Modelling interference between vectors of non-persistently transmitted plant viruses to identify effective control strategies

Aphids are the primary vector of plant viruses. Transient aphids, which probe several plants per day, are considered to be the principal vectors of non-persistently transmitted (NPT) viruses. However, resident aphids, which can complete their life cycle on a single host and are affected by agronomic practices, can transmit NPT viruses as well. Moreover, they can interfere both directly and indirectly with transient aphids, eventually shaping plant disease dynamics. By means of an epidemiological model, originally accounting for ecological principles and agronomic practices, we explore the consequences of fertilization and irrigation, pesticide deployment and roguing of infected plants on the spread of viral diseases in crops. Our results indicate that the spread of NPT viruses can be i) both reduced or increased by fertilization and irrigation, depending on whether the interference is direct or indirect; ii) counter-intuitively increased by pesticide application and iii) reduced by roguing infected plants. We show that a better understanding of vectors’ interactions would enhance our understanding of disease transmission, supporting the development of disease management strategies.     

Dynamics of plant mosaic disease propagation and the usefulness of roguing as an alternative biological control

In this research article, an epidemiological model is formulated for mosaic disease considering plant and vector populations. Plant host population has been divided into three compartments namely healthy, latently infected and infected ones, and vector population is divided into two compartments: non-infective and infective vectors. The system possesses three equilibria: plant-only, disease-free and endemic equilibrium. Plant-only equilibrium is always unstable; disease-free equilibrium is stable when the basic reproduction number, R₀, is less than unity and unstable for when it crosses unity, and ensure existence of an endemic equilibrium which may be stable or can undergo a Hopf bifurcation. Finally, impulse periodic roguing with varied rate and time interval is adopted for cost effective and eco-friendly disease control and future direction of agriculture management. The dynamics of the impulsive system has also been analysed. Detailed numerical simulations are employed to support the analytical results. We found that roguing is most cost effective and useful management for mosaic disease eradication of plants if applied at proper rate and interval.     

A Novel Statistical Model to Estimate Host Genetic Effects Affecting Disease Transmission

There is increasing recognition that genetic diversity can affect the spread of diseases, potentially affecting plant and livestock disease control as well as the emergence of human disease outbreaks. Nevertheless, even though computational tools can guide the control of infectious diseases, few epidemiological models can simultaneously accommodate the inherent individual heterogeneity in multiple infectious disease traits influencing disease transmission, such as the frequently modeled propensity to become infected and infectivity, which describes the host ability to transmit the infection to susceptible individuals. Furthermore, current quantitative genetic models fail to fully capture the heritable variation in host infectivity, mainly because they cannot accommodate the nonlinear infection dynamics underlying epidemiological data. We present in this article a novel statistical model and an inference method to estimate genetic parameters associated with both host susceptibility and infectivity. Our methodology combines quantitative genetic models of social interactions with stochastic processes to model the random, nonlinear, and dynamic nature of infections and uses adaptive Bayesian computational techniques to estimate the model parameters. Results using simulated epidemic data show that our model can accurately estimate heritabilities and genetic risks not only of susceptibility but also of infectivity, therefore exploring a trait whose heritable variation is currently ignored in disease genetics and can greatly influence the spread of infectious diseases. Our proposed methodology offers potential impacts in areas such as livestock disease control through selective breeding and also in predicting and controlling the emergence of disease outbreaks in human populations.     

Opposing effects of allogrooming on disease transmission in ant societies

To prevent epidemics, insect societies have evolved collective disease defences that are highly effective at curing exposed individuals and limiting disease transmission to healthy group members. Grooming is an important sanitary behaviour—either performed towards oneself (self-grooming) or towards others (allogrooming)—to remove infectious agents from the body surface of exposed individuals, but at the risk of disease contraction by the groomer. We use garden ants (Lasius neglectus) and the fungal pathogen Metarhizium as a model system to study how pathogen presence affects self-grooming and allogrooming between exposed and healthy individuals. We develop an epidemiological SIS model to explore how experimentally observed grooming patterns affect disease spread within the colony, thereby providing a direct link between the expression and direction of sanitary behaviours, and their effects on colony-level epidemiology. We find that fungus-exposed ants increase self-grooming, while simultaneously decreasing allogrooming. This behavioural modulation seems universally adaptive and is predicted to contain disease spread in a great variety of host–pathogen systems. In contrast, allogrooming directed towards pathogen-exposed individuals might both increase and decrease disease risk. Our model reveals that the effect of allogrooming depends on the balance between pathogen infectiousness and efficiency of social host defences, which are likely to vary across host–pathogen systems.     

The effect of rouging on the spread of virus diseases in potatoes at Rothamsted in 1946

Experiments on roguing virus-diseased plants from plots of Majestic potatoes, which have been in progress since 1943, were continued in 1946. Plots were rogued in mid-June, early and late July, and plants were lifted from these plots at the end of July, August and September respectively. Roguing had little effect in reducing the spread of rugose mosaic (caused by potato virus Y ). The spread of leaf roll was reduced to half that on unrogued plots by roguing on 14 June. Later roguing did not reduce the spread of leaf roll, unless combined with early lifting. Early lifting increased the effect of early roguing. In spite of these results roguing main crop potatoes in the south of England is not considered a practical control measure.     

The Spread of African Cassava Mosaic Virus into and within Cassava Fields

Only a small proportion of Bemisia tabaci collected in totally infected cassava fields at a site in Côte d'lvoire transmitted African cassava mosaic virus (ACMV) to test plants. Nevertheless, the monthly increase in disease incidence in an experimental planting was directly related to numbers of adult whiteflies counted on plants 6 weeks earlier. In plots at different spacings, the greatest incidence of ACMV expressed as a percentage of the total stand occurred at the lowest plant density. Much speread into the spacing trial and into two other experimental plantings occurred from outside sources and followed downwind gradients. By contrast, spread from ACMV-infected sources within plantings was limited. It occurred in all directions but over distances of only a few metres. These contrasting patterns of spread are attributed to the differentbehavior of B. tabaci above and within the crop canopy. It is concluded that contamination of cassava fields in the coastal forest area of Côte d'Ivoire is due mainly to rapid spread from outside sources which leads to internal foci that contribute to some further, although limited, spread. These findings are discussed in relation to possible control strategies based on the release of healthy cuttings, dense planting and subsequent roguing. Such measures are unlikely to be effectve in the coastal forest region of Côte d'Ivoire and adjacent countriesunless varieties are grown with greater resistance to infection than those currently used.     

Infectious disease in consumer populations: dynamic consequences of resource-mediated transmission and infectiousness

Nonhost species can strongly affect the timing and progression of epidemics. One central interaction—between hosts, their resources, and parasites—remains surprisingly underdeveloped from a theoretical perspective. Furthermore, key epidemiological traits that govern disease spread are known to depend on resource density. We tackle both issues here using models that fuse consumer–resource and epidemiological theory. Motivated by recent studies of a phytoplankton–zooplankton–fungus system, we derive and analyze a family of dynamic models for parasite spread among consumers in which transmission depends on consumer (host) and resource densities. These models yield four key insights. First, host–resource cycling can lower mean host density and inhibit parasite invasion. Second, host–resource cycling can create Allee effects (bistability) if parasites increase mean host density by reducing the amplitude of host–resource cycles. Third, parasites can stabilize host–resource cycles; however, host–resource cycling can also cause disease cycling. Fourth, resource dependence of epidemiological traits helps to govern the relative dominance of these different behaviors. However, these resource dependencies largely have quantitative rather than qualitative effects on these three-species dynamics. Given the extent of these results, host–resource–parasite interactions should become more fundamental components of the burgeoning theory for the community ecology of infectious diseases.     

Optimising and Communicating Options for the Control of Invasive Plant Disease When There Is Epidemiological Uncertainty

Although local eradication is routinely attempted following introduction of disease into a new region, failure is commonplace. Epidemiological principles governing the design of successful control are not well-understood. We analyse factors underlying the effectiveness of reactive eradication of localised outbreaks of invading plant disease, using citrus canker in Florida as a case study, although our results are largely generic, and apply to other plant pathogens (as we show via our second case study, citrus greening). We demonstrate how to optimise control via removal of hosts surrounding detected infection (i.e. localised culling) using a spatially-explicit, stochastic epidemiological model. We show how to define optimal culling strategies that take account of stochasticity in disease spread, and how the effectiveness of disease control depends on epidemiological parameters determining pathogen infectivity, symptom emergence and spread, the initial level of infection, and the logistics and implementation of detection and control. We also consider how optimal culling strategies are conditioned on the levels of risk acceptance/aversion of decision makers, and show how to extend the analyses to account for potential larger-scale impacts of a small-scale outbreak. Control of local outbreaks by culling can be very effective, particularly when started quickly, but the optimum strategy and its performance are strongly dependent on epidemiological parameters (particularly those controlling dispersal and the extent of any cryptic infection, i.e. infectious hosts prior to symptoms), the logistics of detection and control, and the level of local and global risk that is deemed to be acceptable. A version of the model we developed to illustrate our methodology and results to an audience of stakeholders, including policy makers, regulators and growers, is available online as an interactive, user-friendly interface at http://www.webidemics.com/. This version of our model allows the complex epidemiological principles that underlie our results to be communicated to a non-specialist audience.     

Coinfection and the evolution of drug resistance

Recent experimental work in the rodent malaria model has shown that when two or more strains share a host, there is competitive release of drug‐resistant strains upon treatment. In other words, the propagule output of a particular strain is repressed when competing with other strains and increases upon the removal of this competition. This within‐host effect is predicted to have an important impact on the evolution and growth of resistant strains. However, how this effect translates to epidemiological parameters at the between‐host level, the level at which disease and resistance spread, has yet to be determined. Here we present a general, between‐host epidemiological model that explicitly takes into account the effect of coinfection and competitive release. Although our model does show that when there is coinfection competitive release may contribute to the emergence of resistance, it also highlights an additional between‐host effect. It is the combination of these two effects, the between‐host effect and the within‐host effect, that determines the overall influence of coinfection on the emergence of resistance. Therefore, even when competitive release of drug‐resistant strains occurs, within an infected individual, it is not necessarily true that coinfection will result in the increased emergence of resistance. These results have important implications for the control of the emergence and spread of drug resistance.     

Bacteriophage Latent-Period Evolution as a Response to Resource Availability

Bacteriophages (phages) modify microbial communities by lysing hosts, transferring genetic material, and effecting lysogenic conversion. To understand how natural communities are affected it is important to develop predictive models. Here we consider how variation between models—in eclipse period, latent period, adsorption constant, burst size, the handling of differences in host quantity and host quality, and in modeling strategy—can affect predictions. First we compare two published models of phage growth, which differ primarily in terms of how they model the kinetics of phage adsorption; one is a computer simulation and the other is an explicit calculation. At higher host quantities (~10⁸ cells/ml), both models closely predict experimentally determined phage population growth rates. At lower host quantities (10⁷ cells/ml), the computer simulation continues to closely predict phage growth rates, but the explicit model does not. Next we concentrate on predictions of latent-period optima. A latent-period optimum is the latent period that maximizes the population growth of a specific phage growing in the presence of a specific quantity and quality of host cells. Both models predict similar latent-period optima at higher host densities (e.g., 17 min at 10⁸ cells/ml). At lower host densities, however, the computer simulation predicts latent-period optima that are much shorter than those suggested by explicit calculations (e.g., 90 versus 1,250 min at 10⁵ cells/ml). Finally, we consider the impact of host quality on phage latent-period evolution. By taking care to differentiate latent-period phenotypic plasticity from latent-period evolution, we argue that the impact of host quality on phage latent-period evolution may be relatively small.     

Distribution,degree of damage and risk of spread of Trioza erytreae (Hemiptera: Triozidae) in Kenya

The African citrus triozid (ACT), Trioza erytreae Del Guercio, is a destructive pest particularly on citrus, and vectors, “Candidatus” Liberibacter africanus (CLaf), which is the causal agent of the African citrus greening disease. Our study seeks to establish the distribution and host‐plant relationship of ACT across citrus production areas in Kenya. We also modelled the risk of spread using the maximum entropy modelling algorithm with known occurrence data. Our results infer that ACT is widely distributed and causes severe damage to four alternative host plants belonging to the family Rutaceae. The adults, immature stages (eggs and nymphs), galls and the percentage of infested leaves were significantly higher in shaded than unshaded trees. However, adult ACTs preferred Kenyan highlands to Victoria Lake and coastal regions. The average area under the curve of the model predictions was 0.97, indicating an optimal model performance. The environmental variables that most influenced the prediction were the precipitation of wettest quarter, precipitation of wettest month, mean diurnal range, temperature seasonality and mean temperature of the coldest quarter. The current prediction of ACT exceeded its existing range, especially in the Western, Nyanza, Central, Rift valley and Eastern regions of Kenya. The model predicted a contraction of suitable habitats for a potential spread in 2040 with an inland shift to higher altitudes in the cooler regions. The potential for further expansion to climatically suitable areas was more pronounced for the 2080 forecast. These findings provide relevant information to improve monitoring/surveillance and designing IPM strategies to limit its spread and damage.     

Identification of Alternative Hosts of the Fastidious Bacterium Causing Citrus Greening Disease

Citrus greening is a severe disease caused by a fastidious bacterium (GFB) residing in the sieve tubes of its hosts. It is an epidemic disease and is spread by insect vectors. In Asia, the Asian citrus psyllid (Diaphorina citri Kuwayama) is the vector for GFB. For the epidemiological study, an investigation of alternative hosts of GFB was made. Four suitable hosts of the Asian psyllid that are considered as possible alternative hosts of GFB were investigated on graft‐inoculation tests. The multiplication of GFB in plants was monitored by dot hybridization using a GFB‐specific DNA probe developed previously by us. The results demonstrate that GFB can replicate in Chinese box orange (Severinia buxifolia) and wood apple (Limonia acidissima), but not in common jasmin orange (Murraya paniculata var, paniculata) and curry leaf (Murraya euchrestifolia), Chinese box orange is a good host in which GFB replicates as well as it does in its citrus hosts. Wood apple is a transient host in which GFB exists temporarily and disappears several months later. Common jasmin orange and curry leaf are not hosts of GFB as they showed no detectable signals in dot hybridization tests throughout 1 year of experimentation.     

Optimal control of a vectored plant disease model for a crop with continuous replanting

ABSTRACT

Vector-transmitted diseases of plants have had devastating effects on agricultural production worldwide, resulting in drastic reductions in yield for crops such as cotton, soybean, tomato, and cassava. Plant-vector-virus models with continuous replanting are investigated in terms of the effects of selection of cuttings, roguing, and insecticide use on disease prevalence in plants. Previous models are extended to include two replanting strategies: frequencyreplanting and abundance-replanting. In frequency-replanting, replanting of infected cuttings depends on the selection frequency parameter ε, whereas in abundance-replanting, replanting depends on plant abundance via a selection rate parameter also denoted as ε. The two models are analysed and new thresholds for disease elimination are defined for each model. Parameter values for cassava, whiteflies, and African cassava mosaic virus serve as a case study. A numerical sensitivity analysis illustrates how the equilibrium densities of healthy and infected plants vary with parameter values. Optimal control theory is used to investigate the effects of roguing and insecticide use with a goal of maximizing the healthy plants that are harvested. Differences in the control strategies in the two models are seen for large values of ε. Also, the combined strategy of roguing and insecticide use performs better than a single control.     

Genetic structure and biology of Xylella fastidiosa strains causing disease in citrus and coffee in Brazil

Xylella fastidiosa is a vector-borne, plant-pathogenic bacterium that causes disease in citrus (citrus variegated chlorosis [CVC]) and coffee (coffee leaf scorch [CLS]) plants in Brazil. CVC and CLS occur sympatrically and share leafhopper vectors; thus, determining whether X. fastidiosa isolates can be dispersed from one crop to another and cause disease is of epidemiological importance. We sought to clarify the genetic and biological relationships between CVC- and CLS-causing X. fastidiosa isolates. We used cross-inoculation bioassays and microsatellite and multilocus sequence typing (MLST) approaches to determine the host range and genetic structure of 26 CVC and 20 CLS isolates collected from different regions in Brazil. Our results show that citrus and coffee X. fastidiosa isolates are biologically distinct. Cross-inoculation tests showed that isolates causing CVC and CLS in the field were able to colonize citrus and coffee plants, respectively, but not the other host, indicating biological isolation between the strains. The microsatellite analysis separated most X. fastidiosa populations tested on the basis of the host plant from which they were isolated. However, recombination among isolates was detected and a lack of congruency among phylogenetic trees was observed for the loci used in the MLST scheme. Altogether, our study indicates that CVC and CLS are caused by two biologically distinct strains of X. fastidiosa that have diverged but are genetically homogenized by frequent recombination.     

ROGUING POTATO CROPS FOR VIRUS DISEASES

Removing virus-infected plants from plots of Majestic potatoes at Rothamsted on 2 July 1947 did not reduce the spread of leaf roll but reduced rugose mosaic (potato virus Y) to about one-fifth of that in plots rogued on 21 July or left unrogued. Roguing Arran Pilot potatoes on 16 June or 2 July reduced leaf roll to five-sixths of that in unrogued plots; roguing on 16 June reduced rugose mosaic to about half that in plots rogued on 2 July, and about a quarter of that in unrogued plots. Lifting Arran Pilot potatoes in mid-August reduced virus diseases to about two-thirds.
Roguing flattened the gradient (decrease in percentage plants diseased with increasing distance from the source of infection) with rugose mosaic, but had little effect with leaf roll. Evidently any plants prevented by roguing from contracting virus Y were near the initially infected plants.
In 1948, Majestic and King Edward potatoes at three places were rogued during 22–24 June and tubers were dug during 28–30 July and again at the end of the season. Leaf roll spread more in Majestic than in King Edward, and rugose mosaic spread more in King Edward. Roguing reduced the spread of both by about one-fifth at Rothamsted, but had no effect at Sutton Bonington. At Bretton, in the Derbyshire hills, roguing had no effect on leaf roll, but prevented the spread of rugose mosaic.
The small benefit occasionally achieved by roguing in the ware-growing districts of England does not make the practice economically worth while.     

Progress, spread and natural transmission of Bahia bark scaling of citrus in Brazil

Progress, spread and natural transmission of Bahia bark scaling of citrus were evaluated in a trial where 240 screenhouse‐nursed nucellar grapefruit plants –‘Clason’, ‘Little River Seedless’, ‘Red Blush’, ‘Reed’ and ‘Howell Seedless’ cvs – were planted alongside and 5 m apart from a 10‐year‐old symptomatic ‘Marsh Seedless’ grapefruit orchard. Plants were distributed in 16 rows of 15 trees, with three plants of each cultivar per row. Eight trial plants were kept in screen cages. Incidence of symptomatic plants was assessed at 3‐months intervals, for 5 years, and for further 2 years at irregular intervals. Cumulative maps of disease incidence were produced for each assessment date and used in all analyses. Temporal progress was analysed by nonlinear fitting of three disease progress models. Spread was characterised in three levels of spatial hierarchy by the following analyses: ordinary runs, binomial dispersion index, binary power law fitting, isopath mapping and nonlinear fitting of disease gradient models. The first symptomatic plant was detected 2 years after planting. In the last disease assessment, 5 years after the first, 98% of the unprotected plants were symptomatic. None of the screen‐caged trees showed any symptoms. Bahia bark scaling progress was polyetic and best described by the logistic model. Ordinary runs analysis showed little if any evidence of transmission between adjacent trees. Diseased plants showed a very aggregated pattern inside quadrats (D > 5 and b > 1.53). Isopath mapping showed that main spread was only because of the primary inoculum source. Secondary foci were also observed, but they were never dissociated from main initial disease focus. Disease gradient followed wind direction, starting near the original inoculum source and was best described by exponential model. These results support a hypothesis of Bahia bark scaling transmission by air‐borne vectors with limited dispersion ability.     

Within-host population dynamics and the evolution of microparasites in a heterogeneous host population

Abstract Why do parasites harm their hosts? The general understanding is that if the transmission rate and virulence of a parasite are linked, then the parasite must harm its host to maximize its transmission. The exact nature of such trade‐offs remains largely unclear, but for vertebrate hosts it probably involves interactions between a microparasite and the host immune system. Previous results have suggested that in a homogeneous host population in the absence of super‐ or coinfection, within‐host dynamics lead to selection of the parasite with an intermediate growth rate that is just being controlled by the immune system before it kills the host (Antia et al. 1994). In this paper, we examine how this result changes when heterogeneity is introduced to the host population. We incorporate the simplest form of heterogeneity–random heterogeneity in the parameters describing the size of the initial parasite inoculum, the immune response of the host, and the lethal density at which the parasite kills the host. We find that the general conclusion of the previous model holds: parasites evolve some intermediate growth rate. However, in contrast with the generally accepted view, we find that virulence (measured by the case mortality or the rate of parasite‐induced host mortality) increases with heterogeneity. Finally, we link the within‐host and between‐host dynamics of parasites. We show how the parameters for epidemiological spread of the disease can be estimated from the within‐host dynamics, and in doing so examine the way in which trade‐offs between these epidemiological parameters arise as a consequence of the interaction of the parasite and the immune response of the host.     

Human mobility patterns predict divergent epidemic dynamics among cities

The epidemic dynamics of infectious diseases vary among cities, but it is unclear how this is caused by patterns of infectious contact among individuals. Here, we ask whether systematic differences in human mobility patterns are sufficient to cause inter-city variation in epidemic dynamics for infectious diseases spread by casual contact between hosts. We analyse census data on the mobility patterns of every full-time worker in 48 Canadian cities, finding a power-law relationship between population size and the level of organization in mobility patterns, where in larger cities, a greater fraction of workers travel to work in a few focal locations. Similarly sized cities also vary in the level of organization in their mobility patterns, equivalent on average to the variation expected from a 2.64-fold change in population size. Systematic variation in mobility patterns is sufficient to cause significant differences among cities in infectious disease dynamics—even among cities of the same size—according to an individual-based model of airborne pathogen transmission parametrized with the mobility data. This suggests that differences among cities in host contact patterns are sufficient to drive differences in infectious disease dynamics and provides a framework for testing the effects of host mobility patterns in city-level disease data.     

Effect of plant barriers and citrus leaf age on dispersal of Diaphorina citri (Hemiptera: Liviidae)

Studies designed to measure dispersal capacity of Diaphorina citri Kuwayama (Hemiptera: Liviidae) are needed to provide the epidemiological knowledge necessary to improve management of citrus huanglongbing. In this study, a mark–release–recapture technique was used to investigate whether 1) host or non‐host plants of D. citri can act as barriers for dispersing insects and 2) presence or absence of young citrus leaves influence movement of D. citri towards citrus plants. The experimental field consisted of four circular and adjacent areas containing citrus trees, Citrus sinensis (L.) Osbeck cv. ‘Hamlin’, planted in concentric circles at 18, 24 and 30 m from the release centre. Insect activity was monitored by recapturing at each distance using yellow stick traps. Dense plantings of tall non‐host plants of D. citri such as corn had no effect on insect dispersal towards citrus plants when compared to a shorter cover crop such as grass. In contrast, suitable host plants acted as traps decreasing movement of D. citri. Diaphorina citri dispersed at greater speeds in the absence of young leaves reaching 140 m within 6 hours after release, whereas in the presence of young leaves, individuals reached at most 60 m at 1 day after release. Results suggest that D. citri control measures may be more efficient during periods of highest vegetative activity when insects are less active. Moreover, the use of suitable host plants for D. citri as trap plants may be a potential tactic to prevent movement of insects into the crop.     

DNA microarray-based genome comparison of a pathogenic and a nonpathogenic strain of Xylella fastidiosa delineates genes important for bacterial virulence

Xylella fastidiosa is a phytopathogenic bacterium that causes serious diseases in a wide range of economically important crops. Despite extensive comparative analyses of genome sequences of Xylella pathogenic strains from different plant hosts, nonpathogenic strains have not been studied. In this report, we show that X. fastidiosa strain J1a12, associated with citrus variegated chlorosis (CVC), is nonpathogenic when injected into citrus and tobacco plants. Furthermore, a DNA microarray-based comparison of J1a12 with 9a5c, a CVC strain that is highly pathogenic and had its genome completely sequenced, revealed that 14 coding sequences of strain 9a5c are absent or highly divergent in strain J1a12. Among them, we found an arginase and a fimbrial adhesin precursor of type III pilus, which were confirmed to be absent in the nonpathogenic strain by PCR and DNA sequencing. The absence of arginase can be correlated to the inability of J1a12 to multiply in host plants. This enzyme has been recently shown to act as a bacterial survival mechanism by down-regulating host nitric oxide production. The lack of the adhesin precursor gene is in accordance with the less aggregated phenotype observed for J1a12 cells growing in vitro. Thus, the absence of both genes can be associated with the failure of the J1a12 strain to establish and spread in citrus and tobacco plants. These results provide the first detailed comparison between a nonpathogenic strain and a pathogenic strain of X. fastidiosa, constituting an important step towards understanding the molecular basis of the disease.