Host Density as a Factor in Plant Disease Ecology

Burdon, J. J.; Chilvers, G. A.

doi:10.1146/annurev.py.20.090182.001043

Cited by 382 publications

(278 citation statements)

References 49 publications

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“…It permits distinction between invasive and noninvasive growth between discrete nutrient sources and, by analogy, for growth between infected and susceptible hosts. It has long been known that the density of hosts affects the rate of mycelial spread of soil-borne plant pathogens (Gibson, 1956 ;Burdon & Chilvers, 1982). That work treated the effect of host density on the rate of epidemic development as a continuum.…”

Section: mentioning

confidence: 99%

Saprotrophic invasion by the soil‐borne fungal plant pathogen Rhizoctonia solani and percolation thresholds

2000

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In this paper we distinguish between invasive and noninvasive (finite) saprotrophic spread of the soil-borne fungal plant pathogen, Rhizoctonia solani amongst discrete sites of nutrient resource. Using simple concepts of percolation theory, we predict the critical threshold distance, associated with a threshold probability, between donor (colonized) and recipient (uncolonized) nutrient sites at which R. solani can spread invasively by mycelial growth through a population of nutrient sites on a lattice. The critical distance for invasive spread is estimated from colonization profiles derived from placement experiments that summarize the probability of colonization with distance between replicated pairs of colonized and uncolonized sites. Colonization profiles were highly nonlinear, decaying sigmoidally with distance. Thresholds for invasive spread were predicted at inter-site distances of 8.1 mm and 11.8 mm for sites of low and high nutrient agar, respectively. In population experiments with inter-site distances below the predicted thresholds, the spread of the fungus was invasive in all replicates. At large distances ( 10 mm for low, and 14 mm for high nutrient sites) the spread of the fungus was always finite, with the proportion of finite replicates decreasing sharply close to the percolation threshold. Invasive spread did not depend on the furthest extent of growth of the fungus but on distances predicted by the percolation thresholds. Invasive spread of the fungus is also examined in a more natural and variable, nonsterile system involving the growth and colonization of a lattice of poppy seeds over sand. The system is characterized by a decay in the probability of colonization between older poppy seeds, which effectively ' quenches ' saprotrophic spread. Hence in the population experiments with poppy seeds all growth was ultimately finite. The threshold distance, corresponding to the critical percolation probability for invasive growth changed from 18 mm to 4 mm over 21d leading to a switch from invasive to finite growth. We conclude that percolation theory can be used to link the growth of individual mycelial colonies to the formation of patches that result from the colonization of particulate organic matter. The nonlinearity of the colonization profiles combined with the presence of a percolation threshold means that small changes in the distance between nutrient sites can result in large differences in final patch size. The rapid decay of particulate organic matter in a more natural system can have a profound effect on the dynamics of colonization, restricting saprotrophic invasion of the soil. The consequences of invasion thresholds for colony growth of saprotrophic and parasitic fungi in dynamical systems are briefly discussed.

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Section: mentioning

confidence: 99%

Saprotrophic invasion by the soil‐borne fungal plant pathogen Rhizoctonia solani and percolation thresholds

2000

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“…One reason is that, at high densities, pathogens may transmit more efficiently, with the consequence that all individuals become infected and die (Burdon & Chilvers 1982). However, it is also possible that compensating responses might occur, for example, if pathogens only affect the smallest or latest emerging individuals in the population in a manner analogous to asymmetric competition (sensu Weiner 1988).…”

Section: Introductionmentioning

confidence: 99%

Pathogens, density dependence and the coexistence of tropical trees

2006

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There is increasing interest in the role played by density-dependent mortality from natural enemies, particularly plant pathogens, in promoting the coexistence and diversity of tropical trees. Here, we review four issues in the analysis of pathogen-induced density dependence that have been overlooked or inadequately addressed. First, the methodology for detecting density dependence must be robust to potential biases. Observational studies, in particular, require a careful analysis to avoid biases generated by measurement error, and existing studies could be criticized on these grounds. Experimental studies manipulating plant density and pathogen incidence will often be preferable, or should be run in parallel. Second, the form of density dependence is not well understood and, in particular, there are no data indicating whether pathogens cause compensating or overcompensating density responses. Owing to this, we argue that the potential for pathogen-induced density dependence to generate diversity-enhancing outcomes, such as the Janzen-Connell effect, remains uncertain, as coexistence is far more probable if density dependence is overcompensating. Third, there have been few studies examining the relative importance of intra-or interspecific density dependence resulting from pathogens (or, more widely, natural enemies). This is essentially equivalent to asking to what extent pathogens are host-specific. If pathogens are generalists, then mortality rates will respond to overall plant density, irrespective of plant species identity. This will weaken the intraspecific density dependence and reduce the diversity-promoting effects of pathogens. Finally, we highlight the need for studies that integrate observations and experiments on pathogens and density dependence into the whole life cycle of trees, because as yet it is not possible to be certain of the degree to which pathogens contribute to observed dynamics.

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“…A basic premise of epidemiology is that pathogen transmission often increases with host density 12,13 . Densitydependent disease provides a mechanism for the maintenance of plant diversity in natural communities, in which locally uncommon species enjoy a rare-species advantage-based on lower enemy pressure-that mitigates the competitive impacts of dominant species [3][4][5] .…”

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Phylogenetic structure and host abundance drive disease pressure in communities

Parker

Saunders

Bontrager

et al. 2015

Nature

298

325

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Pathogens play an important part in shaping the structure and dynamics of natural communities, because species are not affected by them equally 1,2 . A shared goal of ecology and epidemiology is to predict when a species is most vulnerable to disease. A leading hypothesis asserts that the impact of disease should increase with host abundance, producing a 'rare-species advantage' 3-5 . However, the impact of a pathogen may be decoupled from host abundance, because most pathogens infect more than one species, leading to pathogen spillover onto closely related species 6,7 . Here we show that the phylogenetic and ecological structure of the surrounding community can be important predictors of disease pressure. We found that the amount of tissue lost to disease increased with the relative abundance of a species across a grassland plant community, and that this rare-species advantage had an additional phylogenetic component: disease pressure was stronger on species with many close relatives. We used a global model of pathogen sharing as a function of relatedness between hosts, which provided a robust predictor of relative disease pressure at the local scale. In our grassland, the total amount of disease was most accurately explained not by the abundance of the focal host alone, but by the abundance of all species in the community weighted by their phylogenetic distance to the host. Furthermore, the model strongly predicted observed disease pressure for 44 novel host species we introduced experimentally to our study site, providing evidence for a mechanism to explain why phylogenetically rare species are more likely to become invasive when introduced 8,9 . Our results demonstrate how the phylogenetic and ecological structure of communities can have a key role in disease dynamics, with implications for the maintenance of biodiversity, biotic resistance against introduced weeds, and the success of managed plants in agriculture and forestry.Plant pathogens can be important drivers of community diversity, structure and dynamics 1,2,10,11 . A basic premise of epidemiology is that pathogen transmission often increases with host density 12,13 . Densitydependent disease provides a mechanism for the maintenance of plant diversity in natural communities, in which locally uncommon species enjoy a rare-species advantage-based on lower enemy pressure-that mitigates the competitive impacts of dominant species 3-5 . Reports of density-dependent disease dynamics generally infer the potential effects on communities from studies of one or a few species 2 , while community-level studies 1 are scarce but essential to evaluate whether such a rarespecies advantage predicts patterns of disease across a community.An ongoing debate concerns how community context influences disease, and particularly whether biodiversity suppresses infection and emerging diseases 14,15 . If increasing the number of species in a community reduces the density of competent hosts or the frequency of infected vectors, then biodiversity shows a suppressive 'dilution e...

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Host Density as a Factor in Plant Disease Ecology

Cited by 382 publications

References 49 publications

Saprotrophic invasion by the soil‐borne fungal plant pathogen Rhizoctonia solani and percolation thresholds

Saprotrophic invasion by the soil‐borne fungal plant pathogen Rhizoctonia solani and percolation thresholds

Pathogens, density dependence and the coexistence of tropical trees

Phylogenetic structure and host abundance drive disease pressure in communities

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