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Aspergillus flavus

Aspergillus flavus is a ubiquitous saprophytic fungus in the genus Aspergillus, phylum Ascomycota, known for its role as an opportunistic plant pathogen and producer of aflatoxins, potent hepatocarcinogenic mycotoxins that contaminate agricultural crops. It thrives in warm, humid environments worldwide, particularly in soil and on decaying vegetation, where it acts as a decomposer while also infecting crops such as maize, peanuts, cottonseed, and tree nuts during pre- and post-harvest stages. The fungus features septate hyphae and produces yellow-green conidia in radial patterns on vesicles, forming colonies that mature to olive-green shades, with sclerotia enabling survival under adverse conditions. Approximately 50% of isolates are toxigenic, generating aflatoxins B1 and B2—classified as Group I carcinogens—along with cyclopiazonic acid, leading to significant economic losses in agriculture and posing health risks through food contamination. In human health, A. flavus ranks as the second leading cause of invasive , particularly in immunocompromised individuals, where it can lead to pulmonary infections, , , and cutaneous lesions. It also contributes to allergic reactions and superficial infections, while exposure via contaminated foods increases the risk of and acute toxicity, including and . Ecologically, its ability to spread via conidia carried by and underscores its persistence in agricultural settings, prompting into atoxigenic strains and biocontrol methods to mitigate . The of A. flavus, spanning about 37 million base pairs across eight chromosomes, includes over 13,000 protein-coding genes and multiple biosynthetic clusters regulating production.

Taxonomy and Classification

Etymology and Discovery

The genus was established in 1729 by Italian priest and botanist Pier Antonio Micheli, who named it after the , a liturgical tool resembling a sprinkler used to scatter droplets during religious rites; this reflected the fungus's spore-bearing heads, which Micheli observed under early microscopes and likened to the device's perforated head, derived from the Latin verb aspergere, meaning "to scatter" or "to sprinkle." Micheli's description in Nova plantarum genera marked a foundational moment in , as he was among the first to scientifically illustrate and classify fungal reproductive structures, shifting perceptions from to systematic biology. The species name flavus originates from the Latin adjective for "yellow," alluding to the distinctive golden-yellow hue of the conidia produced by this fungus, a characteristic that distinguishes it within the genus. This epithet highlights the visual trait central to its identification since early observations. Aspergillus flavus was formally described in 1809 by German botanist and mycologist Heinrich Friedrich Link in the Magazin der Gesellschaft Naturforschenden Freunde zu Berlin, where he classified it as a distinct species based on its morphological features observed in natural specimens. Link's work built on Micheli's genus framework, contributing to the emerging field of fungal taxonomy during the early 19th century, when naturalists began cataloging microfungi from diverse substrates. Initial isolations of A. flavus occurred from decaying vegetation and stored grains in Europe, contexts that underscored its saprophytic role in organic matter decomposition.

Phylogenetic Relationships

Aspergillus flavus belongs to the Kingdom Fungi, Phylum Ascomycota, Class Eurotiomycetes, Order Eurotiales, Family Aspergillaceae, Genus Aspergillus, and is placed within Section Flavi of the genus. This taxonomic placement reflects its position among filamentous ascomycete fungi characterized by septate hyphae and asexual conidiation. Section Flavi encompasses species with yellow-green conidia and is distinguished by multilocus phylogenetic analyses using markers such as the (ITS) region, β-tubulin (benA), and (CaM) genes. Within Section Flavi, A. flavus exhibits close phylogenetic relationships to Aspergillus parasiticus, a co-producer of aflatoxins B1 and G1, and Aspergillus oryzae, a domesticated strain utilized in food fermentation processes like soy sauce production. Genetic similarities between A. flavus and these relatives are evident from near-identical ITS sequences, with A. flavus and A. oryzae sharing up to 99.5% nucleotide identity across their genomes, while calmodulin gene sequencing reveals subtle substitutions that delineate species boundaries. Phylogenetic trees constructed from these loci place A. flavus in a monophyletic clade with A. parasiticus, supported by shared syntenic regions and orthologous gene clusters identified in comparative genomics. Evolutionary analyses indicate that A. flavus originated as a saprotroph, decomposing in and debris, with subsequent adaptations enabling opportunistic in plants and animals. Whole-genome sequencing efforts in the , including assemblies from diverse isolates, have characterized the A. flavus as spanning 36-40 Mb, containing approximately 12,000-13,000 protein-coding , and revealing expansions in gene clusters that facilitate production and host colonization. These genomic insights underscore the species' evolutionary flexibility, with lineage-specific variations in recombination and cryptic contributing to its ecological versatility.

Morphology and Growth

Colonial and Microscopic Features

Aspergillus flavus exhibits rapid colonial growth on standard mycological media such as (), typically achieving colony diameters of 4-5 cm after 7 days of at 25-30°C. Colonies appear velvety to powdery in texture, with a yellow-green to olive-green surface coloration and a pale yellow to yellowish reverse. Under microscopic examination, A. flavus produces , septate hyphae measuring 3-12 μm in width. Conidiophores are unbranched, smooth to rough-walled, and range from 300-800 μm in length, terminating in globose to subglobose vesicles of 20-60 μm in diameter. These vesicles bear phialides that are uniseriate or biseriate, giving rise to chains of globose to subglobose conidia, which are 3-6 μm in diameter and possess roughened walls. Morphological variations exist between L- and S-strains of A. flavus, primarily distinguished by sclerotial size and conidial production. The L-strain produces fewer, larger sclerotia (>400 μm in diameter) and more conidia, while the S-strain produces numerous smaller sclerotia (<400 μm) and fewer conidia; conidia are 3-6 μm in both strains. Both strains share the overall colonial and structural characteristics described above.

Reproduction and Sporulation

Aspergillus flavus primarily reproduces asexually through conidiation, a process in which vegetative hyphae differentiate into specialized conidiophores that bear chains of conidia at their tips, serving as the main mechanism for propagation and dissemination. These conidia function as the primary dispersal units, capable of withstanding , UV , and other harsh environmental stresses due to their thick-walled . Although predominantly , rare instances of have been documented in natural populations, involving the formation of ascospore-bearing cleistothecia and meiotic recombination; however, no traditional teleomorph stage akin to Emericella has been confirmed for A. flavus, with sexuality considered cryptic and heterothallic. Evidence of such recombination has been detected through genetic analyses of wild strains. Sporulation in A. flavus is triggered by specific environmental cues, including high relative levels exceeding 85%, temperatures between 25°C and 37°C, and the presence of nutrient-rich substrates such as grains or decaying matter. Under these conditions, conidiophore accelerates, leading to the formation of metulae and phialides that produce multicellular conidia in organized chains, which are subsequently released into the air for dispersal. Optimal sporulation often occurs on carbohydrate-abundant , enhancing conidial and aiding survival in agricultural settings. Conidia of A. flavus exhibit high viability, remaining dormant and infectious for months to over a year in , , or residues, which facilitates long-term persistence in the . Laboratory-induced parasexual cycles, involving formation, diploidization, and , have been demonstrated to enable genetic exchange in controlled settings.

Habitat and Ecology

Natural Environments

Aspergillus flavus primarily functions as a saprophyte in natural environments, playing a key role in the decomposition of organic matter such as soil detritus, plant debris, and compost heaps. This fungus breaks down lignocellulosic materials and contributes to nutrient cycling in terrestrial ecosystems, particularly in warmer regions where organic substrates are abundant. It thrives in warm, arid soils with neutral to slightly alkaline pH levels between 6 and 8, conditions commonly found in semi-arid and tropical landscapes that support its persistence as a soil inhabitant. In microhabitats, A. flavus is frequently associated with the of various plants, where it interacts with root exudates and colonizes decaying vegetation, enhancing its survival through nutrient acquisition from senescing tissues. Population densities in agricultural and natural can reach up to 10^4 to 10^5 conidia per gram, varying with soil type and organic content, which underscores its adaptability to localized hotspots of . These associations allow the to maintain viable propagules in the upper soil layers, facilitating dispersal via or . The species exhibits notable abiotic tolerances that align with its , including drought resistance with a minimum (a_w) threshold of approximately 0.80 for growth, extending to optimal levels up to 0.99 in moist microenvironments. It is thermotolerant, with growth occurring between 12°C and 48°C, peaking at 25–42°C, but shows sensitivity to extreme cold below 10°C and waterlogged, conditions that limit oxygen availability. These tolerances enable A. flavus to persist in fluctuating environments, though prolonged extremes can reduce propagule viability.

Global Distribution and Prevalence

Aspergillus flavus exhibits a but is predominantly prevalent in tropical and subtropical regions across , , and the , where warm temperatures and high favor its proliferation in , air, and plant material. In contrast, it is rare in colder climates, such as those in and , due to its preference for temperatures above 25°C, limiting its establishment in environments with prolonged low temperatures. The fungus spreads primarily through wind-dispersed conidia, which can travel long distances and initiate infections in susceptible crops, as well as via contaminated and of grains and nuts, facilitating its to new areas. Prevalence is notably higher in drought-prone regions, such as the U.S. Southwest and the , where water stress compromises plant defenses and promotes fungal colonization during pre- and post-harvest stages. Recent trends indicate that is expanding A. flavus incidence into temperate zones, with models predicting habitat gains in , , and parts of under warming scenarios, potentially increasing exposure risks. Post-2020 surveys of fields indicate varying contamination rates by A. flavus, with incidences up to 80% reported in some regions of .

Life Cycle and Infection

Asexual Reproduction Cycle

The asexual reproduction of Aspergillus flavus is its dominant mode of propagation, facilitating widespread dissemination through the production of conidia, unicellular spores formed mitotically to maintain clonal lineages. This , which lacks a prominent sexual in natural settings, typically spans 24-48 hours under optimal conditions such as 28-30°C and availability, allowing rapid to environmental niches. The cycle initiates with conidial germination, triggered by moisture and nutrients in media like Czapek-Dox broth. Dormant conidia, measuring approximately 3-4 µm, first exhibit isotropic swelling, increasing in size up to twofold within 0-5 hours, followed by polarized where tubes emerge between 5-10 hours, marking the transition to active . This process involves activation of redox-related genes and is essential for breaking , with completion dependent on and composition. Emerging germ tubes elongate and branch via apical extension, forming a vegetative that colonizes the through hyphal tip growth and septation. This expansive phase, driven by mitotic divisions, establishes developmental competence and typically precedes reproductive structures within 12-24 hours of . From the , specialized aerial hyphae differentiate into conidiophores—stalked structures topped by a vesicle that bears metulae and phialides—under regulatory control of transcription factors like BrlA (initiation), AbaA (phialide maturation), and WetA (conidial wall formation). Sporulation occurs as phialides produce chains of 2-5 µm conidia through repeated mitoses, with maturation yielding green-pigmented spores ready for dispersal by air currents or mechanical disturbance. The full closes as these conidia settle on new surfaces, germinating to perpetuate the process, often observed in laboratory cultures by 48 hours. Environmental cues critically modulate the : depletion, exposure (via blue-light photoreceptors), and adequate oxygen promote conidiophore and sporulation, while from prolonged induces sclerotia—compact, melanized aggregates of hyphae serving as resilient overwintering bodies for until favorable conditions return. Genetically, the preserves clonality through exclusive mitotic propagation, with over 30 identified regulators ensuring coordinated , though rare sexual events have been documented in controlled crosses.

Pathogen-Host Interactions

Aspergillus flavus primarily gains entry into hosts through mechanical wounds, vectors, or natural openings, such as the silks of ears during . Conidia adhere to these sites, germinate under favorable and temperature conditions, and initiate by producing mycelia that penetrate host tissues. This is facilitated by the of hydrolytic enzymes, including cellulases and pectinases, which degrade cell walls composed of and , allowing the to breach epidermal barriers. In crops like and , damage from such as the corn earworm often serves as a critical , exacerbating under abiotic stresses like . Following entry, A. flavus colonizes tissues through a combination of hyphal extension and intracellular growth, preferentially targeting nutrient-rich areas such as the oily and in . The employs toxin-mediated strategies to suppress defenses; aflatoxins, in particular, inhibit plant immune responses by interfering with signaling and inducing in cells, thereby promoting unchecked mycelial proliferation. Additionally, A. flavus can establish latent infections in developing , where conidia or hyphae remain dormant within kernel tissues until post-harvest conditions—such as elevated —trigger sporulation and toxin production during . This persistence underscores the fungus's saprophytic adaptability, enabling long-term survival without immediate symptoms. The host range of A. flavus is notably broad, encompassing cereals like and , oilseeds such as and cottonseeds, and various trees including pistachios and figs. As an opportunistic pathogen, it predominantly targets stressed hosts, where environmental factors like heat, , or nutrient deficiency weaken plant barriers and defenses, facilitating initial and subsequent spread. This versatility allows A. flavus to act as both a primary invader in susceptible crops and a secondary colonizer in damaged tissues across diverse agricultural systems.

Pathogenicity and Diseases

Effects on Plants

Aspergillus flavus is a significant phytopathogen that infects various agricultural crops, leading to pre-harvest and post-harvest diseases that compromise yield and quality. In (Zea mays), it primarily causes Aspergillus ear , where the fungus colonizes developing s, resulting in visible yellow-green to olive-green powdery on the ears and between kernels. This infection often starts at the ear tip or through wounds from insects or mechanical damage, progressing under hot, drought-stressed conditions. In (Arachis hypogaea), A. flavus induces kernel , particularly in pods exposed to soil or during , leading to darkened, shriveled, and rotten seeds often coated with greenish-yellow fungal growth. Symptoms of A. flavus infection in plants typically include tissue discoloration ranging from yellow to brown, kernel shriveling, and overall wilting or chlorosis in affected areas such as roots, stems, or leaves. Under ultraviolet (UV) light, contaminated tissues may exhibit bright greenish-yellow fluorescence, aiding in early detection of infection. Systemic effects extend to seed viability, with contaminated seeds showing significantly reduced germination rates—often leading to complete inhibition depending on toxin levels and exposure duration—due to inhibited enzymatic activity and cellular damage during sprouting. These symptoms are exacerbated in warm, dry environments that favor fungal growth and toxin production. The primary crops impacted by A. flavus include corn, , , and tree nuts such as pistachios and almonds, where infections occur both in the field and during storage. Pre- and post-harvest losses from these diseases can reach 10-50% of yield in severely affected regions, driven by direct tissue destruction and rejection of contaminated produce. Globally, economic impacts from A. flavus-related crop losses and aflatoxin management are substantial, with estimates ranging from $900 million annually in parts of to over $750 million in , contributing to broader worldwide costs in the billions of dollars due to reduced marketability and trade restrictions. The role of aflatoxins in amplifying plant damage is covered in the Toxins and Metabolites section.

Effects on Animals and Humans

Aspergillus flavus primarily affects humans as an opportunistic , causing invasive () in immunocompromised individuals, where it ranks as the second most common etiological agent after A. fumigatus, accounting for approximately 10% of cases worldwide. Invasive infections often manifest as pulmonary disease, with conidia inhaled and germinating in the lungs, leading to tissue invasion, , and dissemination in severe cases; common sites include the lungs, sinuses, and . High-risk groups include patients with AIDS, organ transplant recipients, those undergoing , and individuals with prolonged , with transmission occurring via of airborne conidia from environmental sources. The incidence of , including that caused by A. flavus, is estimated at 1–2 cases per 100,000 population annually , though rates may be higher in endemic regions like . Mortality from A. flavus-induced IA is substantial, with all-cause 30-day case-fatality rates reported at 39.2% and 90-day rates at 47.1%, varying by underlying risk factors, infection site, and co-infections; these rates are often higher than those for A. fumigatus due to A. flavus's propensity for aggressive pleuropulmonary and sino-orbital involvement. Additionally, A. flavus can trigger allergic reactions in susceptible individuals, such as (ABPA), which primarily affects those with or , causing symptoms like wheezing, cough with mucus, fever, and worsening through an immune response to inhaled spores. In animals, A. flavus causes , particularly in , where it contributes to brooder —a respiratory in young chicks characterized by dyspnea, gasping, anorexia, , and increased mortality, often from inhaling spores in contaminated or feed. Transmission in occurs environmentally via aerosolized conidia, not bird-to-bird, with lesions appearing as yellow nodules in lungs and . In , A. flavus is implicated in rare cases of bovine , presenting as a sudden drop in production, firm udder quarters, and normal-appearing , typically linked to contaminated intramammary devices; successful is uncommon. Ingestion of A. flavus-contaminated feed can lead to reduced growth and performance in , including and ruminants, through mycotoxicosis, though primary infections are respiratory. Other animals, such as and marine mammals, may experience localized or systemic from A. flavus, but and represent key agricultural impacts.

Toxins and Metabolites

Aflatoxin Biosynthesis

Aflatoxins are a group of toxic and carcinogenic secondary metabolites produced by Aspergillus flavus, primarily aflatoxins B1 (AFB1), B2 (AFB2), G1 (AFG1), and G2 (AFG2), with AFB1 being the most potent hepatocarcinogen. In A. flavus, only the B-type aflatoxins (B1 and B2) are synthesized, whereas A. parasiticus produces all four types. These compounds are derived from a polyketide biosynthetic pathway initiated by the condensation of acetate units, involving a complex cluster of over 20 genes spanning approximately 75 kb on the fungal chromosome. The gene cluster, highly conserved among aflatoxigenic aspergilli, encodes enzymes such as polyketide synthases, oxidoreductases, and methyltransferases essential for the pathway. The biosynthesis begins with the formation of norsolorinic acid (NOR), the first stable intermediate, from nine acetate units via the encoded by aflA (formerly nor-1) and associated enzymes. NOR is then converted through a series of oxidative and cyclization steps to averantin, averufin, and hydroxyanthraquinones, leading to versicolorin A, a key branching point. Versicolorin A undergoes further modifications, including and esterification, to form sterigmatocystin (ST), a penultimate intermediate and in its own right produced by related fungi. From ST, O-methylation and subsequent rearrangements yield AFB1 and AFB2 in A. flavus, while additional steps produce the G-types in species like A. parasiticus. The pathway requires coordinated expression of clustered genes, with disruptions at any step halting production. Aflatoxin biosynthesis is tightly regulated by environmental factors and genetic elements, with optimal production occurring at 28–30°C under oxidative or stress conditions that activate the pathway. The primary AflR, encoded within the cluster, binds to promoter regions of structural genes to initiate expression, often in concert with the co-activator AflS. Stress responses, such as accumulation, further enhance AflR activity, linking production to fungal survival during host colonization. Detection of aflatoxins typically employs (HPLC) for precise quantification of individual congeners or (ELISA) for rapid screening of total aflatoxins in matrices. Regulatory limits, such as the U.S. Food and Drug Administration's threshold of 20 parts per billion (ppb) for total aflatoxins in human , guide contamination assessments to mitigate health risks. Genetic studies have confirmed the cluster's role through targeted deletions; for instance, inactivation of key genes like aflR or aflD in A. flavus results in atoxigenic strains incapable of production, validating the pathway's genetic basis and supporting biocontrol applications.

Other Secondary Metabolites

Aspergillus flavus produces a diverse array of secondary metabolites beyond aflatoxins, including cyclopiazonic acid (CPA), aspergillic acid, and , which contribute to its ecological fitness and interactions with hosts and competitors. These compounds often exhibit , , and chelating properties, aiding the in niche colonization and defense against other microbes. Production of these metabolites is strain-specific and regulated by environmental factors, global regulators like VeA and LaeA, and biosynthetic gene clusters. Cyclopiazonic acid, a neurotoxic indole-tetramic acid, is synthesized via a hybrid synthase-nonribosomal synthetase (PKS-NRPS) pathway encoded by cluster 55. It functions as an against insects and mammals, reducing feeding by 48-66% in certain bioassays, and plays an ecological role in microbial through potential activity. Approximately 30-50% of A. flavus strains produce CPA, often concurrently with aflatoxins, with variability influenced by and nitrogen sources; for instance, production decreases under low conditions. Detection typically involves liquid chromatography-mass spectrometry (LC-MS), which identifies CPA alongside transcriptomic analysis of the biosynthetic genes. Aspergillic acid, a hydroxamic acid-containing pyrazinone, is biosynthesized by the asa gene cluster, which encodes nonribosomal peptide synthetases and is upregulated in nutrient-rich media like casein peptone. This metabolite exhibits strong antimicrobial activity and iron-chelating properties, enabling A. flavus to sequester iron from the environment and inhibit competing bacteria and fungi during host invasion, such as in maize kernels. Production varies across strains, with robust expression in certain isolates under specific cultural conditions, though exact prevalence percentages are not uniformly reported. LC-MS and high-performance liquid chromatography with diode-array detection (HPLC-DAD-MS) are standard for its identification and quantification. Kojic acid, a γ-pyrone and precursor to fungal pigments, is produced by a featuring the kojA and kojR , with inhibited by and dependent on LaeA. It serves as an and iron chelator, disrupting microbial iron acquisition and providing defense against , while also acting as an in ecological contexts. Strain variability is notable, with some isolates producing kojic acid exclusively without other toxins, though many co-produce it with aflatoxins under glucose-rich conditions. LC-MS remains the primary detection method, often coupled with (NMR) for structural confirmation.

Economic and Health Impacts

Agricultural and Food Safety Issues

Aspergillus flavus poses significant challenges to by contaminating staple crops such as , corn, and , leading to substantial crop losses and export rejections due to levels exceeding international standards. In the , in 2019 approximately 30% of finished lots failed to meet specifications set by the USDA for edible products (15 ppb total aflatoxins), resulting in economic losses from downgrading or rejection. Recent years (2020-2023) have shown lower failure rates of 6% or less. Globally, affects a significant portion of crops, with estimates indicating up to 25% of crops impacted by mycotoxins according to the FAO. High incidence rates are reported in regions like , where improper handling exacerbates the issue. Trade barriers arise from stringent limits, which establish maximum levels of 15 ppb for total aflatoxins in intended for further processing and 10 ppb for ready-to-eat , while the enforces stricter limits of 2 ppb for and 4 ppb for total aflatoxins in ready-to-eat , and 8 ppb for B1 and 15 ppb total for further processing. In November 2025, the Commission adopted a revised to reduce aflatoxins in throughout the . These regulations have historically prevented exports; for instance, saw no formal shipments in the early 1990s due to widespread exceeding acceptable thresholds. Post-harvest conditions further amplify risks, as A. flavus thrives in warm, humid environments, converting low-level pre-harvest into higher concentrations during prolonged storage. Inadequate and in or warehouses allow fungal , particularly in developing countries where is limited, leading to rapid accumulation in crops like corn and . This post-harvest proliferation not only reduces marketable yield but also necessitates costly interventions such as sorting or disposal to comply with safety standards. The global economic burden of A. flavus-induced contamination is estimated at $6-18 billion annually as of 2025, encompassing direct losses from rejected produce, reduced feed value, and disruptions. In the United States alone, corn losses range from $52 million to $1.68 billion per year, driven by contamination events that affect production and . exacerbates these mitigation gaps by expanding suitable habitats for A. flavus, with rising temperatures and droughts projected to increase contamination risks in over 89% of U.S. corn-growing counties, including the , by 2031-2040. Case studies from the U.S. , such as the 2012 drought-induced outbreak, illustrate this trend, where led to widespread aflatoxin exceedances, forcing millions of bushels into lower-value uses and highlighting vulnerabilities in current management practices.

Public Health and Historical Cases

Aspergillus flavus poses significant public health risks primarily through the production of aflatoxins, potent mycotoxins that contaminate food and feed. Aflatoxin B1, the most prevalent and toxic form, is classified as a Group 1 carcinogen by the International Agency for Research on Cancer (IARC), indicating it is carcinogenic to humans, with strong evidence linking it to hepatocellular carcinoma via genotoxic mechanisms that induce DNA adducts in liver cells. Acute exposure to high levels of aflatoxins can cause aflatoxicosis, characterized by severe liver damage, hemorrhage, and rapid death; a notable outbreak in Kenya in 2004 resulted from contaminated maize, affecting 317 individuals and causing 125 deaths with a case fatality rate of 39%. Historical incidents underscore the long-recognized dangers of A. flavus. In the early 1960s, an epidemic known as "Turkey X disease" in led to the deaths of over 100,000 turkey poults, traced to aflatoxin-contaminated groundnut meal; this outbreak prompted the identification of aflatoxins as metabolites of A. flavus and marked the beginning of systematic research into their toxicology. Similarly, the opening of Tutankhamun's tomb in 1922–1923 fueled legends of the "Curse of the Pharaohs" after several workers, including Lord Carnarvon, died from respiratory illnesses; Aspergillus flavus spores, capable of causing invasive in immunocompromised individuals, have been hypothesized as a contributing factor due to the fungus's presence in ancient Egyptian tombs. Epidemiologically, chronic low-level exposure to aflatoxins is widespread in developing countries, where staples like , , and are commonly contaminated, affecting an estimated 4.5 billion people globally and increasing risks of , growth stunting in children, and , particularly in . In animals, aflatoxins similarly induce ; prolonged exposure in dogs via contaminated commercial feeds has been linked to , failure, and , with outbreaks causing numerous fatalities and highlighting vulnerabilities in pet .

Management Strategies

Cultural and Environmental Controls

Cultural and environmental controls for Aspergillus flavus focus on agronomic practices that minimize fungal proliferation and aflatoxin contamination in crops like and by alleviating stress factors and limiting inoculum sources. Crop rotation with non-host plants, such as or , significantly reduces soil propagule density of A. flavus; for instance, continuous corn cropping results in up to 1628 colony-forming units (CFU) per gram of soil, compared to 237–374 CFU/g under or rotations. This practice disrupts the fungal lifecycle and lowers risk, though effects are less pronounced in high-inoculum environments. Breeding and planting drought-tolerant corn hybrids enhance resistance to A. flavus infection by mitigating physiological stress that favors fungal invasion; studies show a positive correlation between drought tolerance traits and reduced aflatoxin accumulation in 20 such lines. However, no fully commercial resistant varieties exist, and efficacy varies by hybrid and environmental conditions. Timely harvest at kernel moisture levels below 28% prevents post-maturity stress and subsequent aflatoxin synthesis, as delayed harvesting under drought can increase contamination by exposing kernels to optimal fungal growth conditions. Early harvesting has been shown to reduce aflatoxin occurrence in pre-harvest peanut kernels without significantly altering Aspergillus section Flavi incidence. Proper strategies reduce stress, a key driver of A. flavus . Deep , such as subsoiling or plowing, buries crop residues and inoculum deeper in the profile, decreasing A. flavus propagule availability for the next season and reducing kernel rates. For post-harvest , storing grains at contents below 13% and temperatures under 15°C inhibits fungal growth and aflatoxin production; at these levels, A. flavus ceases, preventing during . Monitoring techniques aid in early detection and prevention. (UV) light scouting identifies A. flavus-infected ears or kernels by their characteristic blue-green under black light, allowing targeted removal before harvest. (IPM) targets insect vectors like the corn earworm, which facilitate fungal spread by creating entry wounds; controlling these pests through cultural and mechanical means limits A. flavus dissemination in fields. These non-chemical approaches, when integrated, provide sustainable reductions in A. flavus risks without relying on active interventions.

Biological and Chemical Interventions

Biological interventions against Aspergillus flavus primarily involve the application of atoxigenic (non-aflatoxin-producing) strains to outcompete toxigenic populations in agricultural fields. The strain AF36, isolated from cottonseed and featuring a in the gene that prevents biosynthesis, was first registered for limited use in U.S. in 1995 and expanded commercially in 1996. This biocontrol agent is applied as granules or coated seeds, achieving 70-99% reductions in contamination through competitive exclusion, where AF36 displaces toxigenic strains by colonizing crop surfaces and soil, limiting their sporulation and sclerotia formation—the overwintering structures of A. flavus. Similar atoxigenic strains, such as those in vegetative compatibility groups like YV36, have demonstrated efficacy in and by reducing toxigenic fungal prevalence via resource competition. Chemical interventions target A. flavus growth and aflatoxin production using fungicides, particularly azoles applied as seed treatments or foliar sprays. , a , inhibits biosynthesis in fungal membranes, effectively suppressing A. flavus development in and conditions, with studies showing significant reductions in fungal biomass and toxin levels in ears. However, repeated exposure has induced in up to 72% of recovered isolates from treated corn seeds, attributed to in genes like cyp51A, complicating long-term efficacy. Additionally, chemical residues in harvested crops pose regulatory challenges, limiting use in safety-sensitive contexts. Integrated approaches combine biological and chemical methods with adsorbents to address at multiple stages, from field to post-harvest feed. Biocontrol with atoxigenic strains like AF36 in pre-harvest settings pairs effectively with clay-based sorbents, such as hydrated sodium calcium (HSCAS) or , added to animal feeds to bind aflatoxins in the , reducing by 40-90% without affecting nutrient absorption. Recent advancements in the 2020s include /Cas9-edited non-toxigenic A. flavus strains, where targeted deletions of clusters (e.g., via dual systems) create stable mutants with potential for enhanced biocontrol. Preliminary lab studies suggest promise for greater persistence and specificity compared to wild-type atoxigenics. These edited strains show promise in preliminary field tests for greater persistence and specificity compared to wild-type atoxigenics.