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Host Susceptibility (host + susceptibility)
Selected AbstractsCrowding and disease: effects of host density on response to infection in a butterfly,parasite interactionECOLOGICAL ENTOMOLOGY, Issue 5 2009ELIZABETH LINDSEY Abstract. 1. Hosts experiencing frequent variation in density are thought to benefit from allocating more resources to parasite defence when density is high (,density-dependent prophylaxis'). However, high density conditions can increase intra-specific competition and induce physiological stress, hence increasing host susceptibility to infection (,crowding-stress hypothesis'). 2. We studied monarch butterflies (Danaus plexippus) and quantified the effects of larval rearing density on susceptibility to the protozoan parasite Ophryocystis elektroscirrha. Larvae were inoculated with parasite spores and reared at three density treatments: low, moderate, and high. We examined the effects of larval density on parasite loads, host survival, development rates, body size, and wing melanism. 3. Results showed an increase in infection probability with greater larval density. Monarchs in the moderate and high density treatments also suffered the greatest negative effects of parasite infection on body size, development rate, and adult longevity. 4. We observed greater body sizes and shorter development times for monarchs reared at moderate densities, and this was true for both unparasitised and parasite-treated monarchs. We hypothesise that this effect could result from greater larval feeding rates at moderate densities, combined with greater physiological stress at the highest densities. 5. Although monarch larvae are assumed to occur at very low densities in the wild, an analysis of continent-wide monarch larval abundance data showed that larval densities can reach high levels in year-round resident populations and during the late phase of the breeding season. Treatment levels used in our experiment captured ecologically-relevant variation in larval density observed in the wild. [source] Transmission dynamics of an iridescent virus in an experimental mosquito population: the role of host densityECOLOGICAL ENTOMOLOGY, Issue 4 2005Carlos F. Marina Abstract., 1.,The transmission of insect pathogens cannot be adequately described by direct linear functions of host and pathogen density due to heterogeneity generated from behavioural or physiological traits, or from the spatial distribution of pathogen particles. Invertebrate iridescent viruses (IIVs) can cause patent and lethal infection or a covert sub-lethal infection in insects. Aedes aegypti larvae were exposed to suspensions of IIV type 6 at two densities. High larval density increased the prevalence of aggression resulting in potentially fatal wounding. 2.,The overall prevalence of infection (patent + covert) was positively influenced by host density and increased with exposure time in both densities. The survival time of patently infected insects was extended by , 5 days compared with non-infected insects. 3.,Maximum likelihood models based on the binomial distribution were fitted to empirical results. A model incorporating heterogeneity in host susceptibility by inclusion of a pathogen-free refuge was a significantly better fit to data than an all-susceptible model, indicating that transmission is non-linear. The transmission coefficient (,) did not differ with host density whereas the faction of the population that occupied the pathogen-free refuge (,R) was significantly reduced at high host density compared with the low density treatment. 4.,The transmission of free-living infective stages of an IIV in Ae. aegypti larvae is non-linear, probably because of density-related changes in the frequency of aggressive encounters between hosts. This alters host susceptibility to infection and effectively reduces the proportion of hosts that occupy the pathogen-free refuge. [source] Key role of selective viral-induced mortality in determining marine bacterial community compositionENVIRONMENTAL MICROBIOLOGY, Issue 2 2007T. Bouvier Summary Viral infection is thought to play an important role in shaping bacterial community composition and diversity in aquatic ecosystems, but the strength of this interaction and the mechanisms underlying this regulation are still not well understood. The consensus is that viruses may impact the dominant bacterial strains, but there is little information as to how viruses may affect the less abundant taxa, which often comprise the bulk of the total bacterial diversity. The potential effect of viruses on the phylogenetic composition of marine bacterioplankton was assessed by incubating marine bacteria collected along a North Pacific coastal-open ocean transect in seawater that was greatly depleted of ambient viruses. The ambient communities were dominated by typical marine groups, including alphaproteobacteria and the Bacteroidetes. Incubation of these communities in virus-depleted ambient water yielded an unexpected and dramatic increase in the relative abundance of bacterial groups that are generally undetectable in the in situ assemblages, such as betaproteobacteria and Actinobacteria. Our results suggest that host susceptibility is not necessarily only proportional to its density but to other characteristics of the host, that rare marine bacterial groups may be more susceptible to viral-induced mortality, and that these rare groups may actually be the winners of competition for resources. These observations are not inconsistent with the ,phage kills the winner' hypothesis but represent an extreme and yet undocumented case of this paradigm, where the potential winners apparently never actually develop beyond a very low abundance threshold in situ. We further suggest that this mode of regulation may influence not just the distribution of single strains but of entire phylogenetic groups. [source] A dynamic simulation model for powdery mildew epidemics on winter wheat,EPPO BULLETIN, Issue 3 2003V. Rossi A system dynamic model for epidemics of Blumeria graminis (powdery mildew) on wheat was elaborated, based on the interaction between stages of the disease cycle, weather conditions and host characteristics. The model simulates the progress of disease severity, expressed as a percentage of powdered leaf area, on individual leaves, with a time step of one day, as a result of two processes: the growth of fungal colonies already present on the leaves and the appearance of new colonies. By means of mathematical equations, air temperature, vapour pressure deficit, rainfall and wind are used to calculate incubation, latency and sporulation periods, the growth of pathogen colonies, infection and spore survival. Effects of host susceptibility to infection, and of leaf position within the plant canopy, are also included. Model validation was carried out by comparing model outputs with the dynamics of epidemics observed on winter wheat grown at several locations in northern Italy (1991,98). Simulations were performed using meteorological data measured in standard meteorological stations. As there was good agreement between model outputs and actual disease severity, the model can be considered a satisfactory simulator of the effect of environmental conditions on the progress of powdery mildew epidemics. [source] ADVICE OF THE ROSE: EXPERIMENTAL COEVOLUTION OF A TREMATODE PARASITE AND ITS SNAIL HOSTEVOLUTION, Issue 1 2007Britt Koskella Understanding host-parasite coevolution requires multigenerational studies in which changes in both parasite infectivity and host susceptibility are monitored. We conducted a coevolution experiment that examined six generations of interaction between a freshwater snail (Potamopyrgus antipodarum) and one of its common parasites (the sterilizing trematode, Microphallus sp.). In one treatment (recycled), the parasite was reintroduced into the same population of host snails. In the second treatment (lagged), the host snails received parasites from the recycled treatment, but the addition of these parasites did not begin until the second generation. Hence any parasite-mediated genetic changes of the host in the lagged treatment were expected to be one generation behind those in the recycled treatment. The lagged treatment thus allowed us to test for time lags in parasite adaptation, as predicted by the Red Queen model of host,parasite coevolution. Finally, in the third treatment (control), parasites were not added. The results showed that parasites from the recycled treatment were significantly more infective to snails from the lagged treatment than from the recycled treatment. In addition, the hosts from the recycled treatment diverged from the control hosts with regard to their susceptibility to parasites collected from the field. Taken together, the results are consistent with time lagged, frequency-dependent selection and rapid coevolution between hosts and parasites. [source] Evidence for plant viruses in the region of Argentina Islands, AntarcticaFEMS MICROBIOLOGY ECOLOGY, Issue 2 2007Valery Polischuk Abstract This work focused on the assessment of plant virus occurrence among primitive and higher plants in the Antarctic region. Sampling occurred during two seasons (2004/5 and 2005/6) at the Ukrainian Antarctic Station ,Academician Vernadskiy' positioned on Argentina Islands. Collected plant samples of four moss genera (Polytrichum, Plagiatecium, Sanionia and Barbilophozia) and one higher monocot plant species, Deschampsia antarctica, were further subjected to enzyme-linked immunosorbent assay to test for the presence of common plant viruses. Surprisingly, samples of Barbilophozia and Polytrichum mosses were found to contain antigens of viruses from the genus Tobamovirus, Tobacco mosaic virus and Cucumber green mottle mosaic virus, which normally parasitize angiosperms. By contrast, samples of the monocot Deschampsia antarctica were positive for viruses typically infecting dicots: Cucumber green mottle mosaic virus, Cucumber mosaic virus and Tomato spotted wilt virus. Serological data for Deschampsia antarctica were supported in part by transmission electron microscopy observations and bioassay results. The results demonstrate comparatively high diversity of plant viruses detected in Antarctica; the results also raise questions of virus specificity and host susceptibility, as the detected viruses normally infect dicotyledonous plants. However, the means of plant virus emergence in the region remain elusive and are discussed. [source] Pigmentary characteristics and moles in relation to melanoma riskINTERNATIONAL JOURNAL OF CANCER, Issue 1 2005Linda Titus-Ernstoff Abstract Although benign and atypical moles are considered key melanoma risk factors, previous studies of their influence were small and/or institution-based. We conducted a population-based case-control study in the state of New Hampshire. Individuals of ages 20,69 with an incident diagnosis of first primary cutaneous melanoma were ascertained through the New Hampshire State Cancer Registry. Controls were identified through New Hampshire driver's license lists and frequency-matched by age and gender to cases. We interviewed 423 eligible cases and 678 eligible controls. Host characteristics, including mole counts, were evaluated using logistic regression analyses. Our results showed that pigmentary factors, including eye color (OR = 1.57 for blue eyes compared to brown), hair color (OR = 1.85 for blonde/red hair color compared to brown/black), freckles before age 15 (OR = 2.39 for freckles present compared to absent) and sun sensitivity (OR = 2.25 for peeling sunburn followed by no tan or a light tan and 2.42 for sunburn followed by tan compared to tanning immediately), were related to melanoma risk; these associations held after adjustment for sun-related factors and for moles. In analyses confined to skin examination participants, the covariate-adjusted effects of benign and atypical moles were moderately strong. Compared to 0,4 benign moles, risk increased steadily for 5,14 moles (OR = 1.71), 15,24 moles (OR = 3.55) and , 25 moles (OR = 4.33). Risk also increased with the number of atypical moles; compared to none, the ORs for having 1, 2,3, or , 4 atypical moles were 2.08, 1.84 and 3.80, respectively. Although risk was highest for those with multiple benign and atypical moles, the interaction was not of statistical significance. Our findings, arising from the first population- and incidence-based study to evaluate atypical moles in relation to melanoma risk, confirm the importance of host susceptibility, represented by pigmentary factors and the tendency to develop benign or atypical moles, in the etiology of this disease. © 2005 Wiley-Liss, Inc. [source] Experimental periodontitis in mice selected for maximal or minimal inflammatory reactions: increased inflammatory immune responsiveness drives increased alveolar bone loss without enhancing the control of periodontal infectionJOURNAL OF PERIODONTAL RESEARCH, Issue 4 2009A. P. F. Trombone Background and Objective:, Inflammatory immune reactions that occur in response to periodontopathogens are thought to protect the host against infection, but may trigger periodontal destruction. However, the molecular and genetic mechanisms underlying host susceptibility to periodontal infection and to periodontitis development have still not been established in detail. Material and Methods:, In this study, we examined the mechanisms that modulate the outcome of Aggregatibacter (Actinobacillus) actinomycetemcomitans -induced periodontal disease in mice mouse strains selected for maximal (AIRmax) or minimal (AIRmin) inflammatory reactions. Results:, Our results showed that AIRmax mice developed a more severe periodontitis than AIRmin mice in response to A. actinomycetemcomitans infection, and this periodontitis was characterized by increased alveolar bone loss and inflammatory cell migration to periodontal tissues. In addition, enzyme-linked immunosorbent assays demonstrated that the levels of the cytokines interleukin-1,, tumor necrosis factor-, and interleukin-17 were higher in AIRmax mice, as were the levels of matrix metalloproteinase (MMP)-2, MMP-13 and receptor activator of nuclear factor-,B ligand (RANKL) mRNA levels. However, the more intense inflammatory immune reaction raised by the AIRmax strain, in spite of the higher levels of antimicrobial mediators myeloperoxidase and inducible nitric oxide synthase, did not enhance the protective immunity to A. actinomycetemcomitans infection, because both AIRmax and AIRmin strains presented similar bacterial loads in periodontal tissues. In addition, the AIRmax strain presented a trend towards higher levels of serum C-reactive protein during the course of disease. Conclusion:, Our results demonstrate that the intensity of the inflammatory immune reaction is associated with the severity of experimental periodontitis, but not with the control of A. actinomycetemcomitans periodontal infection, suggesting that the occurrence of hyperinflammatory genotypes may not be an evolutionary advantage in the complex host,pathogen interaction observed in periodontal diseases. [source] HOST PARASITE INTERACTIONS BETWEEN FRESHWATER PHYTOPLANKTON AND CHYTRID FUNGI (CHYTRIDIOMYCOTA),JOURNAL OF PHYCOLOGY, Issue 3 2004Bas W. Ibelings Some chytrids are host-specific parasiticfungithat may have a considerable impact on phytoplankton dynamics. The phylum Chytridiomycota contains one class, the Chytridiomycetes, and is composed of five different orders. Molecular studies now firmly place the Chytridiomycota within the fungal kingdom. Chytrids are characterized by having zoospores, a motile stage in their life cycle. Zoospores are attracted to the host cell by specific signals. No single physical,chemical factor has been found that fully explains the dynamics of chytrid epidemics in the field. Fungal periodicity was primarily related to host cell density. The absence of aggregated distributions of chytrids on their hosts suggested that their hosts did not vary in their susceptibility to infection. A parasite can only become epidemic when it grows faster than the host. Therefore, it has been suggested that epidemics in phytoplankton populations arise when growth conditions for the host are unfavorable. No support for such a generalization was found, however. Growth of the parasitic fungus Rhizophydium planktonicum Canter emend, parasitic on the diatom Asterionella formosa Hassal, was reduced under stringent nutrient limitation,because production and infectivity of zoospores were affected negatively. A moderate phosphorous or light limitation favored epidemic development, however. Chytrid infections have been shown to affect competition between their algal hosts and in this way altered phytoplankton succession. There is potential for coevolution between Asterionella and the chytrid Zygorhizidium planktonicum Canter based on clear reciprocal fitness costs, absence of overall infective parasite strains, and possibly a genetic basis for host susceptibility and parasite infectivity. [source] Molecular, ecological and evolutionary approaches to understanding Alternaria diseases of citrusMOLECULAR PLANT PATHOLOGY, Issue 6 2003Kazuya Akimitsu SUMMARY Alternaria fungi cause four different diseases of citrus: Alternaria brown spot of tangerines, Alternaria leaf spot of rough lemon, Alternaria black rot of several citrus fruits and Mancha foliar of Mexican lime. The first three diseases are caused by the small-spored species, Alternaria alternata and the causal agents can only be differentiated using pathogenicity tests, toxin assays or genetic markers. Mancha foliar is caused by the morphologically distinct, large-spored species A. limicola. Substantial progress has been made in understanding the biology, ecology, population biology, systematics, molecular biology and biochemistry of the interactions between these pathogens and citrus. Epidemiological studies have focused on brown spot of tangerines and their hybrids and have contributed to the development of a model of disease development which has improved control and reduced fungicide use. Studies of the population genetics, host specificity and ecology of A. alternata from different ecological niches on citrus have revealed host specific forms of the pathogen which cause disease on different citrus species, the existence of three phylogenetic lineages of the fungus which cause brown spot world-wide, and closely related non-pathogenic isolates which colonize healthy citrus tissue. The role of host-specific toxins in Alternaria diseases of citrus has been extensively studied for over 20 years, and these pathosystems have become model systems for host-pathogen interactions. Recent molecular research has started to unravel the genetic basis of toxin production and the host susceptibility to toxin, and the role of extracellular, degradative enzymes in disease. [source] Seasonal changes in susceptibility of Quercus suber to Botryosphaeria stevensii and Phytophthora cinnamomiPLANT PATHOLOGY, Issue 3 2002J. Luque Monthly inoculations of both intact plants and excised shoots of Quercus suber with the pathogenic species Botryosphaeria stevensii and Phytophthora cinnamomi were performed to investigate seasonal changes in susceptibility of this forest tree species in relation to environmental parameters and plant water status. Infection symptoms were mainly detected on seedlings inoculated from spring to autumn (April through October) with either pathogen. Mean canker sizes also showed a seasonal pattern, the higher values being recorded in the same period as above. Lesion lengths were significantly (P < 0·001) related to environmental minimum temperature. Mean daily minimum temperatures within the range of 5,12°C clearly inhibited lesion development of P. cinnamomi, whereas B. stevensii showed a less pronounced decrease in canker expansion at the same temperature range. In excised shoots of Q. suber inoculated monthly with B. stevensii, a negative linear relationship was found between the studied range of plant relative water content (81,91%) and canker length. In contrast, the lesions caused by P. cinnamomi were not significantly (P = 0·32) related to any seasonal change in water content. Some control measures for the diseases caused by both pathogens are discussed on the basis of the seasonal changes in host susceptibility observed in this study. [source] The expanding realm of heterologous immunity: friend or foe?CELLULAR MICROBIOLOGY, Issue 2 2006Kathleen R. Page Summary Antecedent or current infections can alter the immunopathologic outcome of a subsequent unrelated infection. Immunomodulation by co-infecting pathogens has been referred to as ,heterologous immunity' and has been postulated to play a role in host susceptibility to disease, tolerance to organ transplant, and autoimmune disease. The effect of various infections on heterologous immune responses has been well studied in the context of shared epitopes and cross-reactive T cells. It has been shown that prior infections can modulate protective immunity and immunopathology by forming a pool of memory T cells that can cross-react with antigens from heterologous organisms or through the generation of a network of regulatory cells and cytokines. While it is not feasible to alter a host's history of prior infection, understanding heterologous immune responses in the context of simultaneous unrelated infections could have important therapeutic implications. Here, we outline key evidence from animal and human studies demonstrating the effect of heterologous immunity on the outcome of disease. We briefly review the role of T cells, but expand our discussion to explore other immune mechanisms that may modulate the response to concurrent active infections. In particular, we underscore the role of the innate immune system, polarized responses and regulatory mechanisms on heterologous immune responses. [source] Behavioural changes in Schistocerca gregaria following infection with a fungal pathogen: implications for susceptibility to predationECOLOGICAL ENTOMOLOGY, Issue 3 2001Steven Arthurs Summary 1. Field observations have indicated that infection of locusts and grasshoppers by the fungal entomopathogen Metarhizium anisopliae var. acridum may result in a substantial increase in the host's susceptibility to predation, before death is caused directly by the disease. 2. Laboratory experiments were conducted to examine how the behaviour of the desert locust Schistocerca gregaria Forskål changes following infection by M. anisopliae var. acridum to explore some potential mechanisms underlying this phenomenon. 3. In the first experiment, which involved monitoring general locust activity in small cages throughout the disease incubation period, infected locusts were observed to increase locomotion and bodily movement from 3 days after infection until death (average survival time of 11 days). There was some evidence of reduced feeding and mating behaviour following infection. 4. In a second experiment, locusts were exposed individually to a simulated predator attack and the initiation and strength of any escape responses were measured. Infected locusts were observed to have a reduced escape capability (both the propensity to escape and the strength of the response). In contrast to the relatively early changes in general activity observed in the first experiment, this was only apparent at the late stages of infection shortly before death. 5. Both an increase in movement and general apparency early in the infection process, and reduced escape capability late on, suggest mechanisms whereby the susceptibility of locusts and grasshoppers to predation might be enhanced following infection with M. anisopliae var. acridum. [source] | |||||||||||||||||||||||||