Report of Cherry X-Disease Phytoplasma in the Northern San Joaquin Valley

Mohamed T. Nouri, UCCE Orchard Systems Advisor, San Joaquin County, Stockton, CA
Cristian Olaya, Postdoctoral Researcher, Department of Plant Pathology, University of California, Davis, CA
Mysore R. Sudarshana, Research Biologist, USDA-ARS, Department of Plant Pathology, University of California, Davis, CA

Survey

In June of 2020, we visited a large cherry orchard in Courtland area of Sacramento County with a severe outbreak of cherry buckskin disease, also known as Western X disease phytoplasma. The orchard is 20 years old and roughly 50 percent of trees appeared to be infected. This is a reminder of how devastating this disease is and how quickly it spreads if growers are not on the lookout for the early symptoms. It seems like a good time to review the details of this disease, which is also very likely still present in San Joaquin County (SJC). Infected cherry trees are the most important source of inoculum for the spread of the disease in California. We are working closely with the grower, and providing information on symptoms, scouting, sampling best management practices (see below) to slow of the spread of the disease. We have also informed other neighboring cherry growers and PCAs about the disease because this problem requires community-wide monitoring and management for successful long-term suppression.

Background

Western X disease is caused by a phytoplasma that is spread by leafhoppers. There were major outbreaks in SJC as early as the 1970s. It was brought slowly under control, thanks to a joint research and outreach effort by the University of California and cherry industry to identify the causal agent, vectors, and successful management strategies. Today, we can see the results of diligent management efforts over the past few decades: though still present and the threat of re-infection is still present, it is rarely encountered and no longer the threat it once was to the cherry industry. In the Pacific northwest cherry orchards, there is now a significant outbreak of what they are calling “little cherry” due partly to X-disease as well as two other viruses that frequently occur together.

Cherry X disease Symptoms

Symptoms of X-disease phytoplasma on sweet cherry trees depend on the rootstock. Cherries on Mahaleb rootstock develop different symptoms than cherries on Colt and Mazzard.

On Mazzard or Colt, infection reduces fruit size and quality. Fruits from X-disease infected trees generally have a bitter taste, are small, and color up later (if at all) than fruit on healthy limbs and trees. The fruits are also more pointed and have a shorter stem than normal fruits (Fig. 1A and B). They are unmarketable.  Fruit symptoms of buckskin disease can be confused with those of cherry crinkle leaf and deep suture (Fig. 2).

The best time to scout for trees with such symptoms is in the week or two prior to harvest. Leaves are often smaller than normal with “wavy” margins (Fig. 1C), but these symptoms have other causes and are not a good diagnostic indicator. Foliage symptoms are not obvious in the early infection years. Only a single branch may show symptoms the first year after infection with more branches exhibiting symptoms in subsequent years, which can make disease diagnosis difficult at early stage of the infection. Trees decline over a period of several years. Symptoms may progress as follow:

• Early infection (Year 1): small fruit may be restricted to one branch or cluster, fruit color may develop normally or individual pale fruit may be observed.

• Middle infection (Years 2-3): small fruit observed on multiple or all limbs, and poor color development is pronounced.

• Terminal infection (Years 3-5), characterized by reduced fruit yield, and dieback of limbs.

 Until trees die, they are a potent source of infection for other trees.

On Mahaleb rootstock, tree will die late in the season that they become infected, or early in the following season. Symptoms similar to Phytophthora crown and root rot, Armillaria root rot, or rodent damage can be seen: Leaves are of normal size, but develop a yellow hue, turning bronze to dead as the season progresses. Trees exhibit a sudden decline as a result of a hypersensitive reaction at the graft union. Fruit symptoms do not develop on Mahaleb-rooted trees. In high-worked trees on Mahaleb, only infected scaffold branches develop these symptoms. Another diagnostic feature that can sometimes be seen is a pitting and grooving of wood – somewhat resembling a zipper – under the bark at the graft union. This symptom is different from pits, which develop in the wood of cherry stem pitting infected trees (Fig. 3).

 Causal Organism: Western X Phytoplasma

Western X is not a virus. It is a special type of bacteria called a phytoplasma. The Western X phytoplasma lives and multiplies in phloem cells in the tree’s vascular system, affecting movement of nutrients. Once a tree is infected, the pathogen multiplies and spreads through the phloem to other parts of the tree. The phytoplasma may cease to replicate or dies in the aerial parts of the tree as it goes dormant in winter; surviving phytoplasma overwinters in the roots (except for Mahaleb rootstock). The aerial portions of the tree become re-infected in the spring, as the phytoplasma moves up through the phloem of the tree. On Mazzard and Colt, removing symptomatic branches does not eliminate the phytoplasma since it is already in the root system.

Transmission

Vector: Leafhoppers

The most significant sources of infection in cherry orchards is the tree-to-tree spread of the phytoplasma by insect vectors. The only known vectors of the X-disease phytoplasma are phloem-feeding species of leafhoppers. The most important vectors of buckskin in cherry in California are:

• The cherry leafhopper (Flor’s leafhopper, Fieberiella florii). It thrives on cherries (favored host) and some other woody plants. This leafhopper is considered to be mainly responsible for spreading the phytoplasma from tree to tree within orchards.

• The mountain leafhopper, Colladonus montanus, lives mainly on herbaceous plants and weeds and occasionally feeds on cherries. Mountain leafhopper flies long distances and is thought to be mainly responsible for introducing buckskin disease into cherry orchards from outside rather than spreading it among trees within the orchards

• In Sierra foothill orchards, the leafhopper, Scaphytopius acutus, also appears to be an important vector.

Management Guidelines

Until it dies, a cherry tree that contracts the phytoplasma will remain infected for the rest of its life. Control of this disease requires a community effort because leafhoppers spread it from orchard to orchard. X-disease phytoplasma is still present but generally at low levels in local cherry orchards. Successful management requires a multi-pronged approach. Research in the 1980s and 1990s showed that these must be in combination for effective long-term suppression:

-          Annual surveys: Each year, prior to harvest, systematically inspect orchards on Colt, Mazzard, Gisela, Krymsk or Maxma rootstock for fruit symptoms. For orchards on Mahaleb rootstock, be vigilant throughout the growing season for trees showing leaf symptoms. Examine the graft union of suspect trees for zipper-like grooving and pitting. If X-disease is suspected on any trees, it is possible to confirm a diagnosis further by collecting and submitting samples to a laboratory for a test. If this appears somewhat complicated, you can contact me, your local farm advisor or your PCA for help.

-          Identify and remove diseased trees: Remove infected trees following postharvest treatment for leafhoppers. Infected cherry trees are the most important source of inoculum for the spread of the disease. On high grafted Mahaleb rootstocks, remove the diseased scaffold branches by sawing off below the graft union and then top-work if desired with clean scion wood. Low-grafted trees on Mahaleb or other susceptible cherry rootstocks should be completely removed.

-          Monitor and manage leafhopper vectors: If you have the disease in your own or a nearby orchard, implement a spray program. Between harvest time and leaf fall, leafhopper populations and X-disease phytoplasma concentration in the tree are higher than at other times. See sections of UC IPM on Cherry Leafhopper and Mountain Leafhopper for more information about postharvest treatment of the orchard for leafhopper vectors. Rotate leafhopper products when populations are present, and try to maintain an effective insecticide residue in the orchard from July through October. A spray schedule could be every three to four weeks starting after harvest through late October.

-          Control alternative hosts for phytoplasma and the leafhoppers: Several weed species act as an alternative host for phytoplasmas and leafhoppers; these are mainly clovers, dandelion and curly dock, and they should be removed from the orchard floor.

Fig. 1. Symptoms of X-disease phytoplasma in sweet cherry, A and B. Small, light colored and misshapen fruit with short stems, C. Small, pale-green leaves with “wavy” margins.

Fig. 2. Symptoms of cherry crinkle leaf and deep suture: Small, pointed fruit and distorted leaves.

Fig. 3. Symptoms of pits and grooves at the graft union in cherry wood on Mahaleb rootstock caused by X-disease phytoplasma.