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Vertebrate Hosts (vertebrate + hosts)
Selected AbstractsTesting the energetic equivalence rule with helminth endoparasites of vertebratesECOLOGY LETTERS, Issue 7 2004Mario George-Nascimento Abstract As a general test of the energetic equivalence rule, we examined macroecological relationships among abundance, density and host body mass in a comparative analysis of the assemblages of trophically transmitted endoparasitic helminths of 131 species of vertebrate hosts. Both the numbers and total volume of parasites per gram of host decreased allometrically with host body mass, with slopes roughly consistent with those expected from the allometric relationship between host basal metabolic rate and body mass. From an evolutionary perspective, large body size may therefore allow hosts to escape from the deleterious effects of parasitism. [source] Synthesis of "Trioxaquantel"® Derivatives as Potential New Antischistosomal DrugsEUROPEAN JOURNAL OF ORGANIC CHEMISTRY, Issue 5 2008Sophie A.-L. Abstract Over the past 20 years, praziquantel, a pyrazinoisoquinoline derivative, has become the mainstay for morbidity control of human and animal schistosomiasis. From early in their lives in vertebrate hosts, schistosomes ingest hemoglobin and aggregate the released heme as a dark pigment very similar to the hemozoin produced by Plasmodium in malaria infection. The antimalarial artemisinin derivatives have real, though low, schistosomicide activity. Because of the complementarity of the two drug classes , praziquantel and artemisinin derivatives , we designed new molecules, named trioxaquantels®, that combine the 1,2,4-trioxane unit responsible for the activity of artemisinin, and the pyrazinoisoquinoline moiety of praziquantel within a single drug. The synthesis of these new drugs and their preliminary evaluation in mice infected with Schistosoma mansoni is reported here.(© Wiley-VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2008) [source] UNCOORDINATED PHYLOGEOGRAPHY OF BORRELIA BURGDORFERI AND ITS TICK VECTOR, IXODES SCAPULARISEVOLUTION, Issue 9 2010Parris T. Humphrey Vector-borne microbes necessarily co-occur with their hosts and vectors, but the degree to which they share common evolutionary or biogeographic histories remains unexplored. We examine the congruity of the evolutionary and biogeographic histories of the bacterium and vector of the Lyme disease system, the most prevalent vector-borne disease in North America. In the eastern and midwestern US, Ixodes scapularis ticks are the primary vectors of Borrelia burgdorferi, the bacterium that causes Lyme disease. Our phylogeographic and demographic analyses of the 16S mitochondrial rDNA suggest that northern I. scapularis populations originated from very few migrants from the southeastern US that expanded rapidly in the Northeast and subsequently in the Midwest after the recession of the Pleistocene ice sheets. Despite this historical gene flow, current tick migration is restricted even between proximal sites within regions. In contrast, B. burgdorferi suffers no barriers to gene flow within the northeastern and midwestern regions but shows clear interregional migration barriers. Despite the intimate association of B. burgdorferi and I. scapularis, the population structure, evolutionary history, and historical biogeography of the pathogen are all contrary to its arthropod vector. In the case of Lyme disease, movements of infected vertebrate hosts may play a larger role in the contemporary expansion and homogenization of the pathogen than the movement of tick vectors whose populations continue to bear the historical signature of climate-induced range shifts. [source] WITHIN-HOST POPULATION DYNAMICS AND THE EVOLUTION OF MICROPARASITES IN A HETEROGENEOUS HOST POPULATIONEVOLUTION, Issue 2 2002Vitaly V. Ganusov Abstract Why do parasites harm their hosts? The general understanding is that if the transmission rate and virulence of a parasite are linked, then the parasite must harm its host to maximize its transmission. The exact nature of such trade-offs remains largely unclear, but for vertebrate hosts it probably involves interactions between a microparasite and the host immune system. Previous results have suggested that in a homogeneous host population in the absence of super- or coinfection, within-host dynamics lead to selection of the parasite with an intermediate growth rate that is just being controlled by the immune system before it kills the host (Antia et al. 1994). In this paper, we examine how this result changes when heterogeneity is introduced to the host population. We incorporate the simplest form of heterogeneity,random heterogeneity in the parameters describing the size of the initial parasite inoculum, the immune response of the host, and the lethal density at which the parasite kills the host. We find that the general conclusion of the previous model holds: parasites evolve some intermediate growth rate. However, in contrast with the generally accepted view, we find that virulence (measured by the case mortality or the rate of parasite-induced host mortality) increases with heterogeneity. Finally, we link the within-host and between-host dynamics of parasites. We show how the parameters for epidemiological spread of the disease can be estimated from the within-host dynamics, and in doing so examine the way in which trade-offs between these epidemiological parameters arise as a consequence of the interaction of the parasite and the immune response of the host. [source] Climate change and vector-borne viral diseases potentially transmitted by transfusionISBT SCIENCE SERIES: THE INTERNATIONAL JOURNAL OF INTRACELLULAR TRANSPORT, Issue 1 2009M. Rios Vector-borne diseases occur when infectious agents (virus, protozoa, bacteria, or helminthes) are transmitted to their hosts by a carrier organism. Climate conditions and their changes play a role in the inter-relationship between these agents, the vectors and the host (or hosts). This review is focused on arthropod-borne viruses (Arboviruses). These viruses are transmitted between susceptible vertebrate hosts by blood-feeding arthropods, and may be transmitted by blood transfusion, tissue and organ transplantation and breast feeding. The lifecycle of arboviruses is influenced by changes in temperature, rainfall, humidity, length of day, average daily solar radiation and/or storm patterns, as well as changes in the frequency of rare events such as floods or droughts. A plethora of studies have suggested that climate changes, particularly temperature changes, are likely to be induced by increase in the amount of greenhouse gases, such as methane, carbon dioxide (CO2) and chlorofluorocarbons, which deplete ozone in the atmosphere leading to an increase in ultraviolet radiation. Current models predict that ambient temperature will increase by 3,5°C on average with a doubling in CO2 concentration in the atmosphere. Vectors, pathogens and hosts each survive and reproduce within a range of optimal climatic conditions: temperature and precipitation being most important, while sea level elevation, wind and daylight duration are also important. Climate changes may affect important determinants of vector-borne disease transmission including (i) vector survival and reproduction, (ii) the vector's biting rate, and (iii) the pathogen's incubation rate within the vector organism. Droughts can increase the dissemination of arboviral diseases in urban areas by allowing a boost in the population of mosquitoes in foul water concentrated in catch basins where they breed. Furthermore, eggs can be vertically infected with arboviruses and heat waves speed up the maturation of the mosquitoes and of the viruses within mosquitoes. Droughts also cause a decline in mosquito predators like frogs, darning needles and dragonflies. In addition, birds congregate around shrinking water sites, enhancing circulation of viruses among birds and mosquitoes. In conclusion, the seriousness of some of the recent epidemics like West Nile virus and Dengue appear to has been influenced by climate change. As most of the arboviral infections are asymptomatic in humans, there is an increased opportunity for blood, organ and tissue donations by infected individuals during the viraemic period, resulting in an increased risk of transmission of arboviruses. [source] The inadvertent introduction into Australia of Trypanosoma nabiasi, the trypanosome of the European rabbit (Oryctolagus cuniculus), and its potential for biocontrolMOLECULAR ECOLOGY, Issue 10 2005P. B. HAMILTON Abstract Wild rabbits (Oryctolagus cuniculus) in Australia are the descendents of 24 animals from England released in 1859. We surveyed rabbits and rabbit fleas (Spilopsyllus cuniculi) in Australia for the presence of trypanosomes using parasitological and PCR-based methods. Trypanosomes were detected in blood from the European rabbits by microscopy, and PCR using trypanosome-specific small subunit ribosomal RNA (SSU rRNA) gene primers and those in rabbit fleas by PCR. This is the first record of trypanosomes from rabbits in Australia. We identified these Australian rabbit trypanosomes as Trypanosoma nabiasi, the trypanosome of the European rabbit, by comparison of morphology and SSU rRNA gene sequences of Australian and European rabbit trypanosomes. Phylogenetic analysis places T. nabiasi in a clade with rodent trypanosomes in the subgenus Herpetosoma and their common link appears to be transmission by fleas. Despite the strict host specificity of trypanosomes in this clade, phylogenies presented here suggest that they have not strictly cospeciated with their vertebrate hosts. We suggest that T. nabiasi was inadvertently introduced into Australia in the 1960s in its flea vector Spilopsyllus cuniculi, which was deliberately introduced as a potential vector of the myxoma virus. In view of the environmental and economic damage caused by rabbits in Australia and other islands, the development of a virulent or genetically modified T. nabiasi should be considered to control rabbits. [source] Molluscan and vertebrate immune responses to bird schistosomesPARASITE IMMUNOLOGY, Issue 7-8 2005P. HORÁK SUMMARY There is a growing understanding of risks posed by human contact with the cercariae of bird schistosomes. In general, there are no fundamental biological differences between human and bird schistosomes in terms of their interactions with snail and vertebrate hosts. The penetration of host surfaces is accompanied by the release of penetration gland products and the shedding of highly antigenic surface components (miracidial ciliated plates and cercarial glycocalyx) which trigger host immune reactions. New surface structures are formed during transformation: the tegument of mother sporocysts and the tegumental double membrane of schistosomula. These surfaces apparently serve as protection against the host immune response. Certain parasite excretory,secretory products may contribute to immunosuppression or, on the other hand, stimulation of host immune reactions. Discovery of new species and their life cycles, the characterization of host,parasite interactions (including at the molecular level), the determination of parasite pathogenicity towards the host, the development of tools for differential diagnosis and the application of protective measures are all topical research streams of the future. Regularly updated information on bird schistosomes and cercarial dermatitis can be found at http://www.schistosomes.cz (web pages of Schistosome Group Prague). [source] Host cell-mediated responses to infection with CryptosporidiumPARASITE IMMUNOLOGY, Issue 12 2000V. McDonald The coccidian Cryptosporidium infects epithelial cells of a variety of vertebrate hosts and is the causative agent of cryptosporidiosis. In mammals, including humans and domestic animals, C. parvum infects the gastrointestinal tract producing an acute watery diarrhoea and weight loss. CD4+ T-cell-deficient hosts have increased susceptibility to infection with the parasite and may develop severe life-threatening complications. The host responses which induce protective immunity and contribute to pathogenesis are poorly understood. In the immunological control of infection, recent studies with murine infection models suggest that IFN-, plays a key role in a partially protective innate immunity against infection identified in immunocompromised mice and also in the elimination of infection mediated by CD4+ T-cells. At the mucosal level, CD4+ intraepithelial lymphocytes are involved in the control of cryptosporidial infection, acting at least in part through production of IFN-, which has a direct inhibitory effect on parasite development in enterocytes. Primary infection of ruminants induces an intestinal inflammatory response in which increased numbers of various T-cell subpopulations appear in the villi. In addition, infection results in increased intestinal expression of pro-inflammatory cytokines such as IL-12, IFN-, and TNF-,. Because these cytokines appear to be important in the aetiology of inflammatory bowel disease, it is possible that they are involved in the mucosal pathogenesis of cryptosporidiosis. [source] NMR solution structure and backbone dynamics of domain III of the E protein of tick-borne Langat flavivirus suggests a potential site for molecular recognitionPROTEIN SCIENCE, Issue 6 2006Munia Mukherjee Abstract Flaviviruses cause many human diseases, including dengue fever, yellow fever, West Nile viral encephalitis, and hemorrhagic fevers, and are transmitted to their vertebrate hosts by infected mosquitoes and ticks. Domain III of the envelope protein (E-D3) is considered to be the primary viral determinant involved in the virus,host-cell receptor interaction, and thus represents an excellent target for antiviral drug development. Langat (LGT) virus is a naturally attenuated BSL-2 TBE virus and is a model for the pathogenic BSL-3 and BSL-4 viruses in the serogroup. We have determined the solution structure of LGT-E-D3 using heteronuclear NMR spectroscopy. The backbone dynamics of LGT-E-D3 have been investigated using 15N relaxation measurements. A detailed analysis of the solution structure and dynamics of LGT-E-D3 suggests potential residues that could form a surface for molecular recognition, and thereby represent a target site for antiviral therapeutics design. [source] |