Michael W. Shaw

Fungicide resistance management principles recommend that farmers avoid splitting the total dose applied of a fungicidal mode of action (MoA) across multiple applications per season (‘dose splitting’). However, dose splitting may sometimes be needed to make another proven resistance management tactic—application in mixture with a different MoA—practically achievable, especially in cases where there are limited MoAs available for disease control. Variable effects of dose splitting on selection for resistance have been observed in field experiments, and its effect on selection for partial resistance in fungal pathogens is not well studied. An improved understanding of whether the effect of dose splitting depends on fungicide properties and the type of fungicide resistance is required. We developed a compartmental epidemiological model of Septoria leaf blotch (STB) ( Zymoseptoria tritici ) to investigate the effect of dose splitting on selection for both complete and partial target‐site and non‐target‐site resistance. To solely measure the effects of dose splitting, we restricted the analysis to solo fungicide application (solo use is not recommended in practice). Our results show variable effects of dose splitting: in general, it increased the selection for both target‐site and non‐target‐site resistance. Within the range of dose–response parameters expected for commercial fungicides, dose splitting increased the selection most for partial resistance mechanisms that result in a reduction in fungicide efficacy at low fungicide concentrations but not at high concentrations. We predict that dose splitting of a succinate dehydrogenase inhibitor (SDHI) fungicide (solo) will increase selection for target‐site and non‐target‐site resistance by between 20% and 35%, respectively.

Ditylenchus gigas Vovlas is the dominant species of Ditylenchus nematode on faba bean in the UK. It is normally reported with Botrytis fabae Sardiña, which causes chocolate spot of faba bean. The aim of the work reported here was to estimate how fast isolated infections of D. gigas may spread spatially and how background infection of the host with B. fabae alters multiplication of D. gigas. Spatial spread in field conditions was measured in plants growing in square grids. After establishment, single plants at the centre of each grid were spray inoculated with D. gigas. In summer 2017, D. gigas spread to a distance of at least 1 m, the edge of each 2 m × 2 m plot. Incidence on shoots decreased very slowly with distance beyond 0.4 m. In a repeat experiment harvested in autumn 2018, D. gigas was detected at distances of up to 160 cm in 4 m × 4 m plots. The yield effect and reproduction rate of D. gigas were measured in glasshouse experiments, alone and following brush inoculation with low (10³) or high (10⁶ conidia/mL) doses of B. fabae. At low doses of D. gigas inoculum multiplied by approximately 75‐fold, with lower rates of multiplication as the inoculum dose increased. The reproduction rate of D. gigas was reduced in plants inoculated with B. fabae, especially at high doses of D. gigas. The reduction was approximately proportional to log (B. fabae dose). Seed yield from inoculated plants decreased approximately in proportion to the logarithms of the initial dose of D. gigas and of B. fabae.

The grey mould pathogen Botrytis cinerea forms systemic associations in some hosts, spreading into plant organs produced a considerable time after initial infection. These infections may have no macroscopic symptoms during much of the hosts' lifetime and are at least partially within the host tissue. The aim of the studies reported here was to locate and visualize these infections at a cellular level in Lactuca sativa (lettuce) and Arabidopsis thaliana . Symptomless but infected plants were produced by dry spore inoculation of plants growing in conditions previously shown to result in fungal spread from the initial inoculation site to newly developing plant organs. Tissue taken from inoculated plants was examined using confocal laser scanning microscopy. Two B . cinerea isolates were used: B05.10 and its GFP‐labelled derivative Bcgfp1‐3. Spore germination on leaf surfaces was followed by development of subcuticular inclusions and plant cell damage in single infected epidermal cells and sometimes a few nearby cells. Sparsely branched long hyphae arose and spread from the inclusions, mostly on the outer surface of the epidermal layer but occasionally below the cuticle or epidermal cells, where further inclusions formed. This was consistent with the pattern in time of recovery of B . cinerea from surface‐sterilized leaf tissue. In the late symptomless phase, mycelium arising from internal fungal inclusions formed mycelial networks on the surface of leaves. Symptomless exterior mycelium grew on the roots in A . thaliana .

Brown rot caused by Monilinia spp. is one of the most important diseases in stone fruits worldwide. Latent infections of fruit by the pathogen often manifest once the fruit is ripe, leading to post-harvest rots. Two microbial strains (Bacillus subtilis -B91 and Aureobasidium pullulans - Y126) have shown antagonistic properties against M. laxa in previous studies. This study assessed the reduction in post-harvest rot of cherry by M. laxa when the two biocontrol (BCAs) strains were applied pre-harvest under field conditions to fruit artificially inoculated with M. laxa. The experiment was carried out for two consecutive years in cherry orchards in Kent. When applied pre-harvest, both strains (B91 and Y126) reduced the incidence of post-harvest rots by 30% - 60%. This promising result helps towards the commercialisation of the two strains, which would reduce reliance on fungicides in commercial cherry production.

The global sustainability agenda is increasing the demand for reduction in inputs into agricultural production while maintaining profitable yield of quality products. Plant diseases are a major constraint for both yield and product quality, but often tools for their control are ineffective or lacking. Biological control using antagonistic microorganisms has long been a subject of research resulting in a wide range of products that are now available and marketed in specific territories around the world. These preparations are often niche products with narrow uses. The research effort is intense both to develop new biological control agents (BCAs) and to obtain knowledge of the mechanisms underlying biological disease control. The prospects for biological control are promising. As a minimum, BCAs supplement other sustainable disease management practices such as disease resistance, and present opportunities for controlling diseases for which other approaches are ineffective or unavailable. We can realistically expect increasing use of BCAs to control crop diseases in ways that will benefit the environment. This review paper arose from a webinar held by the British Society for Plant Pathology as part of the International Year of Plant Heath (IYPH2020), at which many of the 300 participants posed or discussed interesting questions. This review is based on that input and the panel members at the webinar are all included as co‐authors in this review.

BACKGROUND: Myclobutanil is one of the most widely used demethylation inhibitor (DMI) fungicides for the management of apple scab, caused by Venturia inaequalis. Strains of V. inaequalis resistant to myclobutanil have been reported across the world. Tebuconazole, another DMI fungicide, has been proposed as an alternative to myclobutanil, and the extent of cross‐resistance with myclobutanil therefore needs to be evaluated. The sensitivity to tebuconazole and myclobutanil of a total of 40 isolates was determined. Half the isolates came from an isolated orchard which had never been sprayed with fungicides and half from orchards sprayed regularly with myclobutanil, but still with disease control problems. The progeny of a tebuconazole resistant (R) × sensitive (S) V. inaequalis cross were analyzed in order to improve understanding of the genetic control of tebuconazole sensitivity.RESULTS: There is cross‐resistance between myclobutanil and tebuconazole (r = 0.91; P < 0.001). Sensitivity to tebuconazole of the progeny of a R × S cross varied quantitatively in a pattern which implied at least two gene loci differing between the parental strains. In addition, the asymmetric distribution of the sensitivity in the progeny implied possible epistatic effects.CONCLUSION: Resistance to myclobutanil and tebuconazole is strongly correlated. At least two genes are involved in the control of tebuconazole resistance in V. inaequalis.

It is important to understand the likely response of plant pathogens to increased temperatures due to anthropogenic climate change. This includes evolutionary change due to selection on genetically based variation in growth rate with temperature. We attempted to quantify this in two ways. First, radial mycelial growth rates in agar culture were determined for a collection of 44 English isolates of Leptosphaeria maculans and 17 isolates of L. biglobosa , at 14 temperatures. For L. maculans the genotypic variances in four parameters were measured: minimum temperature allowing growth, optimum temperature, growth rate at the optimum temperature, and growth rate at the highest usable temperature, 31.8°C. The standard deviations were 0.068°C, 1.28°C, 0.21 mm/day, and 0.31 mm⋅day ⁻¹ ⋅°C ⁻¹ , respectively. For L. biglobosa , these figures were, respectively: immeasurably small, 1.31°C, 0.053 mm/day, and 0.53 mm⋅day ⁻¹ ⋅°C ⁻¹ . In addition, the incidence and severity of phoma stem canker in planta over a natural growing cycle at four temperatures (16, 20, 24, and 28°C) around the average culture optimum were determined. There was no correlation between in vitro and in planta growth, and the decrease in pathogen measures either side of the optimum temperature was much less for in planta growth than for in vitro growth. We conclude that both pathogens have the capacity to evolve to adapt to changes in environmental conditions, but that predictions of the effect of this adaptation, or estimates of heritability in natural conditions, cannot be made from measurements in vitro.

New invading pathogen strains must compete with endemic pathogen strains to emerge and spread. As disease control measures are often non‐specific, that is, they do not distinguish between strains, applying control not only affects the invading pathogen strain but the endemic as well. We hypothesize that the control of the invasive strain could be compromised due to the non‐specific nature of the control. A spatially explicit model, describing the East African cassava mosaic virus‐Uganda strain (EACMV‐UG) outbreak, is used to evaluate methods of controlling both disease incidence and spread of invading pathogen strains in pathosystems with and without an endemic pathogen strain present. We find that while many newly introduced or intensified control measures (such as resistant cultivars or roguing) decrease the expected incidence, they have the unintended consequence of increasing, or at least not reducing, the speed with which the invasive pathogen spreads geographically. We identify the controls that cause this effect and methods in which these controls may be applied to prevent it. We found that the spatial spread of the invading strain is chiefly governed by the incidence at the wave front. Control can therefore be applied, or intensified, once the wave front has passed without increasing the pathogen's rate of spread. When trade of planting material occurs, it is possible that the planting material is already infected. The only forms of control in this study that reduces the speed of geographic spread, regardless of the presence of an endemic strain, are those that reduce the amount of trade and the distance over which trade takes place. Synthesis and applications. The best control strategy depends on the presence of competing endemic strains. Applying or intensifying the control can slow the rate of spread when absent but increase it if present. Imposing trade restrictions before the epidemic has reached a given area and intensifying other control methods only when the wave front has passed is the most effective way of both slowing down spread and controlling incidence when a competing endemic strain is present and is the safest approach when its presence is unknown.