Factors affecting the temporal progress of stem canker (Rhizoctonia solani ) on potatoes (Solanum tuberosum)

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1 Plant Pathology (1997) 46, Factors affecting the temporal progress of stem canker (Rhizoctonia solani ) on potatoes (Solanum tuberosum) S. A. SIMONS* and C. A. GILLIGAN Department of Plant Sciences, University of Cambridge, Cambridge CB2 3EA, UK The effects of different densities of tuber-borne inoculum, selected agronomic treatments (date of planting, irrigation and size of seed tubers) and their interactions on the temporal progress of stem canker (Rhizoctonia solani) on potato plants (Solanum tuberosum) were investigated in a multifactorial experiment. Data comprising stem number and the incidence and severity of stem canker from planting until tuber initiation in two consecutive growing seasons were analysed using linear contrasts, quadratic contrasts and the area under the disease progress or host growth curve. Differences in the incidence and severity of stem canker were dominated by the effect of different densities of tuber-borne inoculum. The majority of disease progress curves were nonmonotonic for the incidence and severity of stem canker with a rapid rise in disease up to and a decline thereafter. Most treatments affected the area under the curve and to a lesser extent the average rate of increase in disease. Of the agronomic treatments, later dates of planting and preemergence irrigation reduced the levels of stem canker whereas size of seed tubers did not affect the progress of disease. Little additional information was revealed by scoring for the severity rather than the incidence of stem canker. INTRODUCTION Stem canker (Rhizoctonia solani) occurs on potato plants (Solanum tuberosum ) wherever the crop is grown (Hide et al., 1985). The symptoms appear as dark brown, necrotic lesions on the lower parts of stems and, in severe cases, infection can totally destroy stems causing extensive gaps in the crop (Hide et al., 1973). Numerous attempts have been made to identify the factors that influence the incidence and severity of stem canker on potatoes (Harrison, 1978). Much of this research has concentrated on the severity of disease in progeny tubers (black scurf ) as an indirect assessment of stem canker, despite the reported difficulties in relating stem canker and black scurf (Bogucka, 1983; Hide et al., 1989). Relatively fewer studies have been concerned with investigating the effects of growing conditions on the development of stem canker from planting onwards (Griffith, 1984). These reports are often contradictory; some indicate a close association between the severity of black scurf on seed tubers at planting and the subsequent development of stem canker (Gudmestad et al., * Present address: Depatrment of Agriculture, University of Reading, Gate, Reading RG6 2AT, UK. Accepted 11 April ; Chand & Logan, 1982; Read et al., 1989) whilst others indicate a more variable relationship (Hide et al., 1973; Adams & Hide, 19; Adams et al., 19). There is evidence that the prevailing environmental conditions at the time of planting may be a stronger influence on the development of stem canker than the severity of tuber-borne inoculum on seed tubers (Adams et al.,19). The objectives of the work described in this paper were: (i) to quantify the effect of different densities of tuber-borne inoculum on the incidence and severity of stem canker and (ii) to determine the effects and interactions of agronomic treatments in combination with different densities of tuber-borne inoculum on the shape of the disease progress curves for stem canker from planting until tuber initiation. Agronomic treatments were selected for their ability to produce a contrasting range of environmental conditions with an emphasis on factors expected to affect host growth and/or disease development prior to emergence. Because the effect of agronomic treatments on disease may vary during the course of a growing season, it is important to monitor disease at regular times throughout a growing season as individual or infrequent assessments of disease may fail to detect significant treatment effects (Werker & Gilligan, 199). In this paper, observations of stem canker

2 Temporal progress of stem canker 643 were made on six occasions during each of two consecutive growing seasons. The effects of density of tuber-borne inoculum, selected agronomic treatments and their interactions on the temporal progress of stem canker are analysed using contrasts to describe the area under disease progress or host growth curve and the rates of disease progress or stem production. METHODS Experimental design A multifactorial experiment was carried out over two consecutive growing seasons at Cambridge University Farm in order to investigate the effects of four main treatments; density of tuber-borne inoculum, date of planting, size of seed tubers and pre-emergence irrigation, as well as the interaction of these factors with the effect of season, on the development of stem canker on the potato variety, Estima. The experiment comprised a randomized block design consisting of 48 plots arranged in two blocks according to variation in the experimental site. The soil-type was a sandy loam with a ph of 7. 5 and a relatively high density of R. solani, i.e. 336 out of 4 soil samples collected prior to planting using a pellet soil-sampler (Henis et al., 1978) were infested with R. solani. The seed tubers consisted of untreated, certified Scottish elite grade seed. Prior to planting, seed tubers were inoculated with contrasting dilutions (high and low) of a sludge containing chopped potato-soil inoculum of R. solani, prepared according to the method described by (Ko & Hora, 1971) as modified by (Benson & Baker, 1974). The isolate of R. solani (anastomosis group 3), originally from a stem canker lesion on the potato variety King Edward, was kindly supplied by Dr G. A. Hide. Samples of inoculum were tested for colonization by R. solani and for absence of contamination by plating out on potato dextrose agar prior to inoculation for each date of planting in each season. In all of the samples tested, the number of propagules of R. solani per g of undiluted chopped potato-soil inoculum was >5. The high density (1%) of inoculum used was undiluted while the lower density (1%) was diluted 1:9 with sterilized, noninfected chopped potato-soil. A sludge was produced by the addition of % distilled water to the dried chopped potato-soil inoculum (v/v). Seed tubers were coated with the sludge and left to drain and air-dry for 1 day before planting. Three dates of planting were selected to provide contrasting growing conditions. In the first season (1987), planting took place on 22 April, 14 May and 1 June. Slightly drier conditions in the following season (1988) allowed earlier dates of planting on the 12 April, 4 May and 26 May. Two sizes of seed tubers were compared: large (75 9 g) and small ( 75 g in 1987 and 3 45 g in 1988). Pre-emergence irrigation was investigated by comparing two levels of irrigation; no irrigation or trickle-irrigating the plots to field capacity from planting until. After planting, irrigation pipes were laid along the ridges of the plots to be irrigated, and all of the plots (irrigated and nonirrigated) were covered with polyethylene sheets so that soil moisture levels were not affected by rainfall. Irrigation was applied daily and adjusted to maintain the soil moisture level at field capacity. Soil water potential was monitored daily at the depth of planting using gypsum blocks and tensiometers. For the nonirrigated plots, the average soil water potential at the time of planting in both seasons was. 6 MPa rising to. 28 mpa at stem emergence in 1987 and. 3 MPa in For the irrigated plots, the average soil water potential at the time of planting in both seasons was. 4 mpa and decreased to. 1 mpa at in 1987 and. mpa in The treatment ended when 9% of the plants at each date of planting had emerged and the polyethylene covers and irrigation pipes were then removed from the plots. Plots were 9 m long and four rows wide with a row spacing of 72 cm. Fertilizer was applied at the recommended rates of 1. 2tha ¹1 of 1% nitrogen, 1% phosphorus, 1% potassium and 4. 5% magnesium together with. 4tha ¹1 of 25% phosphorus and 25% potassium, prior to ridging. Tubers were dibbed by hand into the ridges to a depth of 15 cm and spaced 3 cm apart to give a seed population of 46 plants per ha. After planting and before the polyethylene sheets were laid, the plots were sprayed with paraquat ( Gramoxone ) and terbutryne and terbuthylazine ( Opogard 5L ), at rates of 6 L ha ¹1 and 4 L ha ¹1, respectively, in L ha ¹1 water, using a knapsack sprayer, for the control of pre- and post-emergent weeds. Disease assessment The incidence of R. solani on seed tubers was assessed prior to inoculation. All of the eyes from a subsample of 1 seed tubers were excised, incubated and assessed microscopically for the presence of hyphae of R. solani, using a technique similar to that described by Hide et al. (1968). In each year, the proportion of seed tubers with hyphae of R. solani was less than 5%.

3 644 S. A. Simons & C. A. Gilligan Stem canker was assessed six times during each growing season; five samples were taken at weekly intervals starting 2 weeks after planting for each date of planting, and the sixth sample 4 weeks later, after tuber initiation had occurred. The plants were harvested sequentially from one end of the plot. Each sample consisted of eight plants, two from each of the four adjacent rows. One plant between successive pairs was left to protect the plants for the next disease assessment, to reduce the risk of errors due to compensatory growth. Each sample plant was examined to determine the number of stems, incidence of stem canker (proportion of infected stems per plant) and severity of stem canker on each stem. Stems were assigned a severity score of 1 4 with categories (1) no stem canker; (2) up to one-third of the stem length affected by the lesion; (3) one- to two-thirds of the length affected, and (4) more than two-thirds of the length affected (cf. Adams et al., 19). A weighted estimate of disease severity was computed for each plant as (SX i W i )/(3SX i ) in which X i is the number of stems in each of the four categories and W i takes the values,1,2,3 for i ¼ Three disease variables: incidence of diseased stems (I), a severity score for all stems (S N ) and a severity score for diseased stems (S I ), i.e. with zero classes omitted (Werker & Gilligan, 199), and one host variable: total number of stems (N), were used to quantify the temporal progress of stem canker and to ascertain how the growth of the plant was affected after infection by R. solani. Statistical analysis Three contrast variables were used to summarize the effects of agronomic treatments on disease progress (I, S N,S I ) and host growth (N). These were the area under the curve (AUC), and measures of the average rate of increase (linear) and the degree of curvature (quadratic) for each disease progress or host growth curve. The area under the curve is a measure of the amount of disease or host tissue present over time, which in these analyses is based upon the number of accumulated day-degrees above C relative to the first date of planting, for each of the sample times. The average rate of increase is computed as a linear contrast of the six successive observations for each replicate, reduced to a single value, thereby eliminating the problem of correlated errors associated with repeated observations (Rowell & Walters, 1976). The degree of curvature was similarly computed as a quadratic contrast. Details of computation are given in Werker & Gilligan (199). Each variable was analysed by a factorial analysis of variance (Table 1) in which the total sums of squares were partitioned into block effects, treatment effects, second order interactions between treatment effects and the interaction between season and the second order treatment interactions. Thirdorder and higher interactions and all interactions with blocks were pooled to give the residual sums of squares, on the basis that there was no evidence of nonhomogeneity between the two types of error. Date of planting was the only treatment with more than two levels and for this treatment, the sums of squares were partitioned into linear and quadratic contrasts for correspondingly later dates of planting, based on the accumulated day-degrees above C for the second and third dates of planting relative to the first date of planting. RESULTS Disease progress curves for the incidence and severity (S N ) of stem canker were mostly nonmonotonic with a rapid increase in disease up to and a decline thereafter (Fig. 1). The principal effect of the agronomic treatments was on the vertical displacement of the curves with minor effects on the shape. Density of inoculum in particular had a marked effect on the incidence and severity of stem canker. Substantial amounts of stem canker developed in both seasons on seed tubers treated with the higher density of inoculum (Fig. 1) whereas very low levels of stem canker developed on seed tubers treated with the lower density of inoculum and there was no evidence of any consistent trends in the progress of disease over time. Principal results from analyses of variance for all of the variables under investigation are given in Table 1. Certain interactions were significant because of the dominating effect of inoculum density, however, in the details of treatment effects on individual variables given below, attention is focused on those interactions which were of sufficient magnitude to exhibit epidemiological significance. Stem number The number of stems declined with time in both seasons though the rate of change was negligibly small in 1987 (Fig. 1). All of the agronomic treatments affected stem number to some extent. Inoculum density had only a small effect on the degree of curvature (Table 1) whereas the addition of water in the irrigated plots resulted not only in fewer stems but also a slower rate of decline (Fig. 2). In the

4 Temporal progress of stem canker 645 Table 1 Significant main effects and interactions for the area under the disease progress or host growth curves and linear and quadratic contrasts for the number of stems (N), incidence of stem canker (I), severity of stem canker averaged over all stems (S N ) and severity of stem canker averaged over diseased stems (S I )(P<. 5) Treatment d.f. a auc b lin c quad d Inoculum 1 I,S N,S I I,S N N,I,S N Planting 2 N,I,S N N I,S N Planting lin 1 N,I,S N N I,S N Planting quad 1 I,S N Irrigation 1 N,I,S N N,I,S N N Seedsize 1 N N Season Inoculum 1 I,S N,S I S I Season Planting 2 N,I,S N I,S N S N Season Planting lin 1 N,I,S N I,S N N Season Planting quad 1 S N Inoculum Planting 2 I,S N I,S N Inoculum Planting lin 1 I,S N I Inoculum Planting quad 1 I,S N, S I I,S N Season Irrigation 1 I,S N I,S N Inoculum Irrigation 1 I,S N I,S N Planting Irrigation 2 S I Planting lin Irrigation 1 N Planting quad Irrigation 1 S I Season Seedsize 1 N N Inoculum Seedsize 1 Planting Seedsize 2 S I Planting lin Seedsize 1 I,S N Planting quad Seedsize 1 N,S I Irrigation Seedsize 1 S N I N Season Inoculum Planting 2 I,S N I,S N Season Inoculum Planting lin 1 I,S N I,S N Season Inoculum Planting quad 1 Season Inoculum Irrigation 1 S I N Season Planting Irrigation 2 Season Planting lin Irrigation 1 I,S N Season Planting quad Irrigation 1 Season Inoculum Seedsize 1 N Season Planting Seedsize 2 N Season Planting lin Seedsize 1 N,S I Season Planting quad Seedsize 1 Season Irrigation Seedsize 1 a Error degrees of freedom, 64. b auc, area under the host growth curve for N, and area under the disease progress curve for I, S N and S I. c Linear contrasts. d Quadratic contrasts. absence of irrigation, the approach to the final stem number, after tuber initiation, was more gradual, as indicated by the significant quadratic contrast. More stems developed from the larger seed tubers but the rate of decline in stem number per plant was proportionally faster than from the smaller seed tubers, e.g. from 6. 1to3. 9 with large seed tubers and from 3. 5to2. 7 with small seed tubers. This effect was more pronounced in the second season when the difference in size of seed tubers was greater. Stem number also decreased with later dates of planting but only in the second growing season (1988). Incidence of stem canker Differences in the incidence of stem canker were dominated by the effect of inoculum density (Fig. 1). At the lower density, stem canker did not exceed 1% whereas at the higher density, incidence of

5 I 646 S. A. Simons & C. A. Gilligan 6 (a) Number of stems 5 4 Number of stems 5 4 Severity of stem canker (S ) N Severity of stem canker (S ) 3 2 1, 1,2 (b) 2 2 1, 1,2 (c) 2 2 1, 1,2 1 (d) 2 1, 1,2 I Severity of stem canker (S N ) Severity of stem canker (S ) stem emergence stem emergence 1, 1,2 1, 1,2 1, 1,2 1, 1,2 Fig. 1 Effect of density of tuber-borne inoculum on (a) number of stems, (b) incidence of stem canker, (c) severity of stem canker averaged over all stems (S N ) and (d) severity of stem canker averaged over the number of diseased stems (S I ), in 1987 and 1988: X, low density of inoculum; W, high density of inoculum.

6 Number of stems Temporal progress of stem canker Number of stems , 1,2 2 1, 1,2 Fig. 2 Effect of pre-emergence irrigation on the number of stems in 1987 and 1988: A, no irrigation; B, irrigation to field capacity from planting until. stem canker averaged across seasons ranged from 32. 9% to a maximum of 69. 5% at. All of the other treatments except size of seed tubers also influenced the incidence of stem canker. The effects were most pronounced in the second growing season when disease incidence was considerably higher (Figs 1, 3 and 4). Shortage of water in plots which were not irrigated increased both the incidence (Fig. 3) and linear rate of increase in stem canker. Delayed planting reduced the amount of disease in 1987 but did not affect the average rate of increase or the degree of curvature of the disease progress curves. This effect was repeated for the two later dates of planting in 1988 (Fig. 4). Severity of stem canker (S N ) (averaged over the total number of stems) The shapes of the disease progress curves for, and the effects of treatments on, the severity of stem canker (S N ) were similar to those for the incidence of stem canker (Fig. 1), i.e. the severity of stem canker increased until and thereafter decreased. Thus, significant effects on incidence were almost always matched by significant effects on S N (Table 1) and differences in the severity of stem canker were dominated by the effect of density of inoculum (Fig. 1). Effects on disease severity (S N ) due to delayed planting and irrigation were also similar to those shown in Figs 2 and 3 for disease incidence , 1, , 1,2 Fig. 3 Effect of pre-emergence irrigation on the incidence of stem canker at the higher density of inoculum in 1987 and 1988: A, no irrigation; B, irrigation to field capacity from planting until.

7 648 S. A. Simons & C. A. Gilligan , 1, , 1,2 Fig. 4 Effect of date of planting on the incidence of stem canker at the higher density of inoculum in 1987 and 1988:X, first date of planting; P, second date of planting; B, third date of planting. Severity of stem canker (S I ) (averaged over the number of diseased stems) Trends in the severity of stem canker averaged over diseased stems (S I ) were highly variable suggesting that the multiplication of stem canker on plants within treatments was not consistent over time (see Fig. 1). This variable is therefore not considered to be a sensitive indicator of disease progress or effects of treatments. DISCUSSION The results from this experiment provide clear evidence for the importance of tuber-borne inoculum of R. solani in the development of stem canker on S. tuberosum. In plants inoculated with the lower density of inoculum (1%), development of stem canker was negligible. This finding is in agreement with earlier reports by James & McKenzie (1972), who suggest that when seed tubers have a 5 15% cover by sclerotia, significant levels of stem canker are not usually observed. In contrast, at the higher density of inoculum, the incidence and severity of stem canker were extremely high. Infection of the young stems was also observed to delay plant emergence, and occasionally, plants did not emerge at all, resulting in gaps. These gaps are usually compensated for by neighbouring plants (Hirst et al., 1973), although changes in the distribution of stems and hence stolons, could ultimately affect the number of sites on which progeny tubers could be formed. A particularly striking feature of the disease progress curves associated with the higher density of inoculum was that the incidence and severity of stem canker did not increase after. Van Emden (1965) first proposed the hypothesis that potato stems become resistant to infection by R. solani upon emergence. The nature of this resistance is not understood though it may be a consequence of the switch to autotrophic nutrition at emergence (Hide et al., 1985). The onset of host resistance at should, however, lead only to a plateau in the disease progress curve rather than to the observed decline. Given that the net number of stems declines with time, it may be inferred that the apparent reduction in stem canker after emergence is due to a net loss of diseased stems. Such loss is due primarily to the death of severely diseased stems, however, the decline in disease incidence may also be augmented by a relatively small production of late-emerging, healthy stems. Variation in the shape of the disease progress and host growth curves highlights the importance of comparing treatments at more than one time. Three variables were used to summarize the dynamic features of the disease progress curves. The area under the curve provided a summary of the integral amount of disease over time. Differences in the area under the curve reflect displacement in the average amount of disease or host variable by a treatment. Linear contrasts were used to summarize the average rate of disease progress and quadratic contrasts to describe the degree of curvature of the curves. In practice, most treatments affected the area under the curve, and to a lesser extent, the average rate of increase in disease or host growth whereas relatively few treatments were shown to affect the degree of curvature. Nonlinear models have frequently been used to

8 Temporal progress of stem canker 649 describe the progress of disease. We describe elsewhere the use of nonlinear models to analyse the progress of stem canker disease (Gilligan et al., 1997). Precise estimation of parameters in these models usually requires substantial numbers of observations on the disease progress curve. These models can be used to compare disease progress curves (Gilligan, 199; Gilligan et al., 1997) but techniques for the comparison of parameters in factorial experiments, in which many curves have to be compared, are not well defined because of problems of convergence and interpretation (Gilligan, 1994). The contrast variables used to describe the progress of disease and host growth in this experiment offered greater flexibility than standard analyses of factorial experiments. Nonlinear models have the advantage of having easily interpretable parameters that define processes with clear biological meaning such as intrinsic rates of growth or carrying capacities. Although polynomial contrasts are not as biologically meaningful as many nonlinear parameters, they do provide useful descriptions of the disease progress curves in certain circumstances, particularly where there are large numbers of factorial treatments. Of the three agronomic treatments, only size of seed tubers did not affect the progress of disease. Irrigation resulted in less disease in both seasons as well as an unexpected reduction in the number of stems per plant. This effect was particularly pronounced in 1988 when the soil water potential prior to emergence in the non-irrigated plots was markedly higher than in Most reports suggest that wet soil conditions after planting favour the pathogen (Schaal, 1935; Frank & Leach, 19). However, this experiment supports alternative findings of Clarke & Martin (1935) and Hide et al. (1985) which suggest that stem canker is more severe in dry than in moist soil. The reduction in stem number under moist conditions appears to be unrelated to the incidence of stem canker, although the role of other pathogenic microorganisms in reducing stem number under such moist conditions remains to be ascertained. Biological mechanisms involved in the effect of different dates of planting are more difficult to define although the treatment does provide a good starting point for comparing the influences of soil temperature and moisture on levels of disease in the field. In this experiment, later dates of planting tended to reduce the amounts of stem canker (cf. Schaal, 1935) but the results were variable across seasons (Fig. 4). In 1987, soil temperatures prior to emergence increased with later dates of planting. Thus, the incidence and severity of stem canker decreased as soil temperatures increased. This effect was repeated at the second and third dates of planting in 1988 when overall soil temperatures prior to emergence tended to be lower than in At the first date of planting in 1988, however, the temperature of the soil was substantially higher than in 1987 which could explain the seasonal variation in the effect of date of planting. Similarly, the soil water potential prior to emergence increased with later dates of planting but in this experiment, the effect is confounded by the effect of the irrigation treatment in which all plots were either irrigated to field capacity until or kept artificially dry with polyethylene covers until. Before delayed planting or irrigation are recommended as methods to reduce the amount of stem canker, it will be necessary to ensure that there is a concomitant decrease in black scurf on progeny tubers and that there is no accompanying reduction in yield. On the basis of this experiment, using a severity score for stem canker averaged over the total number of stems (S N ) does not provide much additional information beyond that obtained when only presence or absence of infection is assessed. We conclude therefore that scoring for the severity of infection is unnecessary in studies which are designed to investigate the effect of environmental conditions on stem canker. The increased efficiency of scoring plants for presence or absence of infection also has practical implications in terms of the number of plants which can be sampled at any one time. Sample variation is probably the biggest single obstacle to forecasting this disease (Adams et al., 1985) and increasing the sample size is one possible way to reduce sample variation. Perhaps the easiest way to achieve this is to simplify the system used for scoring the disease. Werker & Gilligan (199) argued that conventional estimates of disease severity, in which the number of healthy stems is included, confounds the incidence of disease (i.e. presence or absence) with the multiplication of disease on an infected plant. They showed that separation of disease severity into a score for the severity of disease averaged over the number of diseased stems (S I ) enabled a more precise estimate of the effect of treatments on the multiplication of the take-all disease on wheat. That we were not able to show this with stem canker suggests that multiplication of disease on infected stems is highly variable. ACKNOWLEDGEMENTS Funding for S.S. was provided by a Postgraduate Studentship from the Potato Marketing Board.

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