Hubbry Logo
Xylella fastidiosaXylella fastidiosaMain
Open search
Xylella fastidiosa
Community hub
Xylella fastidiosa
logo
8 pages, 0 posts
0 subscribers
Be the first to start a discussion here.
Be the first to start a discussion here.
Xylella fastidiosa
Xylella fastidiosa
Xylella fastidiosa
View on Wikipedia
from Wikipedia

Xylella fastidiosa
Scientific classification Edit this classification
Domain: Bacteria
Kingdom: Pseudomonadati
Phylum: Pseudomonadota
Class: Gammaproteobacteria
Order: Lysobacterales
Family: Lysobacteraceae
Genus: Xylella
Species:
X. fastidiosa
Binomial name
Xylella fastidiosa
Wells et al., 1987

Xylella fastidiosa is an aerobic, Gram-negative bacterium of the genus Xylella.[1] It is a plant pathogen, that grows in the water transport tissues of plants (xylem vessels) and is transmitted exclusively by xylem sap-feeding insects such as sharpshooters and spittlebugs.[1][2][3][4] Many plant diseases are due to infections of X. fastidiosa, including bacterial leaf scorch, oleander leaf scorch, coffee leaf scorch (CLS), alfalfa dwarf, phony peach disease, and the economically important Pierce's disease of grapes (PD),[5] olive quick decline syndrome (OQDS),[6][7] and citrus variegated chlorosis (CVC).[8] While the largest outbreaks of X. fastidiosa–related diseases have occurred in the Americas[9] and Europe,[10] this pathogen has also been found in Taiwan,[11] Israel,[12] and a few other countries worldwide.[13][14]

Xylella fastidiosa can infect an extremely wide range of plants, many of which do not show any symptoms of disease.[15] Disease occurs in plant species that are susceptible due to blockage of water flow in the xylem vessels caused by several factors: bacterial obstruction, overreaction of the plant immune response (tylose formation), and formation of air embolisms.[16][17][18] A strain of X. fastidiosa responsible for citrus variegated chlorosis was the first bacterial plant pathogen to have its genome sequenced, in part because of its importance in agriculture.[19] Due to the significant impacts of this pathogen on agricultural crops around the world, there is substantial investment in scientific research related to X. fastidiosa and the diseases it causes.[20]

Taxonomy

[edit]

Xylella fastidiosa is the first-proposed species in the genus Xylella and the only species until 2016. The genus Xyella Wells et al. 1987 currently consists of two species, Xylella fastidiosa Wells et al. 1987 and Xylella taiwanensis Su et al. 2016.[21] Xylella fastidiosa in turn consists of several subspecies, each with own preferred host plants and geographic origin:

  • X. f. subsp. fastidiosa (Wells et al. 1987) Schaad et al. 2009 is defined around the original type strain and is the best-studied so far. It is mainly known for Pierce's disease of grapevines and leaf scorch of almond.[22] It also affects alfalfa and maple.[23] It is thought to have originated in southern Central America.[24]
    • Identical to invalid name "X. f. subsp. piercei" Schaad et al. 2004.[25]
  • X. f. subsp. multiplex Schaad et al. 2009 affects many trees, including stone-fruit ones such as peaches and plums, and is thought to originate in temperate and southern North America.[24] It also affects elm, grape, and sycamore.[23]
  • "X. f. subsp. pauca" Schaad et al. 2004 is believed to have originated in South America. It is the causal agent of citrus variegated chlorosis (CVC) in Brazil.[26] It also affects South American coffee crops, causing coffee leaf scorch.[24]
  • "X. f. subsp. sandyi" Schuenzel et al. 2005 is thought to have originated in the southern part of the United States, and is notable for causing oleander leaf scorch.[24]
  • "X. f. subsp. tashke" Randell et al., 2009 is proposed to include isolates associated with Chitalpa tashkentensis leaf scorch in Southwestern USA. Whether it is causative is unknown. Whether it forms a distinct group that can be called a subspecies is also unknown.[24]
  • "X. f. subsp. morus" Nunney et al. 2014 includes a strain associated with mulberry leaf scorch in the eastern USA and California. It is genetically distinct enough to be its own subspecies.[24]

The three X. fastidiosa subspecies by Schaad et al. were outlined in the same 2004 publication. Two of them were made valid according to the Prokaryotic Code in 2009. No reason was given for not validating the third subspecies, pauca.[27]

X. taiwanensis affects Pyrus pyrifolia in Taiwan, causing leaf scorch. It has not spread to the EU.[28] It was originally proposed to be a subspecies of X. f., but the large divergence lead to the proposal of a separate species.[24]

Pathogen anatomy and disease cycle

[edit]

Xylella fastidiosa is rod-shaped, and at least one subspecies has two types of pili on only one pole; longer, type IV pili are used for locomotion, while shorter, type I pili assist in biofilm formation inside their hosts. As demonstrated using a PD-related strain, the bacterium has a characteristic twitching motion that enables groups of bacteria to travel upstream against heavy flow, such as that found in xylem vessels.[29] It is obligately insect-vector transmitted from xylem-feeding insects directly into xylem, but infected plant material for vegetative propagation (e.g. grafting) can produce mature plants that also have an X. fastidiosa disease.[30] In the wild, infections tend to occur during warmer seasons, when insect vector populations peak. The bacterium is not seed transmitted, but instead is transmitted through "xylem feed-ing, suctorial homopteran insects such as sharpshooter leafhoppers and spittle bugs"[31] and has been historically difficult to culture (fastidious),[32][33] as its specific epithet, fastidiosa, reflects.

X. fastidiosa has a two-part lifecycle, which occurs inside an insect vector and inside a susceptible plant. While the bacterium has been found across the globe, only once the bacterium reaches systemic levels do symptoms present themselves. Once established in a new region, X. fastidiosa spread is dependent on the obligate transmission by xylem-sap feeding insect.[34] Within susceptible plant hosts, X. fastidiosa forms a biofilm-like layer within xylem cells and tracheary elements that can completely block the water transport in affected vessels.[35]

Strains

[edit]

EB92-1 is a significantly less pathogenic strain of X. fastidiosa which is used for biocontrol against its relatives.[36] There is very little genomic distance between pathogenic and EB92-1 strains. However, 10 genes believed to be responsible for causing diseases in plants are missing.[36] EB92-1 not only protects against X. fastidiosa infection; it also protects against Citrus Huanglongbing, which is caused by Liberibacter.[37]

Symptoms

[edit]

Significant variation in symptoms is seen between diseases, though some symptoms are expressed across species. On a macroscopic scale, plants infected with a X. fastidiosa-related disease exhibit symptoms of water, zinc, and iron deficiencies,[38] manifesting as leaf scorching and stunting in leaves turning them yellowish-brown, gummy substance around leaves,[38] fruit reduction in size and quality,[38] and overall plant height. As the bacterium progressively colonizes xylem tissues, affected plants often block off their xylem tissue, which can limit the spread of this pathogen; blocking can occur in the form of polysaccharide-rich gels, tyloses, or both. These plant defenses do not seem to hinder the movement of X. fastidiosa. Occlusion of vascular tissue, while a normal plant response to infection, makes symptoms significantly worse; as the bacterium itself also reduces vascular function, a 90% reduction of vascular hydraulic function was seen in susceptible Vitis vinifera.[39] This bacterium rarely completely blocks vascular tissue. There usually is a slight amount of vascular function that keeps the plant alive, but makes its fruit or branches die, making the specific plant economically nonproductive. This can cause a massive drop on supply of quality fruit.[38] Smaller colonies usually occur throughout a high proportion of xylem vessels of a symptomatic plant.[citation needed]

X. fastidiosa is a Gram-negative, xylem-limited illness that is spread by insects. It can damage a variety of broadleaved tree species that are commonly grown in the United States. X. fastidiosa can be found in about 600 different plant species.[citation needed]

  • Withering and desiccation of branches
  • Leaf chlorosis
  • Dwarfing or lack of growth of the plant
  • Drooping appearance and shorter internodes
  • Shriveled fruits on infected plants
  • Premature fruit abscission
  • gum-like substance on leaves
  • hardening and size reduction of fruit

Pierce's disease

[edit]

(X. f. subsp. fastidiosa) Severe PD symptoms include shriveled fruit, leaf scorching, and premature abscission of leaves, with bare petioles remaining on stems.[40]

Citrus variegated chlorosis

[edit]

(X. f. subsp. pauca) This disease is named after the characteristic spotty chlorosis on upper sides of citrus leaves. Fruits of infected plants are small and hard.[8]

Leaf scorches

[edit]

Some isolates cause Almond leaf scorch, in California that includes CFBP8071 (fastidiosa), M23 (fastidiosa), and M12 (multiplex).[41][42]

(X. f. subsp. pauca) Coffee Leaf Scorch (CLS) is a disease caused by the causal agent Xylella fastidiosa that is economically significant in Brazil.[43] Citrus variegated chlorosis (CVC), another significant disease in this region caused by a strain of X. fastidiosa has been shown to infect coffee plants with CLS. The disease has also been found in Costa Rica's Central Valley where it is referred to as 'crespera' disease by coffee growers.[44] Symptoms of the bacterial infection in coffee plants feature curling leaf margins, chlorosis and irregularly shaped leaves, stunting and reduced plant growth, and branch atrophy.[44] The disease reduced coffee production by up to 30% in plantations across Brazil.[43]

X. fastidiosa was discovered in Apulia, Italy in 2013 for the first time as a destructive disease agent of olive trees and likely came from strains present in asymptomatic plant material imported from Costa Rica. The strains were of a single origin in subspecies pauca.[45]

Environment

[edit]

X. fastidiosa occurs worldwide, though its diseases are most prominent in riparian habitats including the southeastern United States, California, and South America.

Symptoms of X. fastidiosa diseases worsen during hot, dry periods in the summer; lack of water and maximum demand from a full canopy of leaves, combined with symptoms due to disease, stress infected plants to a breaking point. Cold winters can limit the spread of the disease,[33] as it occurs in California, but not in regions with milder winters such as Brazil. Additionally, dry summers seem to delay symptom development of PD in California.[30]

Any conditions that increase vector populations can increase disease incidence, such as seasonal rainfall and forests or tree cover adjacent to crops, which serve as alternate food sources and overwintering locations for leafhoppers.[30]

Alexander Purcell, an expert on X. fastidiosa, hypothesized that plants foreign to X. fastidiosa's area of origin, the neotropical regions, are more susceptible to symptom development. Thus, plants from warmer climates are more resistant to X. fastidiosa disease development, while plants from areas with harsher winters, such as grapes, are more severely affected by this disease.[33]

Host species

[edit]

X. fastidiosa has a very wide host range; as of 2020, its known host range was 595 plant species, with 343 species confirmed by two different detection methods, in 85 botanical families.[46] Most X. fastidiosa host plants are dicots, but it has also been reported in monocots and ginkgo, a gymnosperm. However, the vast majority of host plants remain asymptomatic, making them reservoirs for infection.[citation needed]

Due to the temperate climates of South America and the southeastern and west coast of the United States, X. fastidiosa can be a limiting factor in fruit crop production, particularly for stone fruits in northern Florida and grapes in California.[35] In South America, X. fastidiosa can cause significant losses in the citrus and coffee industries; a third of today's citrus crops in Brazil has CVC symptoms.[40]

X. fastidiosa also colonizes the foreguts of insect vectors,[47] which can be any xylem-feeding insects, often sharpshooters in the Cicadellidae subfamily Cicadellinae.[3][33] After an insect acquires X. fastidiosa, it has a short latent period around 2 hours, then the bacterium is transmissible for a period of a few months or as long as the insect is alive.[48] The bacterium multiplies within its vectors, forming a "bacterial carpet" within the foregut of its host. If the host sheds its foregut during molting, the vector is no longer infected, but can reacquire the pathogen. At present, no evidence shows that the bacterium has any detrimental effect on its insect hosts.

The EFSA maintains a list of plants known to be susceptible to Xylella and updates it regularly. Classification is performed down to the subspecies level if possible. As of May 2025, the latest report is from July 2024, containing information from literature published before 31 December 2023. The lists provided in EFSA's journal article about the update is only a summary; full data is available from the Microstrategy platform of the EFSA.[49][50]

List of subspecies X. f. subsp. fastidiosa-susceptible plants (recreated from EFSA Panel of 2020)[46]
Family Genus
Adoxaceae Sambucus
Amaranthaceae Alternanthera, Chenopodium
Anacardiaceae Rhus, Toxicodendron
Apiaceae Conium, Datura, Daucus, Oenanthe
Apocynaceae Nerium, Vinca
Araliaceae Hedera
Asteraceae Ambrosia, Artemisia, Baccharis, Callistephus, Conyza, Franseria, Helianthus, Lactuca, Solidago, Sonchus, Xanthium
Betulaceae Alnus
Boraginaceae Amsinckia
Brassicaceae Brassica
Cannaceae Canna
Caprifoliaceae Lonicera, Symphoricarpos
Convolvulaceae Convolvulus, Ipomoea
Cyperaceae Cyperus
Fabaceae Acacia, Chamaecrista, Cytisus, Genista, Lathyrus, Lupinus, Medicago, Melilotus, Spartium, Trifolium, Vicia
Fagaceae Quercus
Geraniaceae Erodium, Pelargonium
Juglandaceae Juglans
Lamiaceae Callicarpa, Origanum, Melissa, Mentha, Rosmarinus, Salvia
Lauraceae Persea, Umbellularia
Magnoliaceae Magnolia
Malvaceae Malva
Myrtaceae Eucalyptus, Eugenia, Metrosideros
Oleaceae Fraxinus, Syringa
Onagraceae Epilobium, Fuchsia, Clarkia, Oenothera
Pittosporaceae Pittosporum
Platanaceae Platanus
Poaceae Avena, Bromus, Cynodon, Digitaria, Echinochloa, Eragrostis, Eriochola, Festuca, Holcus, Hordeum, Lolium, Paspalum, Pennisetum, Phalaris, Phleum, Poa, Setaria, Sorghum
Polygonaceae Persicaria, Polygonum, Rheum, Rumex
Portulacaceae Montia, Portulaca
Resedaceae Reseda
Rhamnaceae Rhamnus
Rosaceae Cotoneaster, Fragaria, Photinia, Prunus, Rosa, Rubus
Rubiaceae Coffea, Coprosma
Rutaceae Citrus
Salicaceae Populus, Salix
Sapindaceae Acer, Aesculus
Scrophulariaceae Veronica
Simmondsiaceae Simmondsia
Solanaceae Datura, Lycopersicon, Nicotiana, Solanum
Urticaceae Urtica
Verbenaceae Duranta
Vitaceae Ampelopsis, Parthenocissus, Vitis

Oleander

[edit]

Oleander leaf scorch is a disease of landscape oleanders (Nerium oleander) caused by a X. fastidiosa strain that has become prevalent in California and Arizona, starting in the mid-1990s. This disease is transmitted by a type of leafhopper (insect) called the glassy-winged sharpshooter (Homalodisca coagulata). Oleander is commonly used in decorative landscaping in California, so the plants serve as widely distributed reservoirs for Xylella.[51]

Both almond and oleander plants in the Italian region of Apulia have also tested positive for the pathogen.[52]

Grape vines

[edit]

Pierce's disease (PD) was discovered in 1892[53] by Newton B. Pierce (1856–1916; California's first professional plant pathologist) on grapes in California near Anaheim,[26] where it was known as "Anaheim disease".[54] The disease is endemic in Northern California, being spread by the blue-green sharpshooter, which attacks only grapevines adjacent to riparian habitats. It became a real threat to California's wine industry when the glassy-winged sharpshooter, native to the Southeast United States, was discovered in the Temecula Valley in California in 1996; it spreads PD much more extensively than other vectors.[55]

Symptoms of infection on grape vines

[edit]

When a grape vine becomes infected, the bacterium causes a gel to form in the xylem tissue of the vine, preventing water from being drawn through the vine.[56] Leaves on vines with Pierce's disease turn yellow and brown, and eventually drop off the vine. Shoots also die. After one to five years, the vine itself dies. The proximity of vineyards to citrus groves compounds the threat, because citrus is not only a host of sharpshooter eggs, but also is a popular overwintering site for this insect.[57]

Collaborative efforts for solutions

[edit]

In a unique effort, growers, administrators, policy makers, and researchers are working on a solution for this immense X. fastidiosa threat.[10] No cure has been found,[58] but the understanding of X. fastidiosa and glassy-winged sharpshooter biology has markedly increased since 2000, when the California Department of Food and Agriculture, in collaboration with different universities, such as University of California, Davis; University of California, Berkeley; University of California, Riverside, and University of Houston–Downtown started to focus their research on this pest. The research explores the different aspects of the disease propagation from the vector to the host plant and within the host plant, to the impact of the disease on California's economy. All researchers working on Pierce's disease meet annually in San Diego in mid-December to discuss the progress in their field. All proceedings from this symposium can be found on the Pierce's disease website,[59] developed and managed by the Public Intellectual Property Resource for Agriculture (PIPRA).[60]

Few resistant Vitis vinifera varieties are known, and Chardonnay and Pinot noir are especially susceptible, but muscadine grapes (V. rotundifolia) have a natural resistance.[58] Pierce's disease is found in the Southeastern United States and Mexico. Also, it was reported by Luis G. Jiménez-Arias in Costa Rica, and Venezuela,[61] and possibly in other parts of Central and South America. In 2010, X. fastidiosa became apparent in Europe, posing a serious, real threat.[62] There are isolated hot spots of the disease near creeks in Napa and Sonoma in Northern California.[58] Work is underway at UC Davis to breed PD resistance from V. rotundifolia into V. vinifera. The first generation was 50% high-quality V. vinifera genes, the next 75%, the third 87% and the fourth 94%. In the spring of 2007, seedlings that are 94% V. vinifera were planted.[63]

A resistant variety, 'Victoria Red', was released for use especially in Coastal Texas.[64]

The management of X. fastidiosa, a dangerous plant pathogen, requires a multidisciplinary approach that includes genetic and spatial ecology perspectives.[65][10] Such an approach will improve knowledge on invasive processes and resource allocation, optimizing diagnostic and management efforts. Effective communication with stakeholders is crucial for successful and sustainable management. X. fastidiosa is a great way to study how pathogenicity changes at different levels of biological complexity. This will help scientists come up with better ways to find and control invasive species.[10]

Nerium oleander infected with X. fastidiosa in Phoenix, Arizona

Olive trees

[edit]
An olive grove infested with X. fastidiosa in Puglia, Italy in 2019

In October 2013, the bacterium was found infecting olive trees in the region of Apulia in southern Italy.[52] The disease caused rapid decline in olive grove yields, and by April 2015, was affecting the whole Province of Lecce and other zones of Apulia,[7][66] though it had not previously been confirmed in Europe.[67] The subspecies involved in Italy is X. f. subsp. pauca, which shows a marked preference for olive trees and warm conditions and is thought to be unlikely to spread to Northern Europe.[68]

The cycle in olives has been called olive quick decline syndrome (in Italian: complesso del disseccamento rapido dell'olivo).[67][69] The disease causes withering and desiccation of terminal shoots, distributed randomly at first but then expanding to the rest of the canopy[69] resulting in the collapse and death of trees.[69] In affected groves, all plants normally show symptoms.[69] The most severely affected olives are the century-old trees of local cultivars Cellina di Nardò and Ogliarola salentina.[70]

By 2015, the disease had infected up to a million olive trees in Apulia[71] and Xylella fastidiosa had reached Corsica,[72] By October 2015, it had reached Mainland France, near Nice, in Provence-Alpes-Côte d'Azur, affecting the non-native myrtle-leaf milkwort (Polygala myrtifolia). This is the subspecies X. fastidiosa subsp. multiplex which is considered to be a different genetic variant of the bacterium to that found in Italy.[73][74] On 18 August 2016 in Corsica, 279 foci of the infection have been detected, concentrated mostly in the south and the west of the island.[75] In August 2016, the bacterium was detected in Germany in an oleander plant.[76] In January 2017 it was detected in Mallorca and Ibiza.[77]

Notably, in 2016, olive leaf scorch was first detected in X. fastidiosa's native range, in Brazil.[26]

In June 2017, it was detected in the Iberian peninsula, specifically in Guadalest, Alicante.[78] In 2018, it was detected elsewhere in Spain[79] and Portugal,[80] and in Israel in 2019.[81]

Citrus

[edit]

Xylella infection was detected in South American citrus in the 1980s and subsequently in the USA but had limited spread beyond the Americas until the detection in citrus groves in Portugal in 2023.[82]

Genome sequencing

[edit]

The genome of X. fastidiosa was sequenced in 2000 by a pool of over 30 research laboratories in the state of São Paulo, Brazil, funded by the São Paulo Research Foundation.[83]

See also

[edit]

References

[edit]

Further reading

[edit]
[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Xylella fastidiosa

View on Grokipedia
from Grokipedia
Xylella fastidiosa is a Gram-negative, xylem-limited, fastidious bacterium in the family Xanthomonadaceae that colonizes the vascular tissues of host and is transmitted by xylem-sap-feeding vectors such as sharpshooters. Native to the , it has emerged as a global agricultural threat due to its broad host range exceeding 600 plant species across more than 80 families, causing lethal vascular diseases without effective curative treatments. The pathogen manifests in distinct subspecies—fastidiosa, multiplex, pauca, and sandyi—each associated with specific syndromes like Pierce's disease in grapevines, leaf scorch, and quick decline syndrome (OQDS), the latter devastating Italian olive groves since 2013 with tree mortality rates approaching 100% in affected areas. Transmission occurs non-circulatively through vectors acquiring the bacterium during feeding and inoculating healthy , with biofilms aiding persistence in foreguts and plant , obstructing water flow and inducing symptoms of scorching, , and dieback. Economic impacts are severe, with billions in losses from crop devastation and stringent quarantines, underscoring the need for early detection via PCR and vector management, though challenges persist due to asymptomatic carriers and climate-driven spread. Management relies on preventing introduction through regulatory bans on propagative materials and controlling vectors like the , but no bactericides eradicate established infections, emphasizing resistant cultivars and cultural practices as primary defenses despite limited genetic resistance identified. Genomic studies reveal high plasticity enabling to new hosts, complicating in non-endemic regions like and where outbreaks continue to expand.

Taxonomy and Classification

Discovery and Etymology

The bacterium Xylella fastidiosa was first linked to plant disease in 1892, when American plant pathologist Newton B. Pierce described a destructive condition in grapevines (Vitis vinifera) in , later termed Pierce's disease, characterized by leaf scorching, dieback, and vine decline. Although microscopic observations of xylem-inhabiting bacteria were reported in affected tissues as early as the late , the causal agent was initially misattributed to viral or fungal origins during . Pure cultures of the bacterium were not successfully isolated until 1978 from diseased grapevines using a specialized medium (JDI), enabling definitive identification as a xylem-limited . In 1987, researchers J.M. Wells, B.W. Raju, H.-Y. Chen, L.D. Schulz, R.J. Copeman, and C.L. Chang formally proposed the name Xylella fastidiosa for the species based on strains isolated from grapevines and other hosts, classifying it within the family Xanthomonadaceae. This taxonomic description followed genomic and phenotypic analyses confirming its distinctiveness, marking the first solid cultivation and characterization of the organism despite prior challenges in axenic growth. The genus name Xylella derives from the Greek xýlon () combined with the diminutive suffix -ella, reflecting its exclusive of vessels. The specific epithet fastidiosa is a Latin feminine meaning "fastidious" or "delicate," alluding to the bacterium's nutritional exigency and resistance to laboratory cultivation, which necessitated enriched media with supplements like bovine and for propagation. This nomenclature underscores the organism's biological constraints, observed consistently across strains since its initial isolation.

Subspecies and Strain Diversity

Xylella fastidiosa is classified into five genetically distinct —fastidiosa, multiplex, pauca, sandyi, and morus—differentiated primarily through (MLST), whole-genome sequencing, and host specificity patterns. These subspecies exhibit allopatric origins, with genomic analyses of over 70 strains revealing varying degrees of recombination and divergence that correlate with geographic distribution and pathogenicity. Strain diversity within subspecies is extensive, encompassing dozens of sequence types (STs); for instance, more than 50 STs have been identified globally, each potentially linked to specific pathosystems.
SubspeciesPrimary HostsAssociated Diseases
fastidiosaGrapevines (Vitis spp.), almondsPierce's disease, almond leaf scorch
multiplexBroadleaf plants, including blueberries, maplesLeaf scorch diseases in ornamentals and forest trees
paucaOlives, coffee, citrusOlive quick decline syndrome, coffee leaf scorch, citrus variegated chlorosis
sandyiOleander, coffeeOleander leaf scorch
morusMulberry treesMulberry leaf scorch
Subspecies fastidiosa strains, prevalent in , demonstrate high genetic homogeneity in grape-associated populations but show recombination hotspots that influence virulence factors like adhesins and hemagglutinins. In contrast, pauca strains from and display greater intra-subspecies diversity, with ST53 dominating outbreaks in Italian olives since 2013, though variants like ST80 have emerged in . Multiplex exhibits the broadest host range among subspecies, with North American strains forming distinct clades adapted to temperate hosts via mutations in type III secretion systems. Recent genomic sequencing of sandyi isolates from intercepted coffee plants confirms closed pan-genomes with limited , underscoring niche specialization. Overall, strain typing via MLST loci such as cnp60 and hlpA remains essential for and epidemiological tracking, as phylogenetic clustering often predicts vector competence and severity.

Biology and Pathogenesis

Cellular Structure and Anatomy

Xylella fastidiosa is a Gram-negative, rod-shaped with cells typically measuring 0.25–0.35 μm in and 0.9–3.5 μm in length. As a member of the family Xanthomonadaceae, it possesses a standard Gram-negative cell envelope comprising an inner cytoplasmic membrane, a thin layer in the periplasmic space, and an outer membrane embedded with lipopolysaccharides (LPS). The bacterium is non-flagellate and catalase-positive but oxidase-negative, reflecting adaptations for its aerobic, xylem-limited lifestyle. Motility in X. fastidiosa occurs via twitching, driven by type IV pili that extend and retract to propel cells across surfaces at speeds up to 5 μm per minute against fluid flow, facilitating upstream migration within vessels. Type I pili also contribute to this process, alongside roles in cell-cell aggregation and initiation. The outer features a rhamnose-rich O-antigen in its LPS, which modulates surface charge, adhesion to host tissues, and evasion of immune recognition by delaying innate responses. Additional ultrastructural elements include outer membrane vesicles (OMVs), which are released to influence dynamics and maturation, and exopolysaccharides such as fastidian gum that stabilize aggregates. Afimbrial adhesins, including hemagglutinins, complement pili in mediating attachment to walls without fimbrial structures. These features collectively enable persistent in the nutrient-poor, flow-resistant environment, where the bacterium forms rippled cell walls observable in electron of infected tissues.

Lifecycle, Transmission, and Disease Mechanism

Xylella fastidiosa is a gram-negative, -limited bacterium that reproduces asexually via binary fission within the vessels of susceptible host and the of its vectors. In the host, cells adhere to xylem walls, multiply to high densities, and form biofilms embedded in a matrix of extracellular polymeric substances, enabling persistent colonization from roots to shoots. Bacterial populations can reach 10^6 to 10^9 cells per gram of in advanced infections, with growth rates influenced by host and environmental factors such as optima around 25-30°C. Within vectors, the bacterium colonizes the cuticular surface of the precibarium without invading , multiplying locally to sustain transmission competence for weeks to months. Transmission occurs exclusively through xylem sap-feeding insects, primarily sharpshooter leafhoppers (Cicadellinae subfamily) in the Americas and spittlebugs (Aphrophoridae) in Europe, in a manner that is propagative, persistent, and non-circulative. Acquisition happens during vector feeding on infected plants, where bacteria adhere to and colonize the vector's foregut within hours, with no evidence of multiplication beyond the mouthparts or systemic spread in the insect. Inoculation into a new host requires mechanical injection via the stylet during xylem probing, often within minutes of acquisition, as there is no extrinsic incubation period; efficiency varies by vector species, with some achieving over 50% transmission rates after brief acquisition access. The pathogen does not persist in soil, seeds, or propagate vegetatively without vectors, limiting natural spread to insect-mediated dispersal over distances of tens to hundreds of meters per generation. The disease mechanism centers on xylem dysfunction induced by bacterial colonization, leading to hydraulic failure rather than direct toxin production. formation and bacterial aggregates, augmented by host-derived polymers like and gums, occlude vessels, reducing by up to 80% in symptomatic tissues; this triggers , , and reduced water transport, manifesting as marginal scorch and canopy dieback. Incompatible interactions may involve plant defenses such as or that limit bacterial titers below pathogenic thresholds, while susceptible hosts exhibit minimal resistance, allowing unchecked proliferation. Secondary effects include altered in hosts, promoting tylose and gel formation that exacerbates blockage, with symptom onset typically 3-12 months post-inoculation depending on strain virulence and environmental stress.

Hosts and Vectors

Susceptible Host Plants

Xylella fastidiosa possesses an exceptionally wide host range, infecting more than 600 plant species across over 80 families, including both agricultural crops and or ornamental plants. While many hosts remain and serve as reservoirs for the bacterium, facilitating its spread without overt symptoms, certain species exhibit severe upon , particularly under favorable environmental conditions. The European Food Safety Authority's host plant database, updated through systematic literature reviews, lists 696 species as of December 2023, with 439 confirmed by at least two independent detection methods such as PCR and culture isolation; subsequent updates in 2025 added 14 more naturally infected species. Susceptibility varies by bacterial subspecies and strain, with experimental inoculations demonstrating potential infection in additional species beyond those naturally observed. For example, subsp. fastidiosa predominantly affects North American hosts like grapevines, whereas subsp. pauca shows preference for olives in Mediterranean and South American contexts. Key symptomatic hosts include:
  • Grapevines (Vitis spp.): Primary host for Pierce's disease in California and other U.S. regions, leading to vine decline and reduced yields.
  • Olives (Olea europaea): Causes olive quick decline syndrome (OQDS) in Italy and Brazil, characterized by leaf scorching and tree dieback, with infections confirmed in over 100 cultivars.
  • Citrus (Citrus spp.): Associated with citrus variegated chlorosis (CVC) in Brazil and citrus leaf scorch in Florida, impacting fruit quality and tree longevity.
  • Almonds (Prunus dulcis): Induces almond leaf scorch in California, contributing to premature defoliation and nut crop losses.
  • Oleander (Nerium oleander): Develops oleander leaf scorch, a notable ornamental host with visible wilting and marginal necrosis.
Other hosts encompass ( spp.), blueberries ( spp.), and various species like and plums, where diseases such as phony peach disease occur. Forest and riparian species, including maples (Acer spp.) and sycamores ( spp.), often act as symptomless carriers in natural ecosystems, underscoring the bacterium's role in complex transmission networks. Recent studies have identified potential European hosts in the family, such as poplars ( spp.) and willows (Salix spp.), through experimental challenges, though natural infections remain rare.

Insect Vectors and Transmission Dynamics

Xylella fastidiosa is transmitted semipersistently by xylem-sap-feeding in the families Cicadellidae (s) and Cercopidae (spittlebugs), which acquire the bacterium during feeding on infected plants and inoculate it into healthy hosts via contaminated mouthparts. In its native American range, over 20 species vector the , with the (Homalodisca vitripennis) exhibiting high efficiency in transmitting strains causing Pierce's disease in grapevines, due to its broad host range and dispersal capabilities. The blue-green sharpshooter (Graphocephala atropunctata) also serves as a key vector in vineyards. In , where the bacterium was introduced around 2013, the meadow spittlebug (Philaenus spumarius) is the primary vector for subspecies pauca strains driving quick decline , with nymphs acquiring the from weeds and adults dispersing it to crops. Other spittlebugs, such as Neophilaenus campestris, contribute regionally but with lower efficiency. Transmission occurs propagatively within vectors: bacterial cells, acquired via ingestion, adhere to the —specifically the precibarium and cibarium—form biofilms via cell-cell signaling (e.g., diffusible signal factors), and multiply without entering the or salivary glands. This colonization is lifelong in adults, enabling persistent inoculative transmission during subsequent probing, where bacteria are dislodged into plant vessels within 15–30 seconds of stylet insertion, often without requiring prolonged feeding. Nymphs can acquire X. fastidiosa but transmit at lower rates, as efficiency peaks in adults post-molting; no transstadial or transovarial passage occurs, limiting vertical spread. Vector competence varies by , bacterial strain, and environmental factors, with American sharpshooters showing higher rates for X. fastidiosa subsp. fastidiosa than European spittlebugs for subsp. pauca. Dynamics of spread hinge on vector phenology, density, and host-switching behavior: spittlebug nymphs aggregate on low herbaceous plants in spring, acquiring from reservoir weeds before adults migrate to woody crops in summer, amplifying epidemics in fragmented landscapes. Sharpshooters, by contrast, exhibit more continuous activity and longer dispersal flights (up to 100 km), facilitating rapid regional outbreaks, as modeled in compartmental frameworks incorporating vector population stages and latency. Bacterial disruption in vectors—potentially via quorum-sensing inhibitors—has been proposed to curtail transmission, though field efficacy remains unproven. Empirical studies confirm no mechanical (non-propagative) transmission, underscoring the obligate role of biological vectors in cycles.

Major Diseases and Symptoms

Pierce's Disease in Grapevines

Pierce's disease (PD) is a destructive and lethal bacterial infection primarily affecting grapevines ( and related hybrids), caused by the xylem-limited pathogen subsp. fastidiosa. The bacterium colonizes the plant's water-conducting vessels, forming biofilms and inducing tylose production, which progressively blocks water and nutrient transport, resulting in chronic drought-like stress even under adequate irrigation. Infected vines typically decline and die within 1 to 5 years, with no known cure, though symptom onset can be delayed in cooler climates. Characteristic symptoms emerge in late summer under hot, dry conditions, beginning with marginal scorching or that starts at the tips and edges, often bounded by a green halo. Affected leaves may abscise prematurely while petioles remain attached to the , leading to a "matchstick" appearance; this is distinct from other scorch diseases due to the persistent petiole. On canes, irregular, multifocal lesions develop with dark, sunken areas and gum , while fruit clusters shrivel and dry unevenly. Severe infections cause defoliation, cane dieback from the tips, and , with vines showing delayed bud break and reduced yield in subsequent seasons. Diagnosis is confirmed via laboratory tests like or PCR, as symptoms mimic abiotic stresses or other pathogens. Transmission occurs primarily through xylem-feeding insects, notably sharpshooter leafhoppers such as the (Homalodisca vitripennis) in , which acquire the bacterium from infected plants and inoculate healthy ones during feeding. Long-distance spread happens via infected propagation material, including cuttings and nursery stock. The pathogen's persistence in weed hosts amplifies local epidemics, with disease pressure highest in warm, humid regions below 1,000 meters elevation where vectors thrive. In , PD has caused epidemics since the early 20th century, particularly devastating the southern wine and industries, with annual economic losses exceeding $104 million from reduced yields, vine replacement, and regulatory controls as of 2014 estimates. Public investments in vector and have mitigated further spread, growers approximately $56 million annually by preventing broader outbreaks. relies on vector suppression via systemic insecticides, roguing infected , and planting resistant cultivars like certain Vitis labrusca hybrids or PD-tolerant selections such as '1103 Paulsen' , though no V. vinifera varieties are fully immune. avoiding vector habitats and practices further limit incidence.

Olive Quick Decline Syndrome

Olive Quick Decline Syndrome (OQDS), also known as sindrome del disseccamento rapido dell'olivo (SDRO), is a lethal disease of olive trees (Olea europaea) caused by the bacterium Xylella fastidiosa subsp. pauca (Xfp), particularly sequence type ST53. The pathogen infects the xylem vessels, obstructing water and nutrient transport, which leads to systemic wilt and eventual tree death. First reported in the Salento region of Apulia, southern Italy, in late 2013, the outbreak has since spread to over 1 million hectares of olive groves, prompting EU quarantine measures. Symptoms typically begin with scorching and drying of leaves on twigs and branches in the upper canopy, resembling drought stress or fire damage, followed by defoliation and dieback that progresses downward to the trunk within 1-2 months. Affected trees exhibit reduced fruit yield, with wood cross-sections revealing brown streaking indicative of bacterial colonization. Susceptibility varies by ; highly vulnerable varieties include Ogliarola salentina and Cellina di Nardo, while Leccino shows partial resistance through differential and anatomy that limits bacterial and formation. Co-infections with fungal pathogens like Neofusicoccum spp. can compound symptoms, producing distinct branch cankers. The disease is vectored primarily by the meadow spittlebug (), which transmits Xfp during feeding on , with potential via infected propagation material. In , the epidemic has caused economic losses exceeding €132 million on affected farms, with models projecting up to €5.6 billion in total damages over 50 years if unchecked, including reduced production and landscape degradation. Recent detections in Spain's island highlight ongoing risks of further spread within the Mediterranean basin.

Citrus Variegated Chlorosis

Citrus variegated chlorosis (CVC) is a bacterial disease primarily affecting sweet orange (Citrus sinensis) and other citrus species, caused by Xylella fastidiosa subsp. pauca. The pathogen colonizes the xylem vessels, obstructing water and nutrient transport, which leads to characteristic foliar symptoms and reduced plant vigor. Symptoms were first observed in 1984 in sweet oranges in Alto Paraná, Misiones Province, Argentina, though not identified as CVC until later; the disease was confirmed in São Paulo State, Brazil, in 1987, where it rapidly spread across citrus groves. Early foliar symptoms include interveinal on young leaves, appearing as irregular yellow mottling or that mimics but persists despite fertilization; affected leaves may curl upward and become leathery. As the disease progresses, older leaves exhibit severe with green islands, canopy thinning, twig dieback, and stunting of shoots and overall tree growth. Fruit production declines due to smaller, harder fruits with thicker rinds and higher seed counts, often remaining green and smaller than normal, reducing marketable yield by 10-14% in affected Brazilian orchards. In severe cases, trees show defoliation, branch , and premature decline, with infection rates reaching up to 100% in unmanaged groves. The bacterium is transmitted by xylem-feeding insects, primarily sharpshooter leafhoppers such as Dilobodius spp. and Oncometopia spp. in , which acquire and spread the during feeding. Unlike other X. fastidiosa , the CVC strain induces systemic leading to upward curl and foliar hardening due to callose deposition in , exacerbating hydraulic dysfunction. CVC remains confined largely to and northern , with recent detections in as of 2015, posing risks to global given Brazil's output of over 14 million tons annually, representing more than one-third of worldwide orange supply. relies on via insecticides, rogueing infected trees, and planting on resistant rootstocks like Citrus limonia, though no curative treatments exist and economic losses persist in smallholder farms.

Other Associated Diseases

Xylella fastidiosa causes oleander leaf scorch in Nerium oleander, characterized by yellowing along leaf margins followed by scorching at the tips and edges, progressing to twig dieback and branch cankers, with symptoms often appearing in summer and persisting year-round in mild climates. The disease was first confirmed in in 1993, where the bacterium was isolated from symptomatic plants and fulfilled through inoculation studies demonstrating systemic colonization and symptom induction. Transmission occurs via xylem-feeding insects like Homalodisca vitripennis, with no effective chemical controls, leading to recommendations for removal of infected plants to prevent spread. Almond leaf scorch, prevalent in orchards since the , manifests as marginal leaf with a distinctive golden-yellow band separating scorched tissue from green areas, often termed "golden death" due to premature defoliation and tree decline over 3–5 years. The subsp. fastidiosa strain blocks vessels, inducing water stress, with disease incidence reaching up to 20% in untreated groves by the 1990s before vector management reduced spread. Hosts include Prunus dulcis, with glassy-winged sharpshooters as key vectors; cultural practices like applications targeting vectors have limited economic losses estimated at millions annually in affected regions. Coffee leaf scorch, primarily affecting in , features irregular marginal and apical scorching on mature leaves, accompanied by stunted shoots and , with symptoms emerging on young flushes and leading to reduced yield by up to 30% in infected plantations. Caused by subsp. pauca, the disease was linked to X. fastidiosa in the 1990s through culturing and pathogenicity tests, showing bacterial populations exceeding 10^6 cells per gram of tissue in symptomatic plants. transmit the , with no resistant varieties identified, prompting reliance on rogueing and . Bacterial leaf scorch affects diverse shade trees such as oaks (Quercus spp.), elms (Ulmus spp.), and maples (Acer spp.) in the eastern and , presenting as irregular marginal leaf browning starting on older foliage, with J-shaped discolorations and premature leaf drop recurring annually. The subsp. multiplex colonizes , causing chronic decline over 5–10 years, with detection via or PCR confirming bacterial presence at densities sufficient to occlude vessels. Incidence has risen since the , linked to introduction via nursery stock, with management limited to and injections offering temporary symptom suppression but no cure. Phony peach disease in Prunus persica involves exaggerated vegetative growth ("phony" shoots), small deformed fruit, and leaf mottling, first described in in the 1890s and associated with X. fastidiosa subsp. multiplex through isolation and fulfillment of in controlled inoculations. Symptoms reduce fruit quality and yield by over 50%, with vectors facilitating spread in southeastern U.S. orchards; the disease's persistence despite sanitation efforts underscores the bacterium's broad host range and efficient xylem limitation.

Epidemiology and Distribution

Historical Origins and Spread

Xylella fastidiosa is a xylem-limited bacterium native to the Americas, where it has long been associated with diseases in a wide array of plants including grapes, citrus, and coffee. The earliest documented outbreak occurred in the late 19th century, with Pierce's disease of grapevines first described in 1892 by plant pathologist Newton B. Pierce in southern California, where it devastated vineyards by causing leaf scorch, wilting, and plant death. Pure cultures of the bacterium were not isolated until 1978 from infected grapevines, confirming its role as the causal agent. By the mid-20th century, the pathogen's distribution across North, Central, and South America was well-established, with subspecies such as fastidiosa (affecting grapes and almonds), multiplex (affecting stone fruits and maples), and pauca (affecting coffee and citrus) adapted to regional hosts and vectors like sharpshooter leafhoppers. The bacterium's spread beyond the began in the early through international plant trade, with reporting subsp. fastidiosa in grapevines by 2002. In Europe, X. fastidiosa was first detected in October 2013 in olive trees in Italy's region ( peninsula), marking the initial outbreak of subsp. pauca sequence type ST53, which caused olive quick decline syndrome (OQDS) with symptoms of leaf scorching, branch dieback, and tree mortality. Genetic analysis traced this strain to Central American origins, likely introduced via an ornamental plant imported from around 2008. By 2015, the infection had spread to over 1 million olive trees in , prompting quarantine measures, though containment failed due to efficient local vectors like the spittlebug . Subsequent detections accelerated the pathogen's European footprint: subsp. multiplex was found in Corsica and mainland France in 2015 on ornamental Polygala myrtifolia, subsp. fastidiosa in Mallorca, Spain, in 2016, and further outbreaks in mainland Spain (Alicante, 2017) and Portugal by 2018. These introductions, primarily via asymptomatic host plants, exploited the absence of natural immunity in European flora and favorable climates in the Mediterranean basin, leading to over 20 million infected olive trees across affected regions by 2024. Outside Europe, detections in Israel (2017) and the Middle East highlight ongoing risks from global trade, with no evidence of natural long-distance dispersal absent human-mediated vectors. ![Olive grove affected by Xylella fastidiosa in Surano, Lecce, Italy][float-right]

Current Global Outbreaks and Risk Factors

Xylella fastidiosa is endemic across North, Central, and , where it sustains outbreaks in key crops including grapevines affected by Pierce's disease in and citrus trees with variegated chlorosis in . In , the bacterium was first confirmed in Italy's region in 2013, causing extensive olive decline, and has since been detected in , , and , with subspecies fastidiosa, multiplex, and pauca identified in limited demarcated areas. Recent European developments include new findings in Occitanie, , in 2023 and subsp. fastidiosa in , , in 2024. Emerging detections outside traditional ranges signal expanding threats, with first reports in continental in 2024, and in 2023, on in 2024, and in 2024. Genomic analyses of sequence read archives indicate potential unrecognized infections in and , alongside new host . hosts subspecies fastidiosa and taiwanensis, contributing to regional disease pressure. Primary risk factors for outbreaks and spread center on vector-mediated transmission by xylem-feeding insects, including spittlebugs like in and sharpshooters in the , which acquire the bacterium from infected and inoculate healthy ones during feeding, with winged adults enabling regional dispersal. Human-facilitated introduction via of asymptomatic infected nursery stock and ornamentals drives long-distance incursions, as the pathogen's latency in hosts evades visual inspections. Climatic conditions favoring establishment include subtropical and tropical climates with mild winters and hot, dry summers, where models project high-risk zones primarily in the but potential northward shifts in and elsewhere under scenarios for 2050 and 2070. The bacterium's broad host range exceeding 700 across 88 families amplifies potential in diverse agroecosystems.

Detection and Diagnosis

Laboratory and Field Methods

Laboratory detection of Xylella fastidiosa primarily relies on molecular techniques such as (PCR), which offers high sensitivity for identifying the bacterium in plant tissues, including symptomatic and asymptomatic samples. Real-time PCR and nested PCR variants enable quantification and subspecies differentiation, with protocols standardized for quarantine applications, detecting as few as 10-100 bacterial cells per reaction. (LAMP) provides a faster alternative, amplifying DNA at constant temperature without thermal cycling, suitable for resource-limited labs and validated for X. fastidiosa subspecies. Serological methods like (ELISA) use monoclonal antibodies for antigen detection but exhibit lower sensitivity than PCR, often requiring confirmation. Bacterial isolation on selective media, such as PW or CSAA agar, remains the gold standard for confirmation but is hindered by the pathogen's fastidious growth, taking 10-30 days. Advanced genomic tools, including metagenomic sequencing, allow strain identification from environmental DNA extracts, bypassing cultivation and revealing co-occurring microbes, though they demand bioinformatics expertise and higher costs. Recombinase polymerase amplification (RPA)-based kits, like AmplifyRP XRT+, enable isothermal detection in under 30 minutes with minimal equipment, showing 95-100% accuracy against qPCR in field-collected samples. Sample preparation involves grinding petioles or sap extraction, with DNA yields optimized using kits like CTAB or commercial columns to minimize inhibitors from polyphenolic hosts like . Field methods emphasize visual scouting for symptoms such as leaf scorching, , or dieback, which prompt targeted sampling but can miss latent infections with incubation periods up to 12 months. Portable diagnostics, including lateral flow devices and battery-operated real-time LAMP systems, facilitate on-site testing of crude extracts, achieving detection limits comparable to lab PCR within 1 hour. Insect-based surveillance deploys "spy" vectors like to trap and test for the bacterium via PCR, aiding early spread prediction in high-risk areas. via or multispectral indices (e.g., NDVI, PRI) detects physiological stress in canopies pre-symptomatically, with models classifying infected trees at 85-90% accuracy from drone or data. These approaches integrate with EPPO protocols, recommending combined visual-molecular confirmation to balance speed and specificity in outbreak zones.

Molecular and Genomic Tools

Molecular detection of Xylella fastidiosa primarily relies on (PCR)-based assays targeting conserved genetic regions such as the 16S rRNA gene or -specific sequences. Real-time quantitative PCR (qPCR) methods, including multiplex tetraplex assays, enable simultaneous detection and differentiation of like X. fastidiosa subsp. pauca and multiplex, with sensitivities reaching femtogram levels in extracts. Novel genus-specific qPCR assays, such as X-ComEC targeting the citrate-malate-lyase , provide universal detection of X. fastidiosa and related species like X. taiwanensis, validated across diverse strains with no to non-target . Isothermal amplification techniques, including (LAMP), offer field-deployable alternatives to PCR by requiring minimal equipment and enabling visual detection. Colorimetric LAMP (cLAMP) variants, using hydroxy naphthol dye, allow naked-eye identification of X. fastidiosa in tissues within at constant temperature, achieving detection limits comparable to qPCR in infected orchards. Droplet digital PCR (ddPCR) enhances quantification accuracy in low-titer samples from woody chips, outperforming traditional qPCR in sensitivity for early infections. Genomic tools leverage next-generation sequencing for confirmatory diagnosis and typing beyond initial screening. Metagenomic sequencing directly from or identifies X. fastidiosa and sequence types in under three days, bypassing culture requirements and revealing co-infections. Nanopore-based ampli-seq workflows, combining targeted PCR amplification with portable sequencing, resolve X. fastidiosa at the strain level (e.g., MLST sequence types) from multiple host species, with run times of hours and compatibility for field labs. Targeted enrichment protocols facilitate whole-genome sequencing from crude extracts, enabling phylogenetic and profiling without prior isolation. These approaches, while higher-throughput, complement molecular assays by providing epidemiological resolution during outbreaks.

Economic and Ecological Impacts

Agricultural and Economic Losses

Xylella fastidiosa has inflicted substantial agricultural losses across major crop-producing regions, primarily through diseases like Pierce's disease in grapes, olive quick decline syndrome (OQDS) in , and citrus variegated chlorosis (CVC) in . In , Pierce's disease alone imposes annual costs exceeding $100 million on the winegrape industry, encompassing vine losses, reduced production, and mitigation efforts. Without ongoing control programs funded by growers and taxpayers, these losses could double to $104 million yearly in foregone production and vine replacements. In Italy's Puglia region, OQDS caused by X. f. subsp. pauca has devastated olive orchards, with over one million trees affected and economic losses reaching €132 million on monitored farms in Salento as of recent analyses. Between 2016 and 2018, yield shortfalls equated to 10% of national olive production, costing nearly €390 million, alongside tree removal and replanting expenses. Broader modeling projects potential European-wide impacts up to €20 billion if unchecked spread occurs, driven by production halts and market disruptions. In Brazil, CVC has reduced citrus yields by 10-14% nationally, with pronounced effects on sweet orange production in São Paulo state, the world's largest orange producer. This translates to millions of tons in annual output losses, compounded by higher management costs and tree replacements, though exact monetary figures remain tied to fluctuating global juice markets. Smallholder farms face disproportionate burdens, exacerbating regional economic strain. These cases underscore X. fastidiosa's role in threatening high-value perennial crops, where recovery timelines span decades due to long maturation periods.

Environmental and Biodiversity Effects

Xylella fastidiosa infections, particularly by subspecies pauca in Puglia, Italy, have induced substantial alterations to olive-dominated landscapes, impairing ecosystem service provisioning by 34% in the short term and 30% in the long term. These disruptions encompass diminished regulation of soil erosion, reduced primary production, and degradation of habitats with high conservation value. The bacterium's impact extends to genetic diversity within olive populations, contributing to a projected 28% reduction in overall biodiversity components in affected areas. In urban and semi-natural olive forests, the disease prompts shifts in land use toward uncultivated soils, with approximately 66,475 hectares of historical olive groves in Lecce Province showing severe infection rates, including 51% of monumental trees. This leads to habitat and nursery function losses, adversely affecting associated fauna and local biodiversity. Ecosystem regulation services, such as carbon sequestration—estimated at 2600 kg CO₂ per century-old tree—face interruption, though partial recovery may occur within 30–40 years through replanting efforts. Globally, X. fastidiosa threatens ecosystem health by infecting over 500 plant species, potentially inducing enduring ecological shifts and plant diversity declines, particularly under scenarios that favor vector activity and pathogen proliferation. In introduced European contexts, these effects manifest prominently in Mediterranean agroecosystems with environmental overlap, whereas native North American forests exhibit no reported serious damage, highlighting strain-specific and host-dependent variability in ecological consequences.

Control and Management

Vector and Spread Mitigation

The primary vectors of Xylella fastidiosa are xylem-feeding insects, predominantly sharpshooter leafhoppers (Cicadellidae) in the and spittlebugs (Cercopidae) in . Key species include the (Homalodisca vitripennis), which transmits Pierce's disease to grapes and other hosts across and the southeastern U.S., and the meadow spittlebug (), responsible for outbreaks of olive quick decline syndrome in , , since 2013. These vectors acquire the bacterium from infected plants during feeding and transmit it to healthy ones without a latent period, facilitating rapid local epidemics. Chemical control targets immature stages to minimize adult populations and transmission risk. Neonicotinoid insecticides such as and provide effective suppression of H. vitripennis nymphs in , with applications in early spring to adjacent habitats like groves reducing immigration into vineyards by up to 70% when combined with barriers. In EU regulations, phytosanitary treatments with approved plant protection products are mandated prior to removal of infected plants in demarcated zones, focusing on vector knockdown in infected (50 m radius) and buffer (up to 5 km) areas to curb short-distance spread. Biological control leverages natural enemies for sustainable vector reduction. The predator has been modeled for inundative release against P. spumarius, with lab data showing predation completion in approximately 50 minutes and simulations indicating that 2.25% predator-to-prey ratios (e.g., 4,000 individuals per ) can limit X. fastidiosa incidence to under 10% in orchards within two years, comparable to chemical but with lower environmental impact. Egg parasitoids such as Gonatocerus ashmeadi and G. triguttatus have reduced H. vitripennis populations in field trials, while entomopathogenic fungi like Hirsutella spp. show promise in evaluations. Field validation remains essential for broader adoption. Cultural practices integrated with vector monitoring mitigate spread by disrupting habitats. Weed removal and ploughing in host-free buffer zones target alternative feeding sites for vectors like P. spumarius, reducing nymphal development and adult dispersal in EU containment strategies. In grape-growing regions, managing riparian vegetation curbs populations of related sharpshooters, with regulatory approvals required for efficacy. Area-wide integrated pest management, combining these approaches with annual surveys per EFSA guidelines, emphasizes early intervention to prevent epidemic thresholds, though challenges persist in diverse agroecosystems.

Plant Removal, Quarantine, and Cultural Practices

In regions affected by Xylella fastidiosa, such as Puglia, Italy, where the bacterium causes olive quick decline syndrome, plant removal serves as a primary eradication strategy, involving the uprooting of infected trees and surrounding host plants within a 100-meter radius of outbreaks to interrupt transmission cycles. This approach, mandated under emergency measures since 2015, has led to the destruction of over 300,000 olive trees by 2018 in containment zones, though its efficacy diminishes once the pathogen establishes widespread reservoirs in wild flora. In , for Pierce's disease management, prompt removal of symptomatic upon detection—ideally before vector-mediated spread—limits local epidemics, with programs like the Pierce's Disease Control Program documenting reduced incidence through systematic since 2001. Similarly, in the , , elimination of infected and other hosts in demarcated areas, combined with buffer zones, has contained subsp. multiplex outbreaks as part of annual surveillance protocols updated in 2022. Quarantine protocols form the cornerstone of preventing introduction and interstate or international spread, with X. fastidiosa designated a quarantine pest under EU (EU) 2016/2031, prohibiting the movement of susceptible (over 300 listed, including olives, grapes, and almonds) from infested areas without certification. Implementing (EU) 2020/1201, amended through 2025, enforces demarcated zones with planting bans on hosts and mandatory inspections, enabling containment in where initial outbreaks were traced to imported coffee in 2013. In the United States, USDA APHIS imposes federal on interstate shipment of host materials from infested states like , requiring post-entry and heat treatments for propagation stock to eliminate latent infections, as outlined in recovery plans for like citrus variegated chlorosis. These measures, extended in via state legislation like AB 1861 in 2024, include vector host surveys and material tracing to avert economic losses exceeding $100 million annually from Pierce's . Cultural practices complement removal and by enhancing host resilience and reducing inoculum sources, including through the excision of symptomatic branches and destruction of to minimize bacterial reservoirs in tissues. In groves, adaptive —such as severe cuts to 20-30% of canopy in early stages—has shown limited success in slowing systemic progression of subsp. pauca, with trials in indicating up to 25% reduction in bacterial titers when performed annually from 2016 onward, though regrowth often reinfects without . Optimized and fertilization, shifting from traditional dry-farming to deficit drip systems, bolster tree vigor against stress that exacerbates symptoms, as demonstrated in Balearic zones where balanced delayed decline in 70% of treated almonds by 2022. Dormant-season in grapevines, avoiding wet periods to limit vector activity, further integrates with away from riparian hosts, aligning with integrated guidelines that emphasize certified disease-free planting stock to sustain long-term .

Resistance Breeding and Biotechnological Approaches

Traditional breeding programs have focused on identifying and selecting host plant varieties with natural tolerance or resistance to Xylella fastidiosa, particularly in olives and grapes, where the pathogen causes significant diseases like olive quick decline syndrome and Pierce's disease. In olives, cultivars such as Leccino and FS-17 (also known as Favolosa) exhibit stable resistance characterized by lower bacterial titers and reduced symptom severity following inoculation with X. fastidiosa subsp. pauca, the strain prevalent in Europe. Surveys of natural olive populations under high inoculum pressure have revealed heritable resistance traits in Leccino offspring, supporting ongoing selective breeding efforts to develop commercial resistant hybrids. In grapes, wild Vitis species like V. arizonica demonstrate multigenic resistance, with genome-wide association studies identifying candidate genes involved in defense responses; resistance appears polyphyletic and influenced by environmental factors such as aridity in southwestern U.S. accessions. Breeding populations confirm that multiple genomic regions contribute to reduced vascular colonization and symptom expression, enabling introgression of these traits into cultivated V. vinifera. Biotechnological strategies complement breeding by targeting molecular mechanisms of resistance, though applications specific to X. fastidiosa remain developmental. (RNAi) has been explored to silence pathogen or vector genes, with potential for host-delivered dsRNA to disrupt bacterial adhesion or formation, but field efficacy trials are limited. CRISPR/Cas9 genome editing offers promise for enhancing host resistance through targeted modifications, such as knocking out susceptibility factors or overexpressing defense genes; while successfully applied to vectors like the , direct editing in host plants like grapes and olives is emerging via identification of resistance loci from cross-species transcriptomics and protein interaction networks. In , has produced transgenic varieties resistant to X. fastidiosa-related diseases by altering pathways, providing a model for broader application despite regulatory hurdles. approaches integrating transcriptomics have pinpointed conserved resistance genes across hosts, facilitating precise biotechnological interventions, though multigenic nature and off-target risks necessitate rigorous validation. Challenges include the pathogen's broad host range and vector dependence, underscoring the need for integrated breeding-biotech pipelines over reliance on single-gene edits.

Genomic Research and Advances

Genome Sequencing Milestones

The complete of Xylella fastidiosa strain 9a5c, responsible for citrus variegated chlorosis and belonging to subspecies pauca, was sequenced in 2000 by the , led by A.J.G. Simpson at the São Paulo Center in . This 2.73 million chromosome, published on July 13, 2000, represented the first fully assembled of any plant-pathogenic bacterium, revealing features such as a high proportion of TonB-dependent transporters and two rRNA operons, which informed early understandings of its xylem-limited lifestyle and host adaptation mechanisms. Shortly thereafter, the of X. fastidiosa subsp. fastidiosa strain Temecula-1, associated with Pierce's in grapevines, was completed, spanning approximately 2.73 Mb and deposited in public databases around the same period, enabling initial between strains affecting different crops. This pairwise comparison highlighted genetic similarities in pathogenicity islands while identifying strain-specific virulence factors, such as type IV secretion systems absent in the strain. Subsequent milestones included draft and complete genomes for subsp. multiplex, which affects stone fruits and oaks; for instance, a draft sequence of the Stag's Leap strain (causing Pierce's disease) was released in 2016, followed by complete hybrid assemblies of strains like , LM10, and RH1 in 2020 using Illumina and PacBio data, each around 2.5–2.6 Mb. High-quality draft genomes for subsp. pauca strains from and hosts emerged in 2020, supporting phylogeographic studies of European outbreaks. Advancements in long-read sequencing technologies facilitated a surge in complete, circularized genomes post-2020, including five historic subsp. fastidiosa strains assembled via and Illumina in 2023, and subsp. sandyi strains like CO33 in 2024, enhancing resolution of recombination events and core genome conservation across over 70 strains analyzed by 2019. These efforts have expanded the to over 4,500 orthologous gene clusters, underscoring ongoing without saturation.

Recent Scientific Developments

In 2025, analysis of the NCBI Sequence Read Archive uncovered previously unrecognized genomic data for Xylella fastidiosa, revealing potential new and hotspots in the , , and , thereby expanding knowledge of its global distribution beyond reported outbreaks. Concurrently, complete sequencing of X. fastidiosa subsp. multiplex strains isolated from provided detailed insights into the pathogen's and European origins, aiding in tracing introduction pathways. Studies on pseudogenization processes in X. fastidiosa genomes, published in April 2025, demonstrated how inactivation contributes to host specificity across strains, with pseudogenes accumulating in lineages adapted to particular hosts like olives or almonds, potentially driving pathogenicity . Comparative genomic analyses of subsp. pauca strain ST-74 from , reported in early 2025, highlighted genetic markers of adaptation and dispersal risks, underscoring the pathogen's potential for further continental spread via trade. A June 2025 investigation revealed that X. fastidiosa releases extracellular vesicles laden with small RNAs, DNA-binding proteins, and non-ribosomal RNA-binding proteins, proposing a model where these vesicles modulate in both bacterial and host cells, offering a mechanism for and host manipulation. Additionally, metagenomic-assembled genomes for X. fastidiosa associated with leaf scorch, assembled in September 2025, furnished high-resolution resources for studying subsp. multiplex in nut crops, facilitating targeted diagnostics and resistance strategies. Research on across 94 X. fastidiosa genomes, detailed in September 2024, quantified their role in enhancing pathogenicity through , with prophages and insertion sequences comprising up to 5% of certain strains' genetic content and correlating with expanded host ranges. These findings collectively advance genomic surveillance and inform predictive modeling for outbreak prevention.

Policy and Controversies

Regulatory Responses and Quarantine Debates

![Olivenhain mit Xylella fastidiosa bei Surano LE 190710][float-right] Xylella fastidiosa is classified as a quarantine pest under the European Union's Regulation (EU) 2016/2031 on protective measures against pests of plants, mandating strict controls to prevent its introduction and spread. Following its detection in Italy's Apulia region in 2013, the EU implemented emergency measures via Commission Implementing Decision (EU) 2015/789, which required member states to conduct surveys, demarcate infected zones, and eradicate the bacterium through the destruction of infected plants and those in containment or buffer zones. These measures include prohibitions on moving host plants from affected areas without certification, insecticide applications to control vectors like the spittlebug Philaenus spumarius, and intensified monitoring. In , regional authorities in faced challenges implementing these protocols, leading to the EU Commission referring to the Court of Justice in June 2018 for inadequate eradication efforts, particularly failure to uproot infected trees and establish buffer zones as required. By 2018, over a million trees had been destroyed in containment efforts, yet the disease continued to spread due to delays attributed to legal challenges and public opposition. Italian legislation responded with at least 46 regional laws since 2013 to address monitoring, compensation for farmers, and alternative strategies like experimental treatments, though compliance with EU directives remained contentious. Debates surrounding quarantine measures center on their efficacy and socioeconomic costs, with critics arguing that mandatory tree removal overlooks the cultural value of ancient groves in Puglia, where trees over 500 years old symbolize heritage and livelihoods. EFSA assessments confirm no field-effective curative treatments exist, emphasizing that incomplete eradication allows vector-mediated spread, but proponents of alternatives advocate for integrated approaches including resistant cultivars and biocontrol over aggressive culling. Socio-environmental conflicts have arisen, including protests against demolitions and lawsuits delaying actions, exacerbating the outbreak to affect over 21 million trees by 2021. While policy prioritizes containment to protect broader , Italian stakeholders debate the proportionality of measures, citing limited success in halting subsp. pauca's advance despite billions in damages.

Criticisms of Management Strategies

Management strategies for Xylella fastidiosa have faced criticism for their limited effectiveness in eradicating the once established in host plants, particularly in open-field conditions. The (EFSA) assessed various in planta controls, including chemical treatments like , , and biocomplexes, as well as biological agents such as endophytic microorganisms and bacteriophages, finding they may reduce symptoms temporarily but fail to eliminate the bacterium from tissues. This limitation stems from the pathogen's residence in biofilms within the xylem, rendering antimicrobials inaccessible and ineffective without risking broader environmental harm or . Eradication policies, such as the mandatory removal of infected under EU regulations, have drawn significant backlash for their socioeconomic and cultural impacts, especially in 's Puglia region where the pauca has devastated over 20 million olive trees since 2013. Critics argue that uprooting centenary olive trees—protected by heritage laws—prioritizes over preserving irreplaceable landscapes, leading to delays in implementation that allowed unchecked spread beyond initial zones. The referred to the Court of Justice in 2018 for inadequate enforcement of measures, highlighting how local resistance and logistical challenges undermined efforts to prevent further dissemination. Debates persist over buffer zone sizes, with reductions from 20 km to 5 km under updated EU rules (2020/1201) questioned for potentially insufficiently curbing vector-mediated transmission. Vector control via insecticides targets xylem-feeding insects like spittlebugs but is hampered by the pathogen's transmission by any such insect species, lacking vector specificity, and regulatory bans on neonicotinoids due to pollinator risks. In Puglia, prolonged adult vector activity from May to October limits the temporal window for effective sprays, while alternatives like entomopathogenic fungi remain unproven at scale. These constraints contribute to broader critiques that integrated strategies—relying heavily on monitoring, pruning, and host removal—are reactive and costly for perennial crops with long incubation periods, often failing to restore infected mature trees economically viable. Environmental concerns include the ecological fallout from mass tree removal and insecticide applications, which disrupt biodiversity in affected agroecosystems without guaranteed containment. Some stakeholders have challenged the causal attribution of olive decline solely to X. fastidiosa, citing potential cofactors like drought or prior decline, though scientific consensus affirms the bacterium's primary role based on Koch's postulates fulfillment. Overall, these strategies are viewed as inadequate for endemically established outbreaks, prompting calls for accelerated research into resistant varieties and novel biocontrols over prolonged reliance on suppressive measures.

References

  1. https://www.sciencedirect.com/topics/immunology-and-microbiology/xylella-fastidiosa
  2. https://www.microbiologyresearch.org/content/journal/micro/10.1099/mic.0.001091
  3. https://pmc.ncbi.nlm.nih.gov/articles/PMC8698212/
  4. https://journals.plos.org/plospathogens/article/file?id=10.1371/journal.ppat.1009813&type=printable
  5. https://bsppjournals.onlinelibrary.wiley.com/doi/10.1111/mpp.12585
  6. https://escholarship.org/content/qt7dx2n5mt/qt7dx2n5mt.pdf
  7. https://www.ncbi.nlm.nih.gov/sites/books/NBK390431/
  8. https://www.frontiersin.org/journals/plant-science/articles/10.3389/fpls.2025.1608687/pdf
  9. https://oajournals.fupress.net/index.php/pm/article/download/14171/13117/26615
  10. https://www.aphis.usda.gov/sites/default/files/gwss-ea.pdf
  11. https://nph.onlinelibrary.wiley.com/doi/pdf/10.1111/nph.18089
  12. https://microbiologysociety.org/blog/on-the-horizon-xylella-fastidiosa.html
  13. http://file.lacounty.gov/SDSInter/acwm/1010013_Xyellafastidiosa.pdf
  14. https://www.apsnet.org/publications/plantdisease/backissues/Documents/1990Articles/PlantDisease74n07_522.PDF
  15. https://www.frontiersin.org/journals/plant-science/articles/10.3389/fpls.2017.00944/full
  16. https://lpsn.dsmz.de/species/xylella-fastidiosa
  17. https://www.annualreviews.org/doi/10.1146/annurev-phyto-080417-045849
  18. https://bexylproject.org/what-is-xylella-fastidiosa/
  19. https://apsjournals.apsnet.org/doi/10.1094/PHYTO-05-20-0167-A
  20. https://pmc.ncbi.nlm.nih.gov/articles/PMC6581164/
  21. https://bmcgenomics.biomedcentral.com/articles/10.1186/s12864-019-5565-9
  22. https://pmc.ncbi.nlm.nih.gov/articles/PMC2446567/
  23. https://bsppjournals.onlinelibrary.wiley.com/doi/10.1111/ppa.13248
  24. https://apsjournals.apsnet.org/doi/10.1094/PHYTOFR-01-24-0004-A
  25. https://pmc.ncbi.nlm.nih.gov/articles/PMC6637975/
  26. https://www.microbiologyresearch.org/content/journal/ijsem/10.1099/00207713-37-2-136
  27. https://journals.asm.org/doi/10.1128/jb.187.16.5560-5567.2005
  28. https://pubmed.ncbi.nlm.nih.gov/17322192/
  29. https://pmc.ncbi.nlm.nih.gov/articles/PMC5786101/
  30. https://www.apsnet.org/publications/phytopathology/backissues/Documents/1994Articles/Phyto84n06_591.pdf
  31. https://pmc.ncbi.nlm.nih.gov/articles/PMC11577798/
  32. https://apsjournals.apsnet.org/doi/10.1094/PHYTO-07-18-0239-FI
  33. https://pmc.ncbi.nlm.nih.gov/articles/PMC6835679/
  34. https://academic.oup.com/aesa/article/99/5/884/12172
  35. https://nph.onlinelibrary.wiley.com/doi/10.1111/nph.18089
  36. https://www.nature.com/articles/s41598-019-46092-0
  37. https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1009813
  38. https://www.efsa.europa.eu/en/efsajournal/pub/8477
  39. https://efsa.onlinelibrary.wiley.com/doi/10.2903/j.efsa.2025.9563
  40. https://pmc.ncbi.nlm.nih.gov/articles/PMC7009507/
  41. https://www.cabidigitallibrary.org/doi/full/10.1079/cabireviews202217021
  42. https://www.biorxiv.org/content/10.1101/2022.06.10.495618v1.full-text
  43. https://www.ars.usda.gov/oc/dof/zooming-in-on-sharpshooters-and-spittlebugs/
  44. https://onlinelibrary.wiley.com/doi/10.1111/aen.12397
  45. https://pmc.ncbi.nlm.nih.gov/articles/PMC5320020/
  46. https://pmc.ncbi.nlm.nih.gov/articles/PMC12027782/
  47. https://pmc.ncbi.nlm.nih.gov/articles/PMC341844/
  48. https://apsjournals.apsnet.org/doi/10.1094/PHYTO-05-16-0202-R
  49. https://journals.asm.org/doi/10.1128/aem.01102-24
  50. https://apsjournals.apsnet.org/doi/10.1094/PHYTO-12-22-0460-IA
  51. https://apsjournals.apsnet.org/doi/10.1094/PHYTO-11-22-0428-V
  52. https://academic.oup.com/jipm/article/8/1/12/3745634
  53. https://pmc.ncbi.nlm.nih.gov/articles/PMC6143690/
  54. https://pnwhandbooks.org/plantdisease/host-disease/grape-vitis-spp-pierces-disease
  55. https://www.arec.vaes.vt.edu/content/dam/arec_vaes_vt_edu/alson-h-smith/grapes/pathology/extension/factsheets/pierces_disease.pdf
  56. https://www.sjvtandv.com/blog/pierces-disease-in-the-san-joaquin-valley
  57. https://fieldreport.caes.uga.edu/publications/B1514/pierces-disease-of-grape-identification-and-management/
  58. https://extension.umd.edu/resource/pierces-disease-background-and-management
  59. https://www.cabidigitallibrary.org/doi/full/10.1079/cabicompendium.57195
  60. https://www.apsnet.org/edcenter/apsnetfeatures/Pages/Pierces.aspx
  61. https://extension.okstate.edu/programs/digital-diagnostics/plant-diseases/pierces-disease-of-grape.html
  62. https://www.universityofcalifornia.edu/news/newly-identified-enzyme-may-be-culprit-pierces-disease-grapevine-damage
  63. https://www.business.qld.gov.au/industries/farms-fishing-forestry/agriculture/biosecurity/plants/priority-pest-disease/pierces-disease
  64. https://californiaagriculture.org/article/108923-pierce-s-disease-costs-california-104-million-per-year/attachment/213859.pdf
  65. https://www.researchgate.net/publication/271351252_Pierce%27s_disease_costs_California_104_million_per_year
  66. https://vinecon.ucdavis.edu/blog/new-study-shows-pierces-disease-investment-saves-winegrape-growers-56-million-annually
  67. https://pmc.ncbi.nlm.nih.gov/articles/PMC10609838/
  68. https://botany.one/2021/09/susceptibility-to-olive-quick-decline-syndrome-is-linked-to-xylem-anatomy/
  69. https://www.frontiersin.org/journals/plant-science/articles/10.3389/fpls.2022.968934/full
  70. https://daily.jstor.org/the-a-to-x-of-olive-quick-decline-syndrome/
  71. https://edis.ifas.ufl.edu/publication/IN1165
  72. https://pmc.ncbi.nlm.nih.gov/articles/PMC6345699/
  73. https://www.efsa.europa.eu/en/topics/topic/xylella-fastidiosa
  74. https://bsppjournals.onlinelibrary.wiley.com/doi/abs/10.1111/ppa.13627
  75. https://bsppjournals.onlinelibrary.wiley.com/doi/abs/10.1111/ppa.14069
  76. https://www.pnas.org/doi/10.1073/pnas.1912206117
  77. https://oajournals.fupress.net/index.php/pm/article/view/15891
  78. https://www.cdfa.ca.gov/citrus/pests_diseases/cvc.html
  79. https://crec.ifas.ufl.edu/research/citrus-production/disease-identification/exotic-citrus/citrus-variegated-chlorosis/
  80. https://apsjournals.apsnet.org/doi/10.1094/PDIS-02-19-0302-RE
  81. https://apsjournals.apsnet.org/doi/10.1094/PD-89-0687B
  82. https://www.sciencedirect.com/topics/agricultural-and-biological-sciences/citrus-variegated-chlorosis
  83. https://www.alice.cnptia.embrapa.br/alice/bitstream/doc/748808/1/Current-situation-management-and-economic-impact-of-citrus-variegated-chlorosis-in-Brazil.pdf
  84. https://www.researchgate.net/publication/341393746_Citrus_Variegated_Chlorosis_an_Overview_of_30_Years_of_Research_and_Disease_Management
  85. https://www.researchgate.net/publication/305655544_Citrus_variegated_chlorosis_Xylella_fastidiosa
  86. https://pmc.ncbi.nlm.nih.gov/articles/PMC7555403/
  87. https://apsjournals.apsnet.org/doi/10.1094/PHYTO.1999.89.1.53
  88. https://www.iucngisd.org/gisd/species.php?sc=326
  89. https://ipm.ucanr.edu/agriculture/almond/almond-leaf-scorch/
  90. https://apsjournals.apsnet.org/doi/pdf/10.1094/PDIS.1998.82.1.94
  91. https://pubmed.ncbi.nlm.nih.gov/30857077/
  92. https://extension.msstate.edu/publications/bacterial-leaf-scorch
  93. https://www.missouribotanicalgarden.org/gardens-gardening/your-garden/help-for-the-home-gardener/advice-tips-resources/insects-pests-and-problems/diseases/bacterial-spots/bacterial-leaf-scorch
  94. https://auf.isa-arbor.com/content/isa/33/6/376.full.pdf
  95. https://planthealthportal.defra.gov.uk/assets/uploads/EvidenceStatement-XylellaFastidiosa.pdf
  96. https://apsjournals.apsnet.org/doi/10.1094/PHYTO-03-22-0105-R
  97. https://www.microbiologyresearch.org/content/journal/mgen/10.1099/mgen.0.000727
  98. https://pmc.ncbi.nlm.nih.gov/articles/PMC9742796/
  99. https://apsjournals.apsnet.org/doi/10.1094/PHYTO-08-18-0319-FI
  100. https://www.eppo.int/ACTIVITIES/plant_quarantine/shortnotes_qps/shortnotes_xylella
  101. https://food.ec.europa.eu/plants/plant-health-and-biosecurity/plant-health-rules/control-measures/xylella-fastidiosa/latest-developments-xylella-fastidiosa-eu-territory_en
  102. https://www.promegaconnections.com/a-silent-killer-tracking-the-spread-of-xylella-fastidiosa/
  103. https://neobiota.pensoft.net/article/53208/
  104. https://gd.eppo.int/taxon/XYLEFA/reporting
  105. https://www.agriculture.gov.au/biosecurity-trade/import/industry-advice/2025/01-2025
  106. https://pmc.ncbi.nlm.nih.gov/articles/PMC12542735/
  107. https://www.nature.com/articles/s41598-025-18286-2
  108. https://journals.asm.org/doi/10.1128/AEM.69.7.4249-4255.2003
  109. https://pmc.ncbi.nlm.nih.gov/articles/PMC8547472/
  110. https://pubmed.ncbi.nlm.nih.gov/37249884/
  111. https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0221903
  112. https://pmc.ncbi.nlm.nih.gov/articles/PMC165181/
  113. https://journals.asm.org/doi/10.1128/msystems.00591-21
  114. https://apsjournals.apsnet.org/doi/10.1094/PHYTOFR-03-22-0025-FI
  115. https://www.frontiersin.org/journals/plant-science/articles/10.3389/fpls.2018.02007/full
  116. https://onlinelibrary.wiley.com/doi/10.1111/epp.12923
  117. https://www.mdpi.com/2077-0472/13/2/448
  118. https://www.nature.com/articles/s41598-018-33957-z
  119. https://www.sciencedirect.com/science/article/pii/S003442572200387X
  120. https://pmc.ncbi.nlm.nih.gov/articles/PMC6719857/
  121. https://www.frontiersin.org/journals/plant-science/articles/10.3389/fpls.2019.01732/full
  122. https://link.springer.com/article/10.1007/s13313-025-01051-4
  123. https://www.mdpi.com/2076-3417/15/2/739
  124. https://apsjournals.apsnet.org/doi/10.1094/PDIS-12-24-2568-RE
  125. https://bsppjournals.onlinelibrary.wiley.com/doi/10.1111/ppa.13416
  126. https://www.sciencedirect.com/science/article/abs/pii/S0167701223000532
  127. https://bsppjournals.onlinelibrary.wiley.com/doi/10.1111/ppa.13877
  128. https://bsppjournals.onlinelibrary.wiley.com/doi/10.1111/ppa.14069?af=R
  129. https://www.fsid.co/newsroom/blog/olive-trees-puglia-xylella-fastidiosa-landscape-change/
  130. https://www.bbc.com/news/science-environment-52234561
  131. https://www.sciencedirect.com/science/article/pii/S026121942030452X
  132. https://pmc.ncbi.nlm.nih.gov/articles/PMC6695699/
  133. https://homed-project.eu/getatt.php?filename=cpaa029_2068.pdf
  134. https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0232363
  135. https://ipm.ucanr.edu/agriculture/grape/pierces-disease/
  136. https://food.ec.europa.eu/plants/plant-health-and-biosecurity/plant-health-rules/control-measures/xylella-fastidiosa_en
  137. https://ec.europa.eu/commission/presscorner/api/files/document/print/en/memo_15_5346/MEMO_15_5346_EN.pdf
  138. https://www.sciencedirect.com/science/article/abs/pii/S0261219424002102
  139. https://pmc.ncbi.nlm.nih.gov/articles/PMC9780951/
  140. https://eur-lex.europa.eu/legal-content/EN/TXT/HTML/?uri=CELEX:02020R1201-20250701
  141. https://wineinstitute.org/press-releases/legislation-introduced-to-extend-pierces-disease-control-program/
  142. https://www.frontiersin.org/journals/plant-science/articles/10.3389/fpls.2025.1608687/full
  143. https://www.mdpi.com/2073-4395/12/12/2917
  144. https://pmc.ncbi.nlm.nih.gov/articles/PMC8228964/
  145. https://gardenerspath.com/how-to/disease-and-pests/pierces-disease/
  146. https://pmc.ncbi.nlm.nih.gov/articles/PMC7168594/
  147. https://biovexo.eu/a-new-study-indicates-presence-of-natural-traits-of-resistance-to-xylella-fastidiosa-in-leccino-offspring/
  148. https://www.mdpi.com/2223-7747/14/2/157
  149. https://pmc.ncbi.nlm.nih.gov/articles/PMC10229667/
  150. https://www.nature.com/articles/s42003-023-04938-4
  151. https://news.uci.edu/2023/06/15/study-reveals-potential-breakthrough-in-grapevine-disease-resistance/
  152. https://www.mdpi.com/2076-0817/14/9/840
  153. https://www.nature.com/articles/s41598-022-09990-4
  154. https://bmcplantbiol.biomedcentral.com/articles/10.1186/s12870-025-07102-8
  155. https://www.sciencedirect.com/science/article/pii/S2452072119300991
  156. https://pmc.ncbi.nlm.nih.gov/articles/PMC12337395/
  157. https://pubmed.ncbi.nlm.nih.gov/10910347/
  158. https://pmc.ncbi.nlm.nih.gov/articles/PMC138861/
  159. https://nature.berkeley.edu/almeidalab/wp-content/uploads/2015/11/Retchless141.pdf
  160. https://journals.asm.org/doi/10.1128/genomeA.00240-16
  161. https://apsjournals.apsnet.org/doi/10.1094/PHYTO-05-20-0162-A
  162. https://journals.asm.org/doi/10.1128/MRA.00536-23
  163. https://pmc.ncbi.nlm.nih.gov/articles/PMC9148166/
  164. https://journals.asm.org/doi/10.1128/aem.00913-25
  165. https://pmc.ncbi.nlm.nih.gov/articles/PMC12269432/
  166. https://journals.asm.org/doi/10.1128/aem.02070-24
  167. https://www.researchgate.net/publication/387669658_Comparative_Genomics_of_Xylella_fastidiosa_Subsp_Pauca_and_Insights_on_its_Current_and_Potential_Movements_in_Ecuador
  168. https://pmc.ncbi.nlm.nih.gov/articles/PMC12189769/
  169. https://apsjournals.apsnet.org/doi/10.1094/PHYTOFR-09-24-0103-A
  170. https://bsppjournals.onlinelibrary.wiley.com/doi/10.1111/ppa.13992
  171. https://agriculture.gouv.fr/telecharger/88108?token=a8dacf083ffe576044e040fbeef9729b768a50e4d07d1181286761e777c9a9b5
  172. https://europa.eu/rapid/press-release_IP-18-3805_en.htm
  173. https://www.nature.com/articles/d41586-018-07389-8
  174. https://www.frontiersin.org/journals/forests-and-global-change/articles/10.3389/ffgc.2021.699393/full
  175. https://ejatlas.org/print/the-olive-quick-decline-syndrome-in-apulia
  176. https://www.efsa.europa.eu/en/press/news/190515-0
  177. https://neobiota.pensoft.net/article/67648/
  178. https://www.oliveoiltimes.com/business/europes-evolving-fight-against-xylella-fastidiosa/123648
  179. https://www.efsa.europa.eu/en/efsajournal/pub/5666
  180. https://apsjournals.apsnet.org/doi/10.1094/PHYTO-12-23-0476-KC
  181. https://pmc.ncbi.nlm.nih.gov/articles/PMC8397937/
Add your contribution
Related Hubs
User Avatar
No comments yet.