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THE TRUTH IS OUT THERE: X-DISEASE IN PEACHES AND CHERRIES

(Dave Rosenberger dar22@cornell.edu, Plant Pathology, Highland)

X-disease is causing continued losses in some stone fruit orchards in the Hudson Valley. X-disease often follows a 10—15 year cycle in which extensive losses over a 4 to 6 year period are followed by a gradual decline in disease incidence until the next cycle begins. The reason for this cyclical pattern has never been determined. A significant increase in X-disease was noted in the Hudson Valley in 1997, and losses mounted in 1998 and 1999. The incidence of new X-disease infections may remain high for several more years before the current cycle reaches its zenith.

A general description of X-disease epidemiology and the symptoms that it causes was published in Scaffolds Vol. 8, No. 14, 21 June 1999. Most of that background information will not be repeated here. Instead, this article will include a review of some published literature on X-disease transmission and suggested approaches for reducing the spread of X-disease.

X-disease is caused by a phloem-limited mycoplasma-like organism (XMLO) – a minute pathogenic organism smaller than most bacteria. The XMLO is transmitted by at least eight species of leafhoppers found in New York, but two species predominate. Scaphytopius acutus is the most important vector in the Hudson Valley and Connecticut. Paraphelpsius irroratus ranks a close second. In Michigan, the relative importance of the two species is reversed. (White apple leafhopper, rose leafhopper, and potato leafhopper are not vectors.) X-disease vectors acquire the XMLO while feeding on diseased chokecherry bushes, on infected sweet cherry trees, or on wild seedlings of sweet cherry. They may also acquire XMLO from some broadleaf weeds and grasses, although the importance of weeds in X-disease epidemiology remains unclear. In eastern United States, vectors do NOT acquire the XMLO from diseased peaches, probably because the titer of the disease organism within diseased peach trees is so low that leafhoppers do not encounter the organisms while feeding.

After leafhopper vectors feed on an infected plant, the X-disease organism must grow within the insect for at least 20 days before the insect can transmit X-disease to another plant. Once that 25-day incubation period is completed, however, the leafhoppers with X-disease remain infective for the rest of their lives. In laboratory studies, leafhoppers have often lived for 30—40 days after they become infective. A single infective insect therefore has the potential to infect numerous plants.

In work completed in Connecticut in the late 1970's, McClure (1980a) showed that S. acutus prefers to feed and breed on red clover, strawberry, blackberry and multiflora rose rather than on peach or chokecherry. S. acutus neither fed nor laid eggs on orchard grass. Adult S. acutus apparently move into peach trees from the ground cover or from border areas rather than completing their full life cycle on peaches. McClure (1980b) also showed that the total numbers of adult X-disease vectors in peach trees was dependent on the kind of groundcover in the orchard. Vector populations were at least 50% lower in peach orchards that had a pure grass groundcover than in peach orchards that contained herbaceous host plants for the leafhoppers.

In Michigan, Larsen and Whalon (1987) showed that the vector P. irroratus moves from ground cover into stone fruit trees at dusk, then returns to the ground cover at dawn. P. irroratus breeds on grasses in the ground cover. Nymphs feed on grass stems just above the soil line and therefore often escape exposure to insecticide sprays applied to orchard trees. Both P. irroratus and S. acutus have two generations per year with adult populations peaking in July and again in September.

The role of herbaceous weeds in X-disease epidemiology remains uncertain. Chiykowski and Sinha (1982) conducted greenhouse studies with caged leafhoppers. They showed that P. irroratus could transmit XMLO both to and from ragweed, lambsquarter, black mustard, red clover, Ladino clover, birdsfoot trefoil, narrow-leaf plantain, and several other herbaceous plant species. However, the importance of these potential weed hosts in field spread of X-disease remains undocumented. McClure (1980b) reported that spread of X-disease was lower in orchards that did not have broadleaf weeds, but that difference may be been attributable solely to loss of habitat for vector reproduction.

Researchers in California studied the spread of X-disease in sweet cherry orchards from 1986 to 1990 to determine how removal of diseased trees and use of residual insecticides to control vectors would affect spread of X-disease (VanSteenwyk 1995). They found that removal of diseased trees as soon as infections were identified was the best way to slow spread of the disease. Removal of diseased cherry trees accounted for 75—84% of the reduction in disease spread, whereas insecticide treatment to kill vectors accounted for only about 7% of the reduction. The strain of XMLO in California is slightly different from that in eastern United States, and vector species and orchard ecology (irrigated versus non-irrigated) also differ between the two areas. However, the California work suggests that vector control alone will not provide good control of X-disease in sweet cherries.

The published literature on X-disease leaves many practical questions unanswered. Again, management decisions must be made based on "educated guesses" derived from published studies. I suggest that stone fruit growers in regions of the eastern United States where X-disease is a problem consider the following strategies to minimize losses to X-disease:

1. The most effective protection against X-disease is to isolate peach plantings and new cherry plantings from all of the known woody hosts for X-disease. Woody hosts that can contribute inoculum include older blocks of sweet cherries and tart cherries, as well as chokecherries and volunteer Mazzard seedling trees that may grow in hedgerows. A single infected chokecherry or Mazzard seedling within 500 ft of a young orchard can contribute enough inoculum to cause major losses.

2. The role of broadleaf weeds in X-disease epidemiology remains uncertain. However, weeds have been implicated both as host plants for reproduction of vectors and as potential inoculum sources of the XMLO. Controlling these weeds is relatively inexpensive. Postharvest applications of 2,4-D herbicide to the row middles will eliminate most broadleaf weeds. (In sweet cherries, this application should be made as soon as possible after harvest to eliminate broadleaf weeds before the second generation of vectors matures in September.) Because broad-leaved weeds are the preferred hosts for the S. acutus vector, killing weed hosts with 2,4-D could possibly stimulate movement of vectors into the trees and thereby contribute to the further spread of X-disease. To avoid that possibility, an insecticide that is effective for controlling leafhoppers should probably be applied at the same time that the 2,4-D is applied.

3. Infected cherry trees should be removed as soon as definite X-disease symptoms are noted. This may be difficult with cultivars of cherry that do not produce distinct symptoms. However, failure to remove infected cherries almost guarantees a continuation of the epidemic.

4. In regions where X-disease is endemic, cherry growers may need to consider propagating cherry trees with Mahaleb stem pieces. When sweet cherry trees propagated on Mahaleb rootstock become infected with X-disease, the scion variety dies back to the graft union within about a year after they are inoculated. This occurs because the Mahaleb rootstock is hypersensitive to the XMLO. In California, some sweet cherry growers have used high-budded trees on Mahaleb rootstock. A separate scion bud is used to generate each scaffold limb. In these trees, X-disease in a single scaffold caused death of that scaffold without causing infection or loss of the entire tree.

Sweet cherry trees on Mahaleb rootstock do not perform well in many of our soils. However, it might be possible to use a 12—20-inch Mahaleb stem piece with multiple buds of the scion variety to create sweet cherry trees in which X-disease would be self-eradicating. This approach would be particularly useful for eliminating X-disease from sweet cherry cultivars that produce indistinct symptoms. Propagating multi-piece trees might be cumbersome, but it deserves further research because growers can ill afford to lose young cherry blocks to X-disease just as these trees are coming into production.

In all probability, no single approach will ever provide adequate control of X-disease. An integrated approach that combines all or most of the actions suggested above may be the only effective way to reduce losses to X-disease in the Hudson Valley.

Literature cited:

> 7.10 Insects