The research team, working from Hamelmalo Agricultural College, interviewed 80 farmers recruited through Ministry of Agriculture records using systematic random sampling. Fifty respondents came from the maize-producing highlands of Maekel and Debub, while thirty came from the groundnut-growing semi-arid zones of Anseba. Questionnaires administered in Tigrinya, the predominant local language, probed sociodemographics, awareness of mold contamination, knowledge of mycotoxins, uses of spoilt grain, and control measures. Alongside the interviews, the researchers collected 79 one-kilogram grain samples from household stores meant for human consumption and carried them to the college pathology laboratory for fungal isolation.

The demographic profile of the respondents matters for interpreting the findings. Ninety-one percent of the farmers were male, most were aged between 41 and 50, and farming on plots of three to six acres was the universal economic activity. Education levels were modest: 39 percent had achieved only primary schooling, a full 20 percent had no formal education at all, and just 7.5 percent had reached tertiary level. These figures set the stage for what the knowledge assessment would uncover, because formal schooling is often the primary channel through which rural communities encounter concepts like fungal contamination and toxic metabolites.

On the surface, the farmers showed practical familiarity with spoilage. More than half, 57.5 percent, said they could identify spoilt grains, and they described doing so through rotting, visible insects, and discolouration. All 80 respondents claimed they could distinguish well-dried pods and grain from poorly dried ones, and two-thirds said they cleaned their stores before introducing new harvests. Yet beneath this practical competence lay a deeper ignorance. When asked about the term mycotoxins, not a single farmer had heard of it. Ninety-five percent did not know the risks associated with consuming mold-infected grain, and 67 percent had no knowledge of measures for controlling mold fungal infection in storage.

The consequences of that ignorance are visible in what farmers do with spoilt grain. Roughly 34 percent admitted to consuming contaminated grain themselves, 26 percent fed it to livestock, and 18.4 percent sold it to unsuspecting customers in local markets. Only 12.5 percent sorted their grain after harvest, a practice that removes damaged and moldy cobs before they seed contamination through an entire store. The pattern echoes findings from Tanzania, Malawi and Zambia, where farmers aware of mycotoxin risks continued consuming contaminated grain due to food shortage, but in Eritrea the problem is compounded by the fact that awareness itself is absent.

Statistical analysis revealed a strong positive correlation between farmers’ knowledge of mold fungi and their ability to understand mycotoxin contamination, with a correlation coefficient of 0.804 at a significance level of p ≤ 0.001. This suggests that the two concepts travel together in the farmers’ mental models: those who grasp fungal infection also grasp toxin risk, and those who lack one lack both. Interestingly, education level showed a negative correlation with mold knowledge, likely because most respondents were primary school dropouts or had no basic education, meaning the topic of mycotoxins was never covered in the schooling they did receive. Age correlated positively with mold knowledge, hinting that accumulated farming experience transmits some awareness informally across generations.

Laboratory analysis confirmed the presence of the very fungi that produce the most dangerous mycotoxins. The researchers isolated Aspergillus niger, Aspergillus flavus, Aspergillus parasiticus, Fusarium verticillioides and Penicillium species from both maize and groundnut samples. Aspergillus flavus and A. parasiticus are the principal producers of aflatoxins, carcinogenic compounds associated with liver cancer, immune suppression, and growth retardation in children. Fusarium verticillioides produces fumonisins, which impair nutrient absorption and cause neural tube defects. The isolation of these species from grain destined for human consumption transforms the survey from an academic exercise into a public health warning.

Storage method emerged as a decisive factor in fungal contamination. Grain kept in the traditional Koffo structure showed the highest incidence of mycotoxigenic fungi across all species measured. Aspergillus niger reached 75.8 percent incidence in maize stored in Koffo, compared with 45.8 percent in plastic containers and 62.8 percent in plastic sacks. Fusarium verticillioides hit 45.6 percent in Koffo-stored maize. The researchers attribute the elevated contamination to farmers mixing old grain with new, leaving Koffo structures open for extended periods, and providing entry points for storage pests such as the maize weevil Sitophilus zeamais and the larger grain borer Prostephanus truncatus. Insect damage breaks grain kernels and raises local humidity, creating ideal conditions for fungal colonization.

The quality attributes observed in collected maize reinforce this pest-fungus synergy. Insect damage was the most common marker of poor grain quality, followed by moldy rot and shrivelling. These defects create pathways for inoculum to spread within stores, gradually contaminating entire grain lots over time. Comparable surveys in Togo and Honduras found similar patterns of Aspergillus, Penicillium and Fusarium dominating traditional storage facilities, suggesting that the Eritrean findings reflect a broader Sub-Saharan African challenge where agronomic, storage and climatic conditions conspire to encourage fungal growth and toxin production.

The study’s authors call for tailored interventions through the Eritrean Ministry of Agriculture to promote good agricultural practices aimed at reducing mold and mycotoxin contamination. They recommend awareness campaigns to inform farmers of the threats and effects of mycotoxins on human and animal health, expanded surveillance to monitor contamination levels, improved access to information, and an increase in the number of extension officers who can train farmers on fungal contaminants and management practices. Given that neighboring Uganda loses an estimated 577 million US dollars annually to mycotoxin-related losses, the economic stakes for Eritrea’s subsistent farming communities are considerable. The knowledge gap documented here is not merely an educational deficit but a silent pathway through which carcinogenic compounds enter the food chain, one contaminated grain at a time.

Subject of Research: Farmer awareness of mold infection and mycotoxin contamination in stored maize and groundnut in Eritrea

Article Title: Evaluation of awareness of mold infections in stored maize ( Zea mays L.) and groundnut ( Arachis hypogaea L.) in Anseba, Debub and Maekel Regions (Zoba) of Eritrea

Article References: Okumu, O. O., Sethumadhava, R., Melika, E. Z., Divora, T. M., Samuel, P. G., Even, B. F., Yasmin, S. J., & Abel, T. T. (2024). Evaluation of awareness of mold infections in stored maize (Zea mays L.) and groundnut (Arachis hypogea L.) in Anseba, Debub and Maekel Regions (Zoba) of Eritrea. Innovations in Agriculture, 7, 1-10. https://doi.org/10.3897/ia.2024.132491

Image Credits: AI Generated

DOI: 10.3897/ia.2024.132491

Keywords: mycotoxins, aflatoxin, food safety, Eritrea, maize, groundnut, Aspergillus, storage, agriculture, public health, Evaluation, awareness

The authors ground their argument in an ecological reframing of why fungi make these toxins in the first place. Mycotoxins emerge from specialised biosynthetic machinery, including polyketide synthases, non-ribosomal peptide synthetases and terpenoid pathways, and recent surveys have reported more than 900 new fungal metabolites, predominantly polyketides, terpenoids and peptides. Rather than evolving to poison mammals, aflatoxin production increases the fitness of Aspergillus flavus by up to 26-fold against insect herbivores while suppressing competing soil microorganisms, a trade-off that persists in natural populations. The same biosynthetic continuum yields antibiotics, antifungals and immunosuppressants, suggesting that the line between mycotoxin and pharmaceutical reflects the producer organism and the exposure context rather than any fundamental chemical mechanism. When dietary mycotoxins reach the gut, they therefore encounter a microbial community that treats them much as it treats any xenobiotic, transforming them enzymatically, binding them physically and, in some cases, releasing them back into active forms.

Microbial metabolism governs mycotoxin fate through conserved mechanisms whose relative contributions depend on the chemistry of the toxin and the composition of the microbiome. Detoxification is exemplified by the de-epoxidation of deoxynivalenol, the most prevalent Fusarium trichothecene, into the far less toxic metabolite DOM-1. Bioactivation runs in the opposite direction: zearalenone can be converted by gut bacteria into alpha-zearalenol, a compound with greater estrogenic activity than its precursor. Microbial cell walls, particularly the peptidoglycan of Lactobacillus and Bifidobacterium strains, adsorb aflatoxin B1 and reduce its free absorption in the small intestine. Meanwhile, microbial deconjugation during enterohepatic cycling can prolong systemic exposure, and masked plant-derived mycotoxins, such as deoxynivalenol-glucosides, can be hydrolysed by colonic beta-glucosidases back into their toxic aglycones in species- and site-dependent ways. The authors emphasise that mycotoxin fate is therefore shaped by microbiota-specific metabolic capacity rather than being intrinsically fixed.

Aflatoxin B1, a Group 1 human carcinogen that contaminates maize, peanuts and animal feed in warm climates, illustrates how epithelial injury intersects with microbiome-dependent immune dysfunction. Multiple microbial taxa degrade aflatoxin B1 through reductive and oxidative ring-modifying pathways that diverge fundamentally from hepatic cytochrome P450 bioactivation, including laccase-mediated oxidation from Bacillus licheniformis and Streptomyces species, F420H2-dependent reductases from mycobacteria and peroxidase-mediated degradation from Pleurotus ostreatus. These activities avoid epoxidation into the DNA-reactive aflatoxin B1-8,9-epoxide, the metabolite responsible for hepatic carcinogenicity. Yet the microbiome also amplifies aflatoxin toxicity. In mice, antibiotic-mediated microbiota depletion eliminated aflatoxin-induced splenic pyroptosis, while faecal microbiota transplantation and even sterile faecal filtrate transfer recapitulated hepatic pyroptosis, implicating gut-derived pipecolic acid and norepinephrine as causal microbial mediators that activate TLR4 and NLRP3 inflammasome signalling, driving caspase-1 activation, gasdermin D cleavage and the release of interleukin-1beta and interleukin-18.

Ochratoxin A, classified as a Group 2B possible human carcinogen and found in cereals, dried fruits, coffee, wine and cocoa, poses sustained dietary risk owing to its chemical stability, long biological half-life and renal accumulation. Microbial detoxification proceeds primarily through carboxypeptidase- and peptidase-mediated hydrolysis into the less toxic ochratoxin alpha, together with cell-wall-mediated binding. Fermented food consortia, particularly Tibetan kefir communities enriched in Lactobacillus kefiranofaciens and Kazachstania species, bind and degrade ochratoxin A through multivalent interactions involving cell wall beta-glucans, polysaccharides and peptidoglycans. In vivo, kefir intervention lowered ochratoxin burden, restored tryptophan and NAD+ homeostasis, upregulated tight junction proteins including claudin-1, occludin and ZO-1, and reduced liver enzyme levels, with metabolomics confirming glycerophospholipid rebalancing. Without such protection, ochratoxin A downregulates tight junction proteins through reactive oxygen species, calcium and myosin light chain kinase-dependent signalling, induces mitochondrial ROS and caspase-dependent apoptosis, and depletes tryptophan-metabolising taxa, weakening aryl hydrocarbon receptor signalling and regulatory T cell function while LPS translocation activates hepatic TLR4 and exacerbates inflammation.

Fumonisin B1, prevalent in maize due to Fusarium contamination, competitively inhibits ceramide synthase, disrupting de novo sphingolipid biosynthesis and driving the characteristic elevation in sphinganine-to-sphingosine ratios used as a biomarker of exposure. Gut-associated lactobacilli contribute to detoxification through esterase- and amidase-mediated hydrolysis that removes tricarballylic acid side chains to form hydrolysed fumonisin B1. Among the best-characterised bacteria, Lactobacillus pontis, L. amylovorus and L. ultunensis isolated from porcine caecum converted fumonisin B1 via surface adsorption followed by enzymatic hydrolysis, achieving up to approximately 50 percent conversion within 48 hours in vitro. However, hydrolysed fumonisin B1 retains biological activity and can sustain intestinal and hepatic injury through MAPK- and NF-kappaB-dependent pathways largely independent of sphingolipid disruption. Comparative animal studies demonstrate that both compounds compromise epithelial barrier integrity, alter gut microbial composition, reduce short-chain fatty acid production by 40 to 60 percent and disrupt hepatic metabolism, although effects are generally milder following exposure to the hydrolysed form. Antibiotic treatment eliminated 75 to 80 percent of fumonisin hepatotoxicity, while faecal microbiota transplantation reproduced hepatic injury, confirming the microbiome as a causal determinant of systemic toxicity.

The trichothecenes deoxynivalenol and T-2 toxin exert toxicity primarily through inhibition of translation and activation of ribotoxic stress pathways that phosphorylate eIF2alpha and engage MAPK and NF-kappaB cascades. Deoxynivalenol reshapes intestinal microbial communities and compromises barrier function, and these effects were partially mitigated by selected strains of Bacillus velezensis, which restored tight junction protein expression, suppressed TLR4/NF-kappaB signalling and normalised microbial composition and short-chain fatty acid profiles. Lactobacillus rhamnosus GG binds deoxynivalenol via S-layer proteins and rescues food intake in anorexia models, increasing butyrate and lowering TNF-alpha and interleukin-6. For T-2 toxin, microbiota-dependent activation of interleukin-6/Janus kinase/signal transducer and activator of transcription 1 signalling mediates splenic injury, as the phenotype was abolished by antibiotic treatment and recapitulated by faecal microbiota transplantation. Elemental nano-selenium attenuated this inflammatory response by reducing reactive oxygen species, suggesting that targeting microbiome-immune interactions may represent a viable strategy to reduce trichothecene toxicity. In contrast to aflatoxin and ochratoxin, evidence for binding-mediated sequestration of trichothecenes remains limited, indicating that biotransformation rather than adsorption is the dominant microbial mechanism influencing their toxicity.

Perhaps the most provocative implication concerns antimicrobial resistance. The authors highlight emerging evidence that deoxynivalenol exposure selectively enriches Gram-positive taxa carrying antibiotic resistance genes, particularly those associated with last-resort antibiotics such as daptomycin. Enterococcus faecalis isolated from deoxynivalenol-exposed microbiota showed extensive drug resistance, with resistance exceeding 128 micrograms per millilitre to daptomycin, vancomycin and linezolid. Deoxynivalenol-induced stress promotes genomic plasticity, enhances the co-occurrence and dissemination of resistance genes via mobile genetic elements, and increases reactive oxygen species production and membrane permeability, amplifying resistance phenotypes. Bacterial defence responses to the toxin converge with classical antibiotic resistance mechanisms, including activation of ATP-binding cassette transporters, toxin-detoxifying enzymes and stress-response proteins such as porins, glutathione S-transferases and phosphotransferases. The authors caution that deoxynivalenol is not an antimicrobial in the conventional sense but may act as a selective ecological pressure that favours resistant populations, and they note that evidence that aflatoxin, ochratoxin or zearalenone directly promote horizontal resistance gene transfer remains limited.

The authors are equally candid about the limitations of the evidence base. Most reports of mycotoxin-induced microbiota perturbation remain descriptive, with limited causal or functional resolution, and many experiments use high doses and non-human models whose relevance to real-world conditions, where exposure is usually chronic and low-dose, is uncertain. Reported microbiota responses are inconsistent, with deoxynivalenol, zearalenone and aflatoxin producing opposing shifts in Proteobacteria, Firmicutes and Bacteroidetes across experimental systems, likely reflecting differences in host biology, exposure intensity, duration and matrix composition. Results for Lactobacillus are particularly inconsistent despite its relevance in detoxification, and aflatoxin exposure can even increase Lactobacillus populations, raising mechanistic questions about whether microbial enrichment reflects adaptive detoxification, ecological resilience or selection for intrinsically resistant taxa with altered functional potential. High in vitro degradation or binding rates by probiotics do not necessarily persist in vivo because of gastric pH, transit time, competing food matrices, host metabolism and enterohepatic recirculation.

Looking ahead, Garcia-Cela and Marcon Gasperini call for a shift beyond descriptive microbiota profiling toward integrative frameworks that link microbial ecology, host physiology and metabolomic outputs. Priority areas include in vivo validation of microbial detoxification pathways, systematic comparison of in vitro and dietary exposure models, and strain-level functional characterisation to resolve inter- and intra-species variability in detoxification capacity. Multi-strain consortia, including kefir-like communities, are particularly attractive because they can couple adsorption, biodegradation and ecological competition within a single system. Engineered microbial systems could be designed to express defined detoxification enzymes or high-affinity binding modules, but their deployment will require careful evaluation of containment, regulatory approval and ecological impact. Future studies must also incorporate co-exposure scenarios, enterohepatic cycling and host-specific variables to enhance translational relevance, and mechanistic resolution of feedback loops between epithelial injury and microbial metabolic reprogramming will be essential to understand whether host-microbiome interactions amplify or constrain toxicity over time. The next generation of interventions, the authors suggest, will likely be modular, mechanism-based and tailored to the toxin, matrix and host context rather than dependent on any single probiotic solution.

Subject of Research: Microbiology / Toxicology

Article Title: Mechanistic evidence and assumptions in mycotoxin-gut interaction

Article References: Garcia-Cela, E., & Marcon Gasperini, A. (2026). Mechanistic evidence and assumptions in mycotoxin-gut interaction. Frontiers in Fungal Biology, 7, Article 1855881. https://doi.org/10.3389/ffunb.2026.1855881

Image Credits: AI Generated

DOI: 10.3389/ffunb.2026.1855881

Keywords: mycotoxins, gut microbiota, aflatoxin B1, ochratoxin A, fumonisin B1, deoxynivalenol, T-2 toxin, antimicrobial resistance, intestinal barrier, microbial detoxification, Mechanistic, evidence

Ochratoxin A (OTA) is one of the most concerning mycotoxins in the food supply. Classified by the International Agency for Research on Cancer as a group 2B agent—a possible human carcinogen—it carries nephrotoxic, immunotoxic, and teratogenic properties. While OTA contamination is well documented in cheese, no legal limits for the toxin in cheese currently exist, highlighting an urgent need for effective mitigation strategies. The European Food Safety Authority has identified cheese among the food categories contributing to chronic dietary OTA exposure in some consumer groups, making the search for solutions increasingly pressing.

Enter Debaryomyces hansenii. This yeast is one of the dominant species naturally found on the surfaces of many ripened cheeses, where it contributes positively to flavour development, proteolytic and lipolytic activities, and surface deacidification. It has been included in the European Qualified Presumption of Safety (QPS) framework since 2007, meaning regulators consider it safe for use in food. Previous research has shown that D. hansenii can limit ochratoxigenic fungi in fermented meats, but until now, no study had tested its effectiveness against A. westerdijkiae specifically on a cheese-like matrix.

The research team, led by scientists at the Institute of Sciences of Food Production (CNR-ISPA) in Bari, Italy, tested thirteen strains of A. westerdijkiae—twelve isolated from the surfaces of Italian cave cheeses and one from sorghum—against a single strain of D. hansenii (ITEM 19968), itself originally isolated from cheese. They used a Caciocavallo-based cheese agar medium designed to mimic the actual cheese environment from which the fungal strains were recovered.

The experimental design was straightforward but rigorous. The researchers inoculated the cheese agar with a suspension of D. hansenii at a concentration of 10⁶ cells per millilitre, then spotted fungal spores onto the surface in a symmetrical triangular pattern. Control plates received the fungal spores but no yeast. Plates were incubated for 20 days at 25°C in the dark, and mycelial growth was measured at 5, 10, 15, and 20 days post-inoculation. After the incubation period, the entire plate contents were collected and analysed for OTA using high-performance liquid chromatography with fluorometric detection.

The results revealed a striking temporal pattern. In the first five days, the interaction between the two microorganisms was heterogeneous: five of the thirteen fungal strains actually showed apparent growth stimulation in the presence of the yeast, with inhibition values ranging from −17% to +35%. However, by day 10, all thirteen strains exhibited reduced mycelial growth, with inhibition values ranging from 17% to 31%. These inhibition levels remained relatively stable through days 15 and 20, suggesting a sustained antagonistic effect once the yeast became established.

The most dramatic findings, however, concerned ochratoxin A production. At 20 days post-inoculation, OTA production was reduced by 63% to 100% across all toxin-producing strains. Seven strains—ITEM 9607, ITEM 18032, ITEM 19082, ITEM 19084, ITEM 19092, ITEM 19094, and ITEM 19095—showed complete inhibition, with OTA levels falling below the detection limit of 3 μg/kg. The control group’s baseline OTA production ranged from 5 to 1,603 μg/kg, meaning the yeast suppressed toxin output regardless of how intrinsically toxigenic each fungal strain was.

What makes these results particularly intriguing is that the reduction in OTA was proportionally greater than the reduction in fungal growth. This suggests that D. hansenii does not merely limit fungal proliferation but also directly interferes with the metabolic pathways involved in mycotoxin biosynthesis. Previous work by Gil-Serna and colleagues demonstrated that the yeast may downregulate genes involved in OTA production and adsorb the toxin onto its cell walls. The authors of the current study propose that nutrient competition, accumulation of yeast-derived metabolites, and modifications to the cheese environment’s physicochemical properties—such as lactate utilisation and surface pH increase—may all contribute to the observed antagonistic effects.

The temporal dynamics of the interaction are also noteworthy. The apparent stimulation of some fungal strains during the first five days likely reflects the yeast’s establishment phase, during which it adapts to the substrate and progressively alters local conditions without yet generating conditions restrictive enough to inhibit fungal growth. Once established, however, D. hansenii appears to create an environment hostile to both fungal expansion and toxin synthesis. This suggests that for practical applications in cheese ripening, the yeast would need to be active for at least ten days to exert meaningful biocontrol.

The researchers caution that their work was conducted under controlled laboratory conditions using a cheese-like medium, which may not fully replicate the complexity of real cheese ecosystems. The specific physiological and molecular mechanisms underlying the observed effects were not investigated and warrant further study using transcriptomic, metabolomic, and targeted biochemical approaches. Additionally, the sensory impact of the specific D. hansenii strain on cheese quality remains untested and must be evaluated under actual manufacturing conditions before practical application.

Nevertheless, the findings represent a significant step forward in the search for natural, sustainable solutions to mycotoxin contamination in dairy products. As consumer demand for clean-label foods grows and regulatory pressure on chemical preservatives intensifies, biocontrol approaches using microorganisms with a history of safe use in food fermentation are gaining traction. Debaryomyces hansenii, already a familiar inhabitant of cheese surfaces and a recognised contributor to cheese ripening, may soon play an even more important role—not just in shaping flavour and texture, but in actively protecting consumers from one of the food supply’s most persistent toxic threats.

Subject of Research: Biocontrol of ochratoxigenic Aspergillus westerdijkiae by Debaryomyces hansenii on cheese-like medium

Article Title: Debaryomyces hansenii as potential biocontrol agent against Aspergillus westerdijkiae and its ochratoxin A production on cheese-like medium

Article References: Carella, D., Cervellieri, S., Anelli, P., Gatto, A., De Girolamo, A., Lippolis, V., Moretti, A., & Susca, A. (2026). Debaryomyces hansenii as potential biocontrol agent against Aspergillus westerdijkiae and its ochratoxin A production on cheese-like medium. Current Research in Food Science, Article 101599. https://doi.org/10.1016/j.crfs.2026.101599

Image Credits: AI Generated

DOI: 10.1016/j.crfs.2026.101599

Keywords: Debaryomyces hansenii, Aspergillus westerdijkiae, ochratoxin A, mycotoxins, cheese ripening, biocontrol, food safety, yeast, dairy, biopreservation, Debaryomyces, hansenii

A. fumigatus is the principal cause of aspergillosis, a spectrum of infections ranging from allergic airway disease to life-threatening invasive illness. The fungus produces extremely small conidia that are easily inhaled deep into the respiratory tract, and it can survive and grow across a wide range of environmental conditions, including at and above human body temperature. It also manufactures toxic metabolites known as mycotoxins. In 2022, the World Health Organization designated A. fumigatus a priority fungal pathogen, underscoring the urgent need for global surveillance as resistance to azoles, the first-line class of antifungal agents, continues to rise.

The research team, led by Bianca Gomes of the Center for Ecology, Evolution and Environmental Change at the University of Lisbon and colleagues from several Portuguese institutions, collected 420 samples from five poultry farms comprising 14 poultry pavilions. The matrices included indoor air, electrostatic dust cloths, wood shavings bedding, feed, surface swabs, workers’ filtering respiratory protection devices, and broiler breast tissue. Sampling spanned four stages of the production cycle, from cleaned and disinfected empty pavilions through the first, second, and third weeks of bird growth, across two consecutive production cycles in summer and winter.

Fungal characterization relied on culture-based methods at two temperatures. Plates incubated at 27 degrees Celsius captured the general environmental mycobiota, while incubation at 37 degrees Celsius selected thermotolerant species capable of growing at human body temperature, a critical indicator of pathogenic potential. Detection rates at 37 degrees Celsius reached 95.78 percent across all matrices and production stages, compared with only 14.64 percent at 27 degrees Celsius. Section Fumigati was particularly predominant in air and bedding at the higher temperature, representing more than 79 percent of recovered fungi in both matrices. The team notes that exposure assessments targeting this section should include culture at 37 degrees Celsius, since lower temperatures may promote faster-growing fungi and underestimate the presence of potentially pathogenic Aspergillus species.

From 253 recovered isolates, 173 grew at 37 degrees Celsius and were selected for further analysis. Sub-culturing on Potato Dextrose Agar at 50 degrees Celsius identified 164 putative A. fumigatus isolates, since growth at such elevated temperatures is indicative of A. fumigatus sensu stricto rather than morphologically similar cryptic species within the section. Azole resistance screening followed EUCAST guidelines using the azole-containing agar plate method, with conidial suspensions inoculated onto four-well RPMI-1640 agar plates containing 4 milligrams per liter itraconazole, 2 milligrams per liter voriconazole, and 0.5 milligrams per liter posaconazole. Seven isolates, six from bedding and one from air, showed visual growth on the azole-supplemented wells and were selected for confirmatory testing.

Broth microdilution susceptibility testing according to the EUCAST reference method E.Def 9.4 confirmed pan-azole resistance in all seven isolates. Minimum inhibitory concentrations ranged from 2 to 8 milligrams per liter for itraconazole, 2 to 4 for voriconazole, and 1 to 2 for posaconazole, all exceeding the EUCAST clinical breakpoints. Whole-genome sequencing using Oxford Nanopore technology generated 13.02 million reads and 48.76 gigabases of sequence data, with sequencing depth between 168.7-fold and 313.7-fold and 96 to 98 percent of reads successfully mapped against the A. fumigatus Af293 reference genome. Taxonomic classification using Kraken2 confirmed the predominance of A. fumigatus reads across all datasets, with less than 1 percent of reads remaining unclassified.

Targeted analysis of the cyp51A gene, which encodes the azole target enzyme, identified the TR34/L98H mutation in four isolates. This mutation combines a 34-base-pair tandem repeat insertion in the promoter region with a leucine-to-histidine substitution at position 98 in the coding region, altering the azole target enzyme and reducing antifungal binding affinity. The four TR34/L98H isolates were recovered from bedding and air, with three from bedding and one from air. The remaining three isolates lacked tandem repeats in the promoter but carried the mutations F46Y, M172V, N284T, D255E, and E427K, along with four indels upstream of the promoter. While the functional impact of these distal promoter alterations remains unclear, changes in the cyp51A promoter have been associated with altered gene expression and reduced azole susceptibility, making them candidate genetic features that may contribute to the resistant phenotype. Further studies, including gene expression analysis and functional validation, are required to determine their role.

The environmental use of azole fungicides has been linked to the emergence and dissemination of TR-based resistance mechanisms in A. fumigatus, contributing to the global spread of resistant lineages characterized by multi-azole resistance and increased recombination rates. The TR34/L98H clade frequently harbors the hypermutator variant msh6-G233A, which has been associated with elevated mutation rates and adaptive capacity, potentially facilitating the evolution of antifungal resistance. The presence of this variant was not assessed in the recovered isolates, so its occurrence cannot be established. Nonetheless, the detection of TR34/L98H isolates in poultry farm environments highlights the importance of continued One Health surveillance to monitor the occurrence and potential dissemination of azole-resistant A. fumigatus across environmental, animal, and human interfaces. The common use of wood shavings, possibly treated with azoles, as animal bedding material may promote the emergence of resistant mycobiota within poultry farms, although azole residues in bedding were not assessed in this study.

Cytotoxicity assays were performed on 145 successfully re-isolated section Fumigati isolates using the MTT assay with two cell lines: human alveolar lung carcinoma cells (A549), representing the primary site of exposure to airborne fungal spores, and human hepatocellular carcinoma cells (HepG2), representing potential systemic effects of mycotoxin exposure. A reduction in cell viability below 70 percent was considered indicative of a cytotoxic effect. Overall, 46.20 percent of isolates induced toxicity on HepG2 cells, reducing viability to as low as 34 percent, while 16.55 percent reduced A549 viability to as low as 57 percent. Twelve percent of isolates induced toxicity on both cell lines. Isolates recovered from air samples showed the highest frequency of cytotoxicity in HepG2 cells at 65.8 percent, whereas cytotoxicity in A549 cells was generally less frequent across all matrices.

When the cytotoxicity of fungal isolates was compared with previously obtained cytotoxicity data from their corresponding environmental samples, no significant association was detected. Overall, 76.90 percent of environmental samples induced cytotoxicity, whereas only 10.77 percent of the corresponding isolates exhibited cytotoxic effects, with very low concordance between the two types of samples. This pattern of discordance, dominated by cytotoxic environmental samples with noncytotoxic isolates, suggests that cultivable fungi alone are not the main contributors to the observed toxic profile. The team also screened 38 mycotoxins in environmental samples, detecting deoxynivalenol, fumonisins, and zearalenone across all three matrices. For swine kidney cells, a significant association was detected between cytotoxicity and mycotoxin detection, with cytotoxic samples approximately twice as likely to contain detectable mycotoxins. For A549 cells, no significant association was observed, suggesting that matrix type and production stage may have a greater influence on cytotoxicity than mycotoxin detection alone. Collectively, these findings reinforce the need for integrated surveillance strategies targeting both Aspergillus species and mycotoxins in poultry production, extending to poultry residues and their safe land application, while research into sustainable antifungal alternatives, including plant essential oils, may help reduce reliance on azoles and mitigate the selective pressure driving resistance.

Subject of Research: Microbiology

Article Title: Detection of TR34/L98H pan-azole-resistant Aspergillus fumigatus in poultry farm environments

Article References: Gomes, B., Dias, M., Cervantes, R., Gonçalves, L., Carolino, E., Ramos, M. J. N., Nunes, M., Dias, R., & Viegas, C. (2026). Detection of TR34/L98H pan-azole-resistant Aspergillus fumigatus in poultry farm environments. Frontiers in Fungal Biology, 7, Article 1858050. https://doi.org/10.3389/ffunb.2026.1858050

Image Credits: AI Generated

DOI: 10.3389/ffunb.2026.1858050

Keywords: Aspergillus fumigatus, azole resistance, TR34/L98H, poultry farms, One Health, antifungal resistance, mycotoxins, Detection, TR34, L98H, pan-azole-resistant, Aspergillus

The scale of insect consumption worldwide is staggering. More than 3,000 ethnic groups eat insects, and 2,205 species have been documented as food across 128 countries. In Africa alone, 464 edible species have been reported from 48 countries, with termites, caterpillars, crickets, and grasshoppers among the most widely consumed. Yet while insects deliver high-quality protein, lipids, vitamins, and minerals, the safety landscape surrounding them has remained surprisingly underexplored—particularly when they are incorporated into foods for the most vulnerable consumers: infants and young children.

To fill this gap, the research team analyzed 30 material types: 11 edible-insect products, seven food ingredients, seven insect-enriched formulations, and five commercial complementary flours. The insects included winged termites (Macrotermes subhyalinus), lake-flies (Chaoborus sp.), crickets (Gryllus bimaculatus and Scapsipedus icipe), desert locusts (Schistocerca gregaria), grasshoppers (Ruspolia differens), silkworm pupae (Bombyx mori), wild silk moth caterpillars (Anaphe panda), mopane worms (Gynanisa maja and Gonimbrasia belina), Bunaea alcinoe, and Gonimbrasia zambesina. Fungal isolation comprised 1,080 inoculated culture observations across three independent batches per material type, from which 798 fungal isolates were recovered and identified by culture, microscopy, and internal transcribed spacer (ITS) sequencing.

The results paint a striking picture of fungal prevalence. Aspergillus accounted for 70.7 percent of isolates recovered from insect products, followed by Penicillium at 18.6 percent and Fusarium at 7.4 percent. Penicillium was detected in all 11 insect products, while Fusarium appeared in eight of them. Across all material categories, Aspergillus dominated at 55.3 percent of the 798 recovered isolates, followed by Penicillium at 26.1 percent and Fusarium at 14.5 percent. The distribution of fungal genera differed significantly between material types, with Aspergillus predominating in insects, ingredients, and enriched formulations, while Penicillium was more common in commercial complementary flours.

Beyond mere presence, the researchers probed the toxigenic potential of the recovered fungi using endpoint PCR. Among 44 Aspergillus flavus-like morphotypes, the aflatoxin-biosynthesis genes aflD and aflQ were detected in 32 and 23 isolates, respectively. Among 22 Fusarium-like isolates, the fumonisin-biosynthesis gene FUM1 was detected in 19, and the VERTF intergenic-spacer profile associated with potentially fumonisin-producing Fusarium verticillioides strains appeared in 10. The authors are careful to note that marker detection does not establish gene expression or actual mycotoxin production—but it does provide biological context for the chemical findings that followed.

Using liquid chromatography–tandem mass spectrometry (LC–MS/MS), the team screened 23 mycotoxins in five complementary-food formulations—four insect-fortified and one non-insect control—over three months of storage at approximately 22 degrees Celsius. Six mycotoxins were confirmed: 3-acetyldeoxynivalenol, aflatoxin G1, sterigmatocystin, and fumonisins B1, B2, and B3. Only aflatoxin G1 and fumonisin B1 were quantified above their limits of quantification, at 4.20 µg/kg and 20.31–86.88 µg/kg, respectively. Quantifiable fumonisin B1 occurred more frequently at later storage points and peaked after three months, although the temporal pattern was not uniformly monotonic across formulations. The aflatoxin G1 point estimate fell below the Kenyan total-aflatoxin maximum for processed cereal-based foods for older infants and young children, and the European Union maize-based infant-food fumonisin value was used only as a contextual benchmark, since the formulations were grain-amaranth-based and contained no maize. Neither comparison established compliance or safety.

Notably, fumonisin B1 was detected in all five formulations, including the non-insect control, while the aflatoxin G1 and fumonisin B3 detections occurred only in the control formulation. The findings therefore do not support attribution of the detected mycotoxins specifically to the insect ingredients. Grain amaranth, common to all formulations, may have contributed to the widespread fumonisin occurrence, but the source cannot be assigned because individual ingredient batches were not analyzed separately for mycotoxins. This nuance underscores a broader challenge in multi-ingredient foods: contamination can flow from any component, and pinpointing origins requires ingredient-level surveillance.

The histamine and allergen-related findings add another layer of complexity. Histamine, which forms through microbial decarboxylation of histidine during inadequate handling or storage, is heat-stable and has caused poisoning outbreaks following insect consumption in Thailand. In this study, quantifiable histamine concentrations in 17 insect preparations ranged from 3,108 to 30,232 µg/kg, with the highest values recorded in raw and pan-fried lake flies (Chaoborus spp.). One oven-dried mopane worm preparation (Gonimbrasia belina) exceeded the assay’s upper quantitative limit and was reported as greater than 40,000 µg/kg. Three preparations fell below the assay’s lower limit of quantification. These values are descriptive rather than evidence of regulatory compliance, since no histamine limits currently exist for edible insects or insect-based complementary foods.

On the allergen front, lysozyme-reactive ELISA signals were below 25 µg/kg in all 17 insect preparations, suggesting minimal reactivity with hen’s-egg lysozyme antibodies. However, crustacean-reactive signals exceeded the assay’s upper quantification limit of 400 µg/kg in 16 of 17 preparations, with the remaining oven-dried Gonimbrasia belina result at 382 µg/kg. These signals represent analytical boundaries rather than health-based safety thresholds, and the reacting proteins were not identified. Tropomyosin and arginine kinase are among the arthropod proteins most frequently implicated in cross-reactivity between crustaceans and insects, and previous studies have demonstrated IgE recognition of cricket and grasshopper proteins by shrimp-allergic patients. The authors stress that the ELISA component was exploratory and that confirmation using multiple independently collected batches within each species and processing category is required before clinical conclusions can be drawn.

The study’s conclusions are clear: edible insects remain a promising, sustainable, and nutrient-rich food source, but their safety depends on species, rearing, processing, and storage. The findings support improved hygienic processing, ingredient control, routine fungal and mycotoxin surveillance, prompt post-harvest temperature control, and continued assessment of allergen-related cross-reactivity—particularly when insects are intended for incorporation into complementary foods for infants and young children. As insect-based nutrition scales up across Africa and beyond, this research provides a critical technical foundation for building safe, trustworthy value chains that can deliver on the promise of insects as food without compromising the health of the most vulnerable consumers.

Subject of Research: Fungal contamination, mycotoxins, histamine, and allergen-related immunoreactivity in edible insects and insect-fortified complementary foods

Article Title: Fungal contamination, mycotoxins, histamine, and allergen-related immunoreactivity in edible insects and insect-fortified complementary foods

Article References: Imbumi, M., Okoth, S., Audenaert, K., De Steur, H., Gellynck, X., Tanga, C. M., De Saeger, S., Kimiywe, J., & Raes, K. (2026). Fungal contamination, mycotoxins, histamine, and allergen-related immunoreactivity in edible insects and insect-fortified complementary foods. Frontiers in Fungal Biology, 7, Article 1798430. https://doi.org/10.3389/ffunb.2026.1798430

Image Credits: AI Generated

DOI: 10.3389/ffunb.2026.1798430

Keywords: edible insects, fungal contamination, mycotoxins, histamine, allergen cross-reactivity, complementary foods, food safety, Aspergillus, Fusarium, infant nutrition, Fungal, contamination

The argument rests on a subtle but important distinction that applied mycology has long recognized yet rarely built into risk assessments. Every mycotoxigenic fungus has two overlapping but distinct ecological ranges: its growth window, the full set of temperature and water activity conditions under which it can colonize a substrate, and its toxin-production window, the narrower range in which the biosynthetic machinery for a given toxin is actually switched on. In nearly every species studied, the toxin-permitting range sits inside the growth range like a kernel inside a shell. Most models have treated these boundaries as fixed species properties, measured once on synthetic laboratory media such as potato dextrose agar and applied as constants ever since. Medina argues that this treatment is doubly flawed: fungi experience the food matrix itself as part of their environment, and boundary values measured on agar can differ considerably from those on the actual grain, nut or fruit at risk.

The factor that forced a reconsideration of these fixed windows is carbon dioxide. When elevated CO2 is added to the interaction between temperature and water availability in experimental systems, it does not simply increase toxin output under already favorable conditions. Instead, it widens the range of conditions under which toxin is produced at all, drawing the toxin-production window closer to the growth window. In studies of Aspergillus flavus on maize, interacting elevated CO2 with drought stress and increased temperature raised the expression of aflatoxin biosynthetic genes aflD and aflR and boosted aflatoxin B1 production, in some cases several-fold, under conditions that previously supported growth only. A parallel pattern, in which fungal growth changes little while toxin production expands, has been documented in pistachio-associated A. flavus and grape-associated A. carbonarius, although the degree and direction of the shift vary by species, strain and substrate.

There is also evidence that these windows are not merely plastic but can shift with repeated exposure. Strains of Fusarium langsethiae, F. poae and F. sporotrichioides sub-cultured for ten generations at 1000 parts per million of CO2 altered their subsequent growth and toxin-production responses relative to non-acclimatized strains, suggesting that successive generations can acclimatize to a changing atmosphere. Medina stresses that the direct CO2 effect has so far been demonstrated most convincingly in Aspergillus systems, and that confirming it across the wider fungal community remains a research priority. Still, the emerging picture is that climate change, acting through the interaction of temperature, water activity and CO2, does not merely make existing conditions more frequent. It modifies the ecological space available to toxigenic fungi, and often widens it.

The second half of the argument concerns timescale. Research on climate change and mycotoxins since the early 2000s has focused on combined rather than single factors, because studies varying one variable at a time consistently mis-estimated fungal behavior compared with combined-factor data. What has changed is the frequency with which these factors now cluster within a single cropping season rather than being spread across successive years. A season that once brought a single anomalous event, an early heat spike, a mid-season drought, a late intense rainfall, can now deliver several in sequence in the same field. Meanwhile, crop pests and pathogens have been shifting polewards at a mean rate of 2.7 kilometers per year since 1960, and temperature-dependent infection risk for fungal crop pathogens is projected to rise fastest at higher, increasingly productive latitudes. A framework built around isolated, spaced-out anomalies simply cannot describe a regime in which extremes compound within one crop cycle.

At the community level, this has a counterintuitive consequence. If growth and toxin windows widen and shift for multiple species at once, the previously separate temporal and spatial niches occupied by Fusarium, Aspergillus, Penicillium and Alternaria species within a crop cycle begin to overlap. Species that once took turns now compete for the same favorable conditions, and the outcomes are strain- and species-specific rather than predictable from single-factor data. Wider ecological windows, in other words, do not simply mean more toxin from one fungus. They may mean a larger, more crowded set of species with a genuine opportunity to contribute toxin to the same commodity at the same time. Medina proposes that the degree of overlap between the growth window and the toxin window could serve as a practical ecological metric for anticipating mycotoxin risk under climate change, one that can be estimated for a given species and matrix rather than assumed constant.

If the mechanism is general, its fingerprints should be visible in field surveys that were never designed to test it, and the evidence assembled in the Perspective is strikingly consistent with that prediction. Household maize in Kenya has been found to carry 22 different mycotoxins spanning both Aspergillus and Fusarium products, alongside 31 metabolites of A. flavus, with sharp regional differences between aflatoxin- and fumonisin-dominant areas. Brazilian cocoa has been reported carrying up to 15 mycotoxins from three fungal genera simultaneously. An 11-year survey of northern Italian maize found more than 85 percent of samples contaminated with two or more mycotoxins from Fusarium and Aspergillus jointly, and a seven-year survey across 23 European countries documented co-occurrence rates of 52 to 74 percent between trichothecenes and other Fusarium-derived emerging toxins. A ten-year global screen of 74,821 animal feed samples from 100 countries found that 64 percent of samples tested for three or more toxins contained at least two.

Multi-species coexistence is also visible within single crops, and species substitutions track the changing climate. In maize, hotter, drier conditions favor a shift from Fusarium verticillioides towards Aspergillus flavus dominance, and one modeling study projects a 92 percent increase in aflatoxin B1 risk in European maize under a two-degree warming scenario. PCR surveys of Spanish vineyards have found A. flavus on 67 percent of organically grown berries, A. niger on 44 percent and A. carbonarius on 14 percent, three toxigenic species routinely sharing the same fruit. On cereals, F. graminearum has displaced F. culmorum as the head-blight pathogen of Danish wheat, while Fusarium head blight has intensified under warming in southern England and central China, the latter accompanied by a shift toward a more toxigenic chemotype. The pattern even persists through processing: a UK survey of plant-based meat alternatives found emerging Fusarium toxins in up to 98.9 percent of samples and Alternaria toxins in up to 90.4 percent, while 78 percent of wheat flour samples from Shandong, China, carried deoxynivalenol together with two Alternaria toxins.

Medina is careful to flag the central confounder. Improved analytical capability, particularly broader liquid chromatography tandem mass spectrometry panels, undoubtedly accounts for a substantial share of the co-occurrence now being recorded, and multi-mycotoxin contamination is unlikely to be an entirely new phenomenon. But the same trend appears across independent surveys differing in continent, commodity and study design, which is compatible with a genuine biological contribution layered on top of better detection. Climate change should be viewed as a major interacting driver rather than the sole determinant, since agronomic practices, cultivar choice, trade patterns, storage conditions and sampling strategies all shape what is recorded. The proposed framework is offered explicitly as a plausible hypothesis rather than an established transition.

The practical implications are considerable, because the infrastructure of mycotoxin management remains anchored in a world of single toxins and single species. Predictive models that treat temperature, water activity and CO2 as separate, additive factors will systematically underestimate risk, since it is their interaction that widens the toxin window. Regulatory limits calibrated around single-compound thresholds do not address the toxicological consequences of co-occurring mycotoxins. Medina calls for surveillance to move to routine multi-mycotoxin analysis and near-real-time monitoring, noting that low-cost CO2 sensing has recently been proposed as an early warning signal because fungal CO2 output rises before toxin becomes detectable. Mitigation strategies validated under current conditions need re-testing under interacting future scenarios, and regulators from EFSA to Codex Alimentarius should treat multi-mycotoxin contamination not as an anomaly but as the baseline against which exceptionality is judged. Because the same crops, climate drivers and contaminated commodities flow through livestock and the wider environment, the author frames this as a One Health problem, shared by human, animal and environmental health sectors. The Perspective leaves readers with a memorable reframing: the black swan was never disappearing, it was multiplying, and the flock, not the single bird, is now the more accurate description of the risk.

Subject of Research: Climate change effects on fungal ecology and the risk of multi-mycotoxin contamination of crops and food

Article Title: Beyond the black swan: climate change and the evolving risk of multi-mycotoxin contamination

Article References: Medina, A. (2026). Beyond the black swan: climate change and the evolving risk of multi-mycotoxin contamination. Frontiers in Fungal Biology, 7, Article 1981215. https://doi.org/10.3389/ffunb.2026.1981215

Image Credits: AI Generated

DOI: 10.3389/ffunb.2026.1981215

Keywords: mycotoxins, climate change, fungal ecology, food safety, Aspergillus flavus, aflatoxin, Fusarium, CO2, ecological niche, surveillance, One Health, food contamination

The analytical approach adopted in this study deserves particular attention. By isolating individual strains rather than analyzing bulk soil samples, the researchers were able to attribute toxin production to specific organisms and to link chemical profiles directly to genetically identified species. This distinction matters because bulk-soil analyses, which detect mycotoxins mixed together in a single extract, cannot disentangle whether several toxins originate from one versatile organism or from several specialist strains coexisting in the same soil volume. The strain-by-strain strategy, combined with liquid chromatography coupled to high-resolution mass spectrometry, provides a resolution that allows toxicological risk assessment at the level of the individual genotype, which is ultimately the unit of inheritance and adaptation in fungal populations.

The prevalence of beauvericin and enniatins among the isolates is a finding with considerable food safety relevance. These compounds belong to the class of emerging mycotoxins, so named because they are not routinely monitored and remain largely unregulated despite accumulating evidence of their biological activity. Both are cyclic peptides, and both have been shown in laboratory studies to exert cytotoxic effects through mechanisms that include disruption of cellular ion homeostasis and induction of oxidative stress. Because they frequently co-occur with regulated toxins such as deoxynivalenol and zearalenone in contaminated grain, questions about possible additive or synergistic effects on consumers are increasingly raised in the toxicological literature. The observation that numerous species produced these compounds at very high concentrations in vitro, and in some cases in combinations not previously documented for those species, suggests that the true occurrence of emerging mycotoxins in food and feed may be underestimated when monitoring programs focus exclusively on the traditional, regulated targets.

Equally noteworthy is the lower-than-expected frequency of trichothecene and fumonisin detection. Both toxin families are among the most intensively studied fungal metabolites worldwide, and fumonisins in particular are strongly associated with species within the Fusarium fujikuroi species complex, which includes important ear rot pathogens of maize. Their relative scarcity in the Spanish soil isolates may reflect genuine biogeographical patterns, differences in the crop history of the sampled fields, or the influence of in vitro culturing conditions on the expression of toxin biosynthetic gene clusters. It also serves as a reminder that the presence of a species is not synonymous with the presence of its signature toxin: toxin production depends on the integrity and expression of biosynthetic gene clusters, which can vary substantially between strains even within the same species. Some strains are silent producers under the tested conditions, while others express their full toxicological repertoire.

The identification of species such as Fusarium algeriense, Fusarium brachygibbosum, Fusarium clavum, and Fusarium flagelliforme in Spanish agricultural soils expands the known geographic distribution of these fungi. Species complex taxonomy, which groups morphologically similar species into phylogenetically coherent clusters, has transformed Fusarium systematics over the past two decades. DNA sequence-based identification, typically targeting conserved genomic regions, is now essential because morphological characters alone are frequently insufficient to separate closely related species that may differ markedly in pathogenicity and toxigenic capacity. The detection of species not extensively described in the region may indicate recent introductions through seed movement, soil transport, or plant material trade, although it may equally reflect that previous surveys simply lacked the molecular tools to distinguish them from look-alike taxa.

The finding that species identity, rather than soil environmental characteristics, was the only significant factor shaping multi-mycotoxin profiles aligns with a fundamental principle of fungal secondary metabolism: the genetic capacity to produce a given toxin is inherited, while environmental conditions modulate its expression. Soil pH, organic matter content, nitrogen availability, and texture certainly influence the abundance and community composition of soil fungi, as decades of microbial ecology research have demonstrated. However, once a strain is present, the specific set of secondary metabolites it can synthesize is dictated by its genome. This has practical consequences for risk prediction: knowing which species dominate a soil community allows a first-order prediction of the mycotoxins likely to be produced, whereas soil physicochemical measurements, while valuable for understanding pathogen ecology, do not override that genetic determinism.

The sampling design, spanning vineyards, cereal fields, legume plots, horticultural land, fallow ground, and hop yards across multiple provinces, provides a broad cross-section of the agricultural landscape of the region. Vineyards featured prominently in the collection, which is consistent with the intensive cultivation of wine grapes in northwestern Spain and with previous reports associating grapevines with soilborne Fusarium communities. The inclusion of fallow and diverse crop types strengthens the conclusion that mycotoxigenic Fusarium populations are a general feature of the agricultural soils of the area rather than a phenomenon restricted to a single cropping system. This breadth is important for any future attempts to design regional monitoring strategies, since it suggests that the reservoir function of soil cannot be managed through crop-specific interventions alone.

From a management perspective, the study underscores the difficulty of preventing mycotoxin contamination by targeting soil alone. Because the toxin-producing capacity resides in genetically diverse resident populations, approaches such as crop rotation, soil amendments, and biological suppression may reduce inoculum pressure but are unlikely to eliminate it. Integrated strategies therefore need to consider the entire chain from soil to harvest, combining measures that reduce fungal populations in soil with those that limit infection of crops and post-harvest toxin accumulation. The suppressive properties of soils rich in organic matter and harboring diverse microbial communities offer one possible avenue, since such soils can naturally constrain Fusarium activity through competition and antagonism.

Finally, the study contributes to a growing appreciation of soil as a dynamic component of food safety systems rather than merely a growth medium. The mycotoxin potential documented in these 119 strains demonstrates that toxigenic fungi persist in soils even in the absence of symptomatic crops, quietly maintaining a gene pool from which future epidemics may draw. Continued surveillance of soil-borne Fusarium diversity, coupled with multi-mycotoxin analytical methods capable of capturing both regulated and emerging compounds, will be essential for anticipating shifts in contamination risk as agricultural practices and climatic conditions evolve across the Iberian Peninsula and other Mediterranean production regions.

Subject of Research: Agricultural soils as a potential reservoir of mycotoxigenic Fusarium spp. in northwest Spain

Article Title: Agricultural soils as a potential reservoir of mycotoxigenic Fusarium spp. in northwest Spain

Article References: Montes-Ruiz, R., Masiello, M., Gambacorta, L., De Girolamo, A., Martinez-Reyes, N., Mayo-Prieto, S., Moretti, A., Casquero, P. A., & Gutiérrez, S. (2026). Agricultural soils as a potential reservoir of mycotoxigenic Fusarium spp. in northwest Spain. Frontiers in Fungal Biology, 7, Article 1946828. https://doi.org/10.3389/ffunb.2026.1946828

Image Credits: AI Generated

DOI: 10.3389/ffunb.2026.1946828

Keywords: Fusarium, mycotoxins, beauvericin, enniatins, soil microbiology, plant pathology, emerging mycotoxins, Spain, LC-HRMS, species complexes, food safety, agricultural soils

The team, led by scientists at the Institute of Sciences of Food Production of the Italian National Research Council in Bari together with colleagues at the University of Bari, the University of Turin and ADAMA Agricultural Solutions, combined laboratory assays with two years of field trials in northern Italy. In the lab, they exposed three strains of A. alternata, previously isolated from wheat kernels showing black point symptoms, to eight commercial fungicide formulations spanning several chemical classes: sterol biosynthesis inhibitors such as prothioconazole, difenoconazole, metconazole and tebuconazole; the respiratory uncoupler fluazinam; the multi-site contact fungicide folpet; and two mixtures pairing prothioconazole with difenoconazole or with the strobilurin azoxystrobin. Mycelial growth on treated agar plates, conidial germination under the microscope, and mycotoxin profiles measured by high-performance liquid chromatography together painted a detailed picture of how each molecule affects the pathogen.

The growth data were clear-cut. Difenoconazole was the most potent single active ingredient, halving colony growth at concentrations below 0.375 milligrams per liter, while the prothioconazole–difenoconazole mixture and the prothioconazole–azoxystrobin combination reached similar potency at very low doses, suggesting additive or synergistic inhibition of sterol biosynthesis at different steps of the same pathway. Fluazinam also performed strongly, with EC50 values between 0.1 and 0.5 milligrams per liter across strains. Folpet, by contrast, needed doses up to 50 milligrams per liter to suppress growth by more than 80 percent in the most sensitive strain, making it the least effective of the panel against mycelial expansion.

Conidial germination told a complementary story. At the lowest tested doses, most fungicides left spore germination untouched, but difenoconazole visibly stunted germ tube elongation even at 0.375 milligrams per liter and, at 0.75 milligrams per liter, blocked elongation entirely in roughly 30 percent of conidia. Folpet at 50 milligrams per liter was the standout, preventing germination in more than 80 percent of spores and arresting germ tube development completely within 72 hours. These microscopic effects matter because conidia are the propagules that land on wheat ears and initiate infection; a fungicide that stops germination or cripples germ tubes prevents colonization before it starts.

Yet when the researchers measured mycotoxin production at sub-lethal doses — concentrations that halve growth but do not kill the fungus — the picture inverted dramatically. Prothioconazole alone, at just 0.1 milligrams per liter, triggered massive increases in toxin output: alternariol monomethyl ether rose roughly tenfold in one strain and more than twelvefold in another, while alternariol, altenuene and tenuazonic acid all climbed significantly. Folpet produced even more spectacular inductions, with alternariol monomethyl ether jumping from 14 to nearly 235 micrograms per gram in one strain — an increase of almost 1,700 percent. Altertoxin I, a particularly concerning compound because of its mutagenic potency, was stimulated by prothioconazole, folpet, metconazole, tebuconazole and fluazinam at low doses. In stark contrast, difenoconazole at higher doses pushed several toxins below the detection limit, hinting that even closely related triazoles can diverge sharply in how they modulate fungal secondary metabolism.

The authors interpret this paradox through the lens of fungal hormesis and stress physiology. Sub-lethal chemical pressure can generate intracellular oxidative imbalance, and reactive oxygen species act as signals that reprogram secondary metabolism rather than simply damaging cells. Previous work on Fusarium graminearum showed that triazole exposure raises hydrogen peroxide inside the fungus and up-regulates the trichothecene biosynthetic pathway, boosting deoxynivalenol production. In Alternaria, recent molecular studies have identified regulatory networks — including the GATA transcription factor AaAreA, which links nitrogen status to alternariol biosynthesis genes, and the Slt2–Swi6 cell-wall integrity pathway, which controls production of alternariol, its methyl ether and tenuazonic acid — that plausibly mediate these fungicide-induced shifts. When growth is constrained, cellular resources may be redirected toward defense-related secondary metabolites, so a fungicide can simultaneously shrink a colony and inflate its toxin load.

To see whether these laboratory warnings translate to the field, the team ran split-plot trials over two growing seasons at the University of Turin’s experimental station in Carmagnola, comparing minimum tillage, which leaves maize residues on the soil surface, with conventional ploughing that buries them. They applied difenoconazole, prothioconazole or the two combined at wheat heading, and in half the plots artificially inoculated the ears with an A. alternata conidial suspension at flowering, 48 hours after spraying. The results confirmed prothioconazole’s reputation: it delivered the strongest reduction in Fusarium head blight incidence and severity, cut kernel colonization by Fusarium, and lowered deoxynivalenol by roughly 79 percent and zearalenone by about 77 percent on average. The mixture with difenoconazole performed comparably on mycotoxins and produced the highest grain yield gains, particularly under minimum tillage, where fungicide treatment lifted yield by 32 percent relative to the untreated control.

Conventional tillage itself proved to be a powerful lever against Fusarium. By incorporating maize residues into the soil rather than leaving them as inoculum reservoirs, ploughing reduced deoxynivalenol by 40 percent and zearalenone by 75 percent compared with minimum tillage, and improved grain yield by 16 percent and test weight as well. Notably, however, neither tillage system nor any fungicide treatment significantly altered Alternaria kernel colonization, which stayed below 20 percent in every plot, and no Alternaria toxins were detected in any field sample. Even the artificial inoculation at flowering failed to raise Alternaria contamination, leading the authors to hypothesize that anthesis is not the most susceptible window for Alternaria infection and that black point disease depends on environmental conditions and the competitive interplay among co-occurring fungal species rather than on a single well-defined infection event.

That disconnect between the petri dish and the paddock is the study’s central lesson. In vitro, sub-lethal prothioconazole and folpet clearly stimulated Alternaria toxin biosynthesis, yet under real field conditions — with strong Fusarium competition, variable weather, and an unknown natural timing of Alternaria inoculum — the fungus never reached the population densities or physiological state needed to translate that potential into measurable grain contamination. The authors caution that their field results are limited by the very low Alternaria incidence observed, and they call for follow-up experiments that inoculate at different wheat growth stages and under environmental conditions more favorable to Alternaria development, to pinpoint the phenological windows where the pathogen actually establishes and to determine the optimal fungicide timing for black point control.

The implications reach beyond agronomy into food safety policy. Alternaria toxins are not yet subject to binding maximum levels in wheat, but the European Commission’s 2022 recommendation urges systematic monitoring of alternariol, alternariol monomethyl ether and tenuazonic acid, and toxicological evidence linking these compounds to genotoxicity, cytotoxicity and endocrine disruption continues to accumulate. As climate change and evolving cropping practices reshape fungal communities on cereal ears, the study underscores that integrated disease management — combining residue management through tillage, judicious fungicide choice, and a deeper understanding of fungal ecology — remains the most reliable path to keeping both Fusarium and Alternaria risks in check, and that the compound-specific effects of fungicides on secondary metabolism deserve a permanent place in risk assessments for mycotoxin control.

Subject of Research: Effects of Fusarium head blight fungicides on Alternaria alternata growth and mycotoxin production in wheat

Article Title: In vitro and field response of Alternaria alternata to fungicides applied in soft wheat cropping systems for Fusarium Head Blight control

Article References: Abi Saad, C., Masiello, M., Haidukowski, M., Meloni, R., Somma, S., Maruccia, S., Sanzani, S. M., Ippolito, A., Pollmann, B., Moretti, A., & Blandino, M. (2026). In vitro and field response of Alternaria alternata to fungicides applied in soft wheat cropping systems for Fusarium Head Blight control. Frontiers in Agronomy, 8, Article 1906417. https://doi.org/10.3389/fagro.2026.1906417

Image Credits: AI Generated

DOI: 10.3389/fagro.2026.1906417

Keywords: Alternaria alternata, Fusarium head blight, wheat, mycotoxins, fungicides, prothioconazole, difenoconazole, black point disease, tillage, food safety, sterol biosynthesis inhibitors, hormesis

Maize ear rot is far more than a cosmetic blemish on cobs. The disease reduces yield, degrades grain quality, and — most importantly for human and animal health — opens the door to mycotoxin contamination, the toxic secondary metabolites that Fusarium fungi deposit in infected kernels. Fumonisins, the signature toxins of F. verticillioides, are linked to serious health problems in livestock and are suspected carcinogens in humans, while trichothecenes produced by F. graminearum suppress immune function and cause vomiting and feed refusal. Because contaminated grain cannot simply be cleaned after harvest, understanding which species are present in a production region, and which toxin genes they carry, is the foundation of any rational food-safety strategy.

The researchers collected and analysed 54 Fusarium isolates from maize ears showing ear rot symptoms across Karnataka, a major maize-growing state. Identification began with colony and spore morphology but did not stop there, because Fusarium species are notoriously difficult to separate by appearance alone. The team instead built multilocus phylogenies, sequencing several conserved genetic loci and comparing the resulting DNA fingerprints across isolates to place each strain on an evolutionary tree. This approach resolved the collection into six distinct Fusarium species, but the headline finding was the lopsided composition: F. verticillioides accounted for 43 of the 54 isolates, or 79.63 percent of everything recovered from diseased ears.

That numerical dominance was matched by disease-causing power. When representative isolates were inoculated onto maize, most of the collection produced high pathogenicity, with disease severity exceeding 75 percent. The two most agriculturally important species were tested in detail: F. verticillioides reduced seed germination to 65 percent, and F. graminearum pushed it down to 62 percent, while both caused substantial stalk and ear rot symptoms in the infected plants. In practical terms, the fungi are not merely colonising senescing tissue opportunistically; they are active, aggressive pathogens capable of damaging the crop at multiple stages, from germination of the next season’s seed to the integrity of the developing ear.

The link between prevalence and toxicity emerged when the team screened every isolate for mycotoxin biosynthesis genes. The fumonisin gene cluster in F. verticillioides includes FUM1, the polyketide synthase gene that catalyses a key early step in assembling the fumonisin molecule, and its presence is a reliable indicator of a strain’s potential to produce the toxin. Strikingly, FUM1 was detected in all 43 F. verticillioides isolates — every single one. The genetic potential for fumonisin production is therefore not a minority trait in this population but a universal feature, which helps explain why this species so thoroughly dominates the ear rot complex in the region.

Genetic potential, however, is only meaningful if the toxin actually accumulates in grain. To verify this, the researchers used liquid chromatography coupled with mass spectrometry, or LC–MS, a technique that separates individual metabolites and identifies them by their mass-to-charge signatures with high specificity. Analysis of kernels infected with a tested F. verticillioides isolate confirmed high fumonisin accumulation, closing the loop between gene, pathogen, and chemical hazard. For food-safety monitoring, this is the crucial evidence: the dominant pathogen in Karnataka’s maize is not just present and aggressive, it is demonstrably loading harvested grain with a regulated toxin.

The F. graminearum isolate told a different toxicological story. Rather than fumonisin genes, it carried the genetic machinery for trichothecene biosynthesis, including TRI7 and TRI13 — genes whose sequence characteristics determine which chemotype of trichothecene a strain can produce. The presence of NIV-associated versions of these genes indicates the isolate belongs to the nivalenol chemotype, one of the major trichothecene classes. Although this species was far rarer in the collection than F. verticillioides, its presence matters because trichothecenes and fumonisins pose distinct health risks and are regulated separately, so a shift in the species balance of a region would change the entire contamination profile of the grain supply.

To understand what makes F. verticillioides such an effective pathogen at the molecular level, the team sequenced the whole genome of isolate PMER18. The assembly yielded a genome of roughly 40 megabases — in the typical range for filamentous fungi — and achieved 98.0 percent completeness on the BUSCO benchmark, a quality metric that checks for the presence of a set of single-copy genes expected in any healthy fungal genome. A near-complete assembly means the annotation is trustworthy: the researchers could mine it for gene families involved in disease without worrying that key regions were missing or fragmented.

That mining produced a rich catalogue of virulence-associated features. The genome encodes putative pathogenicity genes, a substantial complement of CAZymes — carbohydrate-active enzymes that degrade plant cell wall polymers such as cellulose, hemicellulose, and pectin, allowing the fungus to physically penetrate and feed on host tissue — alongside membrane transporters that can export toxins and shield the fungus from plant defence compounds, and a set of candidate effector proteins. Effectors are molecules secreted by pathogens to manipulate or suppress host immunity, and identifying candidates in the genome provides a shortlist for future functional studies. Together these elements sketch the mechanistic basis of the species’ success: enzymatic tissue breakdown, chemical self-protection, and immune subversion, all coupled to an intact fumonisin production line.

The broader significance of the study lies in its integration. Diversity surveys, pathogenicity tests, toxin-gene screens, chemical confirmation, and genome analysis are often published separately; by combining them on the same isolate collection, the authors have produced a framework that connects field observation to molecular mechanism and, ultimately, to risk assessment. For plant breeders, the near-universal FUM1 presence in the dominant species argues that fumonisin resistance should be a breeding priority in the region. For regulators and grain handlers, the LC–MS confirmation of kernel contamination defines the monitoring target. And for pathologists, the genome of PMER18 supplies a reference for tracking virulence evolution. As climate patterns shift and maize systems intensify, this kind of unified pathogen profile — knowing exactly which fungi are present, how aggressive they are, what toxins they can make, and which genes enable it all — is precisely the evidence base that integrated disease management requires.

Subject of Research: Diversity, pathogenicity, mycotoxin gene profile, and genomics of Fusarium species causing maize ear rot in Karnataka, India

Article Title: Characterisation of mycotoxin-producing Fusarium species associated with maize ear rot and its pathogenomics and mycotoxin gene profile

Article References: Pallavi, K. N., Prasannakumar, M. K., Harish, J., Karan, R., Manjunatha, C., Devanna, P., & Sarangi, A. N. (2026). Characterisation of mycotoxin-producing Fusarium species associated with maize ear rot and its pathogenomics and mycotoxin gene profile. Scientific Reports. https://doi.org/10.1038/s41598-026-74277-x

Image Credits: AI Generated

DOI: 10.1038/s41598-026-74277-x

Keywords: Fusarium verticillioides, maize ear rot, mycotoxins, fumonisins, FUM1, trichothecenes, plant pathology, whole-genome sequencing, CAZymes, pathogenicity, Karnataka, food safety

The review, which followed the Scale for the Assessment of Narrative Review Articles (SANRA) to ensure methodological rigor, synthesized literature retrieved from PubMed, Scopus, Web of Science, and Google Scholar. Its central conclusion is sobering but constructive: complete elimination of aflatoxins is not feasible given the complexity of the contamination pathways, yet layered interventions applied at successive points in the food chain can dramatically reduce exposure. The authors frame aflatoxin contamination as a persistent global food safety issue that is especially acute in resource-limited regions, where it threatens food security, public health, agricultural productivity, and the sustainability of food systems simultaneously.

The quantitative picture that emerges from the synthesis is striking. Integrated pre-harvest strategies, which combine agronomic practices with biological control, were reported to reduce aflatoxin levels by approximately 51 to 99 percent across individual studies. Post-harvest interventions, including improved drying and storage, achieved reductions of 30 to 94 percent. Advanced sorting technologies, which physically remove contaminated kernels from otherwise acceptable lots, eliminated up to 99 percent of contaminated material. Biological detoxification methods reduced aflatoxin levels by 45 to 99 percent, enzymatic systems achieved degradation rates of up to 95 percent, chemical methods ranged from 20 to 100 percent reduction, and physical treatments delivered 15 to 90 percent reductions depending on the conditions applied.

Crucially, the authors caution that these figures are not pooled estimates and cannot be directly compared with one another. Differences in experimental conditions, commodities, baseline contamination levels, analytical methods, and study settings mean that a 99 percent reduction reported in one laboratory trial of a biocontrol agent on maize cannot be assumed to translate to a smallholder groundnut field in a different climate. This transparency is a notable strength of the review: rather than presenting a single seductive number, it maps the landscape of available evidence and its limits, giving policymakers and food safety managers a realistic sense of what each barrier can and cannot deliver.

The pre-harvest stage is where the contamination cycle begins, and the review emphasizes that prevention at the source is the most sustainable starting point. Agronomic practices such as timely planting, adequate irrigation, pest control, and soil management reduce the plant stress that favors Aspergillus infection, while resistant crop varieties and biological control agents that compete with toxigenic fungal strains can suppress aflatoxin formation before harvest. Biological control in particular has gained traction in recent years, relying on non-toxigenic strains of the same fungi to outcompete their toxin-producing relatives in the field. When these measures are integrated rather than applied in isolation, the reported reductions in aflatoxin accumulation become substantial.

Once crops are harvested, the battle shifts to drying, storage, and handling. Poor post-harvest management is a dominant driver of contamination in tropical and subtropical regions, where high humidity and inadequate infrastructure allow fungi to flourish in stored grain. The review documents how proper drying to safe moisture levels, hermetic storage, improved ventilation, and hygiene measures can cut aflatoxin levels by 30 to 94 percent. These interventions are often low-cost and locally implementable, making them especially relevant for smallholder farmers and community-level food systems where the burden of contamination is heaviest and regulatory testing infrastructure is weakest.

Downstream, technological and biochemical barriers offer additional layers of protection. Advanced optical and electronic sorting systems can detect and eject discolored or mold-damaged kernels at industrial speed, removing up to 99 percent of contaminated material from a processing line. Biological detoxification exploits microorganisms or their products to bind or transform aflatoxins, while enzymatic degradation uses specific enzymes to break down the toxin molecule itself, with reported degradation reaching 95 percent. Chemical treatments, such as ammoniation, and physical treatments, such as irradiation or adsorption onto binding agents, round out the toolkit, each with its own efficacy range, cost profile, and regulatory considerations.

The multi-barrier logic is what elevates the review from a catalog of techniques to a coherent strategy. Each individual barrier is imperfect, and residual contamination passing one stage can be intercepted by the next. By integrating agronomic practices, biocontrol, proper storage, and detoxification across the food chain, the cumulative reduction in exposure can approach the levels needed to protect public health, even where no single measure achieves it alone. The authors argue that this integration can improve food safety and security, reduce post-harvest losses, and promote sustainable agriculture, turning a fragmented set of interventions into a system-level defense.

The implications extend well beyond food chemistry. The review explicitly connects integrated aflatoxin management to the United Nations Sustainable Development Goals, including SDG 2 on Zero Hunger, SDG 3 on Good Health and Well-being, SDG 9 on Industry, Innovation and Infrastructure, SDG 12 on Responsible Consumption and Production, SDG 13 on Climate Action, and SDG 15 on Life on Land. Climate change looms large in this framing: rising temperatures and shifting rainfall patterns are expected to expand the geographic range of aflatoxin-producing fungi into regions previously considered low-risk, making resilient, multi-layered management systems a matter of adaptation as much as prevention. Protecting vulnerable populations, particularly in sub-Saharan Africa and South Asia where exposure is highest, depends on making these strategies accessible and affordable.

As the global food system confronts the twin pressures of a growing population and a changing climate, the review’s message is that aflatoxin management must be treated as a continuous chain of responsibility rather than a series of disconnected fixes. From the seed in the soil to the meal on the plate, every stage offers an opportunity to interrupt contamination, and every stage that is neglected undermines the others. For researchers, the work highlights the need for standardized, comparable studies that can support pooled estimates and evidence-based policy. For farmers, processors, and regulators, it offers a practical blueprint: stack the barriers, match them to local conditions, and treat food safety as a system. In a world where millions of tonnes of grain are lost or degraded to mycotoxin contamination each year, that blueprint may prove one of the most cost-effective public health tools available.

Subject of Research: Farm-to-fork multi-barrier strategies for managing aflatoxin contamination in food systems

Article Title: Sustainable farm-to-fork multi-barrier strategies for aflatoxin management in food systems

Article References: Bereda, G., & Ahamad, J. (2026). Sustainable farm-to-fork multi-barrier strategies for aflatoxin management in food systems. Discover Sustainability. https://doi.org/10.1007/s43621-026-04982-0

Image Credits: AI Generated

DOI: 10.1007/s43621-026-04982-0

Keywords: aflatoxins, food safety, food security, multi-barrier strategies, biocontrol, post-harvest losses, detoxification, sustainable agriculture, mycotoxins, farm-to-fork, SDGs, public health