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A world, where upon waking up, you cannot get that daily dose of caffeine. A world, where you cannot sit in the sun while enjoying a nice glass of wine. Where you do not get enough vitamins, because you cannot drink a nice glass of orange juice. This scenario might seem a bit farfetched, but these crops are all being threatened by one single pathogen: Xylella fastidiosa.

Where It All Began

In 1892, Newton Pierce was researching an epidemic grapevine disease in Southern California, which had huge consequences for the grape industry in that region [1]. Later, this disease became known as Pierce’s disease. At first, it was believed that the causal agent of Pierce’s disease was a virus. It was not until 1978 that they successfully isolated and cultivated this causal agent: a bacterium. They inoculated new grapevine plants which then developed the symptoms of Pierce’s disease. Besides this, they discovered that this pathogenic bacterium was indistinguishable from the bacterial causal agent of almond leaf scorch disease in almonds [2]. In 1987, John Wells isolated 25 strains of this pathogenic bacterium from 10 different diseased plant species: Pierce’s disease of grapevine, periwinkle wilt, phony disease of peach and leaf scorch of almond, plum, elm, sycamore, oak and mulberry. The bacterium was named Xylella fastidiosa [3]. In 2000, X. fastidiosa was the first bacterial plant pathogen to have its complete genome sequenced [4].

Overview of the global spread of X. fastidiosa.
Figure 1: Overview of the global spread of X. fastidiosa. Each dot represents a unique report of an established population.

Small Organism,
Big Consequences

Currently, X. fastidiosa is present all over the globe, as can be seen on the map in Figure 1. In South America, Argentina, Brazil and Venezuela economically important crops are infected with X. fastidiosa, while in North- and Central America the pathogen is present in the United States, Canada, Mexico, Puerto Rico and Costa Rica. In Asia, the bacterium has been found in Taiwan and Iran. Since 2013, the bacterium is present in Europe, mainly the Puglia region of Italy is infected. Since then, X. fastidiosa also has been found in parts of France, Spain and Portugal [5]. The spread of X. fastidiosa in Southern Europe can be seen in the map in Figure 2.

X. fastidiosa infections can have big consequences. When X. fastidiosa is detected in a plant, all possible host plants are eradicated in a 100-meter radius. On top of this, a restricted zone with a 5 km radius is instated, in which no host plants when eradication is needed can be traded for 5 years. This means that a farmer cannot sell or trade any of his crops for five years, which often results in bankruptcy. More importantly, when containment measures are taken, this buffer zone can be expanded up to 10 km in radius [6].

The spread X. fastidiosa in Europe.
Figure 2: Spread of X. fastidiosa in Europe. Each dot represents a unique report of an established population.

The X. fastidiosa strain currently present in Europe is X. fastidiosa pauca, which can infect olive trees, but not grapevines. That is why the most measures and regulations against X. fastidiosa are being taken towards olive trees and not towards grapevines. However, if grapevines in Europe also get infected by X. fastidiosa, the same measures will be taken towards grapevines.

Economic and Cultural Impact

Infections with X. fastidiosa can result in big losses. In 2014 alone, X. fastidiosa cost the State of California approximately 104 million dollar, both due to research into X. fastidiosa and as a result of the disease itself [7]. In Italy, the farmers' organization Coldiretti has reported that 21 million trees are infected by to X. fastidiosa, which has led to damages for the Italian olive-oil producers of up to €1.2 billion. The Puglia region in Italy accounts for 40% of the Italian olive oil production. Moreover, according to this organization, the border of the X. fastidiosa infected region moves at a speed of 2 km a month [8,9,10]. In Italy, the disease is mainly present in the Puglia region, which accounts for 40% of Italy’s olive oil production [11]. In Brazil, X. fastidiosa has devastated the citrus industry. In citruses, the pathogen causes citrus variegated chlorosis, which affects almost all sweet orange cultivars in the country that is responsible for 30% of the worldwide sweet orange supply [12]. In fact, in 2012, X. fastidiosa caused 120 million dollar in damages to the Brazilian citrus tree industry [13].

Olive trees infected with Xylella fastidiosa
Figure 3: Trees and ornamental plants are devastated by X. fastidiosa

However, there are not only economic damages. In Italy, a lot of olive trees are protected as part of the cultural heritage. Some of these trees are over a thousand years old and have become a part of the landscape and the local culture. A lot of olive trees and farms have been providing an income for families for hundreds of years and the farmers often have the olives as their sole source of income [14]. In 2014, the European Union dictated that, to save the Italian olive trees, diseased plants needed to be removed, as well as not infected neighboring trees [15]. However, farmers did not follow these rules. Reason for this was their beliefs in conventional disease treatment methods and their distrust of the government, scientists and the European Union [16]. This lack of action created an opportunity for X. fastidiosa to establish itself as a dominant pathogen in Italy.

arrow_forward To Scientific Background
  • References arrow_downward
    1. Pierce, N. B. (Newton B) (1892). The California vine disease: a preliminary report of investigations (No. 2)
    2. Davis, M. J., Purcell, A. H., & Thomson, S. V. (1978). Pierce’s Disease of Grapevines: Isolation of the Causal Bacterium. Science, 199(4324), 75–77.
    3. Wells, J. M., Raju, B. C., Hung, H.-Y., Weisburg, W. G., Mandelco-Paul, L., & Brenner, D. J. (1987). Xylella fastidiosa gen. nov., sp. nov: Gram-Negative, Xylem-Limited, Fastidious Plant Bacteria Related to Xanthomonas spp. International Journal of Systematic Bacteriology, 37(2), 136–143.
    4. Simpson, A. J. G., Reinach, F. C., Arruda, P., Abreu, F. A., Acencio, M., Alvarenga, R., … Setubal, J. C. (2000). The genome sequence of the plant pathogen Xylella fastidiosa. Nature, 406(6792), 151–157.
    5. CABI. (2019). Xylella fastidiosa (Pierce’s disease of grapevines) (Datasheet). Retrieved from
    6. EFSA. (2019). Xylella fastidiosa - EU legislation. Retrieved from
    7. Tumber, K. P., Alston, J. M., & Fuller, K. B. (2014). Pierce’s disease costs California (04 million per year. California Agriculture, 68(1), 20–29.
    8. Coldiretti. (n.d.-a). Xylella, ecco il primo olio da ulivi resistenti - Coldiretti. Retrieved September 11, 2019, from
    9. Coldiretti. (n.d.-b). Xylella advances by 2km a month, a massacre of 21 million olive trees - Coldiretti. Retrieved September 11, 2019, from
    10. Coldiretti. (2019). Sentenza Corte Ue su Xyella, scaricabarile sono costati 1,2 miliardi - Coldiretti. Retrieved September 11, 2019, from
    11. Strona, G., Carstens, C. J., & Beck, P. S. A. (2017). Network analysis reveals why Xylella fastidiosa will persist in Europe. Scientific Reports, 7(1), 71.
    12. Rodrigues, C. M., de Souza, A. A., Takita, M. A., Kishi, L. T., & Machado, M. A. (2013). RNA-Seq analysis of Citrus reticulata in the early stages of Xylella fastidiosa infection reveals auxin-related genes as a defense response. BMC Genomics, 14(1), 676.
    13. Gonçalves, F. P., Stuchi, E. S., Lourenço, S. A., Hau, B., & Amorim, L. (2012). Relationship between sweet orange yield and intensity of Citrus Variegated Chlorosis. Plant Pathology, 61(4), 641–647.
    14. Borunda, A. (2018). Italy’s Olive Trees Are Dying. Can They Be Saved? Retrieved from
    15. Commission Implementing Decision 2014/87/EU of 13 February 2014 as regards measures to prevent the spread within the Union of Xylella fastidiosa (Well and Raju) ().
    16. Burdeau, C. (2017). Where the Olive Trees Are Dying: A Front-Line Report on Xylella. Retrieved from

Scientific Background

Know Your Enemy
-Sun Tzu

Xylella fastidiosa is phytopathogenic Gram-negative bacterium. It has a thin rod shape that lacks any flagella, but has fimbriae that allows for motility [1]. X. fastidiosa has a very unusual lifestyle, being able to live both inside a plant host and in an insect vector, making it a very successful pathogen. Inside of the plant, X. fastidiosa is limited to the xylem, the plant’s vascular system, that transports water and nutrients from the roots to the leaves. X. fastidiosa is known to have over 350 different plant hosts [2]. About two-thirds of these plant species do not experience a large negative impact from this interaction and will never show symptoms of X. fastidiosa infection. To the remaining one-third, infection has deadly consequences, as large populations of X. fastidiosa block the sap-flow in the xylem. This prevents water from reaching the upper part of plants, causing the plants to dry out and perish.

Dissemination Using The Insect Vector

The xylem is a very inaccessible part of the plant, making it hard for any pathogen to spread to new plant hosts. This is where a unique feature of X. fastidiosa’s lifestyle comes in. By expressing adhesin proteins, the pathogen can adhere to the chitin surfaces of the piercing-sucking mouthparts of insects feeding on X. fastidiosa infected plants [3]. Chitin is an integral building block of the insect’s exoskeleton that is commonly exposed on these mouthparts. Once inside the insect, X. fastidiosa colonizes the insect by establishing a biofilm in the foregut. Using this strategy, it is can remain inside the insect vector for its entire life [4]. Once the insect vector feeds on new, still healthy plants, a part of the established colony dissociates from the biofilm and infects the healthy plant. Transmission does not seem to suffer from a latency period, as transmission can already occur directly after the insect acquires the pathogen [5]. In stark contrast to most insect transmitted pathogens, like plant viruses, X. fastidiosa is not specialized to a specific insect species. This is because the strategy of adhesion and biofilm formation used for colonization, makes use of very general features of these insects, such as the chitin molecules of the exoskeleton. This means that in theory, X. fastidiosa is able colonize most of the xylem feeding insects [6, 7], but insect population dynamics and feeding behaviour have a large impact on the insects ability to efficiently spread the pathogen [8].

X. fastidiosa shielding itself from the plants immune sytsem.
Figure 1: X. fastidiosa shielding itself from the plants immune sytsem.

Inside the Plant Host

While insect vectors provide an important reservoir for (re)infection, the plant xylem is the preferred environment of the pathogen. Which is quite remarkable as the xylem is a harsh environment, in which few microbes can survive, because it is very nutrient poor, containing only water, minerals and some proteins [9]. This provides X. fastidiosa with a niche in which it faces very little competition. Adapted to this habitat, X. fastidiosa is known to grow very slowly, with doubling times between 9 hours and 2.3 days [1]. In order to grow inside the plant undisturbed, X. fastidiosa cleverly avoids detection by the plant’s immune system. Generally, the plant’s immune system recognizes conserved structures found on the outside of invading bacteria, called lipopolysaccharides (LPS). X. fastidiosa also has these features, but disguises them with an O-antigen, shielding the LPS sites from being recognized by plant’s innate immune system [10]. This allows X. fastidiosa to go unnoticed during the first phase of infection, enabling the pathogen to firmly establishes itself inside the plant.

Once established inside the plant, X. fastidiosa spreads aggressively throughout the xylem’s vascular system [11]. The pathogen can travel with and against the sap flow of the xylem using his fimbriae, that allow it to "crawl" over the xylem’s inner lining [12]. For most of the infection period, the plant shows no symptoms, depending on the plant species, this asymptomatic period can take anywhere from a few weeks up to two years. But all this time X. fastidiosa is multiplying and spreading throughout the plant. X. fastidiosa reinforces itself by forming a complex biofilm on the walls of the xylem [13]. At one point the overabundance of the pathogen triggers the plant’s immune system. The plant host starts to form vascular inclusions inside the xylem, in an attempt to block the spread of X. fastidiosa throughout the plant [14]. However, at this point the plant is already too late to fight off the pathogen and the large amount of accumulated X. fastidiosa cells together with the vascular inclusions start to block the vascular flow of the xylem [15]. This prevents water from reaching the upper part of the plant, causing the plant to dry out and perish. Because symptoms show so late in the pathogen’s life cycle, the disease appears to progress very quickly, even though X. fastidiosa is a very slow growing organism.

Overview of the different facets of X. fastidiosa's life cylce
Figure 2: Overview of the different facets of X. fastidiosa's life cylce.

Advanced Survival Strategies

It is shown that the insect vectors have a preference for asymptomatic plants [16, 17]. This gives rise to a delicate balance: more X. fastidiosa cells inside plants, gives a larger chance of insect uptake and thus a more successful pathogen. However if X. fastidiosa grows too much, the plant will show symptoms, greatly reducing the chance of insect feeding on the tree, lowering the pathogens success. To maximize insect transmission efficiency, X. fastidiosa monitors cell density in order to ensure it doesn’t grow so much as to cause symptoms [15]. To achieve this, X. fastidiosa uses a specific kind of quorum sensing molecule. This quorum sensing molecule, called Diffusible Signalling Factor (DSF), is both synthesized and detected by the pathogen itself. At a low cell density, X. fastidiosa exhibits a relatively high growth rate and is actively spreading throughout the vascular system. But once the cell density and thus the DSF concentration, surpasses a certain threshold, X. fastidiosa switches behaviour slowing down its growth. It enters what is called "vector acquisition mode" and starts expressing adhesin proteins that allow it to colonize xylem feeding insects [18]. It was shown that X. fastidiosa colony sizes peak before the plant starts to show symptoms. This means that hosts are most effective at spreading the disease while still asymptomatic [17]. This, together with the quick death of plants after symptoms do show, underlines the importance of early detection and intervention.

arrow_back To General Background
  • References arrow_downward
    1. John M Wells, Boligala C Raju, Hsueh-Yun Hung, William G Weisburg, Linda Mandelco-Paul, and Don J Brenner. Xylella fastidiosa gen. nov., sp. nov: gram-negative, xylem-limited, fastidious plant bacteria related to xanthomonas spp. International Journal of Systematic and Evolutionary Microbiology, 37(2):136–143, 1
    2. European Food Safety Authority (EFSA). Update of a database of host plants of xylella fastidiosa: 20 november 2015. EFSA Journal, 14(2):4378, 2016.
    3. Nabil Killiny and Rodrigo PP Almeida. Xylella fastidiosa afimbrial adhesins mediate cell transmission to plants by leafhopper vectors. Appl. Environ. Microbiol., 75(2):521–528, 2009.
    4. BL Hill, AH Purcell, et al. Acquisition and retention of xylella fastidiosa by an efficient vector, graphocephala atropunctata. Phytopathology, 85(2):209–212, 1995.
    5. Alexander H Purcell and AH Finlay. Evidence for noncirculative transmission of pierce’s disease bacterium by sharpshooter leafhoppers. Phytopathology, 69(4):393–395, 1979.
    6. Rodrigo PP Almeida and Leonard Nunney. How do plant diseases caused by xylella fastidiosa emerge? Plant Disease, 99(11), 2015.
    7. NW Frazier. Xylem viruses and their insect vectors. In Proceedings of the international conference on virus and vectors on perennial hosts, with special reference to Vitis, pages 91–99, 1965.
    8. Michael Jeger and Claude Bragard. The epidemiology of xylella fastidiosa; a perspective on current knowledge and framework to investigate plant host–vector–pathogen interactions. Phytopathology, 109(2):200–209, 2018.
    9. Andreas D Peuke. The chemical composition of xylem sap in vitis vinifera l. cv. riesling during vegetative growth on three different franconian vineyard soils and as influenced by nitrogen fertilizer. American Journal of Enology and Viticulture, 51(4):329–339, 2000.
    10. Jeannette N Rapicavoli, Barbara Blanco-Ulate, Artur Muszynski, Rosa Figueroa- Balderas, Abraham Morales-Cruz, Parastoo Azadi, Justyna M Dobruchowska, Claudia Castro, Dario Cantu, and M Caroline Roper. Lipopolysaccharide o-antigen delays plant innate immune recognition of xylella fastidiosa. Nature communications, 9(1):390, 2018.
    11. C Baccari and SE Lindow. Assessment of the process of movement of xylella fastidiosa within susceptible and resistant grape cultivars. Phytopathology, 101(1):77–84, 2011.
    12. Yizhi Meng, Yaxin Li, Cheryl D Galvani, Guixia Hao, James N Turner, Thomas J Burr, and HC Hoch. Upstream migration of xylella fastidiosa via pilus-driven twitching motility. Journal of bacteriology, 187(16):5560–5567, 2005.
    13. Jeannette Rapicavoli, Brian Ingel, Barbara Blanco-Ulate, Dario Cantu, and Caroline Roper. Xylella fastidiosa: an examination of a re-emerging plant pathogen. Molecular plant pathology, 19(4):786–800, 2018.
    14. Qiang Sun, Yuliang Sun, M Andrew Walker, and John M Labavitch. Vascular occlusions in grapevines with pierce’s disease make disease symptom development worse. Plant physiology, 161(3):1529–1541, 2013.
    15. Anne Sicard, Adam R Zeilinger, Mathieu Vanhove, Tyler E Schartel, Dylan J Beal, Matthew P Daugherty, and Rodrigo PP Almeida. Xylella fastidiosa: Insights into an emerging plant pathogen. Annual review of phytopathology, 56:181–202, 2018.
    16. Andrew J McElrone, James L Sherald, and Irwin N Forseth. Effects of water stress on symptomatology and growth of parthenocissus quinquefolia infected by xylella fastidiosa. Plant Disease, 85(11):1160–1164, 2001.
    17. Matthew P Daugherty, Adam R Zeilinger, and Rodrigo PP Almeida. Conflicting effects of climate and vector behavior on the spread of a plant pathogen. Phytobiomes, 1(1):46– 53, 2017.
    18. Subhadeep Chatterjee, Christina Wistrom, and Steven E Lindow. A cell–cell signaling sensor is required for virulence and insect transmission of xylella fastidiosa. Proceedings of the National Academy of Sciences, 105(7):2670–2675, 2008.