Silverleaf (Chondrostereum purpureum) Effects on Japanese Plum (Prunus salicina).

Silverleaf is an important fungal trunk disease of fruit crops, such as Japanese plum (Prunus salicina). It is known that infection by Chondrostereum purpureum results in discolored wood, "silvered" foliage, and tree decline. However, effects on fruit yield and quality have not been assessed. Therefore, the objectives of this study were to determine C. purpureum pathogenicity on P. salicina and the effects on physiology, fruit yield, and quality, in Chile, in 2019 and 2020. Wood samples from affected plum trees were collected in the Chilean plum productive area. Fungi were isolated by plating wood sections from the necrosis margin on culture media. Morphological and molecular characteristics of the isolates corresponded to C. purpureum (98%). Representative isolates were inoculated from healthy plum plants and after 65-d incubation, wood necrotic lesions and silver leaves were visible. Fungi were reisolated, fulfilling Koch's postulates. To determine Silverleaf effects, xylem water potential and fruit yield and quality were measured in healthy and Silverleaf-diseased plum trees 'Angeleno'. Water potential was altered in diseased trees, and fruit yield was reduced by 51% (2019) and by 41% (2020) compared to fruit from healthy trees. Moreover, cover-colour, equatorial-diameter, and weight were reduced, and fruit were softer, failing to meet the criteria to be properly commercialized and exported to demanding markets.

Overwintering Diseased Plant Parts and Newly Infected Flowers and Fruit as Sources of Inoculum for Colletotrichum acutatum in Sour Cherry.

Production of inoculum of Colletotrichum acutatum from both previously infected and overwintered tissue, as well as newly developed plant tissue of sour cherry (Prunus cerasus), was studied in southern Norway. Plant parts were sampled from commercial, private, or research orchards, and incubated for 2 to 14 days (time depended on tissue type) in saturated air at 20°C. In early spring, abundant sporulation was found on scales of overwintered buds and shoots. A mean of 35% infected buds in four cultivars was observed, with a maximum of 72% of the buds infected in one of the samples. Over 3 years, the seasonal production of overwintered fruit and peduncles of cv. Fanal infected the previous year was investigated. In all three years, the infected plant material was placed in the trees throughout the winter and the following growing season; in two of the years, fruit and peduncles were also placed on the ground in the autumn or the following spring. Old fruit and peduncles formed conidia throughout the season, with a peak in May and June. Spore numbers declined over the season, but the decline was more rapid for plant material on the ground than in the trees. On average over 2 years, 68.7, 24.0, or 7.3% of the inoculum came from fruit placed in the trees, placed on the ground in spring, or placed on the ground the preceding autumn, respectively. The number of fruit and peduncles attached to the trees in a planting of cv. Hardangerkirsebær was followed from February to July one year, and although there was a decline over time, fruit and/or their peduncles were still attached in substantial numbers in July, thus illustrating their potential as sources of inoculum. In observations over 2 years in a heavily infected orchard of cv. Stevnsbær, 75 and 47% of flowers and newly emerged fruit, respectively, were infected. Artificially inoculated flowers and fruit produced conidia until harvest, with a peak in mid-July. It may be concluded that previously infected and overwintered, as well as newly emerged tissue of sour cherry, may serve as sources of inoculum of C. acutatum throughout the growing season.

Colletotrichum acutatum Overwinters on Sweet Cherry Buds.

Either naturally infected or artificially inoculated sweet cherry (Prunus avium) buds on fruit spurs (mainly containing generative buds) and on 1-year-old shoots (mainly containing vegetative buds) were examined for presence of Colletotrichum acutatum prior to the beginning of spring growth in each of 4 years. Artificial inoculations were made during the growing seasons preceding the bud sampling. The plant material was incubated moist for either 14 (fruit spurs) or 21 (1-year-old shoots) days at 20°C. Following moist incubation at 20°C, C. acutatum frequently sporulated on buds of fruit spurs and shoots. The fungus sporulated in orange, short-thread or hornlike structures, mainly on distal parts of the buds, and was usually easily visible with the unaided eye. The incidence of infected buds on naturally infected and inoculated fruit spurs was 2 to 80% and 38 to 79%, respectively. Incidence on naturally infected and inoculated shoots was 0 to 53% and 4 to 45%, respectively. On buds within fruit spurs, the incidence of C. acutatum was significantly higher on generative than on vegetative buds. This investigation shows that buds can host C. acutatum and thus are likely to be an important source of primary inoculum for anthracnose of sweet cherry.

Use of a Plastic Rain Shield Reduces Fruit Decay and Need for Fungicides in Sweet Cherry.

It has been shown previously that covering sweet cherry trees (Prunus avium L.) with rain shields made of polyethylene or other waterproof, light-transmitting material prior to harvest to prevent fruit cracking will reduce fruit decay by various fungi. In the present work, the effects of extending the covering period on fruit decay, fruit quality, and the potential reduction in number of fungicide applications were investigated. In six of eight trials, there were significant reductions in fruit decay in covered fruit compared with fruit that were not covered. The most prevalent fruit-decaying fungi were Monilinia laxa and Botrytis cinerea. Mucor piriformis and Colletotrichum gloeosporioides occurred in high amounts in one trial each. The treatments included covering during rain periods until harvest was over from (i) bloom (bloom-cover), (ii) 6 to 7 weeks prior to harvest (early-fruit-cover), (iii) 3 to 4 weeks prior to harvest (late-fruit-cover), and (iv) not covered. In two trials, the number of fungicide applications was similar between different covering times (bloom-cover not included), and in one trial no fungicides were applied at all (all treatments included). There was a significant effect of covering on fruit decay in all three trials, but there was no difference between covering 6 to 7 and 3 to 4 weeks prior to harvest. In the sprayed fields, the incidence of decay was 48% in fruit that were not covered compared with from 6 to 11% in covered fruit. In the unsprayed field, covering from bloom resulted in 14% fruit decay compared with 23 to 26% in the other two cover treatments. In five trials, all covering regimes were included, and the number of fungicide applications varied with time of covering. The number of fungicide applications for the different treatments were: bloom-cover, 0; early-fruit-cover, 1 to 4; late-fruit-cover, 2 to 5; uncovered, 3 to 6. The mean incidence of fruit decay at harvest for the five trials (range in parentheses) was 3.4 (2.0 to 4.3), 1.8 (0.4 to 4.0), 3.8 (1.8 to 7.7), and 16.5% (2.5 to 39.7), respectively, for the covering times listed. There were no significant differences in decay after storage (3 to 7 days at 4°C followed by 2 to 4 days at 20°C) among the different covering times in the six experiments where fruit were stored. The results indicate that fungicide applications were not needed if fruit were covered during rainy periods from bloom until the end of harvest, and it was possible to omit 1 fungicide application if the covering period was increased from 3 to 4 weeks to 6 to 7 weeks. The fruit quality was not reduced by increasing the covering period from the normal 3 to 4 weeks in any of the experiments.

Cuticular Fractures Promote Postharvest Fruit Rot in Sweet Cherries.

Preharvest cuticular fractures in sweet cherry fruit have been suggested to facilitate pathogen invasion, and a method to classify the mount of cuticular fracturing into five categories (from 1 = no visible fractures to 5 = severe fracturing) has previously been proposed. Sweet cherry fruit of the four cultivars Early Burlat, Lapins, Van, and Vista were sorted into these five categories of cuticular fracturing and inoculated with conidial suspensions of either Botrytis cinerea or Monilinia laxa. After incubating the fruit at 20°C and 100% relative humidity for 4 to 7 days, they were assessed for visible fungal growth. Due to quiescent infections of M. laxa, fruit treated with B. cinerea developed more brown rot than gray mold. However, a significant linear relation (P < 0.05) between the amount of cuticular fracturing and fungal infections was obtained in five of seven trials with B. cinerea and in two of four trials with M. laxa, indicating that fungal infections in sweet cherry fruit may be facilitated by cuticular fractures. Independent of cultivar and year, a significant linear relation was found between the category of cuticular fracturing and percentage of infected fruit after inoculation with both B. cinerea and M. laxa, and in control fruit (P = 0.0001, 0.0183, and 0.0182, respectively). This is the first report quantifying an increase in fungal infection with increasing amount of cuticular fracturing. The mean difference in fruit rot (%) ± standard deviation among fruit in fracturing categories 1 and 5, expressed as the linear contrast of amount of fruit rot in category 5 minus amount of fruit rot in category 1, was 37.2 ± 7.4 (P = 0.0001), 35.4 ± 11.0 (P = 0.0022), 17.0 ± 6.7 (P = 0.0135), and 29.8 ± 4.7 (P = 0.0001), after treatments with B. cinerea, M. laxa, water control, and for all data pooled, respectively.