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Parasite Survival (parasite + survival)
Selected AbstractsPARASITISM OF PHOTOSYNTHETIC DINOFLAGELLATES BY THREE STRAINS OF AMOEBOPHRYA (DINOPHYTA): PARASITE SURVIVAL, INFECTIVITY, GENERATION TIME, AND HOST SPECIFICITY1JOURNAL OF PHYCOLOGY, Issue 3 2002D. Wayne Coats Amoebophrya ceratii (Koeppen) Cachon is an obligate parasite of dinoflagellates and may represent a species complex. However, little is known about the biology and host range of different strains of Amoebophrya Cachon. Here, we determined parasite generation time and dinospore infectivity, survival, and ability to infect nonprimary hosts for strains of Amoebophrya from Akashiwo sanguinea (Hirasaka) G. Hansen et Moestrup, Gymnodinium instriatum (Freudenthal et Lee) Coats comb. nov., and Karlodinium micrum (Leadbeater et Dodge) J. Larsen. Akashiwo sanguinea was readily infected, with parasite prevalence reaching 100% in dinospore:host inoculations above a 10:1 ratio. Parasitism also approached 100% in G. instriatum, but only when inoculations exceeded a 40:1 ratio. Karlodinium micrum appeared partially resistant to infection, as parasite prevalence saturated at 92%. Parasite generation time differed markedly among Amoebophrya strains. Survival and infectivity of dinospores decreased over time, with strains from G. instriatum and A. sanguinea unable to initiate infections after 2 and 5 days, respectively. By contrast, dinospores from Amoebophrya parasitizing K. micrum remained infective for up to 11 days. Akashiwo sanguinea and G. instriatum were not infected when exposed to dinospores from nonprimary Amoebophrya strains. Karlodinium micrum, however, was attacked by dinospores of Amoebophrya from the other two host species, but infections failed to reach maturity. Observed differences in host,parasite biology support the hypothesis that Amoebophrya ceratii represents a complex of host-specific species. Results also suggest that Amoebophrya strains have evolved somewhat divergent survival strategies that may encompass sexuality, heterotrophy during the "free-living" dinospore stage, and dormancy. [source] ORIGINAL ARTICLE: Probability of emergence of antimalarial resistance in different stages of the parasite life cycleEVOLUTIONARY APPLICATIONS (ELECTRONIC), Issue 1 2009Wirichada Pongtavornpinyo Abstract Understanding the evolution of drug resistance in malaria is a central area of study at the intersection of evolution and medicine. Antimalarial drug resistance is a major threat to malaria control and directly related to trends in malaria attributable mortality. Artemisinin combination therapies (ACT) are now recommended worldwide as first line treatment for uncomplicated malaria, and losing them to resistance would be a disaster for malaria control. Understanding the emergence and spread of antimalarial drug resistance in the context of different scenarios of antimalarial drug use is essential for the development of strategies protecting ACTs. In this study, we review the basic mechanisms of resistance emergence and describe several simple equations that can be used to estimate the probabilities of de novo resistance mutations at three stages of the parasite life cycle: sporozoite, hepatic merozoite and asexual blood stages; we discuss the factors that affect parasite survival in a single host in the context of different levels of antimalarial drug use, immunity and parasitaemia. We show that in the absence of drug effects, and despite very different parasite numbers, the probability of resistance emerging at each stage is very low and similar in all stages (for example per-infection probability of 10,10,10,9 if the per-parasite chance of mutation is 10,10 per asexual division). However, under the selective pressure provided by antimalarial treatment and particularly in the presence of hyperparasitaemia, the probability of resistance emerging in the blood stage of the parasite can be approximately five orders of magnitude higher than in the absence of drugs. Detailed models built upon these basic methods should allow us to assess the relative probabilities of resistance emergence in the different phases of the parasite life cycle. [source] Host sex and ectoparasites choice: preference for, and higher survival on female hostsJOURNAL OF ANIMAL ECOLOGY, Issue 4 2007PHILIPPE CHRISTE Summary 1Sex differences in levels of parasite infection are a common rule in a wide range of mammals, with males usually more susceptible than females. Sex-specific exposure to parasites, e.g. mediated through distinct modes of social aggregation between and within genders, as well as negative relationships between androgen levels and immune defences are thought to play a major role in this pattern. 2Reproductive female bats live in close association within clusters at maternity roosts, whereas nonbreeding females and males generally occupy solitary roosts. Bats represent therefore an ideal model to study the consequences of sex-specific social and spatial aggregation on parasites' infection strategies. 3We first compared prevalence and parasite intensities in a host,parasite system comprising closely related species of ectoparasitic mites (Spinturnix spp.) and their hosts, five European bat species. We then compared the level of parasitism between juvenile males and females in mixed colonies of greater and lesser mouse-eared bats Myotis myotis and M. blythii. Prevalence was higher in adult females than in adult males stemming from colonial aggregations in all five studied species. Parasite intensity was significantly higher in females in three of the five species studied. No difference in prevalence and mite numbers was found between male and female juveniles in colonial roosts. 4To assess whether observed sex-biased parasitism results from differences in host exposure only, or, alternatively, from an active, selected choice made by the parasite, we performed lab experiments on short-term preferences and long-term survival of parasites on male and female Myotis daubentoni. When confronted with adult males and females, parasites preferentially selected female hosts, whereas no choice differences were observed between adult females and subadult males. Finally, we found significantly higher parasite survival on adult females compared with adult males. 5Our study shows that social and spatial aggregation favours sex-biased parasitism that could be a mere consequence of an active and adaptive parasite choice for the more profitable host. [source] Mechanisms of pathogenesis and the evolution of parasite virulenceJOURNAL OF EVOLUTIONARY BIOLOGY, Issue 2 2008S. A. FRANK Abstract When studying how much a parasite harms its host, evolutionary biologists turn to the evolutionary theory of virulence. That theory has been successful in predicting how parasite virulence evolves in response to changes in epidemiological conditions of parasite transmission or to perturbations induced by drug treatments. The evolutionary theory of virulence is, however, nearly silent about the expected differences in virulence between different species of parasite. Why, for example, is anthrax so virulent, whereas closely related bacterial species cause little harm? The evolutionary theory might address such comparisons by analysing differences in tradeoffs between parasite fitness components: transmission as a measure of parasite fecundity, clearance as a measure of parasite lifespan and virulence as another measure that delimits parasite survival within a host. However, even crude quantitative estimates of such tradeoffs remain beyond reach in all but the most controlled of experimental conditions. Here, we argue that the great recent advances in the molecular study of pathogenesis provide a way forward. In light of those mechanistic studies, we analyse the relative sensitivity of tradeoffs between components of parasite fitness. We argue that pathogenic mechanisms that manipulate host immunity or escape from host defences have particularly high sensitivity to parasite fitness and thus dominate as causes of parasite virulence. The high sensitivity of immunomodulation and immune escape arise because those mechanisms affect parasite survival within the host, the most sensitive of fitness components. In our view, relating the sensitivity of pathogenic mechanisms to fitness components will provide a way to build a much richer and more general theory of parasite virulence. [source] Characterization of a Leishmania stage-specific mitochondrial membrane protein that enhances the activity of cytochrome c oxidase and its role in virulenceMOLECULAR MICROBIOLOGY, Issue 2 2010Ranadhir Dey Summary Leishmaniasis is caused by the dimorphic protozoan parasite Leishmania. Differentiation of the insect form, promastigotes, to the vertebrate form, amastigotes, and survival inside the vertebrate host accompanies a drastic metabolic shift. We describe a gene first identified in amastigotes that is essential for survival inside the host. Gene expression analysis identified a 27 kDa protein-encoding gene (Ldp27) that was more abundantly expressed in amastigotes and metacyclic promastigotes than in procyclic promastigotes. Immunofluorescence and biochemical analysis revealed that Ldp27 is a mitochondrial membrane protein. Co-immunoprecipitation using antibodies to the cytochrome c oxidase (COX) complex, present in the inner mitochondrial membrane, placed the p27 protein in the COX complex. Ldp27 gene-deleted parasites (Ldp27,/,) showed significantly less COX activity and ATP synthesis than wild type in intracellular amastigotes. Moreover, the Ldp27,/, parasites were less virulent both in human macrophages and in BALB/c mice. These results demonstrate that Ldp27 is an important component of an active COX complex enhancing oxidative phosphorylation specifically in infectious metacyclics and amastigotes and promoting parasite survival in the host. Thus, Ldp27 can be explored as a potential drug target and parasites devoid of the p27 gene could be considered as a live attenuated vaccine candidate against visceral leishmaniasis. [source] Ocular toxoplasmosis: in the storm of the eyePARASITE IMMUNOLOGY, Issue 12 2006L. A. JONES SUMMARY Ocular toxoplasmosis (OT) can occur in the children of mothers infected with Toxoplasma gondii during pregnancy. It is not limited to the congenitally infected, but can also occur following adult-acquired infection or as a result of disease reactivation in immune-compromised and pregnant individuals. Many aspects of immune privilege in the eye, including constitutive TGF-, expression and reduced MHC class 1 expression, would appear at first to favour parasite survival. Conversely, many of the mechanisms that control parasite multiplication in other anatomical sites, such as nitric oxide expression, IFN-, and TNF-,, are known to disrupt immune privilege and are associated with ocular damage. Taking into account the opposing needs of limiting parasite multiplication and minimizing tissue destruction we review the pathogenesis of OT in the murine model. [source] Regulation of innate and acquired immunity in African trypanosomiasisPARASITE IMMUNOLOGY, Issue 10-11 2005J. M. MANSFIELD SUMMARY African trypanosomes are well known for their ability to avoid immune elimination by switching the immunodominant variant surface glycoprotein (VSG) coat during infection. However, antigenic variation is only one of several means by which trypanosomes manipulate the immune system of their hosts. In this article, the role of parasite factors such as GPI anchor residues of the shed VSG molecule and the release of CpG DNA, in addition to host factors such as IFN-,, in regulating key aspects of innate and acquired immunity during infection is examined. The biological relevance of these immunoregulatory events is discussed in the context of host and parasite survival. [source] Isolates of Trichuris muris elicit different adaptive immune responses in their murine hostPARASITE IMMUNOLOGY, Issue 3 2005C. E. Johnston SUMMARY The J and S isolates of Trichuris muris have different infection profiles in C57BL/6 mice; J worms are expelled, S worms survive to chronicity. Building on this, the ability of the J and S isolates to survive, and the quality of the immune response induced was explored in three different strains of mouse. The resistant BALB/c mouse mounted a strong Th2 response against both isolates, which were quickly expelled. The susceptible AKR host mounted a Th1 response and retained both isolates. Despite equivalent worm exposure, mesenteric lymph node cells from AKR mice infected with the S isolate produced significantly higher levels of IL-12 and the intestinal mastocytosis was reduced. IgG1 and IgG2a from S-infected AKR mice recognized low molecular weight antigens not recognized by J-infected mice. Differential expulsion kinetics was observed in the slower-responding C57BL/6 strain; J worms were expelled but S isolate worms were retained. Survival of the S isolate was again associated with elevated IL-12 and decreased Th2 responses. In resistant mouse strains, the outcome of infection is thus dominantly influenced by host genetics. However, in the slower-responding host, isolate-derived factors may play a role in shaping the quality of the adaptive immune response, thus influencing parasite survival. [source] Effect of oxygen radicals and differential expression of catalase and superoxide dismutase in adult Heligmosomoides polygyrus during primary infections in mice with differing response phenotypesPARASITE IMMUNOLOGY, Issue 3 2002A. Ben-Smith Summary The ability of oxygen radicals to kill Heligmosomoides polygyrus adult worms was examined by assessing parasite survival following incubation with hydrogen peroxide and acetaldehyde/xanthine oxidase, generators ofH2O2and H2O2/O2,, respectively. H. polygyrus worms could tolerate levels of < 0·25 mMhydrogen peroxide and < 0·5 mM/20 mU acetaldehyde/xanthine oxidase for 20 h, but, at higher concentrations, marked sex-dependent susceptibility was observed, with males being more sensitive toH2O2and O2,than female worms. The ability to evade free radical-mediated damage was also evaluated by measuring superoxide dismutase (SOD) and catalase levels in worms isolated at different time points from four strains of mice with differing resistance phenotypes. Levels of both catalase and SOD in female worms isolated from ,rapid'[(SWRxSJL)F1], ,fast' (SWR) or ,intermediate' (BALB/c), but not ,slow' (C57BL/10), responder mice showed a strain-dependent increase with time. Moreover, male worms were rejected faster than female worms in the ,rapid', ,fast' and ,intermediate' responder strains of mice. The results suggest that host-derived free radicals can damage adult worms and that female worms can increase production of their scavenging enzymes in response to the immune onslaught that eventually leads to worm expulsion in mice with ,fast', ,rapid' or ,intermediate' response phenotypes. [source] Hypoxia modulates phenotype, inflammatory response, and leishmanial infection of human dendritic cellsAPMIS, Issue 2 2010MAIRA CEGATTI BOSSETO Bosseto MC, Palma PVB, Covas DT, Giorgio S. Hypoxia modulates phenotype, inflammatory response, and leishmanial infection of human dendritic cells. APMIS 2010; 118: 108,14. Development of hypoxic areas occurs during infectious and inflammatory processes and dendritic cells (DCs) are involved in both innate and adaptive immunity in diseased tissues. Our group previously reported that macrophages exposed to hypoxia were infected with the intracellular parasite Leishmania amazonensis, but showed reduced susceptibility to the parasite. This study shows that although hypoxia did not alter human DC viability, it significantly altered phenotypic and functional characteristics. The expression of CD1a, CD80, and CD86 was significantly reduced in DCs exposed to hypoxia, whereas CD11c, CD14, CD123, CD49 and HLA-DR expression remained unaltered in DCs cultured in hypoxia or normoxia. DC secretion of IL-12p70, the bioactive interleukin-12 (IL-12), a cytokine produced in response to inflammatory mediators, was enhanced under hypoxia. In addition, phagocytic activity (Leishmania uptake) was not impaired under hypoxia, although this microenviroment induced infected DCs to reduce parasite survival, consequently controlling the infection rate. All these data support the notion that a hypoxic microenvironment promotes selective pressure on DCs to assume a phenotype characterized by pro-inflammatory and microbial activities in injured or inflamed tissues and contribute to the innate immune response. [source] Host cell lipids control cholesteryl ester synthesis and storage in intracellular ToxoplasmaCELLULAR MICROBIOLOGY, Issue 6 2005Yoshifumi Nishikawa Summary The intracellular protozoan Toxoplasma gondii lacks a de novo mechanism for cholesterol synthesis and therefore must scavenge this essential lipid from the host environment. In this study, we demonstrated that T. gondii diverts cholesterol from low-density lipoproteins for cholesteryl ester synthesis and storage in lipid bodies. We identified and characterized two isoforms of acyl-CoA:cholesterol acyltransferase (ACAT)-related enzymes, designated TgACAT1, and TgACAT1, in T. gondii. Both proteins are coexpressed in the parasite, localized to the endoplasmic reticulum and participate in cholesteryl ester synthesis. In contrast to mammalian ACAT, TgACAT1, and TgACAT1, preferentially incorporate palmitate into cholesteryl esters and present a broad sterol substrate affinity. Mammalian ACAT-deficient cells transfected with either TgACAT1, or TgACAT1, are restored in their capability of cholesterol esterification. TgACAT1, produces steryl esters and forms lipid bodies after transformation in a Saccharomyces cerevisiae mutant strain lacking neutral lipids. In addition to their role as ACAT substrates, host fatty acids and low-density lipoproteins directly serve as Toxoplasma ACAT activators by stimulating cholesteryl ester synthesis and lipid droplet biogenesis. Free fatty acids significantly increase TgACAT1, mRNA levels. Selected cholesterol esterification inhibitors impair parasite growth by rapid disruption of plasma membrane. Altogether, these studies indicate that host lipids govern neutral lipid synthesis in Toxoplasma and that interference with mechanisms of host lipid storage is detrimental to parasite survival in mammalian cells. [source] Motility and infectivity of Plasmodium berghei sporozoites expressing avian Plasmodium gallinaceum circumsporozoite proteinCELLULAR MICROBIOLOGY, Issue 5 2005Rita Tewari Summary Avian and rodent malaria sporozoites selectively invade different vertebrate cell types, namely macrophages and hepatocytes, and develop in distantly related vector species. To investigate the role of the circumsporozoite (CS) protein in determining parasite survival in different vector species and vertebrate host cell types, we replaced the endogenous CS protein gene of the rodent malaria parasite Plasmodium berghei with that of the avian parasite P. gallinaceum and control rodent parasite P. yoelii. In anopheline mosquitoes, P. berghei parasites carrying P. gallinaceum and rodent parasite P. yoelii CS protein gene developed into oocysts and sporozoites. Plasmodium gallinaceum CS expressing transgenic sporozoites, although motile, failed to invade mosquito salivary glands and to infect mice, which suggests that motility alone is not sufficient for invasion. Notably, a percentage of infected Anopheles stephensi mosquitoes showed melanotic encapsulation of late stage oocysts. This was not observed in control infections or in A. gambiae infections. These findings shed new light on the role of the CS protein in the interaction of the parasite with both the mosquito vector and the rodent host. [source] | |||||||||||||