections. In patients with severe malaria, the microbiota shows an enrichment of pathobionts, including pathogens that are known to cause concomitant bloodstream infections. Microbial metabolites have also been detected in the plasma of severe malaria patients, potentially contributing to metabolic acidosis and other clinical complications. However, establishing causal relationships requires intervention studies targeting the gut microbiota.

Root-Knot-Nematode-Encoded CEPs Increase Nitrogen Assimilation.

C-terminally encoded peptides (CEPs) are plant developmental signals that regulate growth and adaptive responses to nitrogen stress conditions. These small signal peptides are common to all vascular plants, and intriguingly have been characterized in some plant parasitic nematodes. Here, we sought to discover the breadth of root-knot nematode (RKN)-encoded CEP-like peptides and define the potential roles of these signals in the plant-nematode interaction, focusing on peptide activity altering plant root phenotypes and nitrogen uptake and assimilation. A comprehensive bioinformatic screen identified 61 CEP-like sequences encoded within the genomes of six root-knot nematode (RKN; Meloidogyne spp.) species. Exogenous application of an RKN CEP-like peptide altered A. thaliana and M. truncatula root phenotypes including reduced lateral root number in M. truncatula and inhibited primary root length in A. thaliana. To define the role of RKN CEP-like peptides, we applied exogenous RKN CEP and demonstrated increases in plant nitrogen uptake through the upregulation of nitrate transporter gene expression in roots and increased 15N/14N in nematode-formed root galls. Further, we also identified enhanced nematode metabolic processes following CEP application. These results support a model of parasite-induced changes in host metabolism and inform endogenous pathways to regulate plant nitrogen assimilation.

Early signals of parasitism expressed through behaviour but modulated by social context

Sickness behaviours are believed to be an adaptive response to infection. However, the degree to which these behaviours can be expressed may be impacted by an individual's social environment. Here we tested, first, whether parasitism reduces the activity behaviour of lambs, Ovis aries , second, whether this occurs prior to other observed costs of parasitism and, third, whether the infection status of other individuals affects the degree to which these behaviours are expressed. Sixty lambs were separated into replicate groups within three treatments: (1) parasitized: all lambs were infected with the parasitic nematode Teladorsagia circumcincta ; (2) nonparasitized; all lambs were dosed with water; (3) mixed: some of the group were infected and some were dosed with water. Activity behaviour was monitored before, during and after parasite infection. Parasitized groups had reduced activity levels following infection, and this occurred before any other impact or measure of parasitism was detected. Infected animals in the mixed groups had reduced activity levels following infection, but the level of change was less than that in animals in the fully parasitized groups. Activity levels remained low until lambs were treated with anthelmintic when activity levels of the groups that had been parasitized returned to the same level as nonparasitized groups. These findings show that parasite-induced behavioural changes occur earlier than other more commonly observed signals of infection, but the infection profile of an individual's group can shape these behavioural responses to infection. • Domestic lambs were experimentally infected with a gastrointestinal nematode. • Parasitized lambs had reduced activity levels following infection. • This occurred before any other measure or impact of parasitism was detected. • However, these behavioural changes were affected by group infection status. • Thus, an individual's social environment can affect their response to infection.

Neophobic behavioural responses of parasitised fish to a potential predator and baited hook

Many juvenile fish show essential avoidance of predators but are also faced with the need to show risky asset-acquiring behaviour, such as trying new food sources, many of which are known to be influenced by parasite infection. Here, we investigated the links between parasite infection, anti-predator behaviour and neophobia towards a novel food presented on a baited hook in fish. Juvenile Spangled perch (Leipotherapon unicolor) undertook two behavioural tests in our laboratory, before being dissected and examined for external and internal parasites. We used an adapted conditioned place avoidance (CPA) paradigm to examine responses to a predator fish and in a separate test, we examined neophobia of a baited hook. Of the 69 Spangled perch studied, 27% of fish were uninfected and at least one of nematodes, Protozoa/Myxozoa or Monogenea were found in the remaining fish. Fish spent less time in the side of the tank where the predator was previously encountered, than before encounters, indicating that fish can learn to avoid locations where predators were previously observed. We found that fish spent longer in the side of the tank where the predator was visible than in the same side of the tank in earlier trials without the predator, supporting previous studies showing that fish actively approach and engage in predator inspection. Fish infected with Protozoa/Myxozoa and camallanid nematodes were less likely to enter the side of the tank with the predator than uninfected fish, suggesting a reluctance to approach a predator in these infected fish. However, Protozoa/Myxozoa and camallanid infected fish bit the baited hook sooner than uninfected fish, possibly indicating less neophobia of the baited hook in fish with these infections. Avoiding to approach a predator yet reduced neophobia to novel foods in some infected fish suggest that parasites do not exert a general, overall, effect on risk aversiveness. Instead, changes in neophobic behaviour appear complex and we discuss the possibility that parasite-induced changes in fish behaviour may be modulated by altered hunger levels and reduced locomotion brought about by illness.

Host Manipulation, Gene Editing, and Non-Traditional Model Organisms: A New Frontier for Behavioral Research?

Insects and parasites dominate the biosphere, in terms of known biodiversity and mode of life, respectively. Consequently, insects play a part in many host-parasite systems, either as parasite, host, or both. Moreover, a lot of these systems involve adaptive parasite-induced changes of host phenotype (typically behavior or morphology), which is commonly known as host manipulation. While many host manipulation systems have been described within the last few decades, the proximate mechanisms that underpin host phenotypic change are still largely unknown. Given the intimate co-evolutionary history of host-parasite systems, teasing apart the intricate network of biochemical reactions involved in host manipulation requires the integration of various complementary technologies. In this perspective, we stress the importance of multidisciplinary research on host manipulation, such as high-throughput sequencing methods (genomics and transcriptomics) to search for candidate mechanisms that are activated during a manipulation event. Then, we argue that gene editing technologies, specifically the CRISPR-Cas9 system, are a powerful way to test for the functional roles of candidate mechanisms, in both the parasite and the host. Finally, given the sheer diversity of unique host-parasite systems discovered to date, there is indeed a tremendous potential to create novel non-traditional model systems that could greatly expand our capacity to test the fundamental aspects of behavior and behavioral regulation.

Praziquantel Reduces Maternal Mortality and Offspring Morbidity by Enhancing Anti-Helminthic Immune Responses.

Alongside the wide distribution throughout sub Saharan Africa of schistosomiasis, the morbidity associated with this chronic parasitic disease in endemic regions is often coupled with infection-driven immunomodulatory processes which modify inflammatory responses. Early life parasite exposure is theorized to drive immune tolerance towards cognate infection as well as bystander immune responses, beginning with in utero exposure to maternal infection. Considering that 40 million women of childbearing-age are at risk of infection worldwide, treatment with Praziquantel during pregnancy as currently recommended by WHO could have significant impact on disease outcomes in these populations. Here, we describe the effects of anthelminthic treatment on parasite-induced changes to fetomaternal cross talk in a murine model of maternal schistosomiasis. Praziquantel administration immediately prior to mating lead to clear re-awakening of maternal anti-parasite immune responses, with persistent maternal immune activation that included enhanced anti-schistosome cytokine responses. Clearance of parasites also improved capacity of dams to endure the additional pressure of pregnancy during infection. Maternal treatment also drove lasting functional alterations to immune system development of exposed offspring. Prenatal anthelminthic treatment skewed offspring immune responses towards parasite clearance and reduced morbidity during cognate infection. Maternal treatment also restored offspring protective IgE antibody responses directed against schistosome antigens, which were otherwise suppressed following exposure to untreated maternal infection. This was further associated with enhanced anti-schistosome cytokine responses from treatment-exposed offspring during infection. In the absence of cognate infection, exposed offspring further demonstrated imprinting across cellular populations. We provide further evidence that maternal treatment can restore a more normalized immune profile to such offspring exposed in utero to parasite infection, particularly in B cell populations, which may underlie improved responsiveness to cognate infection, and support the WHO recommendation of anthelminthic treatment during pregnancy.

Are amphipodsOrchestia grillus(Bosc, 1802) (Amphipoda: Talitridae) infected with the trematodeLevinseniella byrdi(Heard, 1968) drawn to the light?

AbstractA parasite can change its host’s behavior in spectacular ways. When the saltmarsh amphipod Orchestia grillus (Bosc, 1802) is infected with the trematode Levinseniella byrdi (Heard, 1968) it is bright orange and is found in the open unlike uninfected individuals. I tested the hypothesis that infected amphipods are found in the open because L. byrdi reverses their innate photophobia. During daytime treatments and when placed in a dark chamber, 0% of the uninfected and 20% of the infected amphipods, on average, moved to the light chamber after 30 minutes. When placed in a light chamber, 91% of the uninfected and 53% of the infected amphipods, on average, went to the dark side after 30 minutes. These results clearly indicate that O. grillus is normally photophobic, but not drawn to light when infected with L. byrdi. Instead, L. byrdi appears to neutralize the amphipod’s photophobia. Uninfected O. grillus are typically found under vegetation. I hypothesize that O. grillus with L. byrdi infections wander into open, unvegetated habitats randomly. In addition, 94% of infected amphipods could be touched by a finger in the field suggesting they can be easily caught by predators. Levinseniella byrdi infects at least three other amphipod hosts, Chelorchestia forceps (Smith & Heard, 2001), Uhlorchestia spartinophila (Bousfield & Heard, 1986), and U. uhleri (Shoemaker, 1930). The parasite-manipulation hypothesis suggests that the parasite-induced changes (conspicuous body color and neutralized light response) are adaptive for L. byrdi to make amphipod hosts more susceptible to bird predators, the definitive hosts. This hypothesis remains to be tested.

ATP Purinergic Receptor P2X1-Dependent Suicidal NETosis Induced by Cryptosporidium parvum under Physioxia Conditions.

Simple SummaryCryptosporidium parvum, a zoonotic apicomplexan, is one of the leading causes of severe diarrheal disease worldwide and a major contributor to early infant and neonatal mortality. In vivo, sporozoites of C. parvum must invade enterocytes where they develop in a unique intracellular extracytoplasmic niche. Polymorphonuclear neutrophils (PMN) are the most common leukocytes in the immune defense system of the host, the first to be transferred to C. parvum-infected gut mucosa, and are increasingly recognized as important cells in the fight against other intestinal parasites. We investigated the role of ATP purinergic receptor P2X1, glycolysis, plasma membrane monocarboxylate transporters (MCTs) of lactate, extracellular acidification rates (ECAR), and mitochondrial oxygen consumption rates (OCR), as well as Notch signaling in C. parvum-triggered NETs formation in exposed bovine PMN under intestinal physioxic (5% O2) as well as hyperoxic (21% O2) conditions. Both C. parvum stages, i.e., sporozoites and oocysts, strongly induce suicidal NETosis in a P2X1-dependent manner, suggesting anti-cryptosporidial effects not only through firm sporozoite entrapment and hampered sporozoite excystation, but also probably through direct exposure to NETs-derived toxic molecules.Cryptosporidiosis is a zoonotic intestinal disease that affects humans, wildlife, and neonatal cattle, caused by Cryptosporidium parvum. Neutrophil extracellular traps (NETs), also known as suicidal NETosis, are a powerful and ancient innate effector mechanism by which polymorphonuclear neutrophils (PMN) battle parasitic organisms like protozoa and helminths. Here, C. parvum oocysts and live sporozoites were utilized to examine suicidal NETosis in exposed bovine PMN under both 5% O2 (physiological conditions within small intestinal tract) and 21% O2 (normal hyperoxic conditions in research facilities). Both sporozoites and oocysts induced suicidal NETosis in exposed PMN under physioxia (5% O2) and hyperoxia (21% O2). Besides, C. parvum-induced suicidal NETosis was affirmed by total break of PMN, co-localization of extracellular DNA decorated with pan-histones (H1A, H2A/H2B, H3, H4) and neutrophil elastase (NE) by means of confocal- and immunofluorescence microscopy investigations. C. parvum-triggered NETs entrapped sporozoites and impeded sporozoite egress from oocysts covered by released NETs, according to scanning electron microscopy (SEM) examination. Live cell 3D-holotomographic microscopy analysis visualized early parasite-induced PMN morphological changes, such as the formation of membrane protrusions towards C. parvum while undergoing NETosis. Significant reduction of C. parvum-induced suicidal NETosis was measured after PMN treatments with purinergic receptor P2X1 inhibitor NF449, under both oxygen circumstances, this receptor was found to play a critical role in the induction of NETs, indicating its importance. Similarly, inhibition of PMN glycolysis via 2-deoxy glucose treatments resulted in a reduction of C. parvum-triggered suicidal NETosis but not significantly. Extracellular acidification rates (ECAR) and oxygen consumption rates (OCR) were not increased in C. parvum-exposed cells, according to measurements of PMN energetic state. Treatments with inhibitors of plasma membrane monocarboxylate transporters (MCTs) of lactate failed to significantly reduce C. parvum-mediated NET extrusion. Concerning Notch signaling, no significant reduction was detected after PMN treatments with two specific Notch inhibitors, i.e., DAPT and compound E. Overall, we here describe for the first time the pivotal role of ATP purinergic receptor P2X1 in C. parvum-mediated suicidal NETosis under physioxia (5% O2) and its anti-cryptosporidial properties.

Schistosoma haematobium infection is associated with alterations in energy and purine-related metabolism in preschool-aged children.

Helminths are parasitic worms that infect over a billion people worldwide. The pathological consequences from infection are due in part, to parasite-induced changes in host metabolic pathways. Here, we analyse the changes in host metabolic profiles, in response to the first Schistosoma haematobium infection and treatment in Zimbabwean children. A cohort of 83 schistosome-negative children (2–5 years old) as determined by parasitological examination, guardian interviews and examination of medical records, was recruited at baseline. Children were followed up after three months for parasitological diagnosis of their first S. haematobium infection, by detection of parasite eggs excreted in urine. Children positive for infection were treated with the antihelminthic drug praziquantel, and treatment efficacy checked three months after treatment. Blood samples were taken at each time point, and capillary electrophoresis mass spectrometry in conjunction with multivariate analysis were used to compare the change in serum metabolite profiles in schistosome-infected versus uninfected children. Following baseline at the three-month follow up, 11 children had become infected with S. haematobium (incidence = 13.3%). Our results showed that infection with S. haematobium was associated with significant increases (>2-fold) in discriminatory metabolites, linked primarily with energy (G6P, 3-PG, AMP, ADP) and purine (AMP, ADP) metabolism. These observed changes were commensurate with schistosome infection intensity, and levels of the affected metabolites were reduced following treatment, albeit not significantly. This study demonstrates that early infection with S. haematobium is associated with alterations in host energy and purine metabolism. Taken together, these changes are consistent with parasite-related clinical manifestations of malnutrition, poor growth and poor physical and cognitive performance observed in schistosome-infected children.

Brain-encysting trematodes (Euhaplorchis californiensis) decrease raphe serotonergic activity in California killifish (Fundulus parvipinnis).

ABSTRACTModulation of brain serotonin (5-HT) signalling is associated with parasite-induced changes in host behaviour, potentially increasing parasite transmission to predatory final hosts. Such alterations could have substantial impact on host physiology and behaviour, as 5-HT serves multiple roles in neuroendocrine regulation. These effects, however, remain insufficiently understood, as parasites have been associated with both increased and decreased serotonergic activity. Here, we investigated effects of trematode Euhaplorchis californiensis metacercariae on post-stress serotonergic activity in the intermediate host California killifish (Fundulus parvipinnis). This parasite is associated with conspicuous behaviour and increased predation of killifish by avian end-hosts, as well as inhibition of post-stress raphe 5-HT activity. Until now, laboratory studies have only been able to achieve parasite densities (parasites/unit host body mass) well below those occurring in nature. Using laboratory infections yielding ecologically relevant parasite loads, we show that serotonergic activity indeed decreased with increasing parasite density, an association likely indicating changes in 5-HT neurotransmission while available transmitter stores remain constant. Contrary to most observations in the literature, 5-HT activity increased with body mass in infected fish, indicating that relationships between parasite load and body mass may in many cases be a real underlying factor for physiological correlates of body size. Our results suggest that parasites are capable of influencing brain serotonergic activity, which could have far-reaching effects beyond the neurophysiological parameters investigated here.

Behavioural mechanisms underlying parasite-mediated competition for refuges in a coral reef fish

Parasites have been increasingly recognized as participants in indirect ecological interactions, including those mediated by parasite-induced changes to host behaviour (trait-mediated indirect interactions or TMIIs). In most documented examples, host behaviours altered by parasites increase susceptibility to predation because the predator is also a host (host-manipulation). Here, we test for a TMII in which a parasitic copepod modifies the predator-prey interaction between a small goby host and several larger predatory fish. Gobies compete for crevices in the reef to avoid predation and goby mortality increases more rapidly with increasing refuge shortage for parasitized gobies than for those free of parasites. We found interactive effects of refuge shortage and parasitism on two behaviours we predicted might be associated with parasite-mediated competition for refuges. First, as refuge-shortage increases, the rate of aggression among gobies increases and parasitism intensifies this interaction. Second, goby proximity to refuges increases as refuges become scarce, but parasitism nullifies this increase. In combination, these parasite-induced changes in behaviour may explain why parasitized gobies are poor competitors for refuges. Because the parasite is not trophically transmitted via host manipulation, these altered behaviours in parasitized gobies are likely coincidental to infection.

The secreted kinase ROP17 promotes Toxoplasma gondii dissemination by hijacking monocyte tissue migration.

The protozoan parasite Toxoplasma gondii is thought to exploit monocyte trafficking to facilitate dissemination across endothelial barriers such as the blood-brain barrier. Here we analyzed the migration of parasitized monocytes in model endothelial and interstitial environments. We report that infection enhanced monocyte locomotion on the surface of endothelial cells, but profoundly inhibited monocyte transmigration across endothelial barriers. In contrast, infection robustly increased monocyte and macrophage migration through collagen-rich tissues in a Rho/ROCK-dependent manner consistent with integrin-independent interstitial migration. We further demonstrated that the secreted T. gondii protein kinase ROP17 was required for enhanced tissue migration. In vivo, ROP17-deficient parasites failed to upregulate monocyte tissue migration and exhibited an early dissemination delay, leading to prolonged mouse survival. Our findings indicate that the parasite-induced changes in monocyte motility likely facilitate the transport of T. gondii through tissues and promote systemic dissemination, rather than shuttle parasites across the blood-brain barrier via extravasation.

Inter-population variation in the intensity of host manipulation by the fish acanthocephalan Pomphorhynchus tereticollis: are differences driven by predation risk?

Many trophically-transmitted parasites induce behavioural alteration in their intermediate hosts that tend to increase host vulnerability to predation. Inter-population variability in parasite-induced alterations is expected to arise from variable local opportunities for trophic transmission. Yet, this hypothesis has not been investigated so far. We addressed the issue in four populations of the fish parasite Pomphorhynchus tereticollis (Acanthocephala), using variable fish biomass density as a proxy for transmission opportunities. We found variation in the intensity of parasite-induced changes in phototaxis and refuge use among populations. Two of the populations with the lowest predator biomass exhibited the highest levels of behavioural manipulation and prevalence, as expected at low transmission opportunities. They also exhibited micro-habitat segregation between infected and uninfected gammarids in the field. In addition, infection had variable effects on two physiological defence systems, immunity and antioxidant capacity, and on total protein content. Overall, our study brings partial support to the prediction that host manipulation and prevalence should be higher at low predator biomass. Although stronger evidence should be sought by increasing population replicates, our study points to the importance of the ecological context, specifically transmission opportunities brought about by predation pressure, for the evolution of parasite manipulation in trophically-transmitted parasites.

Nutrient availability affects the prevalence of a microsporidian parasite.

Defining the relationship between nutrients and parasitism is complicated by shifts in host physiology and population density, which can both mediate the effects of host diet on parasites and vice versa. We examined the relationship between nutrient availability and an abundant parasite capable of both horizontal and vertical transmission (Hamiltosporidium tvaerminnensis) of a planktonic crustacean, Daphnia magna, in rock pools on Baltic Sea Skerry islands. We found that the relative availability of nutrients directly affected infection prevalence; parasite prevalence was higher in pools with higher particulate N:P ratios. Infection prevalence was not related to Daphnia population densities. A complementary experiment that examined host responses to an N:P gradient in mesocosms indicated that high N:P ratios can increase spore load in the hosts. We surmise that high N:P food increases Daphnia feeding rate, which increases their contact with parasite spores and leads to higher prevalence and more intense infections. We found no direct evidence that parasite-induced changes in host nutrient use affected nutrient dynamics in pools. However, the relationship between diet N:P and the parasite's prevalence and load is consistent with previously documented patterns of this parasite's effect on host nutrient use. Taken together, this study suggests that high N:P ratios in food may benefit the parasite in multiple ways and could create environments that favour horizontal transmission over vertical transmission for parasites capable of both transmission routes. If so, nutrient limitation could have long-term consequences for host-parasite evolution.

Positive phototropism is accelerated in Biomphalaria glabrata snails by infection with Schistosoma mansoni

Parasite-induced behavioral changes in their hosts favor to complete the lifecycle of parasites. Schistosome infection is also known to cause physiological changes in infected freshwater snail intermediate hosts. Here, we report, a novel phenomenon in which Schistosoma mansoni, a highly debilitating worm affecting millions of people worldwide, alters the phototropic behavior of Biomphalaria glabrata, the vector snail. S. mansoni-infection enhanced positive phototropism of vector snails and infected snails spent significantly more time in light. Possibly, these behavioral changes help the parasite to be released efficiently from the infected intermediate hosts, and to infect mammalian hosts.

Infection, specificity and host manipulation of Australapatemon sp. (Trematoda, Strigeidae) in two sympatric species of leeches (Hirudinea).

Factors that drive parasite specificity and differences in infection dynamics among alternative host species are important for ecology and evolution of host-parasite interactions, but still often poorly known in natural systems. Here, we investigated spatiotemporal dynamics of infection, host susceptibility and parasite-induced changes in host phenotype in a rarely explored host-parasite system, the Australapatemon sp. trematode infecting two sympatric species of freshwater leeches, Erpobdella octoculata and Helobdella stagnalis. We show significant variation in infection abundance between the host species in both space and time. Using experimental infections, we also show that most of this variation likely comes from interspecific differences in exposure rather than susceptibility. Moreover, we demonstrate that the hiding behaviour of E. octoculata, but not that of H. stagnalis, was impaired by the infection irrespective of the parasite abundance. This may increase susceptibility of E. octoculata to predation by the final avian host. We conclude that differences in patterns of infection and in behavioural alterations among alternative sympatric host species may arise in narrow spatial scales, which emphasises the importance of local infection and transmission dynamics for parasite life cycles.

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.

Naris deformation in Darwin’s finches: Experimental and historical evidence for a post-1960s arrival of the parasite Philornis downsi

The rate of evolution depends on the strength of selection, which may be particularly strong for introduced parasites and their naive hosts. Because natural selection acts on phenotypes and because parasites can alter host phenotype, one fruitful starting point to measure the impact of novel pathogens is to quantify parasite-induced changes to host phenotype. Our study system is Darwin’s finches on Floreana Island, Galápagos Archipelago, and the virulent fly larvae of Philornis downsi that were first discovered in Darwin’s finch nests in 1997. We use an experimental approach and measure host phenotype in parasitized and parasite-free chicks in Darwin’s small ground finch (Geospiza fuliginosa). Beak size did not differ between the two treatment groups, but naris size was 106% larger in parasitized chicks (∼3.3 mm) versus parasite-free chicks (∼1.6 mm). To test if P. downsi was present prior to the 1960s, we compared naris size in historical (1899–1962) and contemporary birds (2004–2014) on Floreana Island in small ground finches (G. fuliginosa) and medium tree finches (Camarhynchus pauper). Contemporary Darwin’s finches had significantly larger naris size (including extreme deformation), whereas historical naris size was both smaller and less variable. These findings provide the first longitudinal analysis for the extent of P. downsi-induced change to host naris size and show that Darwin’s finches, prior to the 1960s, were not malformed. Thus natural selection on altered host phenotype as a consequence of P. downsi parasitism appears to be contemporary and novel.

Bold, Sedentary Fathead Minnows Have More Parasites.

Parasites that rely on trophic transmission can manipulate the behavior of an intermediate host to compromise the host's antipredator competence and increase the probability of reaching the next host. Selection for parasite manipulation is diminished when there is significant risk of host death to causes other than consumption by a suitable definitive host for the parasite. Consequently, behavioral manipulation by parasites can be expected to be subtle. Ornithodiplostomum ptychocheilus (Op) is a trematode parasite that has a bird-snail-fish host life cycle. Fathead minnows are a common intermediate host of Op, where metacercariae encyst in the minnow brain. In this study, we report a link between metacercarial intensity and behavior in fathead minnows. In the field, we found that roaming distance by free-living minnows over 24 h was negatively correlated with parasite intensity. In the laboratory, we found that boldness in an open field test was positively correlated with parasite intensity. These parasite-induced behavioral changes may render infected minnows more susceptible to predators, which would serve to facilitate trophic transmission of parasites to the bird host.

Host-seeking behaviors of mosquitoes experimentally infected with sympatric field isolates of the human malaria parasite Plasmodium falciparum: no evidence for host manipulation

Previous studies have shown that Plasmodium parasites can manipulate mosquito feeding behaviours such as motivation and avidity to feed on vertebrate hosts, in ways that increase the probability of parasite transmission. These studies, however, have been mainly carried out on non-natural and/or laboratory based model systems and hence may not reflect what occurs in the field. We now need to move closer to the natural setting, if we are to fully capture the ecological and evolutionary consequences of these parasite-induced behavioral changes. As part of this effort, we conducted a series of experiments to investigate the long and short-range behavioural responses to human stimuli in the mosquito Anopheles coluzzii during different stages of infection with sympatric field isolates of the human malaria parasite Plasmodium falciparum in Burkina Faso. First, we used a dual-port olfactometer designed to take advantage of the whole body odor to gauge mosquito long-range host-seeking behaviors. Second, we used a locomotor activity monitor system to assess mosquito short-range behaviors. Compared to control uninfected mosquitoes, P. falciparum infection had no significant effect neither on long-range nor on short-range behaviors both at the immature and mature stages. This study, using a natural mosquito-malaria parasite association, indicates that manipulation of vector behavior may not be a general phenomenon. We speculate that the observed contrasting phenotypes with model systems might result from coevolution of the human parasite and its natural vector. Future experiments, using other sympatric malaria mosquito populations or species are required to test this hypothesis. In conclusion, our results highlight the importance of following up discoveries in laboratory model systems with studies on natural parasite–mosquito interactions to accurately predict the epidemiological, ecological and evolutionary consequences of parasite manipulation of vector behaviors