Phomopsis viticola (Phomopsis cane and leaf spot)

The distinctive symptoms commonly attributed to Phomopsis cane and leaf spot on grapevine include dark fissure-like lesions on canes, bleaching of canes and small dark spots on leaves that are surrounded by yellow halos (Pine, 1959; Taylor and Mabbitt, 1961; Hewitt and Pearson, 1988). The strain recognized in Australia as Taxon 2 produces the severe symptoms attributed to P. viticola in other regions of the world, whereas the other strain common in Australia, Taxon 1, does not. Both taxa are considered here.Symptoms in springLeaf symptoms appear in spring on lower leaves of shoots and consist of small dark brown spots, usually less than 1 mm in diameter, surrounded by a 2-3 mm yellow halo (Taylor and Mabbitt, 1961; Hewitt and Pearson, 1988). The leaves can be distorted and parts of leaves are killed when the spots are numerous (Taylor and Mabbitt, 1961; Creecy and Emmett, 1990). Spots that become necrotic darken and drop out, giving the leaves a 'shot-hole' appearance (Hewitt and Pearson, 1988). Affected leaves, particularly those with spots on their petioles, can turn yellow and abscise (Bugaret, 1990; Creecy and Emmett, 1990). Severely affected basal leaves may also be stunted (Emmett et al., 1992a).The first evidence of Phomopsis infection on emerging shoots is small spots with black centres. They usually occur on the basal portion of the shoots (Taylor and Mabbitt, 1961; Moller et al., 1981) within 15 days of bud opening and growth is often inhibited (Bugaret, 1990). Similar spots may appear on the flower cluster stems and if badly infected, the clusters wither (Moller et al., 1981; Creecy and Emmett, 1990), may become necrotic, dry and fall off (Gärtel, 1972; Hewitt and Pearson, 1988).No symptoms are observed with Taxon 1 infection although budburst may be reduced and ascomata have been observed on unburst buds (Whisson and Brant, 1998).Symptoms in summerLesions on the shoots expand and elongate and the epidermal layers crack to form black lesions up to 3-6 mm long. Where lesions are numerous, they coalesce, giving a brown-black scabby appearance to parts of the shoots (Taylor and Mabbitt, 1961; Hewitt and Pearson, 1988). The lesions can become up to 5 cm long and 2 cm wide, and their cracked surfaces become roughened as the canes swell and harden (Emmett et al., 1992a). Girdled shoots can fail to mature, or become stunted and die. As infected canes grow and harden, shoot breakage may occur in areas of heavy scabbing and lesion development. Severely scarred shoots may break off at the base or just below the clusters in strong winds or at harvest (Moller et al., 1981; Bugaret, 1990; Emmett et al., 1992a). Occasionally young grapes dry up and fall off, if necrosis spreads as far as their point of attachment (Bugaret, 1990).As the season progresses, the symptoms become obscured by vine growth and leaf cover. Normal leaves develop on subsequent nodes, hiding the distorted basal leaves, so diseased vines may appear normal (Taylor and Mabbitt, 1961; Moller et al., 1981). Cracks in the epidermis and cortex of the shoots tend to heal and become rough as the tissues mature (Hewitt and Pearson, 1988).Taxon 1 infection is asymptomatic, but the shoots may appear weakened or stunted, and may not set bunches (Scheper et al., 1997a).Symptoms in autumn and winterIn cool weather, late in the season, the fruit may become infected by Taxon 1 or Taxon 2. While such infection is rare, it mainly occurs through lesions on the bunch or berry stem, although some particularly susceptible varieties may be infected directly through the skin of the young berry (Hewitt and Pearson, 1988). Usually only isolated bunches are affected, but if rain occurs just before harvest, berries can develop light brown spots which enlarge, darken (Moller et al., 1981; Lal and Arya, 1982) and produce conidiomata through the skin (Bugaret, 1990). These exude yellowish spore masses before finally shrivelling and becoming mummified (Taylor and Mabbitt, 1961; Gärtel, 1972; Moller et al., 1981). Infected berries may abscise from the pedicel, leaving a dry scar (Hewitt and Pearson, 1988).In winter, the conidiomata become prominent in the cortex of diseased 1-year-old canes, spurs, rachis stubs and old tendrils (Hewitt and Pearson, 1988). As the dormant season progresses, the bark of infected canes and spurs bleaches white in the areas between the lesions, particularly round the nodes on the basal portions of the canes, and becomes speckled with tiny black conidiomata (Taylor and Mabbitt, 1961; Moller et al., 1981). Severely infected canes or spurs exhibit irregular dark brown to black patches intermixed with bleached areas. Bleaching appears to be due to the production of numerous conidiomata which lift the epidermal layer, admitting air beneath it (Hewitt and Pearson, 1988). Severely affected canes and spurs are more sensitive to low temperatures than healthy tissue; this can result in extensive killing of the spurs and weakening of the canes (Moller et al., 1981).Taxon 1 infection also exhibits distinctive white or bleached areas during winter, particularly round the nodes, which are speckled with small black conidiomata. No crack-like lesions are observed. Occasionally the bleached areas contain irregular patches delineated by thin black lines. Black spots may be found within this zone, which have been identified as either the conidiomata or ascomata (Merrin et al., 1995; Scheper et al., 1995; 1997b; 1999).

Cultural Control

Resistant grapevine cultivars are not available. In France, only Pinot Meunier is judged to be resistant to Phomopsis (Doazan, 1974).

When establishing new vines, use disease-free budwood, cuttings and rootlings. Infected cane material reduces the rate of success of grafting and cutting propagation, and can allow Phomopsis to become established in a vineyard. If permitted, propagation material can be disinfected with 8-hydroxyquinoline sulphate to avoid introducing P. viticola to new vineyards (Hewitt and Pearson, 1988). Alternatively, hot water treatment (Hamilton, 1997) may be used but is less effective and loss of vine material can occur if the procedure is not followed carefully.

Once the disease has appeared, avoid using diseased canes and spurs to develop vine frameworks. Diseased and dead wood should be removed during pruning, and the material ploughed into the soil, or destroyed by burning (Hewitt and Pearson, 1988; Emmett et al., 1992a) to prevent carry-over of spores into the next season.

Pruning methods may significantly affect the amount of disease present in a vineyard. Cane pruning appears more effective than spur pruning in minimizing the potential for Phomopsis infection or spread, because it removes the basal part of the shoots where Phomopsis most commonly occurs. Avoid hedge pruning and minimal pruning of grapevines, because this generally leaves more wood on the vine than hand-pruning, and the incidence of disease can increase in the next season if the vines are already infected. Dead canes continue to produce inoculum for at least 3 years, increasing the amount of inoculum from year to year (Pscheidt and Pearson, 1989a; Pearson, 1990).

In most years, the economic loss due to Phomopsis infection is minor. However, the fungus has considerable potential to reduce yields where preventive control has been ineffective, or when the disease has remained unidentified over a number of seasons. In years when vineyards are severely infected, losses can occur from reduced vigour of shoots early in the growing season, leading to stunting of grapevines (Bugaret, 1990) and lowering vine productivity by reducing potential bunch numbers. Breakage of the canes at severely scarred regions reduces cluster number and yield and diseased mature berries (Lal and Arya, 1982) should not be harvested. If berries are infected, post-harvest storage in cool temperatures at high humidity can lead to losses. Canes or spurs infected with Phomopsis are prone to frost damage and infection reduces the amount of healthy wood for new shoot growth the following season. The fungus can weaken mature vines and kill grafted and other nursery stock (Hewitt and Pearson, 1988).

In the USA, Pscheidt and Pearson (1989b) reported a total crop loss estimate of 35.7% due to Phomopsis infection of the rachis and subsequent girdling of clusters which caused whole clusters to fall on the ground. This occurred during a 3-year period of successive wet spring weather. Experiments have shown that there is a correlation between disease severity and yield but the effect of chemical treatments on yield is not clear (Cucuzza and Sall, 1982) and depends on the weather, the growth stage of the vine at the time of application, the method of pruning and whether the vines have been pruned or not (Taylor and Mabbitt, 1961; Pscheidt and Pearson, 1989a,b). Although Taxon 1 is commonly found in vineyards in Australia, there has been no clearly documented evidence of loss of yield due to infection.