Most X. fastidiosa-related diseases appear as marginal leaf necrosis and scorching of the leaves. In the case of PD, X. fastidiosa can also cause desiccation of berries (termed 'raisining'), irregular periderm development and abnormal abscission of petioles. In olive trees affected with OQDS, leaves exhibit marginal necrosis and defoliation, and overall tree decline occurs. Plants with ALS and OLS also exhibit the characteristic leaf scorch symptoms. Not all X. fastidiosa-related diseases exhibit the typical leaf scorch symptoms. These include CVC and Phony Peach disease, amongst others. In the case of CVC, symptoms include foliar wilt and interveinal chlorosis on the upper surfaces of the leaves (similar to zinc deficiency), which correspond to necrotic, gum-like regions on the undersides of the leaves. Additional symptoms of CVC include defoliation, dieback and hardening of fruits. Plants infected with Phony Peach disease exhibit a denser, more compact canopy (as a result of shortened internodes, darker green leaves and delayed leaf senescence), premature bloom and reduced fruit size. Some occlusions occur in the xylem vessels, but there are no foliar wilting, chlorosis or necrosis symptoms . USEFUL WEBSITES: http://www.piercesdisease.org/; https://pubmlst.org/xfastidiosa/; http://www.xylella.lncc.br/; https://nature.berkeley.edu/xylella/; https://ec.europa.eu/food/plant/plant_health_biosecurity/legislation/emergency_measures/xylella-fastidiosa_en.

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Xylella fastidiosa is a gram-negative bacterium that causes Pierce’s disease (PD) in grapevine. X. fastidiosa is xylem-limited and interfaces primarily with pit membranes (PMs) that separate xylem vessels from one another and from adjacent xylem parenchyma cells. PMs are composed of both pectic and cellulosic substrates, and dissolution of PMs is facilitated by X. fastidiosa cell wall-degrading enzymes. A polygalacturonase, which hydrolyzes the pectin component of PMs, is required for both movement and pathogenicity in grapevines. Here, we demonstrate that two X. fastidiosa β-1,4-endoglucanases (EGases), EngXCA1 and EngXCA2, also play a role in how X. fastidiosa interfaces with grapevine PMs. The loss of EngXCA1 and EngXCA2 in tandem reduces both X. fastidiosa virulence and population size and slows the rate of PD symptom development and progression. Moreover, we demonstrate that single and double EGases mutants alter the rate of PD progression differently in two grapevine cultivars, Cabernet Sauvignon and Chardonnay, and that Chardonnay is significantly more susceptible to PD than Cabernet Sauvignon. Interestingly, we determined that there are quantitative differences in the amount of fucosylated xyloglucans that make up the surface of PMs in these cultivars. Fucosylated xyloglucans are targets of the X. fastidiosa EGases, and xyloglucan abundance could impact PM dissolution and affect PD symptom development. Taken together, these results indicate that X. fastidiosa EGases and the PM carbohydrate composition of different grape cultivars are important factors that influence PD symptom development and progression.

Ralstonia cause wilt diseases by colonizing xylem vessels and disrupting water transport. The dogma is that bacterial biomass clogs vessels and reduces the flow of xylem sap due to Ralstonia abundance. However, the physiological mechanism of xylem disruption during bacterial wilt is untested. Using a tomato and Ralstonia pseudosolanacearum GMI1000 model, we visualized and quantified spatiotemporal dynamics of xylem disruption during bacterial wilt. First, we measured stomatal conductance of leaflets on mock-inoculated and wilt-symptomatic plants. Wilted leaflets had reduced stomatal conductance, as did turgid leaflets on the same petiole as wilted leaflets. Next, we used X-ray microcomputed tomography (X-ray microCT) and light microscopy to differentiate between mechanisms of xylem disruption: blockage by bacterial biomass, blockage by vascular tyloses, or sap displacement by gas embolisms. We imaged intact plant stems to quantify embolized vessels. Embolized vessels were rare, but infected plants with low bacterial populations had a non-significant trend of more vessel embolisms. To test that vessels are clogged during bacterial wilt, we imaged excised stems after brief dehydration. Most vessels in mock-infected plants emptied their contents after excision, but non-conductive clogged vessels were abundant in infected plants by 2 days post infection. At wilt onset when bacterial populations exceeded 5x108 cfu/g stem tissue, approximately half of the vessels were clogged with electron-dense bacterial biomass. We found no evidence of tyloses in X-ray microCT reconstructions or from light microscopy of preserved stems. Therefore, bacterial blockage of vessels appears to be the principal cause of xylem disruption during Ralstonia wilt.

Xylella fastidiosa causes devasting diseases to several critical crops. Because X. fastidiosa colonizes and infects many plant species, it is important to understand whether the genome of X. fastidiosa has genetic determinants that underlie specialization to specific host plants.

This study presents a sensor strip for user-friendly, naked-eye detection of Xylella fasitdiosa, the bacterial causal agent of Pierce's disease in grapevine. This sensor uses anti- X. fastidiosa antibodies conjugated to a polydiacetylene layer on a polyvinylidene fluoride strip to generate specific color transitions and discriminate levels of the pathogen. The detection limit of the sensor is 0.8 × 10 cells/mL, which is similar to bacterial load in grapevine 18 days following bacterial inoculation. This sensor enables equipment-free detection that is highly desirable for in-field diagnostic tools in resource-limited settings.

Plant pathogenic Ralstonia cause wilt diseases by colonizing xylem vessels and disrupting water transport. Due to the abundance of Ralstonia cells in vessels, the dogma is that bacterial biomass clogs vessels and reduces the flow of xylem sap. However, the physiological mechanism of xylem disruption during bacterial wilt disease is untested. Using a tomato and Ralstonia pseudosolanacearum GMI1000 model, we visualized and quantified the spatiotemporal dynamics of xylem disruption during bacterial wilt disease. First, we measured stomatal conductance of leaflets on mock-inoculated and wilt-symptomatic plants. Wilted leaflets had reduced stomatal conductance, as did turgid leaflets located on the same petiole as wilted leaflets. Next, we used X-ray microcomputed tomography (X-ray microCT) and light microscopy to differentiate between mechanisms of xylem disruption: blockage by bacterial biomass, blockage by vascular tyloses, or sap displacement by gas embolisms. We imaged stems on plants with intact roots and leaves to quantify embolized vessels. Embolized vessels were rare, but there was a slight trend of increased vessel embolisms in infected plants with low bacterial population sizes. To test the hypothesis that vessels are clogged during bacterial wilt, we imaged excised stems after allowing the sap to evaporate during a brief dehydration. Most xylem vessels in mock-infected plants emptied their contents after excision, but non-conductive clogged vessels were abundant in infected plants by 2 days post infection. At wilt onset when bacterial populations exceeded 5x108 cfu/g stem tissue, approximately half of the xylem vessels were clogged with electron-dense bacterial biomass. We found no evidence of tyloses in the X-ray microCT reconstructions or light microscopy on the preserved stems. Bacterial blockage of vessels appears to be the principal cause of vascular disruption during Ralstonia wilt.