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Susceptible Hosts (susceptible + hosts)
Selected AbstractsEvidence for the importance of odour-perception in the parasitoid Rhopalicus tutela (Walker) (Hym., Pteromalidae)JOURNAL OF APPLIED ENTOMOLOGY, Issue 6 2001E. M. Pettersson Possible host location mechanisms in the chalcid wasp Rhopalicus tutela (Walker) (Hym., Pteromalidae), a parasitoid of the eight-spined spruce bark beetle, Ips typographus (L.) (Col., Scolytidae), were examined. This was carried out in order to repeat and complement former studies on parallel parasitoid,scolytid systems that had contradictory results. Morphological examinations of the parasitoid antennae were made using both scanning and transmission electron microscopy. Possible functions of the sensilla placodea (multiporous plate sensillum), and other sensilla present on the antennae, have been indicated. For the first time, the placoid sensilla in a pteromalid parasitoid have shown porous walls and numerous innervations, which are typical characteristics for chemoreceptors. Previously the placoid sensilla have been suggested to be an infrared receptor. In order to test the chemoreceptive ability of R. tutela females and males, a synthetic reference blend was analysed by combined gas chromatography and electroantennographic detector (GC-EAD). Their sensitivity to host-related volatiles (such as certain pheromone components and oxygenated monoterpenes) was significantly greater than that for host-tree-related compounds (monoterpene hydrocarbons). Employing an infrared thermo-scanner, the current study failed to detect ,hot spots' associated with susceptible hosts beneath the bark. Results from electrophysiology and electron microscopy revealed clear odour-perceptive functions of the parasitoid antennae. These results strongly support the major importance of volatiles in host location by the bark beetle parasitoid R. tutela. [source] Two species of feminizing microsporidian parasite coexist in populations of Gammarus duebeniJOURNAL OF EVOLUTIONARY BIOLOGY, Issue 3 2003J. E. Ironside Abstract The amphipod crustacean Gammarus duebeni hosts two species of vertically transmitted microsporidian parasites, Nosema granulosis and Microsporidium sp. A. Here it is demonstrated that these co-occurring parasite species both cause infected females to produce female-biased broods. A survey of European G. duebeni populations demonstrates that these two parasites co-occur in six of 10 populations. These findings contrast with the theoretical prediction that two vertically transmitted feminizing parasites should not coexist in a panmictic population of susceptible hosts at equilibrium. Possible explanations for the co-occurrence of the two feminizing microsporidia in G. duebeni include the recent invasion of a new parasite, horizontal transmission of one or both parasites and the spread of alleles for resistance to the dominant parasite in host populations. [source] The inflammatory cytokine, interleukin-1 beta, mediates loss of astroglial glutamate transport and drives excitotoxic motor neuron injury in the spinal cord during acute viral encephalomyelitisJOURNAL OF NEUROCHEMISTRY, Issue 4 2008Natalie A. Prow Abstract Astrocytes remove glutamate from the synaptic cleft via specific transporters, and impaired glutamate reuptake may promote excitotoxic neuronal injury. In a model of viral encephalomyelitis caused by neuroadapted Sindbis virus (NSV), mice develop acute paralysis and spinal motor neuron degeneration inhibited by the AMPA receptor antagonist, NBQX. To investigate disrupted glutamate homeostasis in the spinal cord, expression of the main astroglial glutamate transporter, GLT-1, was examined. GLT-1 levels declined in the spinal cord during acute infection while GFAP expression was preserved. There was simultaneous production of inflammatory cytokines at this site, and susceptible animals treated with drugs that blocked IL-1, release also limited paralysis and prevented the loss of GLT-1 expression. Conversely, infection of resistant mice that develop mild paralysis following NSV challenge showed higher baseline GLT-1 levels as well as lower production of IL-1, and relatively preserved GLT-1 expression in the spinal cord compared to susceptible hosts. Finally, spinal cord GLT-1 expression was largely maintained following infection of IL-1,-deficient animals. Together, these data show that IL-1, inhibits astrocyte glutamate transport in the spinal cord during viral encephalomyelitis. They provide one of the strongest in vivo links between innate immune responses and the development of excitotoxicity demonstrated to date. [source] Anti-adhesive activity of sulphated exopolysaccharides of microalgae on attachment of red sore disease-associated bacteria and Helicobacter pylori to tissue culture cellsLETTERS IN APPLIED MICROBIOLOGY, Issue 6 2000M.A. Guzman-Murillo Because of the affinity of certain bacterial species for sulphated glycoconjugates exposed on the epithelial cells of susceptible hosts, we hypothesized that sulphated exopolysaccharides of microalgae can be used in anti-adhesive therapies against bacterial infections, both in cold- and warm-blooded animals. In this study we found that adhesion of the human pathogen Helicobacter pylori to the HeLa S3 cell line, and adhesion of the fish pathogens Vibrio campbellii, V. ordalii, Streptococcus saprophyticus, and Aeromonas veronii to spotted sand bass primary tissue culture cells, can be effectively blocked with the various sulphated exopolysaccharides used. [source] A mycobacterial virulence gene cluster extending RD1 is required for cytolysis, bacterial spreading and ESAT-6 secretionMOLECULAR MICROBIOLOGY, Issue 6 2004Lian-Yong Gao Summary Initiation and maintenance of infection by mycobacteria in susceptible hosts are not well understood. A screen of Mycobacterium marinum transposon mutant library led to isolation of eight mutants that failed to cause haemolysis, all of which had transposon insertions in genes homologous to a region between Rv3866 and Rv3881c in Mycobacterium tuberculosis, which encompasses RD1 (Rv3871,Rv3879c), a known virulence gene cluster. The M. marinum mutants showed decreased virulence in vivo and failed to secrete ESAT-6, like M. tuberculosis RD1 mutants. M. marinum mutants in genes homologous to Rv3866-Rv3868 also failed to accumulate intracellular ESAT-6, suggesting a possible role for those genes in synthesis or stability of the protein. These transposon mutants and an ESAT-6/CFP-10 deletion mutant all showed reduced cytolysis and cytotoxicity to macrophages and significantly decreased intracellular growth at late stages of the infection only when the cells were infected at low multiplicity of infection, suggesting a defect in spreading. Direct evidence for cell-to-cell spread by wild-type M. marinum was obtained by microscopic detection in macrophage and epithelial monolayers, but the mutants all were defective in this assay. Expression of M. tuberculosis homologues complemented the corresponding M. marinum mutants, emphasizing the functional similarities between M. tuberculosis and M. marinum genes in this region that we designate extRD1 (extended RD1). We suggest that diminished membranolytic activity and defective spreading is a mechanism for the attenuation of the extRD1 mutants. These results extend recent findings on the genomic boundaries and functions of M. tuberculosis RD1 and establish a molecular cellular basis for the role that extRD1 plays in mycobacterial virulence. Disruption of the M. marinum homologue of Rv3881c, not previously implicated in virulence, led to a much more attenuated phenotype in macrophages and in vivo, suggesting that this gene plays additional roles in M. marinum survival in the host. [source] Distribution of the anther-smut pathogen Microbotryum on species of the CaryophyllaceaeNEW PHYTOLOGIST, Issue 1 2010Michael E. Hood Summary ,Understanding disease distributions is of fundamental and applied importance, yet few studies benefit from integrating broad sampling with ecological and phylogenetic data. Here, anther-smut disease, caused by the fungus Microbotryum, was assessed using herbarium specimens of Silene and allied genera of the Caryophyllaceae. ,A total of 42 000 herbarium specimens were examined, and plant geographical distributions and morphological and life history characteristics were tested as correlates of disease occurrence. Phylogenetic comparative methods were used to determine the association between disease and plant life-span. ,Disease was found on 391 herbarium specimens from 114 species and all continents with native Silene. Anther smut occurred exclusively on perennial plants, consistent with the pathogen requiring living hosts to overwinter. The disease was estimated to occur in 80% of perennial species of Silene and allied genera. The correlation between plant life-span and disease was highly significant while controlling for the plant phylogeny, but the disease was not correlated with differences in floral morphology. ,Using resources available in natural history collections, this study illustrates how disease distribution can be determined, not by restriction to a clade of susceptible hosts or to a limited geographical region, but by association with host life-span, a trait that has undergone frequent evolutionary transitions. [source] Inheritance of insensitivity to culture filtrate of Pyrenophora tritici-repentis, race 2, in wheat (Triticum aestivum L.)PLANT BREEDING, Issue 3 2006P.K. Singh Abstract Tan spot of wheat is caused by the fungus Pyrenophora tritici-repentis. On susceptible hosts, P. tritici-repentis induces two phenotypically distinct symptoms, tan necrosis and chlorosis. This fungus produces several toxins that induce tan necrosis and chlorosis symptoms in susceptible cultivars. The objectives of this study were to determine the inheritance of insensitivity to necrosis-inducing culture filtrate of P. tritici-repentis, race 2, and to establish the relationship between the host reaction to culture filtrate and spore inoculation with respect to the necrosis component. The F1, F2, and BC1F1 plants and F2:8 lines of five crosses involving resistant wheat genotypes ,Erik', ,Red Chief', and line 86ISMN 2137 with susceptible cultivars ,Glenlea' and ,Kenyon' were studied. Plants were spore-inoculated at the two-leaf stage. Four days later, the newly emerged uninoculated third leaf was infiltrated with a culture filtrate of isolate Ptr 92,164 (race 2). Reactions to the spore inoculation and the culture filtrate were recorded 8 days after spore inoculation. The segregation observed in the F2 and BC1F1 generations and the F2:8 lines of all crosses indicated that a single recessive gene controlled insensitivity to necrosis caused by culture filtrate. This gene also controlled resistance to necrosis induced by spore inoculation. [source] Differential modulation of innate immune cell functions by the Burkholderia cepacia complex: Burkholderia cenocepacia but not Burkholderia multivorans disrupts maturation and induces necrosis in human dendritic cellsCELLULAR MICROBIOLOGY, Issue 10 2008Kelly L. MacDonald Summary Burkholderia cepacia complex (BCC) bacteria cause pulmonary infections that can evolve into fatal overwhelming septicemia in chronic granulomatous disease or cystic fibrosis patients. Burkholderia cenocepacia and Burkholderia multivorans are responsible for the majority of BCC infections in cystic fibrosis patients, but B. cenocepacia is generally associated with a poorer prognosis than B. multivorans. The present study investigated whether these pathogens could modulate the normal functions of primary human monocyte-derived dendritic cells (DCs), important phagocytic cells that act as critical orchestrators of the immune response. Effects of the bacteria on maturation of DCs were determined using flow cytometry. DCs co-incubated for 24 h with B. cenocepacia, but not B. multivorans, had reduced expression of costimulatory molecules when compared with standard BCC lipopolysaccharide-matured DCs. B. cenocepacia, but not B. multivorans, also induced necrosis in DCs after 24 h, as determined by annexin V and propidium iodide staining. DC necrosis only occurred after phagocytosis of live B. cenocepacia; DCs exposed to heat-killed bacteria, bacterial supernatant or those pre-treated with cytochalasin D then exposed to live bacteria remained viable. The ability of B. cenocepacia to interfere with normal DC maturation and induce necrosis may contribute to its pathogenicity in susceptible hosts. [source] Proteases in pathogenesis and plant defenceCELLULAR MICROBIOLOGY, Issue 10 2004Yiji Xia Summary Plant pathogens deliver a variety of virulence factors to host cells to suppress basal defence responses and create suitable environments for their propagation. Plants have in turn evolved disease resistance genes whose products detect the virulence factors as a signal of invasion and activate effective defence responses. Understanding how a virulence effector contributes to virulence on susceptible hosts but becomes an avirulence factor that triggers defence responses on resistance hosts has been a major focus in plant research. Recent studies have shown that a growing list of pathogen-encoded effectors functions as proteases that are secreted into plant cells to modify host proteins. In addition, several plant proteases have been found to function in activation of the defence mechanism. These findings reveal that post-translational modification of host proteins through proteolytic processing is a widely used mechanism in regulating the plant defence response. [source] | ||||||||||