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Botrytis cinerea
Botrytis cinerea infection on strawberry
Scientific classification Edit this classification
Kingdom: Fungi
Division: Ascomycota
Class: Leotiomycetes
Order: Helotiales
Family: Sclerotiniaceae
Genus: Botrytis
Species:
B. cinerea
Binomial name
Botrytis cinerea
Pers. (1794)

Botrytis cinerea is a necrotrophic fungus that affects many plant species, including wine grapes. In viticulture, it is commonly known as "botrytis bunch rot"; in horticulture, it is usually called "grey mould" or "gray mold".

The fungus gives rise to two different kinds of infections on grapes. The first, grey rot, is the result of consistently wet or humid conditions, and typically results in the loss of the affected bunches. The second, noble rot, occurs when drier conditions follow wetter, and can result in distinctive sweet dessert wines, such as Sauternes, the Aszú of Tokaji, or Grasă de Cotnari.[1] The species name Botrytis cinerea is derived from the Latin for "grapes like ashes"; the "grapes" refers to the bunching of the fungal spores on their conidiophores, while "ashes" refers to the greyish colour of the spores en masse.[citation needed] The fungus is usually referred to by its anamorph (asexual form) name, because the sexual phase is rarely observed. The teleomorph (sexual form) is an ascomycete, Botryotinia fuckeliana, also known as Botryotinia cinerea (see taxonomy box).

Etymology

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Botrytis is derived from the Ancient Greek botrys (βότρυς) meaning "grapes",[2] combined with the Neo-Latin suffix -itis for disease. Botryotinia fuckeliana was named by mycologist Heinrich Anton de Bary in honor of another mycologist, Karl Wilhelm Gottlieb Leopold Fuckel. Synonyms for the sexual stage are:

  • Botrytis fuckeliana N.F. Buchw., (1949)
  • Botrytis gemella (Bonord.) Sacc., (1881)
  • Botrytis grisea (Schwein.) Fr., (1832)
  • Botrytis vulgaris (Pers.) Fr., (1832)
  • Haplaria grisea Link, (1809)
  • fuckeliana de Bary
  • Phymatotrichum gemellum Bonord., (1851)
  • Polyactis vulgaris Pers., (1809)
  • Sclerotinia fuckeliana (de Bary) Fuckel, (1870)

Hosts and symptoms

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Hosts

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The disease, gray mold, affects more than 200 dicotyledonous plant species and a few monocotyledonous plants found in temperate and subtropical regions, and potentially over a thousand species.[3][4] Serious economic losses can be a result of this disease to both field and greenhouse grown crops. The causal agent, Botrytis cinerea can infect mature or senescent tissues, plants prior to harvest, or seedlings. There is a wide variety of hosts infected by this pathogen including protein crops, fiber crops, oil crops, and horticultural crops. Horticultural crops include vegetables (examples are chickpeas, lettuce, broccoli, and beans) and small fruit crops (examples are grape, strawberry, raspberry, and blackberry[5]), these are most severely affected and devastated by gray mold.[3] Plant organs affected include fruits, flowers, leaves, storage organs, and shoots.

Symptoms and signs

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Symptoms vary across plant organs and tissues. B. cinerea is a soft rot that will have a collapsed and water soaked appearance on soft fruit and leaves. Brown lesions may develop slowly on undeveloped fruit.[6] Twigs infected with gray mold will die back. Blossoms will cause fruit drop and injury, such as ridging on developing and mature fruit.[7] Symptoms are visible at wound sites where the fungus begins to rot the plant. Gray masses with a velvety appearance are conidia on the plant tissues are a sign of plant pathogen.[7] These conidia are asexual spores that will continue to infect the plant and surrounding hosts throughout the growing season making this a polycyclic disease.

Plants can produce localized lesions when a pathogen attacks. An oxidative burst causes hypersensitive cell death called a hypersensitive response (HR).[8] This soft rot can trigger HR to assist in colonization. Botrytis cinerea, as a necrotrophic pathogen, exploits the dead tissue for its pathogenicity or its ability to cause disease. Susceptible plants cannot use the HR to protect against B. cinerea.

Biology

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Conidiophore
Petri dish with a ring of visible sclerotia (dark brown balls)

Botrytis cinerea is characterized by abundant hyaline conidia (asexual spores) borne on grey, branching tree-like conidiophores. The fungus also produces highly resistant sclerotia as survival structures in older cultures. It overwinters as sclerotia or intact mycelia, both of which germinate in spring to produce conidiophores. The conidia, dispersed by wind and by rain-water, cause new infections. B. cinerea performs an asexual cycle over the summer season.[citation needed]

Gliocladium roseum is a fungal parasite of B. cinerea.[9]

The hypothetical protein BcKMO was shown to positively regulate growth and development. It showed a great similarity to the kynurenine 3-monooxygenase encoding gene in eukaryotes.[citation needed]

Overexpression of the gene atrB produces altered versions of the transcription factor mrr1, which in turn confer a multiple fungicide resistance phenotype known as MDR1.[5] An even higher overexpression yields mrr1 composed partly of Δ497V/L, yielding MDR1h phenotypes with even more anilinopyrimidine- and phenylpyrrole- resistance.[5]

Environment

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Gray mold favors moist, humid, and warm environmental conditions between 65–75 °F (18–24 °C).[10] Temperature, relative humidity, and wetness duration produce a conducive environment that is favorable for inoculation of mycelium or conidia.[11] Controlled environments, such as crop production greenhouses, provide the moisture and high temperatures that favor the spreading and development of the pathogen B. cinerea.

Standing water on plant leaf surfaces provides a place for spores to germinate.[12] Humid conditions can result from improper irrigation practice, plants placed too close together, or the structure of the greenhouse not allowing for efficient ventilation and air flow. Ventilation at night significantly reduces the incidence of gray mold.[13]

Melanized sclerotium allows B. cinerea to survive for years in the soil. Sclerotia and the asexual conidia spores contribute to the widespread infection of the pathogen.[14]

A low pH is preferred by the gray mold to perform well. B. cinerea can acidify its environment by secreting organic acids, like oxalic acid.[14] By acidifying its surroundings, cell wall degrading enzymes (CWDEs) are enhanced, plant-protection enzymes are inhibited, stomatal closure is deregulated, and pH signaling is mediated to facilitate its pathogenesis.[14]

Viticulture

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Manifesting as noble rot on Riesling grapes
Manifesting as noble rot on Riesling

In the Botrytis infection known as noble rot, the fungus removes water from the grapes, leaving behind a higher percent of solids, such as sugars, fruit acids and minerals. This results in a more intense, concentrated final product. The wine is often said to have an aroma of honeysuckle and a bitter finish on the palate.

A distinct fermentation process initially caused by nature, the combination of geology, climate and specific weather led to the particular balance of beneficial fungus while leaving enough of the grape intact for harvesting. The Chateau d'Yquem is the only Premier Cru Supérieur Sauternes, largely due to the vineyard's susceptibility to noble rot.

Botrytis complicates the fermentation process during winemaking. Botrytis produces an anti-fungal compound that kills yeast and often results in the fermentation stopping before the wine has accumulated sufficient levels of alcohol.[15]

Botrytis bunch rot is another condition of grapes caused by B. cinerea that causes great losses for the wine industry. It is always present on the fruitset, however, it requires a wound to start a bunch rot infection. Wounds can come from insects, wind, accidental damage, etc. To control botrytis bunch rot there are a number of fungicides available on the market. Generally, these should be applied at bloom, bunch closure and veraison (the most important being the bloom application). Some winemakers are known to use the German method of fermentation and prefer having a 5% bunch rot rate in their grapes and will usually hold the grapes on the vine a week longer than normal.

Horticulture

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Botrytis cinerea affects many other plants.

Strawberries

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It is economically important on soft fruits such as strawberries and bulb crops.[16] Unlike wine grapes, the affected strawberries are not edible and are discarded. To minimize infection in strawberry fields, good ventilation around the berries is important to prevent moisture being trapped among leaves and berries. A number of bacteria have been proven to act as natural antagonists to B. cinerea in controlled studies.[16]

Other plants

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Botryotinia fuckeliana on a Goudreinet apple

In greenhouse horticulture, Botrytis cinerea is well known as a cause of considerable damage in tomatoes.

The infection also affects rhubarb, snowdrops, white meadowfoam, western hemlock,[17] Douglas-fir,[18] cannabis,[19][20] and Lactuca sativa.[21] UV-C treatment against B. cinerea was investigated by Vàsquez et al., 2017. They find it increases phenylalanine ammonia-lyase activity and production of phenolics. This in turn decreases L. sativa's susceptibility.[21] Potassium bicarbonate-based fungicide may be used.[citation needed]

Human disease

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Botrytis cinerea mold on grapes may cause "winegrower's lung", a rare form of hypersensitivity pneumonitis (a respiratory allergic reaction in predisposed individuals).

Mycoviruses of Botrytis cinerea

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Mycoviruses

As well as being an infective agent, Botrytis cinerea also hosts several mycoviruses itself. A range of phenotypic alterations due to the mycoviral infection have been observed from symptomless to mild impact, or more severe phenotypic changes including reduction in pathogenicity, growth/suppression of mycelia, sporulation and sclerotia production, formation of abnormal colony sectors (Wu et al., 2010[22]) and virulence.

Management

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Botrytis cinerea can be managed through cultural, chemical, and biological practices.[23]

There are no resistant species to the gray mold rot. Gray mold can be culturally controlled by monitoring the amount and timing of fertilizer applications to reduce the amount of fruit rot. Excessive application of nitrogen will increase the incidence of disease while not improving yields.[6]

Not planting cultivars that have an upright or dense growth habit can reduce disease as these limit airflow and are favorable for the pathogen. Spacing of plants so they are not touching will increase airflow allowing the area to dry out and reduce the spread of disease. Pruning or purposeful removal of diseased, dead, or overgrown limbs on a regular schedule can also help to improve air movement.[7]

Sanitation by removing dead or dying plant tissue in the fall will decrease inoculum levels as there is no debris for the sclerotium or mycelia to overwinter. Removing debris in the spring will remove inoculum from the site. Disposal of berries during harvest that have signs and symptoms of gray mold will reduce inoculum for the following year.

Biochar, a form of charcoal, can be applied as a soil amendment to strawberry plants to reduce the severity of the fungal disease by stimulating defense pathways within the plant.[24]

Gray mold can be chemically controlled with well-timed fungicide applications starting during the first bloom. Timing can reduce the chance of resistance and will save on costs.[6]

Biological controls or microbial antagonists[citation needed] used for disease suppression, have been successfully used in Europe and Brazil in the form of fungi-like Trichoderma harzianum Rifai and Clonostachys rosea f. rosea Bainier (syn. Gliocladium roseum).[24] Trichoderma species especially, have been shown to control gray mold.

Multiple fungicide resistance is a problem in many production areas.[5]

See also

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References

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[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Botrytis cinerea

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from Grokipedia
Botrytis cinerea is a necrotrophic ascomycete belonging to the family Sclerotiniaceae, renowned for causing gray mold disease—a widespread phytopathology affecting over 500 dicotyledonous plant species, including economically vital crops such as grapes, strawberries, tomatoes, and ornamentals. This pathogen initiates infection through airborne conidia that germinate on host surfaces, particularly under humid conditions, leading to tissue necrosis via the secretion of cell wall-degrading enzymes, , and other factors that facilitate nutrient acquisition by killing host cells. While predominantly destructive, B. cinerea exhibits a dual lifestyle: in specific microclimates with alternating wet and dry periods, it induces "" in grape berries, concentrating sugars and flavors to produce prestigious botrytized wines like Sauternes and . Taxonomically, B. cinerea is classified within the phylum , class Leotiomycetes, order Helotiales, and genus , which encompasses 32 species; its teleomorph (sexual stage) is Botryotinia fuckeliana, though is rare in nature and primarily observed under laboratory conditions via mating-type loci MAT1 and MAT2. The fungus's , sequenced from strain B05.10, spans 41.2 megabases across 18 chromosomes with approximately 10,701 protein-coding genes and a 42.75% , enabling its adaptability as a generalist with a broad host range exceeding 1,400 plant species worldwide. dominates its life cycle, producing abundant conidia on branched conidiophores and dormant sclerotia (up to 4 mm in diameter) for overwintering and long-term survival in soil or plant debris. Ecologically, B. cinerea thrives in temperate and subtropical regions, ubiquitous in agricultural settings where high (>90%) and moderate temperatures (15–25°C) favor conidial and through wounds, stomata, or floral parts like stigmas and anthers, which provide nutrient-rich entry points. It transitions from an initial biotrophic phase, where it minimally damages host tissue, to a destructive necrotrophic stage, rapidly colonizing and rotting organs; this versatility allows persistence as a saprophyte on dead matter when hosts are unavailable. Environmental factors, such as and UV exposure, can suppress its spread, while its development of resistance to multiple classes—accounting for 8% of the global market—complicates . The economic ramifications of B. cinerea are profound, inflicting annual global crop losses estimated at $10–100 billion through reduced yields and post-harvest decay, with notable impacts like a 36% decline in strawberry production from 2007–2016, equating to $250 million in yearly damages. Ranked as the second most scientifically and economically significant fungal pathogen, it poses ongoing challenges in greenhouse , fruit production, and , prompting integrated strategies including resistant cultivars, biological controls, and cultural practices to mitigate its threat. Conversely, its beneficial role in winemaking underscores a unique agro-economic value, where controlled infections enhance wine quality and command premium prices in specialized markets.

Taxonomy and Nomenclature

Etymology

The genus name Botrytis derives from the word botrys (βότρυς), meaning "cluster of grapes" or "bunch," which alludes to the grape-like clustering of the fungus's conidia. This nomenclature reflects the morphological resemblance observed in early mycological studies. The specific epithet cinerea originates from the Latin cinereus, denoting "ash-gray" or "ash-colored," a description of the distinctive grayish spore masses produced by the . The name Botrytis cinerea was first proposed by the Dutch mycologist Christiaan Hendrik Persoon in 1794, in his publication Neues Magazin für die Botanik, where he described the fungus based on observations of its clusters. It received a formal description by the Swedish botanist Elias Magnus Fries in 1832, in volume 3 of Mycologicum, solidifying its place in fungal taxonomy. Early 19th-century mycologists, including Otto Fuckel, contributed to understanding the fungus's life cycle by linking the anamorph B. cinerea to its teleomorph stage, initially named Peziza fuckeliana by in 1866 and later reclassified as Sclerotinia fuckeliana by Fuckel in 1870.

Taxonomy and Classification

Botrytis cinerea belongs to the kingdom Fungi, Ascomycota, class Leotiomycetes, order Helotiales, Sclerotiniaceae, and Botrytis. This positioning reflects its placement among ascomycete fungi characterized by apothecial fruiting bodies in the teleomorphic state. The exhibits a pleomorphic life cycle, with Botrytis cinerea as the anamorph (asexual stage) producing conidia, and Botryotinia fuckeliana as the teleomorph (sexual stage) forming apothecia from sclerotia. The teleomorph was established with the Peziza fuckeliana de Bary (1866), later transferred to Botryotinia by Whetzel in 1945. The type specimen for B. cinerea was described by Persoon in 1797, based on material from rotten fruits of Cucurbita and stems of Brassica oleracea. Synonyms include Botryotinia fuckeliana and forms such as Botrytis cinerea f. coffeae Henderson (1939). Following the 2011 International Code of Nomenclature for algae, fungi, and plants adoption of the "one fungus, one name" principle, the anamorph-teleomorph connection was unified under the name Botrytis cinerea as the accepted holomorph nomenclature. This decision was endorsed by the Botrytis research community in 2013, prioritizing the widely used anamorph name due to its type species status and extensive literature. Historical variants like Botrytis cinerea f. botrytis have been subsumed under this unified classification. The current accepted nomenclature is maintained by databases such as Index Fungorum.

Morphology and Biology

Morphology

Botrytis cinerea exhibits a typical fungal morphology characterized by septate hyphae that are cylindrical, branched, and measure approximately 3–5 μm in width, appearing but may appear light brown to in older cultures. These hyphae form an extensive that can appear white initially and turn gray to brown as sporulation occurs, contributing to the characteristic fuzzy appearance of infected tissues. The asexual reproductive structures include erect, branched conidiophores that are slender, straight, and measure 0.5 to 1 mm in length and 10 to 15 μm wide at the base, narrowing toward the apex with enlarged apical cells. These conidiophores are to grayish and produce conidia in dense clusters or chains, often up to 30 conidia long, facilitated by disjunctors. Conidia of B. cinerea are unicellular, to slightly brownish, ovoid to ellipsoidal, smooth-walled, and typically measure 10 to 12 μm in length by 8 to 10 μm in width, though sizes can vary slightly with substrate. These spores form abundant grayish powdery masses on host surfaces, aiding in the visual identification of gray mold. For survival, B. cinerea produces sclerotia, which are hard, black, irregular resting structures ranging from 1 to 5 mm in diameter, initially white and turning dark due to accumulation in the outer cortex. The teleomorph stage, Botryotinia fuckeliana, features cup-shaped apothecia that are brownish and pedicellate, measuring 3 to 10 mm (up to 25 mm) in height, containing cylindrical asci with eight oblong to elliptical, hyaline ascospores per ascus, sized 6 to 9 μm long by 5 to 6 μm wide.

Life Cycle and Reproduction

Botrytis cinerea primarily reproduces asexually through the production and dispersal of conidia, which serve as the main inoculum for infection. Conidia germinate under moist conditions, producing germ tubes that typically measure 20-50 μm in length before forming appressoria for host penetration. These germ tubes enable direct penetration of intact host tissues via hyphal growth or entry through wounds, initiating colonization as a necrotroph that kills host cells to obtain nutrients. Following tissue necrosis, the fungus produces new conidiophores on dead material, releasing conidia that are dispersed by wind or rain splash to perpetuate the cycle. Sexual reproduction in B. cinerea is rare and heterothallic, occurring when compatible fuse during sclerotial development under cool, moist conditions. Sclerotia germinate to form apothecia, stalked fruiting bodies that release ascospores as secondary inoculum. These ascospores can initiate new infections, though they play a minor role compared to asexual conidia due to the infrequency of sexual events. The fungus overwinters mainly as sclerotia in soil or plant debris, providing long-term survival with viability maintained for up to 360 days or more under favorable conditions. This resting structure ensures persistence across seasons. B. cinerea exhibits a polycyclic life history, capable of completing multiple cycles within a single in environments supporting repeated production and dispersal.

Genetics and Molecular Aspects

Genome Structure

The genome of Botrytis cinerea is approximately 39–45 Mb in size, distributed across 18 chromosomes, with the reference strain B05.10 initially assembled at 39 Mb in using combined with transcriptomic data from multiple growth conditions. This assembly identified 11,701 protein-coding genes, representing about 40% of the genome, with an average of 42% and repetitive elements comprising roughly 7%, including low levels of transposable elements in the reference strain. A gapless, chromosome-level assembly of B05.10 was later achieved in using a combination of PacBio long-read sequencing, , and analysis, expanding the total size to 42.6 Mb while confirming the 18-chromosome structure and refining gene annotations to 11,701 complete models. Sequencing efforts have since expanded to multiple isolates, revealing significant strain-to-strain variability that underscores B. cinerea's adaptability as a generalist . Strains are broadly classified into two groups based on content: group I (vacuma), characterized by few or no active transposons and inability to produce the botrydial, and group II (transposa), which harbor high transposon activity (up to 20% of the in some cases) and typically produce botrydial, contributing to differences in and evolutionary dynamics. analyses of diverse isolates, including resequencing of over 80 strains, have identified a core genome of about 9,000 genes shared across populations, with accessory genes (up to 20% variability) often involving expansions in effector families, clusters, and transposon-associated regions that drive host adaptation and resistance. These studies highlight how dispensable genomic regions, including accessory chromosomes (e.g., chromosomes 17–19 varying in size and content among strains), enable rapid without disrupting core functions. Recent sequencing milestones include high-quality assemblies of isolates from agricultural settings, such as four strains from strawberries and blueberries in released in 2025, with genome sizes ranging from 41.9 to 44.9 Mb and completeness exceeding 98%, providing resources for tracking regional and resistance traits. These assemblies, generated via hybrid short- and long-read approaches, further expand the by revealing isolate-specific effector gene duplications and transposon insertions, emphasizing B. cinerea's genomic plasticity as a model for necrotrophic pathogens.

Pathogenicity Mechanisms

Botrytis cinerea employs a necrotrophic , actively killing host plant cells to acquire nutrients, primarily through the secretion of cell wall-degrading enzymes (CWDEs) and phytotoxins. Key CWDEs include polygalacturonases, which break down in plant cell walls, and cutinases, which degrade the waxy to facilitate penetration. These enzymes enable tissue colonization and nutrient release, with proteomic analyses identifying over 100 such secreted proteins during . Phytotoxins like botrydial, a , and botcinins, polyketide-derived compounds, further contribute by inducing and suppressing plant defenses; botrydial is governed by a dedicated , while botcinins exhibit redundancy in enhancement across strains.00245-X) The fungus secretes approximately 150-200 effector proteins that manipulate host immunity, with BcSpl1, a cerato-platanin member, exemplifying this strategy by eliciting a while suppressing basal defenses to promote . These effectors are often clustered with genes for secondary metabolites, such as those producing botrydial and botcinins, integrating delivery with immune evasion. pathways, particularly (MAPK) cascades, regulate these processes; the BcSak1 MAPK pathway responds to stress signals, coordinating conidial , hyphal growth, and infection structure formation essential for . Recent research highlights four molecular strategies for saponin tolerance—efflux pumping, , membrane reinforcement, and antioxidant activation—enabling B. cinerea to counter host compounds during invasion.00245-X) B. cinerea manipulates host physiology by inducing (ROS) accumulation and (PCD), exploiting these responses to expand necrotic lesions. Phytotoxins and effectors trigger ROS bursts that overwhelm plant antioxidants, leading to PCD and nutrient accessibility, while fungal antioxidants mitigate excessive ROS to protect invading hyphae. Additionally, RNAi-based interactions allow bidirectional regulation; host-derived small RNAs can silence fungal genes like those in the TOR pathway, reducing , though B. cinerea counters this via its own sRNA effectors that target plant immunity genes. These mechanisms, encoded within the ~40 Mb , underscore the fungus's adaptability as a broad-spectrum pathogen.00245-X)

Hosts and Symptoms

Host Range

Botrytis cinerea is renowned for its polyphagous nature, capable of infecting a vast array of plant , with records indicating susceptibility in over 1,600 hosts spanning multiple taxonomic groups. This broad host range encompasses 447 genera of (primarily dicotyledons), 128 genera of monocots, 20 genera of gymnosperms, 15 genera of pteridophytes, 6 genera of , and even 1 genus of bryophytes. The predominantly targets dicotyledonous plants, reflecting its evolutionary adaptation to a wide variety of dicot tissues, while infections in monocots are less common but documented. Among economically significant hosts, (grapes), Fragaria × ananassa (strawberries), and Solanum lycopersicum (tomatoes) stand out as major crops affected by gray mold, leading to substantial agricultural losses in , berry production, and vegetable cultivation. Other notable economic and ornamental hosts include roses (Rosa spp.), cannabis (Cannabis sativa), and limited monocots such as onions (Allium cepa), where the fungus exploits wounded or senescing tissues for entry. Non-agricultural hosts play a critical role as reservoirs for B. cinerea, including various weeds and ornamental that sustain populations between crop seasons and facilitate . These wild and decorative species, often dicotyledonous, harbor the without immediate economic impact but contribute to inoculum buildup in agroecosystems. Host specificity in B. cinerea is not strict, but aggressiveness varies by strain and host type; for instance, strains isolated from exhibit higher on tomato tissues compared to those from , while environmental strains show broader but variable aggressiveness across hosts like soft fruits. This strain-dependent underscores the pathogen's flexibility, enabling efficient on diverse substrates such as soft, decaying fruits.

Disease Symptoms and Signs

Initial symptoms of Botrytis cinerea infection typically manifest as water-soaked lesions on leaves, stems, and flowers, which rapidly progress to browning and soft rot within hours to days under humid conditions. These lesions often appear as irregular tan to gray spots that enlarge quickly, leading to tissue collapse and wilting. In advanced stages, the infection produces characteristic gray, fuzzy masses of and conidia, commonly known as gray mold, which become prominent on infected surfaces during high . Sclerotia, small black resting structures, may form on decayed tissues in later stages, aiding survival. Organ-specific effects include blossom blight, where flowers develop white or light-colored flecks that expand into rotted petals; fruit rot characterized by a velvety gray coating and internal decay; stem cankers featuring lesions that cause wilting above the infection site; and, in hosts such as cannabis (Cannabis sativa), bud rot in dense inflorescences during late flowering. In cannabis, the infection frequently begins internally within the compact bud structure, resulting in rapid deterioration of bracts, leaves, and floral tissues, with symptoms including sudden yellowing or death of associated leaves, gray fuzzy mold visible inside or on the bud, dark gray to brown internal rot, dusty conidial spores, mushy texture, and a musty odor. These signs progress quickly under high humidity (>70% RH) and moderate temperatures (17–24 °C), often in weeks 6–8 of flowering. Bud rot can be distinguished from natural senescence (normal fade), which involves gradual and uniform yellowing or browning of fan leaves (typically lower or older ones first) without mold, rot, odor, or mushy texture. Diagnosis of bud rot may involve gently splitting suspicious buds to reveal internal mycelium, decay, or sporulation. For instance, on grapes, these effects contribute to bunch rot with similar gray sporulation. Diagnostic confirmation involves microscopic examination revealing branched, erect conidiophores bearing chains of oval, conidia, often using 8-10x or humid chambers to induce sporulation. PCR-based methods, such as real-time quantitative PCR, enable sensitive detection of B. cinerea DNA in infected tissues, even during latent phases. The latency period, during which symptoms appear post-infection, typically ranges from 5 to 8 days under optimal conditions of high and moderate temperatures.

Environmental Influences

Favorable Conditions for Infection

Botrytis cinerea thrives under specific abiotic conditions that facilitate conidial , mycelial growth, and host penetration. Optimal temperatures for range from 15 to 25°C, supporting high rates of conidial (up to 75-80% incidence after 36 hours of wetness) and mycelial development (>90% incidence at 100% relative ). Fungal activity diminishes below 0°C, where halts, and above 30°C, where incidence drops to 20-35% even with prolonged wetness. High relative exceeding 90-93% or the presence of free water on host surfaces is critical, with conidia requiring 12-24 hours of continuous wetness to germinate and initiate penetration. No occurs below 65% relative , as dry conditions prevent spore activation. Microenvironmental factors further enhance infection risk. Poor air circulation, often exacerbated by dense plant canopies, maintains elevated levels around susceptible tissues, promoting spore deposition and development. Physical wounds or naturally senescing tissues provide essential entry points, increasing incidence by 1.5 to 5 times under moderate (80% relative humidity) or short wetness durations (6-12 hours). Seasonally, B. cinerea epidemics are most common during cool, wet periods in spring and fall, when prolonged humidity and moderate temperatures align with host vulnerability. Host physiology interacts with these conditions, showing heightened susceptibility during flowering and fruit ripening stages, as accumulating sugars and softening tissues facilitate pathogen establishment. is altering these dynamics, with warming temperatures and shifting precipitation patterns potentially expanding the pathogen's range poleward and into previously less favorable warmer regions, increasing disease pressure in new areas.

Survival and Dissemination

Botrytis cinerea persists through adverse environmental conditions primarily via specialized survival structures, including sclerotia and . Sclerotia, compact masses of hardened , form in , plant debris, or mummified fruits and provide resilience against , extreme temperatures, and microbial antagonists due to their melanized rind and protective β-glucan matrix. These structures can remain viable for up to one year in or plant residues, with some persisting through multiple seasons under favorable microhabitats. survives saprophytically within infected plant tissues, colonizing dead and serving as a secondary inoculum source. Overwintering occurs through mycelial colonization of plant structures such as buds and vascular tissues, particularly in hosts like grapevines, where latent infections in dormant buds enable resurgence in spring. Overwintering debris, including necrotic leaves and rachises, harbors mycelium that produces conidia throughout the subsequent . transmission is rare, as the infrequently colonizes viable seeds, limiting this as a primary overwintering route. Dissemination of B. cinerea relies on conidia as the principal propagules, dispersed primarily by over long ranges and by splash for short distances. carries lightweight conidia from sporulating lesions, enabling travel of several kilometers under favorable airflow, while splash propels them up to 1 meter horizontally within canopies. Insect vectors contribute occasionally to local spread, though this is not a dominant mechanism. Long-distance dissemination occurs through human-mediated pathways, such as the trade of contaminated materials like cuttings, grafts, or seeds, and the of infected . Infested or adhering to and vehicles further facilitates inter-field and international movement of the pathogen. Recent research has demonstrated the robustness of B. cinerea isolates in storage, underscoring their potential for long-term survival. A 2025 study evaluated 125 isolates stored for 2 to 6 years using methods including at −18°C and , finding viability rates of 64–78% after 6 years with , and over 90% of viable isolates retaining full pathogenicity on fruits. These findings highlight the pathogen's durability even under artificial preservation, relevant to laboratory and field contexts.

Impacts in Agriculture

Viticulture and Noble Rot

Botrytis cinerea plays a dual role in , acting as a destructive causing bunch rot while also enabling the beneficial process essential for premium sweet wines. In its pathogenic form, the fungus induces gray mold, leading to significant yield losses in production, particularly during wet vintages where infections can reduce harvests by 10-50% or more through berry rot and premature drop. Globally, the economic toll of B. cinerea on viticulture is estimated at $10-100 billion annually, stemming from direct crop reductions and quality degradation that affects wine value. Under specific environmental conditions, B. cinerea transforms into (pourriture noble), a controlled process that enhances quality for sweet wine production. This occurs in regions like Sauternes in and Tokaji in , where alternating periods of humidity and dry, sunny weather allow the fungus to penetrate skins without causing destructive decay, resulting in water evaporation that concentrates sugars and flavors. The mechanism involves fungal metabolism that dehydrates berries over 10-20 days, elevating sugar levels to 300-500 g/L while preserving aromatic compounds. Certain grape varieties exhibit heightened susceptibility to B. cinerea, influencing both disease risk and potential. Thin-skinned white cultivars such as are particularly prone due to their tight clusters and delicate skins, which facilitate fungal entry and spread under humid conditions. In botrytized wine production, management practices like selective pruning to thin clusters and promote , combined with controlled misting to maintain humidity, help induce and sustain while minimizing unwanted bunch rot. The historical significance of traces back to the 16th century, when producers in first documented the intentional use of botrytized grapes (aszú) for sweet wines, a practice born from delayed harvests during regional conflicts. This innovation spread to Sauternes in the , establishing as a cornerstone of elite sweet winemaking. During the process, B. cinerea induces key chemical changes, including a marked increase in (up to 7-10 g/L) for enhanced mouthfeel and a decrease in total acidity (to ~8 g/L) through degradation, balancing the elevated sugars. Recent climate variability poses challenges to noble rot incidence, as shifting patterns of rainfall and temperature disrupt the precise humid-dry cycles required for beneficial infection. Warmer, drier conditions in traditional regions like and Sauternes reduce opportunities for noble rot development, potentially lowering yields of botrytized grapes and threatening the production of these iconic wines.

Horticulture and Specific Crops

Botrytis cinerea poses significant challenges in , particularly affecting a range of non-grape crops through gray mold infections that lead to rot and . In strawberries, the pathogen causes fruit gray mold and crown rot, resulting in yield losses that can exceed 50% in unmanaged fields, while post-harvest decay remains a major issue during storage and due to latent infections that develop under cool, humid conditions. In tomatoes and peppers, B. cinerea induces stem lesions and cankers, often originating from wounds or infections, which are prevalent in settings where high humidity fosters epidemics; these lesions can girdle stems, leading to plant wilt and death, alongside fruit rot that softens tissues. production amplifies these risks due to enclosed environments that promote dispersal and . Among other horticultural crops, roses suffer from flower , where B. cinerea causes petal spotting and browning that progresses to full decay, especially in cut-flower production; a 2024 review highlights the pathogen's reliance on high and wounding for in this crop. In , bud rot caused by B. cinerea emerges as a destructive issue in cultivation. The disease typically presents with sudden onset in late flowering, featuring rapid yellowing or death of leaves on dense buds within 1-2 days, gray or white fuzzy mold on or inside the buds, internal dark gray or brown rot with dusty spores, mushy texture, and musty odor. Infection frequently begins inside the bud and spreads rapidly under high humidity (>60% RH) and moderate temperatures (17–24°C), resulting in substantial reductions in yield and quality. Bud rot can be distinguished from natural senescence (normal late-flowering fade), which involves gradual yellowing and browning of fan leaves—often beginning with lower or older ones first—uniformly across the plant, without mold, rot, musty odor, or mushy texture, and with buds remaining firm as the plant reallocates nutrients for ripening. Differentiation involves examining suspicious buds by gently splitting them open; the presence of mold or rot internally confirms bud rot, whereas the absence of fungal signs supports normal senescence. Soft fruits like are also impacted, with post-harvest gray mold causing rot; recent genomic analyses of isolates from fields reveal genetic diversity that influences pathogenicity in these small-fruit hosts. The economic toll of B. cinerea in is substantial, with global losses estimated between $10 billion and $100 billion annually across affected produce, including a heavy emphasis on post-harvest decay in ornamentals like roses and such as tomatoes. These losses are exacerbated in high-density plantings common to and intensive horticultural systems, where reduced airflow and increased humidity elevate incidence compared to spaced-out cultivations.

Human Health Implications

Infections in Humans

Botrytis cinerea primarily affects but can rarely cause opportunistic infections in humans through of spores or exposure via wounds, leading to pulmonary or cutaneous manifestations. These infections are uncommon and typically occur in immunocompromised individuals, such as those with , organ transplants, or underlying conditions like , though cases in apparently healthy persons have been documented. is the primary route for respiratory involvement, while wound exposure may result in localized cutaneous infections, though such reports are scarce. Pulmonary infections present as pneumonia, cavitary nodules, or plastic bronchitis, with symptoms including persistent cough and atelectasis. For instance, a 2019 case involved a 62-year-old immunocompetent man with a cavitary nodule identified incidentally, confirmed as Botrytis elliptica (a close relative) via culture and genetic sequencing from resected tissue. Similarly, a 2020 pediatric case reported plastic bronchitis and in a 5-year-old boy, diagnosed through fluid analysis using next-generation sequencing, revealing B. cinerea. Allergic reactions, such as (known as wine grower's lung or berry sorter's lung), arise from repeated inhalation and manifest as respiratory distress with fever and dyspnea. Diagnosis relies on clinical presentation, imaging (e.g., CT scans showing nodules or ), and microbiological confirmation, including fungal culture from biopsies or lavage exhibiting characteristic gray mold growth, often supplemented by molecular methods like multilocus . Invasive mycoses are rare, with only a handful of confirmed cases reported in the literature since the , predominantly pulmonary. Treatment involves antifungal agents such as azoles (e.g., ) for systemic infections, alongside supportive measures like surgical resection for localized lesions; in the 2019 adult case, wedge resection alone sufficed without recurrence, while the pediatric case resolved with and bronchoscopic cast removal. Outcomes are generally favorable with prompt intervention, though delayed in vulnerable patients can lead to complications. Occupational exposure heightens risk, particularly among grape handlers, wine workers, and greenhouse employees sorting moldy produce, where high spore concentrations during harvest or processing trigger sensitization and hypersensitivity reactions. Sensitization to B. cinerea is a concern in horticultural settings, underscoring the need for protective measures like masks in endemic areas.

Associated Mycoviruses

Mycoviruses infecting Botrytis cinerea primarily consist of double-stranded RNA (dsRNA) or positive-sense single-stranded RNA (+ssRNA) viruses, with notable examples including Botrytis cinerea hypovirus 1 (BcHV1), a +ssRNA virus with a genome of approximately 10 kb, and botycimaviruses, which belong to a proposed new family featuring bisegmented +ssRNA genomes of 2–3 kb per segment. Other common types include dsRNA viruses like Botrytis cinerea RNA virus 1 (BcRV1), with an 8.9 kb genome encoding two overlapping open reading frames. These viruses often exist as latent infections in field populations, with over 90 mycoviruses documented across diverse isolates. Infection by hypovirulence-associated mycoviruses such as BcHV1 and BcRV1 typically impairs fungal fitness, inducing hypovirulence that significantly reduces mycelial growth, sporulation, and development on host ; for instance, BcRV1-infected strains exhibit attenuated pathogenicity on fruits, with smaller diameters compared to virus-free controls. Reductions in sporulation and size can reach 30–70% in affected strains, depending on viral accumulation levels and host isolate compatibility, though some mycoviruses cause infections without altering . These effects stem from disruptions in fungal metabolic pathways, including interference with cushion formation essential for penetration. Transmission of B. cinerea mycoviruses occurs mainly intracellularly via hyphal between vegetatively compatible strains, enabling horizontal spread within fungal populations; vertical transmission through conidia or ascospores is possible but less efficient and rare for extracellular release. Hyphal fusion barriers, such as vegetative incompatibility, can limit dissemination, though certain viruses overcome these to some extent. The association of mycoviruses with B. cinerea was first reported in the late with dsRNA elements, but hypovirulence-linked viruses gained attention from 2003 onward, with BcHV1 formally identified in 2018 from symptomatic field isolates. Recent research (2023–2025) has characterized extensive mycoviral diversity in field populations and identified novel hypovirulence candidates through . Owing to their hypovirulence effects, B. cinerea mycoviruses offer biocontrol potential by vectoring viruses into virulent wild strains via , thereby reducing fungal aggressiveness and disease severity in crops without relying on chemical fungicides. Strategies involve fusion or compatible donor strains to facilitate spread, with ongoing studies evaluating stability in agricultural settings.

Management Strategies

Cultural and Biological Controls

Cultural practices play a crucial role in preventing Botrytis cinerea infections by minimizing environmental conditions favorable to the , such as high and poor . and canopy management, including shoot thinning and leaf removal in the fruit zone, improve air circulation and reduce canopy density, thereby decreasing moisture retention on surfaces. Removal of plant debris and sclerotia at the end of the season eliminates overwintering inoculum sources, while avoiding overhead irrigation prevents leaf wetting that promotes . Timing harvests to occur during dry periods further reduces post-harvest humidity exposure, limiting spread in crops like grapes and . Biological control agents offer sustainable alternatives by introducing natural antagonists that compete with or inhibit B. cinerea growth. strains, such as T-39, antagonize the through nutrient competition, production of compounds, and induction of defenses, achieving up to 50% reduction in tomato gray mold incidence in field trials. and related species, like B. velezensis, produce lipopeptides such as surfactin and fengycin that disrupt fungal membranes, with preharvest applications in vineyards showing 25-37% average efficacy against bunch rot over multiple seasons. Mycoviruses, including those inducing hypovirulence in B. cinerea strains, represent an emerging biological approach, where infected fungal isolates exhibit reduced and can potentially spread the within populations to suppress epidemics. Breeding and selection of resistant plant varieties enhance long-term management by incorporating traits that deter infection. Grape cultivars like 'Beta' (Vitis riparia × Vitis labrusca) demonstrate high resistance to gray mold due to robust berry skins and antifungal berry compounds, while Baco Blanc shows notable tolerance linked to unique grape chemistry. Varieties such as Cabernet Sauvignon and certain clones with thicker skins or elevated phenolic content provide partial resistance, reducing susceptibility in viticulture without eliminating the need for complementary practices. Integrated approaches combine multiple non-chemical methods for broader efficacy, particularly in controlled environments. UV-C irradiation in greenhouses inactivates B. cinerea conidia on surfaces, with doses followed by a dark period enhancing fungal killing by up to several logs in trials. Plant-derived essential oils, such as from or from cloves, inhibit germination and mycelial growth when applied pre- or post-harvest, maintaining quality in grapes and apples. Recent 2025 epidemiology studies on bud rot emphasize rigorous , including debris removal and humidity control below 70%, to curb rapid decay under moderate temperatures (17-24°C). Monitoring airborne conidia levels enables proactive decision-making to predict outbreaks. Volumetric spore traps, such as Hirst-type or microtiter immunospore devices, quantify B. cinerea propagules in the air, correlating spore counts with environmental factors like to forecast risks in vineyards and greenhouses. Selective media in these traps facilitate specific isolation and , supporting timely cultural interventions.

Chemical Fungicides and Resistance

Chemical fungicides, often referred to as botryticides, play a central role in managing Botrytis cinerea infections in agriculture, targeting the pathogen's growth and spore production through various modes of action. Common single-site botryticides include iprodione, a dicarboximide that inhibits lipid biosynthesis, fenhexamid, a hydroxyanilide that blocks ergosterol synthesis, and boscalid, a succinate dehydrogenase inhibitor (SDHI) from the FRAC Group 7 that disrupts fungal respiration. Multi-site protectants like chlorothalonil, which interfere with multiple metabolic processes, provide broad-spectrum control with lower resistance risk. These fungicides are typically applied preventively, such as pre-flowering sprays in crops like grapes and strawberries, to establish protective residues before infection occurs. Rotation among different fungicide classes is essential to delay resistance development, with guidelines recommending no more than two consecutive applications of the same mode of action. Efficacy trials indicate that many of these compounds achieve 70-90% disease control under optimal conditions, as summarized in environmental horticulture experiments evaluating preventive applications. Fungicide resistance in B. cinerea has emerged as a major challenge, driven by mechanisms such as target-site mutations, efflux pumps, and overexpression of detoxification enzymes. For SDHIs like boscalid, point mutations in genes (e.g., SdhB, SdhC, SdhD) alter the , conferring high-level resistance; similar mutations affect other classes, including anilinopyrimidines and QoI s. Efflux-mediated multidrug resistance (MDR), involving ATP-binding cassette transporters, enables strains to expel multiple unrelated s, contributing to cross-resistance across FRAC groups. Multiple resistant strains, exhibiting reduced sensitivity to three or more classes, are widespread, with reports from over 50 countries including the , , , , , and others, complicating control in , , and production. Sensitivity monitoring programs in strawberries and tomatoes reveal increasing resistance frequencies, often exceeding 80% for certain classes like benzimidazoles and QoIs in field populations. Recent developments include the introduction of new SDHI molecules like , which offers enhanced activity against some resistant strains due to its unique pyridinylethylbenzamide structure, though baseline sensitivity studies show emerging mutations reducing its efficacy. Innovative approaches such as (RNAi) sprays target fungal genes like Dicer-like proteins (BcDCL1/2) or trehalose-related genes for silencing, demonstrating up to 70% reduction in disease severity in trials on strawberries and tomatoes, as reviewed in studies. Ongoing sensitivity monitoring in key crops like strawberries and tomatoes informs rotation strategies, emphasizing integration with multi-site fungicides to maintain effective control. Regulatory measures have restricted certain fungicides to curb environmental and health risks, such as the European Union's 2021 ban on mancozeb, a multi-site protectant previously used against B. cinerea, due to its and endocrine-disrupting properties. This has prompted shifts toward (IPM) mandates in the EU and elsewhere, requiring rotation and reduced reliance on high-risk chemicals to sustain long-term efficacy.

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