Understanding disease control: influence of epidemiological and economic factors

We present a local spread model of disease transmission on a regular network and compare different control options ranging from treating the whole population to local control in a well-defined neighborhood of an infectious individual. Comparison is based on a total cost of epidemic, including cost of palliative treatment of ill individuals and preventive cost aimed at vaccination or culling of susceptible individuals. Disease is characterized by pre- symptomatic phase which makes detection and control difficult. Three general strategies emerge, global preventive treatment, local treatment within a neighborhood of certain size and only palliative treatment with no prevention. The choice between the strategies depends on relative costs of palliative and preventive treatment. The details of the local strategy and in particular the size of the optimal treatment neighborhood weakly depends on disease infectivity but strongly depends on other epidemiological factors. The required extend of prevention is proportional to the size of the infection neighborhood, but this relationship depends on time till detection and time till treatment in a non-nonlinear (power) law. In addition, we show that the optimal size of control neighborhood is highly sensitive to the relative cost, particularly for inefficient detection and control application. These results have important consequences for design of prevention strategies aiming at emerging diseases for which parameters are not known in advance

Improving epidemic control strategies by extended detection

The majority of epidemics eradication programs work in a preventive responsive way. The lack of exact information about the epidemiological status of individuals makes responsive actions less efficient. Here, we demonstrate that additional tests can significantly increase the efficiency of “blind” treatment (vaccination or culling). Eradication strategy consisting of “blind” treatment in very limited local neighbourhood supplemented by extra tests in a little bit larger neighbourhood is able to prevent invasion of even highly infectious diseases and to achieve this at a cost lower than for the “blind” strategy. The effectiveness of the extended strategy depends on such parameters as the test efficiency and test cost

The Effect of Forest Management Options on Forest Resilience to Pathogens

Invasive pathogens threaten the ability of forests globally to produce a range of valuable ecosystem services over time. However, the ability to detect such pathogen invasions—and thus to produce appropriate and timely management responses—is relatively low. We argue that a promising approach is to plan and manage forests in a way that increases their resilience to invasive pathogens not yet present or ubiquitous in the forest. This paper is based on a systematic search and critical review of empirical evidence of the effect of a wide range of forest management options on the primary and secondary infection rates of forest pathogens, and on subsequent forest recovery. Our goals are to inform forest management decision making to increase forest resilience, and to identify the most important evidence gaps for future research. The management options for which there is the strongest evidence that they increase forest resilience to pathogens are: reduced forest connectivity, removal or treatment of inoculum sources such as cut stumps, reduced tree density, removal of diseased trees and increased tree species diversity. In all cases the effect of these options on infection dynamics differs greatly amongst tree and pathogen species and between forest environments. However, the lack of consistent effects of silvicultural systems or of thinning, pruning or coppicing treatments is notable. There is also a lack of evidence of how the effects of treatments are influenced by the scale at which they are applied, e.g., the mixture of tree species. An overall conclusion is that forest managers often need to trade-off increased resilience to tree pathogens against other benefits obtained from forests

A study of some mutations in a strain of Rhizobium trifolii

RESP-459

Small-World Networks: Links with long-tailed distributions

Small-world networks (SWN), obtained by randomly adding to a regular structure additional links (AL), are of current interest. In this article we explore (based on physical models) a new variant of SWN, in which the probability of realizing an AL depends on the chemical distance between the connected sites. We assume a power-law probability distribution and study random walkers on the network, focussing especially on their probability of being at the origin. We connect the results to L\'evy Flights, which follow from a mean field variant of our model.Comment: 11 pages, 4 figures, to appear in Phys.Rev.

A statistical network analysis of the HIV/AIDS epidemics in Cuba

The Cuban contact-tracing detection system set up in 1986 allowed the reconstruction and analysis of the sexual network underlying the epidemic (5,389 vertices and 4,073 edges, giant component of 2,386 nodes and 3,168 edges), shedding light onto the spread of HIV and the role of contact-tracing. Clustering based on modularity optimization provides a better visualization and understanding of the network, in combination with the study of covariates. The graph has a globally low but heterogeneous density, with clusters of high intraconnectivity but low interconnectivity. Though descriptive, our results pave the way for incorporating structure when studying stochastic SIR epidemics spreading on social networks

Finding and evaluating community structure in networks

We propose and study a set of algorithms for discovering community structure in networks -- natural divisions of network nodes into densely connected subgroups. Our algorithms all share two definitive features: first, they involve iterative removal of edges from the network to split it into communities, the edges removed being identified using one of a number of possible "betweenness" measures, and second, these measures are, crucially, recalculated after each removal. We also propose a measure for the strength of the community structure found by our algorithms, which gives us an objective metric for choosing the number of communities into which a network should be divided. We demonstrate that our algorithms are highly effective at discovering community structure in both computer-generated and real-world network data, and show how they can be used to shed light on the sometimes dauntingly complex structure of networked systems.Comment: 16 pages, 13 figure

A Cellular Automata Model for Citrus Variagated Chlorosis

A cellular automata model is proposed to analyze the progress of Citrus Variegated Chlorosis epidemics in S\~ao Paulo oranges plantation. In this model epidemiological and environmental features, such as motility of sharpshooter vectors which perform L\'evy flights, hydric and nutritional level of plant stress and seasonal climatic effects, are included. The observed epidemics data were quantitatively reproduced by the proposed model varying the parameters controlling vectors motility, plant stress and initial population of diseased plants.Comment: 10 pages, 10 figures, Scheduled tentatively for the issue of: 01Nov0

One Is Enough: In Vivo Effective Population Size Is Dose-Dependent for a Plant RNA Virus

Effective population size (Ne) determines the strength of genetic drift and the frequency of co-infection by multiple genotypes, making it a key factor in viral evolution. Experimental estimates of Ne for different plant viruses have, however, rendered diverging results. The independent action hypothesis (IAH) states that each virion has a probability of infection, and that virions act independent of one another during the infection process. A corollary of IAH is that Ne must be dose dependent. A test of IAH for a plant virus has not been reported yet. Here we perform a test of an IAH infection model using a plant RNA virus, Tobacco etch virus (TEV) variants carrying GFP or mCherry fluorescent markers, in Nicotiana tabacum and Capsicum annuum plants. The number of primary infection foci increased linearly with dose, and was similar to a Poisson distribution. At high doses, primary infection foci containing both genotypes were found at a low frequency (<2%). The probability that a genotype that infected the inoculated leaf would systemically infect that plant was near 1, although in a few rare cases genotypes could be trapped in the inoculated leaf by being physically surrounded by the other genotype. The frequency of mixed-genotype infection could be predicted from the mean number of primary infection foci using the independent-action model. Independent action appears to hold for TEV, and Ne is therefore dose-dependent for this plant RNA virus. The mean number of virions causing systemic infection can be very small, and approaches 1 at low doses. Dose-dependency in TEV suggests that comparison of Ne estimates for different viruses are not very meaningful unless dose effects are taken into consideration

Virus Infection Suppresses Nicotiana benthamiana Adaptive Phenotypic Plasticity

Competition and parasitism are two important selective forces that shape life-histories, migration rates and population dynamics. Recently, it has been shown in various pathosystems that parasites can modify intraspecific competition, thus generating an indirect cost of parasitism. Here, we investigated if this phenomenon was present in a plant-potyvirus system using two viruses of different virulence (Tobacco etch virus and Turnip mosaic virus). Moreover, we asked if parasitism interacted with the shade avoidance syndrome, the plant-specific phenotypic plasticity in response to intraspecific competition. Our results indicate that the modification of intraspecific competition by parasitism is not present in the Nicotiana benthamiana – potyvirus system and suggests that this phenomenon is not universal but depends on the peculiarities of each pathosystem. However, whereas the healthy N. benthamiana presented a clear shade avoidance syndrome, this phenotypic plasticity totally disappeared when the plants were infected with TEV and TuMV, very likely resulting in a fitness loss and being another form of indirect cost of parasitism. This result suggests that the suppression or the alteration of adaptive phenotypic plasticity might be a component of virulence that is often overlooked