scholarly journals Epidemiology in Mixed Host Populations

1999 ◽  
Vol 89 (11) ◽  
pp. 984-990 ◽  
Author(s):  
K. A. Garrett ◽  
C. C. Mundt
Keyword(s):  
Plant Competition ◽  
Natural Populations ◽  
Host Density ◽  
Host Population ◽  
Host Genotype ◽  
Susceptible Host ◽  
Disease Epidemiology ◽  
Host Diversity ◽  
Classic Model ◽  
Diversity Effects

Although plant disease epidemiology has focused on populations in which all host plants have the same genotype, mixtures of host genotypes are more typical of natural populations and offer promising options for deployment of resistance genes in agriculture. In this review, we discuss Leonard's classic model of the effects of host genotype diversity on disease and its predictions of disease level based on the proportion of susceptible host tissue. As a refinement to Leonard's model, the spatial structure of host and pathogen population can be taken into account by considering factors such as autoinfection, interaction between host size and pathogen dispersal gradients, lesion expansion, and host carrying capacity for disease. The genetic composition of the host population also can be taken into account by considering differences in race-specific resistance among host genotypes, compensation, plant competition, and competitive interactions among pathogen genotypes. The magnitude of host-diversity effects for particular host-pathogen systems can be predicted by considering how the inherent characteristics of a system causes it to differ from the assumptions of the classic model. Because of the limited number of studies comparing host-diversity effects in different systems, it is difficult at this point to make more than qualitative predictions. Environmental conditions and management decisions also influence host-diversity effects on disease through their effect on factors such as host density and epidemic length and intensity.

scholarly journals The Effects of Host Diversity and Other Management Components on Epidemics of Potato Late Blight in the Humid Highland Tropics

2001 ◽  
Vol 91 (10) ◽  
pp. 993-1000 ◽  
Author(s):  
K. A. Garrett ◽  
R. J. Nelson ◽  
C. C. Mundt ◽  
G. Chacón ◽  
R. E. Jaramillo ◽  
...  
Keyword(s):  
Late Blight ◽  
Potato Production ◽  
Potato Late Blight ◽  
Planting Density ◽  
Susceptible Host ◽  
Host Diversity ◽  
Progress Curve ◽  
Commercial Potato ◽  
Diversity Effect ◽  
Diversity Effects

A field study at three highland sites near Quito, Ecuador, was conducted to determine whether host-diversity effects on potato late blight would be as important as recently found in studies conducted in temperate areas. We compared three potato mixtures and use of mixtures in combination with different planting densities and two fungicide regimes. Treatment comparisons were made by absolute and relative measures of host-diversity effects and incorporating a truncated area under the disease progress curve as a means of standardizing comparisons across sites. Potato-faba intercrops consisting of only 10% potato provided an estimate of the effects of dilution of susceptible host tissue. Host-diversity effects were very different across study sites, with a large host-diversity effect for reduced disease only at the site most distant from commercial potato production. Planting density had little influence on host-diversity effects or on late blight in single-genotype stands. Fungicide use in combination with potato mixtures enhanced a host-diversity effect for reduced late blight. Potato-faba intercrops produced only a small decrease in potato late blight. Effects of host diversity on yield were variable, with the greatest increase in yield for mixtures treated with fungicides at the site most distant from commercial potato production. The effects of host diversity on late blight severity may be less consistent in the tropical highlands than in the temperate zone, but can contribute to integrated disease management.

scholarly journals Poor maternal environment enhances offspring disease resistance in an invertebrate

2005 ◽  
Vol 272 (1581) ◽  
pp. 2601-2607 ◽  
Author(s):  
Suzanne E Mitchell ◽  
Andrew F Read
Keyword(s):  
Environmental Conditions ◽  
Natural Populations ◽  
Disease Outbreaks ◽  
Host Population ◽  
Optimal Resource Allocation ◽  
Host Genotype ◽  
Evolutionary Response ◽  
Optimal Resource ◽  
Maternal Responses ◽  
The Impact

Natural populations vary tremendously in their susceptibility to infectious disease agents. The factors (environmental or genetic) that underlie this variation determine the impact of disease on host population dynamics and evolution, and affect our capacity to contain disease outbreaks and to enhance resistance in agricultural animals and disease vectors. Here, we show that changes in the environmental conditions under which female Daphnia magna are kept can more than halve the susceptibility of their offspring to bacterial infection. Counter-intuitively, and unlike the effects typically observed in vertebrates for transfer of immunity, mothers producing offspring under poor conditions produced more resistant offspring than did mothers producing offspring in favourable conditions. This effect occurred when mothers who were well provisioned during their own development then found themselves reproducing in poor conditions. These effects likely reflect adaptive optimal resource allocation where better quality offspring are produced in poor environments to enhance survival. Maternal exposure to parasites also reduced offspring susceptibility, depending on host genotype and offspring food levels. These maternal responses to environmental conditions mean that studies focused on a single generation, and those in which environmental variation is experimentally minimized, may fail to describe the crucial parameters that influence the spread of disease. The large maternal effects we report here will, if they are widespread in nature, affect disease dynamics, the level of genetic polymorphism in populations, and likely weaken the evolutionary response to parasite-mediated selection.

Parasite infection and host dynamics in a naturally fluctuating rodent population

2012 ◽  
Vol 90 (9) ◽  
pp. 1149-1160 ◽  
Author(s):  
J.C. Winternitz ◽  
M.J. Yabsley ◽  
S.M. Altizer
Keyword(s):  
Population Density ◽  
Experimental Studies ◽  
Host Density ◽  
Positive Association ◽  
Population Cycles ◽  
Host Population ◽  
Reproductive Status ◽  
Vole Cycles ◽  
Host Infection ◽  
The Impact

Parasites can both influence and be affected by host population dynamics, and a growing number of case studies support a role for parasites in causing or amplifying host population cycles. In this study, we examined individual and population predictors of gastrointestinal parasitism on wild cyclic montane voles ( Microtus montanus (Peale, 1848)) to determine if evidence was consistent with theory implicating parasites in population cycles. We sampled three sites in central Colorado for the duration of a multiannual cycle and recorded the prevalence and intensity of directly transmitted Eimeria Schneider, 1875 and indirectly transmitted cestodes from a total of 267 voles. We found significant associations between host infection status, individual traits (sex, age, and reproductive status) and population variables (site, trapping period, and population density), including a positive association between host density and cestode prevalence, and a negative association between host density and Eimeria prevalence. Both cestode and Eimeria intensity correlated positively with host age, reproductive status, and population density, but neither parasite was associated with poorer host condition. Our findings suggest that parasites are common in this natural host, but determining their potential to influence montane vole cycles requires future experimental studies and long-term monitoring to determine the fitness consequences of infection and the impact of parasite removal on host dynamics.

scholarly journals Parasite variation and the evolution of virulence in a Daphnia-microparasite system

Parasitology ◽  
2007 ◽  
Vol 135 (3) ◽  
pp. 303-308 ◽  
Author(s):  
T. J. LITTLE ◽  
W. CHADWICK ◽  
K. WATT
Keyword(s):  
Genetic Variation ◽  
Rank Order ◽  
Genetic Relationships ◽  
Natural Populations ◽  
Host Genotype ◽  
Relative Growth ◽  
Trade Off ◽  
Relative Growth Rates ◽  
Pasteuria Ramosa ◽  
Evolution Of Virulence

SUMMARYUnderstanding genetic relationships amongst the life-history traits of parasites is crucial for testing hypotheses on the evolution of virulence. This study therefore examined variation between parasite isolates (the bacterium Pasteuria ramosa) from the crustacean Daphnia magna. From a single wild-caught infected host we obtained 2 P. ramosa isolates that differed substantially in the mortality they caused. Surprisingly, the isolate causing higher early mortality was, on average, less successful at establishing infections and had a slower growth rate within hosts. The observation that within-host replication rate was negatively correlated with mortality could violate a central assumption of the trade-off hypothesis for the evolution of virulence, but we discuss a number of caveats which caution against premature rejection of the trade-off hypothesis. We sought to test if the characteristics of these parasite isolates were constant across host genotypes in a second experiment that included 2 Daphnia host clones. The relative growth rates of the two parasite isolates did indeed depend on the host genotype (although the rank order did not change). We suggest that testing evolutionary hypotheses for virulence may require substantial sampling of both host and parasite genetic variation, and discuss how selection for virulence may change with the epidemiological state of natural populations and how this can promote genetic variation for virulence.

scholarly journals Causation without correlation: parasite-mediated frequency-dependent selection and infection prevalence

2021 ◽  
Author(s):  
Curtis M Lively ◽  
Julie Xu ◽  
Frida Ben-Ami
Keyword(s):  
Genetic Diversity ◽  
Natural Populations ◽  
Infection Prevalence ◽  
Strong Positive Correlation ◽  
Frequency Dependent ◽  
Frequency Dependent Selection ◽  
Host Diversity ◽  
Host Genetic ◽  
Host Parasite

Parasite-mediated selection is thought to maintain host genetic diversity for resistance. We might thus expect to find a strong positive correlation between host genetic diversity and infection prevalence across natural populations. Here we used computer simulations to examine host-parasite coevolution in 20 simi-isolated clonal populations across a broad range of values for both parasite virulence and parasite fecundity. We found that the correlation between host genetic diversity and infection prevalence can be significantly positive for intermediate values of parasite virulence and fecundity. But the correlation can also be weak and statistically non-significant, even when parasite-mediated frequency-dependent selection is the sole force maintaining host diversity. Hence correlational analyses of field populations, while useful, might underestimate the role of parasites in maintaining host diversity.

scholarly journals Anaplasma marginale Superinfection Attributable to Pathogen Strains with Distinct Genomic Backgrounds

2014 ◽  
Vol 82 (12) ◽  
pp. 5286-5292 ◽  
Author(s):  
Eduardo Vallejo Esquerra ◽  
David R. Herndon ◽  
Francisco Alpirez Mendoza ◽  
Juan Mosqueda ◽  
Guy H. Palmer
Keyword(s):  
High Throughput Sequencing ◽  
Anaplasma Marginale ◽  
Host Population ◽  
Content Type ◽  
Tropical Regions ◽  
Disease Epidemiology ◽  
Infectious Disease Epidemiology ◽  
Perfect Sequence ◽  
Significant Difference ◽  
High Prevalence

ABSTRACTStrain superinfection occurs when a second pathogen strain infects a host already infected with a primary strain. The selective pressures that drive strain divergence, which underlies superinfection, and allow penetration of a new strain into a host population are critical knowledge gaps relevant to shifts in infectious disease epidemiology. In regions of endemicity with a high prevalence of infection, broad population immunity develops againstAnaplasma marginale, a highly antigenically variant rickettsial pathogen, and creates strong selective pressure for emergence of and superinfection with strains that differ in their Msp2 variant repertoires. The strains may emerge either bymsp2locus duplication and allelic divergence on an existing genomic background or by introduction of a strain with a differentmsp2allelic repertoire on a distinct genomic background. To answer this question, we developed a multilocus typing assay based on high-throughput sequencing of non-msp2target loci to distinguish among strains with different genomic backgrounds. The technical error level was statistically defined based on the percentage of perfect sequence matches of clones of each target locus and validated using experimental single strains and strain pairs. Testing ofA. marginale-positive samples from tropical regions whereA. marginaleinfection is endemic identified individual infections that contained unique alleles for all five targeted loci. The data revealed a highly significant difference in the number of strains per animal in the tropical regions compared to infections in temperate regions and strongly supported the hypothesis that transmission of genomically distinctA. marginalestrains predominates in high-prevalence areas of endemicity.

Effects of goldfish (Carassius auratus) population size and body condition on the transmission of Gyrodactylus kobayashii (Monogenea)

Parasitology ◽  
2017 ◽  
Vol 144 (9) ◽  
pp. 1221-1228 ◽  
Author(s):  
SHUN ZHOU ◽  
HONG ZOU ◽  
SHAN G. WU ◽  
GUI T. WANG ◽  
DAVID J. MARCOGLIESE ◽  
...  
Keyword(s):  
Population Size ◽  
Body Condition ◽  
Host Density ◽  
Host Population ◽  
Laboratory Model ◽  
Constant Density ◽  
Contact Rates ◽  
Effective Contact ◽  
Rate Of Increase ◽  
Population Sizes

SUMMARYField surveys indicate that host population size, rather than density, is the most important determinant of monogenean infection dynamics. To verify this prediction, epidemic parameters were monitored for 70 days at five host population sizes held at constant density using a goldfish – Gyrodactylus kobayashii laboratory model. During the first 20 days, the rate of increase of prevalence and mean abundance was faster in small host populations. Total mean prevalence and total mean abundance throughout the experiment were not significantly affected by host population sizes. Higher transmission rates were detected in larger host populations. However, there were no significant differences in effective contact rates among the five host populations on each sampling day during the first 20 days, implying that contact rates may be saturated at a sufficiently high host density. These results demonstrate that the epidemic occurs more quickly in smaller host populations at the beginning of the experiment. However, the epidemic is independent of the host population size due to the similar effective contact rates in the five population sizes. Significant negative influence of the initial body condition (Kn) of uninfected goldfish on total mean abundance of parasites suggests that susceptibility of hosts is also a determinant of parasite transmission.

Epidemiology and optimal foraging: modelling the ideal free distribution of insect vectors

Parasitology ◽  
2000 ◽  
Vol 120 (3) ◽  
pp. 319-327 ◽  
Author(s):  
D. W. KELLY ◽  
C. E. THOMPSON
Keyword(s):  
Host Species ◽  
Disease Transmission ◽  
Ideal Free Distribution ◽  
Host Population ◽  
Control Effort ◽  
Susceptible Host ◽  
Vector Density ◽  
Free Distribution ◽  
Blood Sucking ◽  
Ideal Free

Existing models of the basic case reproduction number (R0) for vector-borne diseases assume (i) that the distribution of vectors over the susceptible host species is homogenous and (ii) that the biting preference for the susceptible host species rather than other potential hosts is a constant. Empirical evidence contradicts both assumptions, with important consequences for disease transmission. In this paper we develop an Ideal Free Distribution (IFD) model of host choice by blood-sucking insects, predicated on the argument that vectors must have evolved to choose the least defensive hosts in order to maximize their feeding success. From a re-analysis of existing data, we demonstrate that the interference constant, m, of the IFD can vary between host species. As a result, the predicted distribution of insects over hosts has 2 desirable and intuitively plausible behaviours: that it is heterogeneous both within and between host species; and that the intensity of heterogeneity varies with host and vector density. When the IFD model is incorporated into R0, the relationship with the vector: host ratio becomes non-linear. If correct, the IFD could add considerable realism to models which seek to predict the effect of these ecological parameters on disease transmission as they vary naturally (e.g. through seasonality in vector density or host population movement) or as a consequence of artificial manipulation (e.g. zooprophylaxis, vector control). It raises the possibility of targeting transmission hot spots with greater accuracy and concomitant reduction in control effort. The robustness of the model to simplifying assumptions is discussed.

scholarly journals Epidemic thresholds in dynamic contact networks

2008 ◽  
Vol 6 (32) ◽  
pp. 233-241 ◽  
Author(s):  
Erik Volz ◽  
Lauren Ancel Meyers
Keyword(s):  
Dynamic Networks ◽  
Dynamic Contact ◽  
Host Population ◽  
Initial Increase ◽  
Epidemic Threshold ◽  
Susceptible Host ◽  
Mixing Parameter ◽  
Social Mixing ◽  
Fundamental Quantity ◽  
Simple Class

The reproductive ratio, R 0 , is a fundamental quantity in epidemiology, which determines the initial increase in an infectious disease in a susceptible host population. In most epidemic models, there is a specific value of R 0 , the epidemic threshold, above which epidemics are possible, but below which epidemics cannot occur. As the complexity of an epidemic model increases, so too does the difficulty of calculating epidemic thresholds. Here we derive the reproductive ratio and epidemic thresholds for susceptible–infected–recovered (SIR) epidemics in a simple class of dynamic random networks. As in most epidemiological models, R 0 depends on two basic epidemic parameters, the transmission and recovery rates. We find that R 0 also depends on social parameters, namely the degree distribution that describes heterogeneity in the numbers of concurrent contacts and the mixing parameter that gives the rate at which contacts are initiated and terminated. We show that social mixing fundamentally changes the epidemiological landscape and, consequently, that static network approximations of dynamic networks can be inadequate.

scholarly journals Synthesizing within-host and population-level selective pressures on viral populations: the impact of adaptive immunity on viral immune escape

2010 ◽  
Vol 7 (50) ◽  
pp. 1311-1318 ◽  
Author(s):  
Igor Volkov ◽  
Kim M. Pepin ◽  
James O. Lloyd-Smith ◽  
Jayanth R. Banavar ◽  
Bryan T. Grenfell
Keyword(s):  
Evolutionary Dynamics ◽  
Immune Escape ◽  
Adaptive Immune Response ◽  
Population Level ◽  
Analytical Framework ◽  
Host Population ◽  
Host Immunity ◽  
Host Cells ◽  
Susceptible Host ◽  
The Impact

The evolution of viruses to escape prevailing host immunity involves selection at multiple integrative scales, from within-host viral and immune kinetics to the host population level. In order to understand how viral immune escape occurs, we develop an analytical framework that links the dynamical nature of immunity and viral variation across these scales. Our epidemiological model incorporates within-host viral evolutionary dynamics for a virus that causes acute infections (e.g. influenza and norovirus) with changes in host immunity in response to genetic changes in the virus population. We use a deterministic description of the within-host replication dynamics of the virus, the pool of susceptible host cells and the host adaptive immune response. We find that viral immune escape is most effective at intermediate values of immune strength. At very low levels of immunity, selection is too weak to drive immune escape in recovered hosts, while very high levels of immunity impose such strong selection that viral subpopulations go extinct before acquiring enough genetic diversity to escape host immunity. This result echoes the predictions of simpler models, but our formulation allows us to dissect the combination of within-host and transmission-level processes that drive immune escape.

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