A Hopland strain of Pierce’s disease survives winters better than a Central Valley strain

MENDOCINO CO., 9/26/2026  — On May 4, 2021, a team of five people spent one day in a vineyard at the Hopland Research and Extension Center, pricking grapevines with a needle. Each vine got two droplets of liquid. Most of those droplets carried the bacteria that cause Pierce’s disease.

Of the 477 vines, 348 were inoculated on purpose. Half got a strain isolated in Hopland. The other half got a strain from Bakersfield, about 310 miles away. The remaining 129 got a mock inoculation, as controls.

Then the researchers watched for three years to see which infections made it through the winter.

The Hopland strain of bacteria did much better. Across two winters, 52% of its infections survived, compared with 12% for the Bakersfield strain. The authors call that a 77% decrease in fitness for the strain from out of town. Monica Donegan, of UC Berkeley’s Department of Environmental Science, Policy, and Management, and colleagues published the study Sept. 16 in the journal Applied and Environmental Microbiology.

Pierce’s disease can kill a grapevine within a few years. The bacterium, Xylella fastidiosa, gets into the vessels that carry a vine’s sap, and between bacterial clumps and the plant’s own defenses, those vessels block up. Sharpshooter insects carry it from vine to vine. The disease has plagued California grapes for more than a century.

Cold is the grapevine’s ally. In colder grape country, an infected vine that sits through a hard enough winter can recover completely, the paper says. Hopland is at the northern edge of where Pierce’s disease occurs in California, with colder winters than the Central Valley.

The field study suggests the Hopland bacteria have adapted to that. “The two Xf strains tested here are both from CA and within the same subspecies, yet showed vastly different outcomes in a colder viticulture region in CA,” the authors wrote.

The trial used 13 varieties grown mainly in the Mediterranean, from Portugal to Italy, and uncommon in California. The vineyard was planted in 2011, so the vines were 10 years old when the trial began.

The research center’s staff ran the vineyard with standard commercial practices, including pesticide sprays against the insects that spread the bacteria. Only one of the 129 control vines ever tested positive, and the authors presume it was inoculated by mistake. They say the negative results in the other 128 indicate no spread within or into the vineyard.

The bacteria also changed while the researchers watched. The team sequenced the genomes of 58 bacterial isolates cultured from the vines. By 2023, 42 of 43 isolates carried mutations in one small cluster of genes, and bacteria descended from both strains had mutations in that same gene cluster. The authors read that as a sign of rapid adaptation in the field.

The other direction

A second study, published online July 15 in the journal Evolutionary Applications, tested strains from both regions in both places.

The team infected potted cabernet sauvignon and ciliegiolo vines in a UC Berkeley greenhouse, then moved them for the winter, about six and a half months, to screened enclosures at either the Hopland research center or the UC Cooperative Extension office in Bakersfield.

Again, the infections from cold-climate Hopland strains were more likely to survive the winter.

But after a mild winter in Bakersfield, vines infected with the Hopland strains had severe symptoms the following season, and some died. In the first of the two runs, 10 of the 31 vines in that group died. The authors describe the Hopland strains as showing “hypervirulence” when moved to a warmer climate.

Their proposed explanation has two parts. Sharpshooters prefer vines that don’t show symptoms, so a strain that kills its vine too fast hurts its own chances of spreading. And a strain from the north may have evolved to grow fast during short warm stretches, building a big enough population to survive a cold winter. The authors say the vines possibly died from excessive bacterial growth.

The authors call that a proposal, and they note the pattern held only partly. The local strains survived winter better in Hopland, but the Bakersfield strains showed no such home advantage in Bakersfield. The field trial also compared just two strains.

Both studies were supported by the California Department of Food and Agriculture.

The researchers argue that many models used to predict where Pierce’s disease will spread account for climate but ignore differences between strains of the bacteria. Telling the strains apart, they wrote, would improve forecasting and inform quarantine decisions.

By their reading, there seems to be minimal risk from warm-climate strains moving north. They see the risk running the other way. An introduction of cold-climate strains to warm areas “may be devastating in the short term,” the Evolutionary Applications paper says, depending on how the bacteria balance harming vines against spreading, and unless they evolve further.