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Powdery mildew

Powdery mildew is a common fungal disease affecting a wide array of , characterized by the appearance of white to gray, powdery fungal growth on the surfaces of leaves, stems, flowers, and sometimes fruits, caused by obligate biotrophic fungi in the order that require living host tissue for survival and reproduction. These fungi, belonging to genera such as Erysiphe, Golovinomyces, Podosphaera, and Blumeria, are highly specialized, with most species infecting only specific host plants, though collectively they impact thousands of angiosperm species including crops, ornamentals, and wild plants. The powdery appearance results from chains of asexual conidia produced on the surface of the host, which spread via wind and germinate without the need for free water, enabling infection in dry conditions. Symptoms typically begin as small white patches that expand to cover larger areas, leading to (yellowing), , leaf distortion, premature defoliation, and reduced , which can significantly lower crop yields and aesthetic value in ornamental . Unlike downy mildews, powdery mildew fungi grow epiphytically on the surface without penetrating deeply into tissues, though they form haustoria to extract nutrients, creating localized "green islands" of sustained host vitality amid infection. The disease thrives in warm daytime temperatures (around 20–30°C or 68–86°F) with cooler nights and high relative (above 95%), but low light and poor air circulation exacerbate outbreaks; it is particularly problematic in semi-arid regions and greenhouses. Economically, powdery mildew poses a major threat to , affecting key crops like cereals (Triticum aestivum, Hordeum vulgare), cucurbits (Cucumis sativus, Cucurbita spp.), peas (Pisum sativum), grapes, and roses, with global losses estimated in billions due to reduced productivity and the need for applications. Overwintering occurs through dormant sexual structures (chasmothecia) or in plant debris, with primary infections in spring leading to secondary spread via conidia throughout the . relies on cultural practices like improving airflow, using resistant varieties, and targeted fungicides, while research focuses on host-pathogen interactions and biocontrol to mitigate its widespread impact.

Overview

Definition and characteristics

Powdery mildew refers to a group of diseases caused by obligate biotrophic fungi in the order of the phylum , characterized by the formation of conspicuous white, powdery mycelial growth on the surfaces of infected tissues such as leaves, stems, and fruits. These fungi cannot survive on dead material or in soil and rely entirely on living host plants for nutrients, making them highly host-specific pathogens that infect a wide range of angiosperms across agricultural, horticultural, and natural ecosystems. The disease manifests as superficial, effuse patches of fungal hyphae that give the affected areas a dusty, flour-like appearance, often leading to reduced and plant vigor. Key morphological features of powdery mildew fungi include their predominantly epiphytic mycelium, which spreads across the host surface without penetrating deeply into tissues, and specialized haustoria that form intracellularly within epidermal cells to absorb nutrients. Asexual reproduction occurs through chains or single conidia—hyaline, barrel-shaped spores—that serve as the primary means of dispersal via wind, enabling rapid epidemic spread under favorable conditions. In the sexual phase, fungi produce cleistothecia, closed, flask-shaped fruiting bodies containing asci and ascospores, which overwinter and facilitate long-distance dissemination when ejected or carried by rain splash. Unlike , which is caused by pathogens that produce sporangia on the plant's lower surfaces and require free water for , powdery mildew develops externally on both sides, enters cells directly without using stomata, and thrives in warm, dry environments with high at night. This superficial growth and environmental preference distinguish powdery mildew as a true fungal disease adapted to arid conditions, contrasting with the more invasive, moisture-dependent nature of . Powdery mildew imposes substantial economic burdens globally by diminishing crop yields, quality, and market value in sectors like , , and , with annual management costs exceeding hundreds of millions of dollars in major production regions such as vineyards. For instance, in grape production alone, the disease can reduce quality and necessitate intensive applications, highlighting its role as one of the most economically significant foliar pathogens.

Historical significance

Early observations of powdery mildew appear in ancient texts, with in the BCE describing symptoms such as white coatings on leaves in his work on , marking one of the earliest recorded recognitions of the disease. However, specific identification of powdery mildew as a fungal occurred much later, with formal taxonomic classification advancing in the through mycologists like Fries, who in his Systema Mycologicum (1821–1832) described and named numerous species in the genus Erysiphe, establishing the foundational nomenclature for powdery mildews within the . These efforts shifted perceptions from vague "blights" to structured , enabling targeted study. The pivotal historical event for grape powdery mildew (Erysiphe necator, formerly Uncinula necator) was its introduction to Europe from North America, first reported in England in 1845 and independently identified in France in 1847 by researchers like William Tucker and Miles Joseph , who described it as a novel cryptogamic parasite devastating vineyards. This outbreak, paralleling the concurrent crisis, triggered widespread decline across Europe in the mid-19th century and prompting empirical remedies like dusting—initially a folklore practice adapted from earlier uses on peaches in 1821. The epidemic underscored the vulnerability of European Vitis vinifera to exotic pathogens, accelerating the transition from traditional remedies to scientific pathology during the 1800s. Key contributions from figures like furthered this evolution; in 1863, he elucidated the of a powdery mildew species (Sphaerotheca castagnei), including the role of haustoria in nutrient absorption from host plants, solidifying fungi as causal agents of disease. By the 20th century, severe epidemics of cereal powdery mildews, such as Blumeria graminis on , ravaged intensive cropping systems in and , driving innovations in development like benzimidazoles in the 1960s, though early resistance emerged by 1969. These events highlighted the pathogen's economic impact, with losses exceeding 20% in untreated fields, and spurred integrated management strategies. Post-2000 genomic studies have revolutionized understanding, revealing extensive and evolutionary history; for instance, analyses of 172 B. graminis genomes traced its global spread along trade routes, uncovering ancient variants that inform resistance breeding. This molecular era builds on historical milestones, emphasizing powdery mildews' from the onward.

Symptoms and Diagnosis

Visible symptoms

The primary visible symptom of powdery mildew infection is the appearance of white to gray powdery patches on the surfaces of leaves, stems, flowers, and fruits, consisting of fungal and conidia. These patches often develop on both the upper and lower leaf surfaces, though they are more prominent on the upper side in many hosts. The powdery growth gives the affected parts a dusty or flour-like coating, which can be easily rubbed off in early stages. As the infection progresses, the initial small, circular spots expand and coalesce into larger patches, leading to chlorosis (yellowing) of the surrounding leaf tissue. In severe infections, powdery mildew can cause and of host tissue, though it primarily affects the surface without deep penetration. Infected leaves may curl upward or become distorted, particularly in warm, dry conditions, and severe infections can cause premature defoliation as leaves wither and drop. This reduces the plant's photosynthetic capacity, contributing to overall weakening. On fruits, symptoms include superficial russeting—a rough, brownish discoloration—or cracking of the skin, especially in crops like apples and cucurbits. Symptom expression varies by host plant and tissue age, with denser fungal growth typically observed on young, actively growing tissues such as new leaves and shoots, which are more susceptible due to thinner cuticles. On mature tissues, infections are less common and sparser. In conditions of high relative humidity, which favor the despite requiring dry leaf surfaces for spore , the powdery growth remains characteristic. Secondary effects of visible symptoms include stunted growth and significant yield reductions, with losses reaching up to 50% in severely affected susceptible crops like or cucurbits. These impacts arise from impaired and resource allocation to infected areas, but the disease does not typically kill the host outright.

Diagnostic methods

Field diagnosis of powdery mildew typically begins with visual inspection for the characteristic white, powdery fungal growth on surfaces, such as leaves, stems, or fruits. This superficial and conidia can be confirmed using a rub-off test, where gently rubbing the affected area with a finger or tape transfers the powdery residue, distinguishing it from non-fungal coatings. For more precise field-level verification, microscopic examination is essential. Using a dissecting or compound , diagnosticians observe conidiophores—specialized hyphae bearing chains or single conidia on the surface—and haustoria, which are intracellular feeding structures penetrating epidermal cells. Clear tape pressed onto infected can collect samples for slide preparation, allowing identification of fungal without destroying the specimen. In laboratory settings, molecular methods like (PCR) targeting the (ITS) regions of provide species-specific identification with high sensitivity, detecting latent infections before symptoms appear. Quantitative real-time PCR (qPCR) further enables pathogen quantification, achieving detection limits as low as 1 pg/μL of fungal DNA. Serological assays, such as (ELISA), detect specific fungal antigens in plant extracts, offering rapid results though requiring specialized equipment. Advanced diagnostic tools enhance resolution and early detection. Transmission or scanning electron microscopy reveals ultrastructural details, such as conidial surface wrinkles or haustorial interactions with cells, aiding taxonomic confirmation in research contexts. , using wavelengths from 400–1000 nm, non-invasively detects early infection (3–6 days post-inoculation) through changes in , with partial models achieving over 82% accuracy in severity assessment. Challenges in include differentiating powdery mildew from similar white coatings caused by pests like mealybugs, which produce waxy secretions and may be accompanied by or , unlike the uniform fungal powder. Molecular methods like provide high accuracy for , though amplification failures can occur in some taxa due to variability.

Causative Agents

Taxonomy

Powdery mildew fungi belong to the phylum , class Leotiomycetes, order , and primarily the Erysiphaceae, which encompasses over 900 species distributed across 19 genera. These obligate biotrophic fungi form a monophyletic within the , characterized by their unique ectoparasitic lifestyle and production of superficial mycelia. The Erysiphaceae is the sole family in the order , with all known powdery mildew species classified therein following extensive taxonomic revisions. Among the key genera, Erysiphe represents the largest, comprising more than 50% of the (approximately 450) with a broad taxonomic scope that has incorporated former genera such as Microsphaera and Uncinula through emendation. Blumeria is notable for its specialized adaptation, encompassing primarily on grasses, while Podosphaera includes taxa on rosaceous , and the former Uncinula (now synonymous with Erysiphe) features on grapes. Other significant genera include Golovinomyces, Phyllactinia, and Sawadaea, contributing to the family's diversity through distinct morphological traits in their anamorphic and teleomorphic stages. Phylogenetic studies, particularly those utilizing nuclear ribosomal DNA sequences such as 18S rDNA and (ITS) regions, have confirmed the of the and delineated its internal structure into major lineages. Early molecular analyses divided the order into subgroups I-IV based primarily on variations in (chasmothecial) appendages and conidial morphology, with subsequent refinements identifying five principal clades corresponding to traditional tribes: Erysipheae (lacking appendages), Microsphaereae (with mycelioid appendages), Uncinuleae (with uncinate appendages), Cystotheceae (with bullate basal appendages), and Phyllactinieae (with rigid, dichotomously branched appendages). These subdivisions highlight in appendage simplification and underscore the order's ancient divergence, estimated at around 76 million years ago. The nomenclature of powdery mildews traces back to Linnaean beginnings, with the first binomial name, Mucor erysiphe L. (1753), later reassigned to Phyllactinia guttata based on Linnaeus's description in . Early classifications relied on morphological features like appendages, as detailed in monographs by (1900) and (1987), which recognized about 515 species. Post-1990s revolutionized the field, leading to generic recircumscriptions—such as the expansion of Erysiphe and establishment of new genera like Neoerysiphe—and a comprehensive update in and Cook's 2012 monograph, which cataloged approximately 820 species. Recent multi-locus phylogenetic studies (2024-2025) continue to describe new species and refine classifications, such as in the ongoing series on Erysiphe and Podosphaera lineages. Ongoing revisions, incorporating multi-locus data, continue to refine this framework, emphasizing the integration of morphological and genetic evidence.

Diversity of species

Powdery mildew fungi encompass over 900 described in the Erysiphaceae, all biotrophs that cannot be cultured on artificial and rely entirely on living host for growth and reproduction. These demonstrate remarkable in host specificity, with roughly 700 infecting dicotyledonous hosts—such as those in the , , and families—and about 150 targeting monocotyledonous , primarily in the . This distribution underscores their evolutionary adaptations to diverse plant lineages, enabling colonization of over 10,000 angiosperm worldwide while maintaining narrow ecological niches in most cases. A key aspect of their diversity lies in varying degrees of host range adaptation, ranging from monophagous species restricted to single host genera or families to polyphagous ones capable of infecting multiple plant families. For instance, Blumeria graminis, a monophagous pathogen, primarily infects cereal crops within the Poaceae family, with distinct formae speciales adapted to specific hosts like barley (f. sp. hordei) or wheat (f. sp. tritici). In contrast, Golovinomyces cichoracearum exhibits polyphagous behavior, infecting hosts across families including Asteraceae, Solanaceae, and Cucurbitaceae, which facilitates broader dispersal and adaptation to varied environments. Notable examples include Erysiphe necator, which specifically targets grapevines (Vitis spp.) in the Vitaceae, causing significant economic losses in viticulture; Podosphaera mors-uvae (formerly Sphaerotheca mors-uvae), a specialist on strawberries (Fragaria spp.) and other Rosaceae; and Erysiphe diffusa (formerly Microsphaera diffusa), which affects sunflowers (Helianthus spp.) and other Asteraceae. These adaptations highlight how species-level traits, such as conidial morphology and germination patterns, align with host physiology and environmental conditions. Genetic diversity within powdery mildew species further enhances their adaptability, driven by intraspecific variation in that regulate sexual recombination and generate novel genotypes. Post-2010 genomic studies have illuminated this variation, revealing mosaic genome structures with expanded gene families encoding effectors and factors; for example, sequencing of genomes has mapped avirulence genes linked to recognition and mapped quantitative loci for aggressiveness. Similarly, analyses of Golovinomyces spp. have identified polymorphisms in mating-type idiomorphs (MAT1-1 and MAT1-2) that promote genetic exchange, contributing to rapid of under selection pressure from resistant . Such insights from high-throughput sequencing underscore the role of genomic in sustaining and pathogenicity across powdery mildews.

Life Cycle

Infection process

The infection process of powdery mildew begins when wind-dispersed conidia land on a susceptible host plant surface, such as leaves or stems. These asexual spores adhere to the host and germinate rapidly under high relative (above 85%) but without requiring free , typically within 2-4 hours at optimal temperatures of 15-25°C. involves the emergence of a primary germ tube, followed by a secondary germ tube that differentiates into an within 6-12 hours, which generates to facilitate penetration. Penetration occurs directly through the host epidermal via a peg from the , usually within 24-48 hours post-inoculation, without killing the host cells. Inside the host cell, the forms haustoria—specialized feeding structures that invaginate the and absorb nutrients—typically within 24-48 hours of . Following successful , superficial spreads across the host surface, colonizing epidermal cells while remaining ectoparasitic, enabling nutrient uptake and colony expansion without deep tissue invasion. The latency period, from conidial to the appearance of visible symptoms like white mycelial patches, lasts 3-7 days under favorable conditions of 15-25°C and high . During this phase, the establishes and multiplies internally before external growth becomes evident. Dispersal primarily occurs through -blown conidia released from mature colonies, capable of traveling up to several kilometers to initiate secondary infections on nearby or distant hosts. spread can also happen via air currents or means, but long-distance dissemination relies on favorable patterns.

Reproduction

Powdery mildew fungi primarily reproduce asexually during the , producing conidia in chains at the tips of specialized hyphae called conidiophores that emerge from the surface . These conidia, typically barrel- or oval-shaped, are released in large numbers and dispersed by wind, enabling rapid colonization of nearby tissues under favorable conditions. Each conidiophore can generate 1-2 conidia per day per , with production optimized in warm (15–25°C) and dry weather that promotes quick and infection without free water. Sexual reproduction occurs later in the season when hyphae of opposite (MAT1-1 and MAT2-1) fuse, forming an ascogonium and that develop into dikaryotic hyphae. These structures mature into cleistothecia, compact, spherical fruiting bodies containing multiple asci filled with ascospores, which serve as durable overwintering propagules. Cleistothecia formation is triggered by environmental cues such as shortening day lengths and cooling temperatures (below 15°C) in late summer or fall, allowing the to survive adverse winter conditions. The reproductive cycle of powdery mildew is polycyclic, with multiple overlapping generations occurring within a single growing season due to the short latent period (3–7 days) from conidial to new spore production. In temperate regions with extended warm periods, 10–20 cycles can occur, amplifying epidemic potential through repeated asexual dissemination. Mating type compatibility (one MAT1-1 and one MAT2-1 per cleistothecium) ensures during the sexual phase, enhancing adaptability. While most powdery mildew species exhibit both reproductive modes, variation exists; for instance, some populations of f. sp. hordei in warmer or tropical regions may lack a functional sexual stage, relying solely on conidia for persistence and spread.

DNA repair

Powdery mildew fungi, as obligate biotrophs, rely on robust mechanisms to counteract damage from environmental stressors like (UV) radiation and (ROS) generated by host plants during infection. These pathways ensure genomic stability, supporting survival, reproduction, and in nutrient-limited intracellular environments. Primary mechanisms include (NER) for UV-induced lesions, (HR) for accurate repair during , and (NHEJ) for rapid ligation of double-strand breaks (DSBs). Photolyase-mediated repair, a light-dependent variant of NER, plays a prominent role in repairing cyclobutane (CPDs) caused by UV exposure. In the tomato powdery mildew pathogen Pseudoidium neolycopersici, NER and photolyase activity enable conidial recovery from UV-C damage (254 nm), with the photolyase PnPHR1 (a class I CPD photolyase) upregulated within 4 hours post-exposure. This enzyme, binding (FAD) and methenyltetrahydrofolate (MTHF) cofactors, uses /UV-A (365–454 nm) to split dimers, restoring viability and infection potential. HR facilitates precise DSB repair using homologous templates, essential during meiotic recombination for generating in ascospores, while NHEJ provides error-prone but fast closure of breaks, often leading to insertions or deletions. These pathways are conserved in ascomycete fungi, including powdery mildews, though obligate parasitism correlates with relaxed selection on some repair components. Environmental triggers like UV irradiation activate photolyase, while host-derived ROS during haustorial penetration likely induce HR and NHEJ to mitigate oxidative DSBs. Genomic studies between 2015 and 2020 on , the causal agent of grape powdery mildew, identified over 20 core genes, but revealed extensive losses in mismatch repair (MMR) components, with E. necator lacking nine MMR genes such as MLH3, EXO1, and PMS2. Similar losses occur in other powdery mildews, like 21 in Erysiphe pisi and five in , leading to elevated rates, longer microsatellites, and an A|T bias. These deficiencies impair post-replication error correction but enhance adaptability in stable host niches. In , efficient repair supports haustorial development under ROS stress, with incomplete repair fostering genomic variability that boosts ; for instance, MMR losses correlate with accelerated sequence divergence, potentially reducing individual by increasing instability but enabling population-level gains in host adaptation. The proficiency of these repair systems, coupled with tolerated gene losses, underpins the rapid emergence of fungicide resistance in powdery mildews. Elevated mutation rates from MMR deficits facilitate adaptive variants against demethylation inhibitors (DMIs) and quinone outside inhibitors (QoIs), as seen in diverse E. necator populations. This mutational hypervariability, rather than hyper-repair, drives resilience, highlighting DNA repair's dual role in maintaining core functions while permitting evolutionary flexibility for pathogen persistence.

Environmental Factors

Conditions promoting disease

Powdery mildew fungi exhibit optimal development within moderate ranges, with germination and most efficient at 20–26°C. Disease progression is significantly inhibited below 10°C, where is minimal, and above 35°C, which can arrest fungal growth or kill . These preferences align with and fall conditions in many temperate zones, allowing multiple cycles during favorable periods. Unlike water-dependent pathogens such as those causing , powdery mildew requires high relative humidity (70–95%) for initial infection and conidial but favors dry foliar surfaces and low humidity during the day for sporulation and dispersal. Nighttime high humidity, often exceeding 90%, combined with daytime dryness, creates ideal microclimates that enhance pathogen survival and spread without free water, which actually inhibits . This humidity dynamic contrasts sharply with obligately wet-loving fungi, enabling powdery mildew to thrive in arid or semi-arid environments where other diseases falter. Additional abiotic factors amplify disease risk, including moderate to low light levels that favor fungal growth in shaded areas, as light suppresses sporulation. Poor air circulation within dense canopies traps and reduces dispersal barriers, promoting localized epidemics. Elevated from excessive fertilization boosts susceptibility by stimulating lush, tender growth that serves as a preferred for . Climate change exacerbates these conditions; a modeling study on winter wheat in China projected that warmer temperatures and shifting humidity patterns could increase powdery mildew epidemics by approximately 13–14% (with ranges up to 21%) by the 2050s under various climate scenarios, particularly through extended periods of favorable nighttime warmth that align with infection windows. Such shifts may intensify outbreaks in susceptible crops like wheat, where historical data already link rising temperatures to higher disease incidence. As of 2025, new host records continue to expand the documented range, with 29 additional records reported in Taiwan, highlighting ongoing discoveries in pathogen-host interactions.

Host range and susceptibility

Powdery mildew fungi exhibit an exceptionally broad host range, infecting more than 10,000 species of angiosperms across numerous plant families, including economically important groups such as , , , and . This diversity encompasses both herbaceous and woody plants, with some fungal species showing high specificity limited to a single or , while others display wider adaptability across multiple families. No gymnosperms are known hosts for these pathogens. Susceptibility to powdery mildew infection is influenced by several host plant factors, with young, actively growing tissues such as emerging leaves and buds being particularly vulnerable due to their thinner cell walls and delayed defense responses. Genetic traits also play a key role; for instance, the Mildew Locus O (MLO) genes in susceptible hosts facilitate fungal penetration by regulating cellular processes like vesicle trafficking and , thereby promoting infection. In non-susceptible or resistant , pre-formed physical barriers, such as waxy cuticles or surface structures, can impede initial and appressorial formation. Post-invasion resistance mechanisms further contribute to host variability, including the rapid deposition of callose—a β-1,3-glucan —in papillae at sites, which reinforces cell walls and halts hyphal advancement. Elevated early callose accumulation has been shown to confer complete in certain interactions. These defenses, along with hypersensitive and pattern-triggered immunity, effectively limit powdery mildew establishment in non- plants. Powdery mildew fungi are cosmopolitan in distribution, occurring worldwide on susceptible angiosperms, with highest species diversity reported in the , particularly in regions like . Endemic species are noted in tropical areas, and the pathogens' spread via ornamental plants has led to concerns, as new host associations can introduce them to previously unaffected regions.

Management Strategies

Cultural practices

Cultural practices are essential non-chemical strategies for preventing and managing powdery mildew by reducing inoculum sources, improving environmental conditions, and enabling timely interventions at the farm level. These methods focus on agronomic adjustments that disrupt the pathogen's and limit its spread across various hosts like , fruits, and ornamentals. plays a critical role in minimizing overwintering spores and secondary infections. Removing and destroying infected debris, such as fallen leaves and pruned shoots, prevents the buildup of inoculum that can initiate new infections in subsequent seasons. excess or infected foliage during the dormant period or early in the enhances air circulation, reducing the humid microclimates favored by the . Proper spacing, guided by the mature size of the , further promotes and penetration, decreasing relative around foliage and lowering disease incidence by up to 30-50% in well-managed orchards and fields. Timing of cultural activities is key to avoiding conditions that exacerbate powdery mildew. Overhead should be avoided or timed for mid-morning to allow foliage to dry quickly, as prolonged leaf wetness, though not required for , can indirectly favor spore dispersal in humid environments. Planting in full sun and during optimal seasons with lower pressure, combined with mulching to regulate and support plant vigor without creating excess humidity, helps suppress early-season outbreaks. Crop with non-host plants breaks the pathogen's by eliminating continuous sources of inoculum over multiple seasons. Regular through weekly field allows growers to detect early symptoms, such as small white powdery spots on leaves, enabling proactive management before widespread infection occurs. Action thresholds vary by but often include at the first sign of or when 1 in 50 older leaves shows symptoms in susceptible like cucurbits. Integrated cultural approaches, combining , spacing, , and , can provide substantial protection, with reductions in disease severity leading to 20-40% less loss in low-pressure areas when implemented consistently.

Chemical controls

Chemical controls for powdery mildew primarily involve fungicides that act as protectants or , targeting the fungal 's growth and reproduction on host plants. Sulfur-based fungicides, used since the mid-19th century, serve as contact protectants that prevent spore by disrupting fungal metabolism through multi-site action. These compounds achieve 70-90% efficacy in field trials against various powdery mildew , particularly on grapes and cucurbits, when applied preventively. Systemic triazoles, such as , represent a key class of demethylation inhibitors (DMIs) that block biosynthesis in fungal cell membranes, halting pathogen development post-infection. These provide curative and protective effects with efficacies often exceeding 85% on cereals and fruits when applied early. Non-conventional options include mineral-based agents like , a approved for use that raises to disrupt fungal cell walls and kill spores rapidly upon . Horticultural and neem oils function by smothering spores and interfering with membrane integrity, offering moderate control (50-70% efficacy) as supplements in low-pressure scenarios. To mitigate , rotation among classes—such as alternating DMIs with multi-site protectants like —is recommended, as single-mode agents like QoI have shown widespread in over 50% of field isolates by 2020. Foliar applications of these chemicals occur at 7- to 14-day intervals, starting before symptom onset and integrated within IPM programs to minimize usage. Regulatory restrictions, such as measures tightening approvals for certain DMIs due to endocrine disruption concerns since , have prompted shifts toward lower-risk alternatives. Environmental challenges include to pollinators; for instance, DMIs like impair bee flight muscles at sublethal doses, and as of 2025, studies show synergistic when combined with insecticides like broflanilide, underscoring the need for targeted applications to avoid non-target impacts.

Biological controls

Biological controls for powdery mildew involve the use of living organisms as natural enemies to suppress the , offering an alternative to synthetic fungicides. These agents include hyperparasites, predators, and antagonistic microbes that target the powdery mildew , , or reproductive structures directly or indirectly through competition and induced plant defenses. Hyperparasitic fungi, such as Ampelomyces quisqualis, are among the most studied biocontrol agents, parasitizing the of powdery mildew fungi and significantly reducing conidial production. A. quisqualis infects powdery mildew hyphae intracellularly, colonizing up to 80% of the host's conidiophores and thereby limiting dispersal by degrading the 's cellular structure. Commercial formulations like AQ10, based on A. quisqualis strain CNCM I-807, have been developed for foliar application and demonstrate efficacy against powdery mildews on crops such as grapes and cucumbers. Predatory arthropods also contribute to control by consuming powdery mildew spores and . Certain mites, including iolinid like Pronematus spp., actively feed on fungal structures, suppressing infection levels in settings. Similarly, such as the lady Psyllobora vigintimaculata (Coleoptera: ) graze on conidia and hyphae, with larvae capable of consuming thousands of spores daily, providing notable reductions in disease severity on cucurbits and ornamentals. Antagonistic bacteria, exemplified by , exert control through the production of antifungal compounds such as lipopeptides and enzymes that inhibit powdery mildew growth. Strains like B. subtilis UMAF6639 colonize surfaces, outcompeting the for nutrients and space while triggering systemic in hosts like . Field applications of B. subtilis-based products have shown compatible integration with other controls. The primary mechanisms of these biocontrol agents include mycoparasitism, where hyperparasites like A. quisqualis secrete cell wall-degrading enzymes such as chitinases and proteases to penetrate and lyse host hyphae, and nutrient competition, as seen with Bacillus spp. that produce siderophores to limit iron availability to the fungus. Predators employ direct consumption, reducing viable inoculum. In greenhouse and field trials, these agents have achieved 50-70% disease control on crops like strawberries and grapes, particularly when applied preventively. Recent advances in the 2020s emphasize endophytic microbes for enhanced sustainability, with strains like YN201732 colonizing plant tissues internally to provide long-term protection against powdery mildew via induced systemic resistance and direct antagonism. As of 2025, studies demonstrate the efficacy of incorporating biofungicides into fungicide rotations for powdery mildew control in vineyards, achieving consistent reductions over multiple years (2023-2024) when alternated with conventional programs. These approaches are increasingly integrated into (IPM) programs, combining biocontrol with cultural practices to minimize chemical inputs and promote ecological balance in .

Genetic resistance

Genetic resistance to powdery mildew in plants is categorized into qualitative and quantitative types, with qualitative resistance mediated by single dominant R-genes that confer race-specific, vertical resistance, often leading to hypersensitive responses that halt pathogen growth early. In contrast, quantitative resistance involves multiple polygenic loci contributing to partial, race-non-specific horizontal resistance, which is generally more durable due to its additive effects and lower likelihood of being overcome by pathogen evolution. A prominent example of qualitative resistance is the Mla locus in barley, where alleles like Mla6 encode nucleotide-binding leucine-rich repeat (NLR) receptors that recognize specific avirulence effectors from the pathogen Blumeria graminis f. sp. hordei, triggering immunity. Breeding strategies for powdery mildew resistance leverage (MAS) to introgress quantitative trait loci (QTLs), such as the Ren1 locus in grapevines (), which provides partial by limiting hyphal proliferation and sporulation through a cluster of gene analogs. Since 2015, /Cas9 editing has enabled precise insertion or modification of R-genes, as demonstrated in where knockout of the susceptibility SlMLO1 generated non-transgenic resistant lines, and in grapevines where dual editing of MLO6 and MLO7 homologs enhanced without yield penalties. Similar applications in have targeted Pm0 loci to produce transgene-free varieties with broad-spectrum . As of 2024, /Cas9-driven double modification of grapevine MLO6-7 and NPR3 has imparted enhanced to both powdery and . Notable examples include grape cultivars like 'Kishmish vatkana' and 'Dzhandzhal kara' harboring the Ren1 locus, which have been used in breeding programs to develop partially resistant hybrids, though monogenic qualitative resistances like those at Mla can be rapidly overcome by adaptation, necessitating pyramiding with quantitative traits for longevity. Such genetic approaches yield 20-50% improvements in yield stability by mitigating infection-related losses, as seen in resistant lines that maintain productivity under moderate disease pressure. Global breeding programs, such as those at the International and Improvement Center (CIMMYT), incorporate wild relatives like Dasypyrum villosum to transfer durable resistance genes (e.g., Pm21) into elite , enhancing polygenic backgrounds for sustainable control.

Impacts on Specific Hosts

Cereals

Powdery mildew affects major crops such as , , oats, and , primarily caused by the obligate biotrophic fungus and its host-specific formae speciales. The most economically significant pathogens are B. graminis f. sp. tritici on and , and f. sp. hordei on , with additional formae speciales like f. sp. avenae for oats and f. sp. secalis for rye, each adapted to specific cereal hosts within the family. These pathogens thrive in temperate climates, where cool, humid conditions favor and , leading to epidemics that can reduce yields by 10-40% in susceptible varieties during severe outbreaks. Symptoms typically begin as small, white, powdery patches of mycelium and conidia on the upper surfaces of young leaves, spreading to cover extensive areas of foliage, stems, and occasionally heads as the disease progresses. This dense fungal growth interferes with photosynthesis and nutrient uptake, weakening plants and causing chlorosis, premature senescence, and reduced tillering; severe infections can lead to stem lodging due to compromised structural integrity and kernel shriveling from diminished assimilate allocation to developing grains. Historical epidemics in Europe during the 1970s, particularly in the Netherlands and surrounding regions, highlighted the disease's destructive potential, with widespread infections in winter wheat and barley fields driven by favorable weather and susceptible cultivars, resulting in substantial yield reductions across the continent. It can lead to estimated annual yield losses of 7.6–19.9% in wheat, underscoring its role as a persistent threat to food security in temperate grain-growing areas. Management of powdery mildew in cereals relies on integrated approaches tailored to host-specific pathogens, including the deployment of resistant varieties such as the , which carries the mlo resistance gene for broad-spectrum, durable protection against B. graminis f. sp. hordei. Chemical controls, particularly strobilurin (QoI) fungicides like , provide effective preventive and curative action by inhibiting mitochondrial respiration in the fungus, often applied at key growth stages to suppress epidemics in and . is altering disease dynamics, with warmer winters in temperate zones potentially enhancing overwintering survival of B. graminis ascospores on volunteer and debris, thereby increasing primary inoculum and extending epidemic risks into new regions.

Grapes

Powdery mildew of grapes is caused by the obligate biotrophic fungus (synonym ), which primarily infects green tissues such as leaves, shoots, and berries, leading to the characteristic white, powdery fungal growth on the surfaces. The pathogen penetrates host cells via haustoria, disrupting and nutrient allocation, which can result in defoliation, reduced berry size, and skin cracking on fruits. In severe cases, infections cause yield losses of 20-30% by impairing fruit set and ripening, while also predisposing berries to secondary infections like bunch rot from . Historically, E. necator devastated European vineyards starting in the 1840s, with widespread epidemics by the 1850s that threatened the industry's survival until sulfur was found effective against it around 1845, based on earlier observations in peach orchards. This led to the widespread adoption of sulfur dusting and spraying, marking one of the earliest large-scale uses of chemical control in agriculture. The disease's arrival, likely from North America via imported plant material, facilitated bunch rot outbreaks by weakening berry integrity, exacerbating losses during humid post-infection periods. Beyond yield reduction, powdery mildew significantly degrades wine quality by altering composition, imparting off-flavors such as bitter, musty, or mushroom-like notes due to fungal metabolites and impaired accumulation. Management in emphasizes canopy management practices, such as removal and shoot positioning, to enhance airflow and UV exposure, thereby suppressing . Chemical controls include demethylation (DMI) fungicides like , which target biosynthesis in the fungus, often applied preventively in rotation to mitigate . Breeding efforts incorporate genes, such as Run1 from Muscadinia rotundifolia, into rootstocks and scions to provide durable protection without relying solely on sprays. Powdery mildew is a widespread affecting vineyards globally, with most Vitis vinifera cultivars being highly susceptible, posing particular challenges for production in humid regions where sulfur efficacy diminishes under prolonged moisture, necessitating integrated approaches like biological agents and predictive modeling.

Legumes

Powdery mildew affects a range of legume crops, including food legumes such as beans, peas, chickpeas, and soybeans, as well as forage legumes like alfalfa. In beans and peas, the primary pathogen is Erysiphe polygoni (syn. Microsphaera diffusa for some hosts), which produces white, powdery fungal growth on leaves, stems, and pods, leading to chlorosis, premature leaf drop, and reduced photosynthesis. For chickpeas, Leveillula taurica is the main causal agent, causing internal mycelial growth and external conidial production that results in yellowing, necrosis, and defoliation, particularly under warm, dry conditions. Severe infections across these hosts can lead to defoliation, which disrupts pod development and reduces pod set by up to 20-30% in susceptible varieties, as seen in field studies on peas and beans where early-season infection shortened the reproductive phase. Key legume crops experience notable production losses from powdery mildew. In soybeans (Glycine max), the disease, primarily caused by Microsphaera diffusa, emerges in mid- to late season and can cause up to 10% yield reduction in the United States through defoliation and decreased seed fill, especially in susceptible cultivars under dense canopies. Alfalfa (Medicago sativa), a major , suffers from powdery mildew caused by Erysiphe baeumleri or related species, resulting in reduced leaf retention, lower , and declined nutritional quality due to increased fiber content and decreased protein levels from repeated defoliation. In chickpeas (Cicer arietinum), L. taurica infections can reduce yields by 20-40% in severe cases by limiting pod formation and increasing susceptibility to secondary pathogens. The disease is particularly severe in warm, dry subtropical regions, where high daytime temperatures (25-35°C) and low humidity favor spore dispersal without needing free water, as observed in chickpea and bean fields in tropical and subtropical climates. Integrated management emphasizes varietal resistance; for example, soybean lines derived from resistant germplasm like PI 230970 exhibit partial resistance through delayed symptom development and reduced spore production, combined with cultural practices such as and avoiding overhead . Economic impacts are significant for these protein-rich crops, with global losses estimated in millions of dollars annually due to reduced seed quality and yield; post-2010, breakdowns in single-gene resistances (e.g., er loci in peas) have prompted shifts toward pyramided resistance strategies to counter evolving races.

Vegetables (onions, squashes, strawberries)

Powdery mildew on onions is primarily caused by the Leveillula taurica, which produces white to pale yellow lesions on older leaves that develop into powdery growth, reducing and potentially leading to smaller sizes. Severe can result in losses of up to 20%, particularly when the disease develops early in the season. The pathogen thrives in dry, warm conditions with high relative at night, allowing spores to spread via to nearby susceptible hosts. In squashes and other cucurbits, Podosphaera xanthii (synonym Podosphaera fusca) is the main causal agent, manifesting as white powdery spots on leaves, stems, and that coalesce to cover surfaces. Infections on lead to russeting—a rough, brownish discoloration of the skin—that significantly reduces marketability by up to 30%, as affected produce is less appealing for fresh consumption. Overall yield declines occur due to premature , smaller size, and delayed , with losses potentially reaching 20% or more in unmanaged fields. Strawberry powdery mildew, incited by Podosphaera aphanis, affects leaves, flowers, fruits, and runners, producing a characteristic white, felt-like growth on the undersides of leaves and causing upward curling and reddish blotches. Fruit infections result in scarring and deformation, rendering berries unmarketable and contributing to yield reductions of 15-50% in severe outbreaks, especially under humid, moderate-temperature conditions (15-27°C). Runner infections are particularly problematic, as the fungus spreads systemically through propagation material, perpetuating the disease in new plantings. Day-neutral varieties, such as 'Seascape' and 'Albion', exhibit heightened susceptibility compared to short-day types, necessitating vigilant monitoring during extended production cycles. Management of powdery mildew across these relies on preventive applications of -based products, including dusts and wettable powders, which are effective when initiated before symptoms appear and repeated at 7-10 day intervals. For strawberries, emphasis on day-neutral varieties involves integrating with cultural practices like improved air circulation to mitigate runner propagation of the .

Fruits (apples, pears)

Powdery mildew on fruits such as apples and pears is primarily caused by the fungal Podosphaera leucotricha, an biotroph that infects buds, leaves, shoots, , and . The overwinters as within dormant buds, with primary infections emerging in on young tissues, where conidia are produced and dispersed by to initiate secondary infections under warm (50–77°F) and humid conditions. This cycle is particularly severe in humid environments, such as those near water bodies, where prolonged wetness and high favor rapid spread during the . Bud infections by P. leucotricha lead to stunted shoot growth and dwarfing, while blossom and fruit infections result in russeting, characterized by net-like scars on , potentially causing 10–20% yield losses in susceptible cultivars. Overall, the disease reduces tree vigor and winter hardiness, contributing to irregular fruit set and bearing patterns, as infected buds open later and fail to support consistent production. Historically, powdery mildew has posed significant challenges to U.S. production, where traditional varieties are highly susceptible, exacerbating management issues in eastern regions. Management in apple and pear orchards emphasizes early-season interventions, such as applications of at the tight cluster stage to suppress overwintering inoculum and prevent initial infections. Planting resistant cultivars, including Liberty apple, which exhibits moderate to high resistance to P. leucotricha, is a key genetic strategy to minimize disease pressure and reduce reliance on chemical controls. are similarly susceptible, often requiring integrated approaches to limit inoculum from nearby apple trees.

Ornamentals (Syringa, Acer, Berberis)

Powdery mildew infections on ornamental plants such as lilac ( spp.), maple ( spp.), and barberry ( spp.) primarily cause aesthetic damage, reducing their visual appeal in landscapes and gardens where appearance is paramount. These woody ornamentals are commonly used in hedges, borders, and specimen plantings, making visible symptoms like white fungal coatings particularly detrimental to their ornamental value. The disease thrives in conditions of high humidity with moderate temperatures, often appearing in late summer and spreading via airborne spores, which can introduce infections through nursery stock traded across regions. On lilac ( spp.), powdery mildew is primarily caused by Erysiphe syringae, resulting in a white, mealy fungal growth on leaf surfaces that distorts foliage and creates an unsightly appearance in landscape settings. This pathogen favors cool nights and warm days with high , leading to infections that, while rarely lethal, mar the plant's elegance during its blooming period and into fall. In western , E. syringae co-occurs with related species like Phyllactinia syringae, exacerbating the cosmetic impact on cultivated varieties. For (Acer spp.), powdery mildew is incited by fungi such as Sawadaea tulasnei on Norway maple (A. platanoides) or Uncinula circinata on other species, producing white powdery patches on leaves that can induce premature yellowing or reddening, mimicking early fall coloration and diminishing the tree's aesthetic quality. Severe infections in humid environments lead to leaf distortion and drop, contributing to up to noticeable reductions in nursery salability due to reduced vigor and visual appeal, though overall plant health is seldom severely compromised. These symptoms are especially problematic in dense plantings where dispersal is rapid. Barberry (Berberis spp.) suffers from powdery mildew caused by Microsphaera (now Erysiphe) berberidis, which forms white blotches on leaves, stunting growth, causing reddening or scorching, and promoting premature defoliation that undermines the shrub's dense, hedge-forming structure. This defoliation directly affects the plant's value as a barrier or ornamental , as sparse foliage exposes the thorny branches and reduces screening effectiveness. Infections are more pronounced on young leaves in shaded, humid sites, amplifying visibility issues in garden designs. The high visibility of powdery mildew symptoms in these ornamentals heightens their impact in public and private gardens, where even minor infections can prompt removal or replacement. Spread occurs readily through international and domestic of infected nursery stock, introducing pathogens to new areas and complicating management. In the , regulatory restrictions on certain synthetic fungicides, driven by environmental and health concerns, limit chemical control options, pushing reliance on cultural practices and emerging biological agents for suppression.

Other crops (sunflowers, Cannabis)

Powdery mildew on sunflowers () is primarily caused by the Erysiphe cichoracearum, which produces white, powdery fungal growth on leaves, stems, and heads, particularly under conditions of high humidity and moderate temperatures. Head infections are especially damaging, leading to significant reductions in seed yield and oil content, with losses estimated at 20-30% in severe cases due to impaired and premature . The disease has become more prevalent in tropical and subtropical regions, where it can cause 30-75% severity on susceptible varieties. Management of powdery mildew in sunflowers relies on the use of resistant hybrids developed through breeding programs that incorporate genes from wild relatives for enhanced tolerance. For instance, lines such as R-GM-41 and R-GM-49 have shown resistance under field conditions, allowing for the creation of hybrids that maintain yield stability without heavy reliance on fungicides. Integrated approaches, including and timely fungicide applications like , further reduce disease incidence by up to 90% when combined with resistant varieties. In (), powdery mildew is caused by species of Golovinomyces, including G. cichoracearum and G. ambrosiae, which thrive in the dense canopies of indoor environments, leading to rapid dispersal and visible white patches on leaves and buds. The disease impairs plant vigor, reduces overall yield by up to 50% in untreated infestations, and lowers content by damaging resin glands and photosynthetic tissues. The legalization and expansion of production since the have amplified these challenges, as high-value indoor grows create ideal microclimates for pathogen proliferation. Control strategies for cannabis powdery mildew emphasize non-chemical methods suited to controlled environments, such as daily exposure to UV-C light at doses of 3-6 mJ/cm², which damages fungal DNA and suppresses development by 45% or more without residues on harvestable material. Emerging research also highlights breeding for resistance using markers like PM2, alongside environmental controls to limit humidity below 50%. Climate-driven shifts are increasing powdery mildew risks in non-traditional growing areas for both crops, as warmer temperatures and altered patterns favor and spread in regions previously less affected. For sunflowers, this may expand disease pressure in subtropical zones, while indoor operations face heightened vulnerability from inconsistent climate controls.

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