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PubMedDate not supplied

Some haematological parameters in plasmodial parasitized HIV-infected Nigerians.

BACKGROUND: Nigeria is highly burdened by malaria and HIV-infection, yet researchers know little about the impact of this co-infection on the haematological profile of HIV-infected adult Nigerians. This case control study is an attempt to investigate the effect that HIV/malaria co-infection has on some haematological parameters of HIV-infected Nigerians. METHODS: Complete blood count (CBC) of 30 plasmodium parasitized HIV-infected subjects and 70 non-parasitized controls were studied. RESULTS: Of the 30 parasitized subjects, 28 (93.3%) were positive for falciparum malaria and 2 (6.7%) for vivax malaria. The incidence of anaemia, thrombocytopenia, neutropenia and leucopenia were significantly higher in parasitized subjects compared to non-parasitized controls 66.7%, 60%, 36.7% and 63.3% versus 32.9%, 42.9%, 24.3% and 24.3% respectively. A statistically significant difference was observed between the haemoglobin, platelet count and the erythrocyte sedimentation rate (ESR) of parasitized and non- parasitized individuals (p < 0.05) respectively. A significant positive correlation was observed between the level of parasitaemia and anaemia (r = 0.37, p < 0.04) in parasitized subjects. The incidence of anaemia was two times higher in parasitized subjects compared to non-parasitized controls (66.7% versus 32.9%). Red cell morphology showed a normocytic and normochromic picture in 40% and 67.1% of parasitized and non- parasitized individuals respectively. Microcytic, hypochromic picture was observed in 60% and 23% respectively in parasitized and non- parasitized individuals. Striking eosinophilia was seen in 5 (16.7%) of parasitized and 3 (4.3%) of non-parasitized individuals. CONCLUSION: Incidence of cytopenia appear significantly higher in parasitized subjects compared to non-parasitized control and bring to bare the need for regular anti-malaria prophylaxis for HIV-infected patients particularly in Nigeria.

AIDS-Related Opportunistic Infections↗

PubMed2002

The glucogenic response of a parasitized insect Manduca sexta L. is partially mediated by differential nutrient intake.

Induction of gluconeogenesis is accelerated in larvae of the insect Manduca sexta L. parasitized by Cotesia congregata (Say), maintaining the concentration of the blood sugar trehalose, an important nutrient for parasite development. Investigation has demonstrated that when host larvae are offered a choice of diets with varying levels of sucrose and casein, parasitized insects consume a different balance of these nutrients, principally due to a decrease in protein consumption. The result is metabolic homeostasis, with normal unparasitized and parasitized larvae exhibiting similar levels of gluconeogenesis and blood sugar level. In the present study, normal unparasitized and parasitized larvae were maintained on individual chemically defined diets having the balance of protein and carbohydrate consumed by each when offered a dietary choice. Total dietary nutrient, the sum of carbohydrate and protein, was provided at six levels, composed of three pairs of diets. Each diet pair consisting of diets having equivalent overall nutrient ratios of 2:1 and 1:1 casein/sucrose. Host growth and diet consumption were significantly affected by dietary nutrient level and the magnitude of these effects was influenced by parasitism. Due to the effects of dietary nutrient level on diet consumption, none of the unparasitized and parasitized larvae within any of the three diet pairs consumed protein and carbohydrate at the levels predicted by the earlier choice experiments. Among insects on all of the diets, however, two groups of unparasitized and parasitized larvae consumed the expected levels of protein and carbohydrate. In each case, gluconeogenesis, as measured by 13C nuclear magnetic resonance spectroscopy (NMR) analysis of pyruvate cycling and trehalose synthesis from [2-13C]pyruvate, was evident in unparasitized and parasitized insects, confirming the conclusions of the earlier experiments. Generally, all larvae that consumed less than approximately 250 mg of sucrose over the 3-day feeding period, were gluconeogenic, regardless of diet. Differential carbohydrate consumption, therefore, was an important factor in inducing gluconeogenesis in both unparasitized and parasitized insects. The selective 13C enrichment in trehalose displayed by non-gluconeogenic larvae on some diets demonstrated trehalose formation from [2]pyruvate. The absence of net carbohydrate synthesis in these insects was likely due to an elevation of glycolysis. There was no significant effect of diet consumption or parasitism on blood trehalose level. Parasitized larvae displayed higher levels of gluconeogenesis than did unparasitized insects, a finding consistent with the conclusion that blood sugar is rapidly sequestered by developing parasites. The parasite burden, the total number of parasites developing within host larvae, as well as the number of parasites emerging from host larvae to complete development, was significantly less at the lowest dietary nutrient level, but was otherwise similar at all dietary nutrient levels. Moreover, the number of parasites that emerged increased with increasing diet consumption as reflected by host final weight.

Animals↗

PubMed1987

Host effector mechanisms against parasites.

The first part of this presentation considers some of the complexities of parasitic infections and parasite-specific effector mechanisms which have hampered the development of practical methods of immunisation against parasitic diseases. In the second part, an outline is given of the effector mechanisms involved in immunity of cattle to the protozoan parasite Theileria parva. Parasites are antigenically complex organisms which often have distinct developmental stages, sometimes with different predilection sites within the host. Antigenic polymorphism between strains is a common feature of parasites and sometimes results in strain-specific immunity. Certain parasites have also evolved mechanisms of modulating surface antigens which allow them to escape host effector mechanism. Effector mechanisms which control parasitic infections may operate by preventing establishment of the parasites, by eliminating the parasites once they have established or by affecting growth or fecundity of the parasites. In addition to specific antibody and cell-mediated immune responses, inflammatory or physiological responses play an important role in the control of some parasites. Current evidence suggests that effector mechanisms against T.parva parasites operate at two levels. First, antibodies produced against the infective stage of the parasite, the sporozoite, can, by neutralising infectivity, reduce the numbers of organisms which establish in the host. Second, cytotoxic T cells directed against parasitised lymphoblasts cause destruction of parasites following their establishment in the host. Moreover, in situations where immunity is parasite strain-specific, the cytotoxic T cell responses have also been found to be strain-specific. The elucidation of these effector mechanisms has indicated potential new strategies of immunisation against T.parva.

Animals↗

PubMed1997

The malaria parasite supplies glutathione to its host cell--investigation of glutathione transport and metabolism in human erythrocytes infected with Plasmodium falciparum.

Malaria-infected red blood cells are under a substantial oxidative stress. Glutathione metabolism may play an important role in antioxidant defense in these cells, as it does in other eukaryotes. In this work, we have determined the levels of reduced and oxidized glutathione (GSH and GSSG, respectively) and their distributions in the parasite, and in the host-cell compartments of human erythrocytes infected with the malaria parasite Plasmodium falciparum. In intact trophozoite-infected erythrocytes, [GSH] is low and [GSSG] is high, compared with the levels in normal erythrocytes. Normal erythrocytes and the parasite compartment display high GSH/GSSG ratios of 321.6 and 284.5, respectively, indicating adequate antioxidant defense. This ratio drops to 26.7 in the host-cell compartment, indicating a forceful oxidant challenge, the low ratios resulting from an increase in GSSG and a decline in GSH concentrations. On the other hand, the concentrations of GSH and GSSG in the parasite compartment remain physiological and comparable to their concentrations in normal red blood cells. This results from de novo glutathione synthesis and its recycling, assisted by the intensive activity of the hexose monophosphate shunt in the parasite. A large efflux of GSSG from infected cells has been observed, its rate being similar from free parasites and from intact infected cells. This result suggests that de novo synthesis by the parasite is the dominating process in infected cells. GSSG efflux from the intact infected cell is more than 60-fold higher than the rate observed in normal erythrocytes, and is mediated by permeability pathways that the parasite induces in the erythrocyte's membrane. The main route for GSSG efflux through the cytoplasmic membrane of the parasite seems to be due to a specific transport system and occurs against a concentration gradient. Gamma-glutamylcysteine [Glu(-Cys)] and GSH can penetrate through the pathways from the extracellular space into the host cytosol, but not into that of the parasite. This implies that the parasite membrane is impermeable to these peptides, and that the host cannot supply GSH to the parasite as suggested previously. Exogenous Glu(-Cys) is not converted into GSH in the host cell, arguing that GSH synthetase may not be functional. Compartment analysis of Mg2+ in infected erythrocytes revealed that the host compartment exhibits a low concentration of Mg2+ (0.5 mM) in comparison with the parasite compartment (4 mM) and the normal erythrocytes (1.5-3 mM). The drop in [Mg2+] results in cessation of Glu(-Cys) synthesis, and hence of GSH synthesis in the host-cell compartment. The decrease in [Mg2+] can affect other Mg2+-ATP-dependent functions, such as Na+ and Ca2+ active efflux. The present investigation confirms that the host-cell compartment is oxidatively distressed, whereas the parasite is efficiently equipped with anti-oxidant means that protect the parasite from the oxidative injury. The parasite has a huge capacity for de novo synthesis of GSH and for the reduction of GSSG. Part of the GSSG that is actively extruded from the parasite is reduced to GSH in the host cell whose own GSH synthesis is crippled.

Animals↗

PubMedDate not supplied

Correlation between concentration of hemolymph nutrients and amount of fat body consumed in lightly and heavily parasitized hosts (Pseudaletia separata).

Two states of parasitization in the Pseudaletia separata-Cotesia kariyai system were examined: one that was lightly parasitized and one that was heavily parasitized. We predicted that the consumption of fat body and hemolymph nutrients depends on the number of parasitoid larvae in the host. Lightly parasitized hosts (average clutch size+/-S.E.: 42.5+/-16.2, N=15) and heavily parasitized hosts (average clutch size+/-S.E.: 230.2+/-8.8, N=15) were prepared artificially. Eight days after parasitization, perivisceral fat body was depleted in the heavily parasitized host, although peripheral fat body was not yet consumed, but by day 10 most of the peripheral fat body was consumed. In lightly parasitized hosts, perivisceral fat body was not consumed by day 10. The parasitoid larvae deplete the perivisceral fat body first and then consume the peripheral fat body in the heavily parasitized host. The amount of trehalose, the major carbohydrate in the hemolymph, was related to the number of parasitoid larvae developing in the host. In a heavily parasitized host, trehalose concentrations remained low. However, in lightly parasitized hosts, the amount of trehalose increased 8 days after parasitization and then decreased by day 10. Protein and total lipid concentrations in the hemolymph of the heavily parasitized host were significantly lower than in lightly parasitized host on day 10, suggesting that the large number of parasitoid larvae depleted the fat body and hemolymph nutrients by day 10. High concentrations of total lipid on day 8 and 10 in lightly parasitized hosts and on day 8 in heavily parasitized host are likely to be attributed to the teratocytes.

Adipose Tissue↗

PubMed2004

Parasite biodiversity and its determinants in coastal marine teleost fishes of Brazil.

Recent studies of the forces behind the diversification of parasite assemblages have shed light on many aspects of parasite biodiversity. By using only parasite species richness as their measure of diversity, however, previous investigations have ignored the relatedness among parasite species and the taxonomic structure of the assemblages, which contain much information about their evolutionary origins. Here, we performed a comparative analysis across 50 species of fish from the coast of Brazil; we evaluated the effects of several host traits (body size, social behaviour, feeding habits, preference for benthic vs. pelagic habitats, depth range, and ability to enter brackish waters) on the diversity of their assemblages of metazoan parasites. As measures of diversity, we used parasite species richness, as well as the average taxonomic distinctness of the assemblage and its variance; the latter measures are based on the average taxonomic distance between any two parasite species in an assemblage. Unlike parasite species richness, taxonomic distinctness was unaffected by the number of host individuals examined per species. Fish body length proved to be the main predictor of parasite species richness, even when controlling for the confounding influences of host phylogeny and sampling effort, although it did not correlate with measures of parasite taxonomic distinctness. Predatory fish also had higher parasite species richness than planktivores, but this trend could not be confirmed using phylogenetically independent contrasts between host taxa. The main host feature associated with the taxonomic diversity of parasites was schooling behaviour, with schooling fish having more taxonomically diverse parasite assemblages than those of their non-schooling relatives. When focusing on endoparasite species only, both predatory feeding habits and a broad depth range were associated with the taxonomic distinctness of parasites. Our results suggest that certain host traits (i.e. body size) determine how many parasite species a host can accumulate over evolutionary time, whereas different host features influence the processes causing the taxonomic diversification of parasite assemblages.

Animals↗

PubMed1988

The population biology of parasite-induced changes in host behavior.

The ability of parasites to change the behavior of infected hosts has been documented and reviewed by a number of different authors (Holmes and Bethel, 1972; Moore, 1984a). This review attempts to quantify the population dynamic consequences of this behavior by developing simple mathematical models for the most frequently recorded of such parasite life cycles. Although changes in the behavior of infected hosts do occur for pathogens with direct life cycles, they are most commonly recorded in the intermediate hosts of parasites with complex life cycles. All the changes in host behavior serve to increase rates of transmission of the parasites between hosts. In the simplest case the changes in behavior increase rates of contact between infected and susceptible conspecific hosts, whereas in the more complex cases fairly sophisticated manipulations of the host's behavioral repertory are achieved. Three topics are dealt with in some detail: (1) the behavior of the insect vectors of such diseases as malaria and trypanosomiasis; (2) the intermediate hosts of helminths whose behavior is affected in such a way as to make them more susceptible to predation by the definitive host in the life cycle; and (3) the behavior and fecundity of molluscs infected with asexually reproducing parasitic flatworms. In each case an expression is derived for R0, the basic reproductive rate of the parasite when first introduced into the population. This is used to determine the threshold numbers of definitive and intermediate hosts needed to maintain a population of the pathogen. In all cases, parasite-induced changes in host behavior tend to increase R0 and reduce the threshold number of hosts required to sustain the infection. The population dynamics of the interaction between parasites and their hosts are then explored using phase plane analyses. This suggests that both the parasite and intermediate host populations may show oscillatory patterns of abundance. When the density of the latter is low, parasite-induced changes in host behavior increase this tendency to oscillate. When intermediate host population densities are high, parasite population density is determined principally by interactions between the parasites and their definitive hosts, and changes in the behavior of intermediate hosts are less important in determining parasite density. Analysis of these models also suggests that both asexual reproduction of the parasite within a host and parasite-induced reduction in host fecundity may be stabilizing mechanisms when they occur in the intermediate hosts of parasite species with indirect life cycles.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1989

[Parasitic zoonoses in Japan, with special reference to the current topics].

The present situation of parasitic zoonoses in Japan is reviewed. A total of 51 species, i.e., 6 species of protozoan parasites, 14 species of trematode parasites, 11 species of cestode parasites, 18 species of nematode parasites and 2 species of acanthocephalan parasites are potential zoonotic parasites. Most (11 species) of the zoonotic nematodes provoke larva migrans. Habitats of zoonotic parasites vary greatly depending upon individual species. Some parasites cause heterotopic parasitism (e.g., Paragonimus westermani) and metastasis (Entamoeba histolytica). In larva migrans, parasites migrate through various parts of body tissues, affecting multiple organs (gnathostomiasis and sparganosis mansoni). The majority of parasitic zoonoses are food-borne infections. Some of them are an arthropod-borne (or -mediated) infection (dirofilariasis, thelaziasis and moniliformiasis), or acquired by percutaneous infection with cercariae (schistosome cercarial dermatitis) or 3rd-stage infective larvae (hookworm diseases). The diagnosis of parasitic zoonoses, especially larva migrans, is difficult; although some unique clinical symptoms and the presence of eosinophilia and/or increased level of serum IgE antibody are frequently seen in larva migrans, the application of various immunodiagnostic methods is usually required. For the prevention and control of parasitic zoonoses, the ingestion of not only strange food (e.g., snakes, frogs, slugs, etc.) but also raw fish and cuttlefish (sashimi) must be prohibited. Fishes and the meat of wild animals (e.g., bear and wild boar) should be frozen or thoroughly cooked before eating. Pets and domestic animals play an important role as a direct or indirect source of infection with various parasitic zoonoses. The treatment of those animals and/or the eradication of intermediate hosts (or vectors) of the parasites are thus required.

Animals↗

PubMed2005

Cytokine and chemokine responses in patients co-infected with Entamoeba histolytica/dispar, Necator americanus and Mansonella perstans and changes after anti-parasite treatment.

This study examined the impact of concurrent parasite infections (amoebiasis, filariasis, necatoriasis) and the effect of anti-parasite treatment on cytokine and chemokine responses in singly and poly-parasitized patients. Cellular reactivity and parasite-specific Th1- and Th2-type cytokine and chemokine profiles were investigated before and six weeks after treatment. In those patients infected with three parasite species, cellular secretion of interleukin 5 (IL-5) and IL-12p40 by PBMC was strongly diminished (p<0.005) but IL-10 was elevated in parasite-infected patients (p<0.0001) in response to protozoa- and helminth-specific as well as bacteria-specific antigens. Macrophage inflammatory chemokines (MIP-1alpha/CCL3 and MIP-1beta/CCL4), macrophage-derived chemokine (MDC/CCL22) and neutrophil activating chemokine (IL-8/CXCL8) were produced by PBMC in similar amounts in endemic controls and singly and poly-parasitized patients, but thymus and activation-regulated chemokine (TARC/CCL17) was produced the highest by PBMC from patients with triple parasite infections (p<0.0001). Following anti-parasite therapy, secretion of IL-12p40 and IL-5 augmented significantly in treated patients while IL-10, MDC, MIP-1alpha, TARC and IL-8 substantially diminished (all p<10(-5)) when their PBMC were activated with parasite- and bacteria-specific antigens. In summary, PBMC from poly-parasitized patients responded to protozoa- and helminth-specific antigens with a compromised IL-5 and IL-12p40 but high IL-10 and a substantial chemokine release. Chemokines may attract and activate effector cells in peri-parasitic tissues to limit parasite proliferation and dissemination, while depressed IL-5 and IL-12p40 but prominent IL-10 may prevent eosinophil and cytotoxic cell-mediated inflammatory processes and pathogenesis to the host. The changes in this profile following anti-parasite therapy disclosed the dynamics of an immune adaptation associated with parasite accumulation and also with clearance of parasite infections.

Adult↗

PubMed2006

Hosts and parasites as aliens.

Over the past decades, various free-living animals (hosts) and their parasites have invaded recipient areas in which they had not previously occurred, thus gaining the status of aliens or exotics. In general this happened to a low extent for hundreds of years. With variable frequency, invasions have been followed by the dispersal and establishment of non-indigenous species, whether host or parasite. In the literature thus far, colonizations by both hosts and parasites have not been treated and reviewed together, although both are usually interwoven in various ways. As to those factors permitting invasive success and colonization strength, various hypotheses have been put forward depending on the scientific background of respective authors and on the conspicuousness of certain invasions. Researchers who have tried to analyse characteristic developmental patterns, the speed of dispersal or the degree of genetic divergence in populations of alien species have come to different conclusions. Among parasitologists, the applied aspects of parasite invasions, such as the negative effects on economically important hosts, have long been at the centre of interest. In this contribution, invasions by hosts as well as parasites are considered comparatively, revealing many similarities and a few differences. Two helminths, the liver fluke, Fasciola hepatica, of cattle and sheep and the swimbladder nematode, Anguillicola crassus, of eels are shown to be useful as model parasites for the study of animal invasions and environmental global change. Introductions of F. hepatica have been associated with imports of cattle or other grazing animals. In various target areas, susceptible lymnaeid snails serving as intermediate hosts were either naturally present and/or were introduced from the donor continent of the parasite (Europe) and/or from other regions which were not within the original range of the parasite, partly reflecting progressive stages of a global biota change. In several introduced areas, F. hepatica co-occurs with native or exotic populations of the congeneric F. gigantica, with thus far unknown implications. Over the fluke's extended range, in addition to domestic stock animals, wild native or naturalized mammals can also serve as final hosts. Indigenous and displaced populations of F. hepatica, however, have not yet been studied comparatively from an evolutionary perspective. A. crassus, from the Far East, has invaded three continents, without the previous naturalization of its natural host Anguilla japonica, by switching to the respective indigenous eel species. Local entomostrac crustaceans serve as susceptible intermediate hosts. The novel final hosts turned out to be naive in respect to the introduced nematode with far reaching consequences for the parasite's morphology (size), abundance and pathogenicity. Comparative infection experiments with Japanese and European eels yielded many differences in the hosts' immune defence, mirroring coevolution versus an abrupt host switch associated with the introduction of the helminth. In other associations of native hosts and invasive parasites, the elevated pathogenicity of the parasite seems to result from other deficiencies such as a lack of anti-parasitic behaviour of the naïve host compared to the donor host which displays distinct behavioural patterns, keeping the abundance of the parasite low. From the small amount of available literature, it can be concluded that the adaptation of certain populations of the novel host to the alien parasite takes several decades to a century or more. Summarizing all we know about hosts and parasites as aliens, tentative patterns and principles can be figured out, but individual case studies teach us that generalizations should be avoided.

Air Sacs↗

PubMed2002

A double test of the parasite manipulation hypothesis in a burrowing bivalve.

The parasite manipulation hypothesis predicts that parasites should be selected to manipulate host behaviour to facilitate transmission to the next host. The bivalve Macoma balthica burrows less deep when parasitized by the trematode Parvatrema affinis. Shallow burrowing increases the likelihood of ingestion by birds, their final hosts, and therefore this has been interpreted as manipulation by the parasite. When unparasitized, M. balthica displays seasonal changes in burrowing depth, becoming less accessible to predators in winter. If shallow burrowing of parasitized individuals is due to direct manipulation by the parasite, the availability of parasitized individuals should be high throughout the year, or at least especially in the season when most birds are present and potential transmission rates are highest. We compared burrowing depths of parasitized and unparasitized individuals in a single population during seven consecutive years. Parasitized individuals showed reduced burrowing depths but, in contrast to the prediction, the effect of parasites on availability to predators was smallest, not largest, in the season with the highest bird numbers. The parasite P. affinis competes for energy with the host, and M. balthica with low energy stores are known to reduce depth of burrowing. When we included size-corrected somatic ash-free dry mass (as an estimate of the energy stores) in our statistical analysis, the effect of infection on burrowing depth disappeared. Thus the effect of infection on burrowing depth is likely to be an unavoidable, indirect effect of the channelling of energy towards the parasite, causing the starving individual to take greater risks in the acquisition of food. Since both the seasonal pattern and the magnitude of increased availability of parasitized individuals are inadequate, the increased exposure of parasitized M. balthica to the final host does not seem to represent an example of adaptive host manipulation by the parasite.

Animals↗

PubMed2006

The scaling of total parasite biomass with host body mass.

The selective pressure exerted by parasites on their hosts will to a large extent be influenced by the abundance or biomass of parasites supported by the hosts. Predicting how much parasite biomass can be supported by host individuals or populations should be straightforward: ultimately, parasite biomass must be controlled by resource supply, which is a direct function of host metabolism. Using comparative data sets on the biomass of metazoan parasites in vertebrate hosts, we determined how parasite biomass scales with host body mass. If the rate at which host resources are converted into parasite biomass is the same as that at which host resources are channelled toward host growth, then on a log-log plot parasite biomass should increase with host mass with a slope of 0.75 when corrected for operating temperature. Average parasite biomass per host scaled with host body mass at a lower rate than expected (across 131 vertebrate species, slope=0.54); this was true independently of phylogenetic influences and also within the major vertebrate groups separately. Since most host individuals in a population harbour a parasite load well below that allowed by their metabolic rate, because of the stochastic nature of infection, it is maximum parasite biomass, and not average biomass, that is predicted to scale with metabolic rate among host species. We found that maximum parasite biomass scaled isometrically (i.e., slope=1) with host body mass. Thus, larger host species can potentially support the same parasite biomass per gram of host tissues as small host species. The relationship found between maximum parasite biomass and host body mass, with its slope greater than 0.75, suggests that parasites are not like host tissues: they are able to appropriate more host resources than expected from metabolically derived host growth rates.

Animals↗

PubMed2001

Genetic variation in a host-parasite association: potential for coevolution and frequency-dependent selection.

Models of host-parasite coevolution assume the presence of genetic variation for host resistance and parasite infectivity, as well as genotype-specific interactions. We used the freshwater crustacean Daphnia magna and its bacterial microparasite Pasteuria ramosa to study genetic variation for host susceptibility and parasite infectivity within each of two populations. We sought to answer the following questions: Do host clones differ in their susceptibility to parasite isolates? Do parasite isolates differ in their ability to infect different host clones? Are there host clone-parasite isolate interactions? The analysis revealed considerable variation in both host resistance and parasite infectivity. There were significant host clone-parasite isolate interactions, such that there was no single host clone that was superior to all other clones in the resistance to every parasite isolate. Likewise, there was no parasite isolate that was superior to all other isolates in infectivity to every host clone. This form of host clone-parasite isolate interaction indicates the potential for coevolution based on frequency-dependent selection. Infection success of original host clone-parasite isolate combinations (i.e., those combinations that were isolated together) was significantly higher than infection success of novel host clone-parasite isolate combinations (i.e., those combinations that were created in the laboratory). This finding is consistent with the idea that parasites track specific host genotypes under natural conditions. In addition, correspondence analysis revealed that some host clones, although distinguishable with neutral genetic markers, were susceptible to the same set of parasite isolates and thus probably shared resistance genes.

Animals↗

PubMed2007

Dispersal ecology versus host specialization as determinants of ectoparasite distribution in brood parasitic indigobirds and their estrildid finch hosts.

Brood parasitic birds offer a unique opportunity to examine the ecological and evolutionary determinants of host associations in avian feather lice (Phthiraptera). Brood parasitic behaviour effectively eliminates vertical transfer of lice between parasitic parents and offspring at the nest, while at the same time providing an opportunity for lice associated with the hosts of brood parasites to colonize the brood parasites as well. Thus, the biology of brood parasitism allows a test of the relative roles of host specialization and dispersal ecology in determining the host-parasite associations of birds and lice. If the opportunity for dispersal is the primary determinant of louse distributions, then brood parasites and their hosts should have similar louse faunas. In contrast, if host-specific adaptations limit colonization ability, lice associated with the hosts of brood parasites may be unable to persist on the brood parasites despite having an opportunity for colonization. We surveyed lice on four brood parasitic finch species (genus Vidua), their estrildid finch host species, and a few ploceid finches. While Brueelia lice were found on both parasitic and estrildid finches, a molecular phylogeny showed that lice infesting the two avian groups belong to two distinct clades within Brueelia. Likewise, distinct louse lineages within the amblyceran genus Myrsidea were found on estrildid finches and the parasitic pin-tailed whydah (Vidua macroura), respectively. Although common on estrildid finches, Myrsidea lice were entirely absent from the brood parasitic indigobirds. The distribution and relationships of louse species on brood parasitic finches and their hosts suggest that host-specific adaptations constrain the ability of lice to colonize new hosts, at least those that are distantly related.

Adaptation, Physiological↗

PubMedDate not supplied

[The parasite capacity of the host population].

The estimation of parasitic pressure on the host populations is frequently required in parasitological investigations. The empirical values of prevalence of infection are used for this, however the latter one as an estimation of parasitic pressure on the host population is insufficient. For example, the same prevalence of infection can be insignificant for the population with high reproductive potential and excessive for the population with the low reproductive potential. Therefore the development of methods of an estimation of the parasitic pressure on the population, which take into account the features the host population, is necessary. Appropriate parameters are to be independent on view of the researcher, have a clear biological sense and be based on easily available characteristics. The methods of estimation of parasitic pressure on the host at the organism level are based on various individual viability parameters: longevity, resistance to difficult environment etc. The natural development of this approach for population level is the analysis of viability parameters of groups, namely, the changing of extinction probability of host population under the influence of parasites. Obviously, some critical values of prevalence of infection should exist; above theme the host population dies out. Therefore the heaviest prevalence of infection, at which the probability of host population size decreases during the some period is less than probability of that increases or preserves, can serve as an indicator of permissible parasitic pressure on the host population. For its designation the term "parasite capacity of the host population" is proposed. The real parasitic pressure on the host population should be estimated on the comparison with its parasite capacity. Parasite capacity of the host population is the heaviest possible prevalence of infection, at which, with the generation number T approaching infinity, there exists at least one initial population size ni(0) for which the probability of size decrease through T generations is less than the probability of its increase. [formula: see text] The estimation of the probabilities of host population size changes is necessary for the parasite capacity determination. The classical methods for the estimation of extinction probability of population are unsuitable in this case, as these methods require the knowledge of population growth rates and their variances for all possible population sizes. Thus, the development methods of estimate of extinction probability of population, based on the using of available parameters (sex ratio, fecundity, mortality, prevalence of infection PI) is necessary. The population size change can be considered as the Markov process. The probabilities of all changes of population size for a generation in this case are described by a matrix of transition probabilities of Markov process (pi) with dimensions Nmax x Nmax (maximum population size). The probabilities of all possible size changes for T generations can be calculated as pi T. Analyzing the behaviour matrix of transition at various prevalence of infection, it is possible to determine the parasite capacity of the host population. In constructing of the matrix of transition probabilities, should to be taken into account the features the host population and the influence of parasites on its reproductive potential. The set of the possible population size at a generation corresponds to each initial population size. The transition probabilities for the possible population sizes at a generation can be approximated to the binomial distribution. The possible population sizes at a generation nj(t + 1) can be calculated as sums of the number of survived parents N1 and posterities N2; their probabilities--as P(N1) x P(N2). The probabilities of equal sums N1 + N2 and nj(t + 1) > or = Nmax are added. The number of survived parents N1 may range from 0 to (1-PI) x ni(t). The survival probabilities can be estimated for each N1 as [formula: see text] The number of survived posterities N2 may range from 0 to N2max (the maximum number of posterities). N2max is [formula: see text] and the survival probabilities for each N2, is defined as [formula: see text] where [formula: see text], ni(t) is the initial population size (including of males and infected specimens of host), PI is the prevalence of infection, Q1 is the survival probabilities of parents, Pfemales is the frequency of females in the host population, K is the number of posterities per a female, and Q2 is the survival probabilities of posterities. When constructing matrix of transition probabilities of Markov process (pi), the procedure outlined above should be repeated for all possible initial population size. Matrix of transition probabilities for T generations is defined as pi T. This matrix (pi T) embodies all possible transition probabilities from the initial population sizes to the final population sizes and contains a wealth of information by itself. From the practical point of view, however, the plots of the probability of population size decrease are more suitable for analysis. They can be received by summing the probabilities within of lines of matrix from 0 to ni--1 (ni--the population size, which corresponds to the line of the matrix). Offered parameter has the number of advantages. Firstly, it is independent on a view of researcher. Secondly, it has a clear biological sense--this is a limit of prevalence, which is safe for host population. Thirdly, only available parameters are used in the calculation of parasite capacity: population size, sex ratio, fecundity, mortality. Lastly, with the availability of modern computers calculations do not make large labour. Drawbacks of this parameter: 1. The assumption that prevalence of infection, mortality, fecundity and sex ratio are constant in time (the situations are possible when the variability of this parameters can not be neglected); 2. The term "maximum population size" has no clear biological sense; 3. Objective restrictions exist for applications of this mathematical approach for populations with size, which exceeds 1000 specimens (huge quantity of computing operations--order Nmax 3*(T-1), work with very low probabilities). The further evolution of the proposed approach will allow to transfer from the probabilities of size changes of individual populations to be probabilities of size changes of population systems under the influence of parasites. This approach can be used at the epidemiology and in the conservation biology.

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PubMed2006

Experimental evolution of resistance in Paramecium caudatum against the bacterial parasite Holospora undulata.

Host-parasite coevolution is often described as a process of reciprocal adaptation and counter adaptation, driven by frequency-dependent selection. This requires that different parasite genotypes perform differently on different host genotypes. Such genotype-by-genotype interactions arise if adaptation to one host (or parasite) genotype reduces performance on others. These direct costs of adaptation can maintain genetic polymorphism and generate geographic patterns of local host or parasite adaptation. Fixation of all-resistant (or all-infective) genotypes is further prevented if adaptation trades off with other host (or parasite) life-history traits. For the host, such indirect costs of resistance refer to reduced fitness of resistant genotypes in the absence of parasites. We studied (co)evolution in experimental microcosms of several clones of the freshwater protozoan Paramecium caudatum, infected with the bacterial parasite Holospora undulata. After two and a half years of culture, inoculation of evolved and naive (never exposed to the parasite) hosts with evolved and founder parasites revealed an increase in host resistance, but not in parasite infectivity. A cross-infection experiment showed significant host clone-by-parasite isolate interactions, and evolved hosts tended to be more resistant to their own (local) parasites than to parasites from other hosts. Compared to naive clones, evolved host clones had lower division rates in the absence of the parasite. Thus, our study indicates de novo evolution of host resistance, associated with both direct and indirect costs. This illustrates how interactions with parasites can lead to the genetic divergence of initially identical populations.

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PubMed2002

Dose-dependent infection rates of parasites produce the Allee effect in epidemiology.

In many epidemiological models of microparasitic infections it is assumed that the infection process is governed by the mass-action principle, i.e. that the infection rate per host and per parasite is a constant. Furthermore, the parasite-induced host mortality (parasite virulence) and the reproduction rate of the parasite are often assumed to be independent of the infecting parasite dose. However, there is empirical evidence against those three assumptions: the infection rate per host is often found to be a sigmoidal rather than a linear function of the parasite dose to which it is exposed; and the lifespan of infected hosts as well as the reproduction rate of the parasite are often negatively correlated with the parasite dose. Here, we incorporate dose dependences into the standard modelling framework for microparasitic infections, and draw conclusions on the resulting dynamics. Our model displays an Allee effect that is characterized by an invasion threshold for the parasite. Furthermore, in contrast to standard epidemiological models a parasite strain needs to have a basic reproductive rate that is substantially greater than 1 to establish an infection. Thus, the conditions for successful invasion of the parasite are more restrictive than in mass-action infection models. The analysis further suggests that negative correlations of the parasite dose with host lifespan and the parasite reproduction rate helps the parasite to overcome the invasion constraints of the Allee-type dynamics.

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PubMed1993

Effects of parasitism by the braconid wasp Cotesia congregata on host hemolymph proteins of the tobacco hornworm, Manduca sexta.

Parasitism by the braconid wasp Cotesia congregata causes major alterations in the hemolymph proteins of host tobacco hornworm larvae. Earlier studies showed that the total amount of hemolymph protein is reduced during parasitism, beginning almost immediately after the host is parasitized. Simultaneously, parasitism induces synthesis of large amounts of novel proteins that appear in the blood as early as 1-2 h post-parasitization. The present report confirms earlier studies describing the presence of novel proteins in last instar hosts, and also characterizes the effects of parasitism in altering the titers of several endogenous host hemolymph proteins normally produced by the fat body and other tissues. Analysis of hemolymph plasma using SDS-PAGE and densitometry, as well as immunodiffusion assays, showed that in terminal stage fifth instar host larvae, the titers of serpins and arylphorin were dramatically reduced relative to the levels of these proteins detected in nonparasitized gate II fifth instar larvae of the same age. The relative differences between parasitized and nonparasitized larvae increased with time following ecdysis to the fifth instar, so that the day 4 nonparasitized larvae had arylphorin titers of c. 30 mg/ml, whereas parasitized day 4 larvae with newly emerged wasps had only one sixth that amount of storage protein circulating in the hemolymph. Similarly, in nonparasitized larvae the hemolymph serpin concentration increased from c. 200 micrograms/ml (on day 0) to > 600 micrograms/ml (on day 4) in prewandering gate II larvae, but in parasitized larvae the hemolymph serpin concentration was maintained in the range of 100-200 micrograms per ml hemolymph until the pharate third instar parasites emerged from the host larva on day 4. In contrast, the level of hemolymph lipophorin was unaffected by parasitism, and lipophorin increased from c. 1.3 to > 3 mg/ml during the time interval between days 0 and 4 in both nonparasitized and parasitized larvae. Hemolymph titers of insecticyanin also were not significantly different in parasitized vs nonparasitized larvae, and in both types of larvae the concentration of this pigment decreased by c. 50% during the same time interval when lipophorin was increased significantly. Instead of causing a generalized inhibition of host hemolymph protein synthesis, parasitism causes a complex array of changes in the hemolymph protein profile of Manduca sexta, possibly via the mediation of hormonal modulators of host protein synthesis, or transcriptional or translational regulation of host gene expression by factors associated with the polydnavirus or molecules secreted by the parasites.(ABSTRACT TRUNCATED AT 400 WORDS)

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