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You must have seen peanuts or copra or other food items getting infested with fungus like in the above pictures several times. Then what have you done? Thrown away these things? Good. But If you think you can just scrape away the fungus, wash them and use the products, think again. Because you are putting yourself and your loved ones in a dangerous situation. Surprised? Then read on...

This fungus is called Aspergillus flavus. It produces aflatoxin into the food substances you eat.

The above pictures are of Penicillium and Penicillium infested fruits. This fungus too produces mycotoxins.

Heard about these harmful things in foods? No? Then, go ahead and read all about them...

A mycotoxin (from Greek: mykes, mukos = "fungus" and toxikon = "poison") is a toxic secondary metabolite (organic compounds that are not directly involved in the normal growth, development, or reproduction of an organism but often play an important role in interspecies defenses) produced by organisms of the fungi kingdom, commonly known as moulds. The term 'mycotoxin' is usually reserved for the toxic chemical products produced by fungi that readily colonize crops and infest food products.

Mycotoxins are secondary metabolites produced by fungi that are capable of causing disease and death in humans and other animals. Because of their pharmacological activity, some mycotoxins or mycotoxin derivatives have found use as antibiotics, growth promotants, and other kinds of drugs; still others have been implicated as chemical warfare agents. Here I am only focusing on the most important ones associated with human and veterinary diseases, including aflatoxin, citrinin, ergot akaloids, fumonisins, ochratoxin A, patulin, trichothecenes, and zearalenone.

The term mycotoxin was coined in 1962 in the aftermath of an unusual veterinary crisis near London, England, during which approximately 100,000 turkey poults died. When this mysterious turkey X disease was linked to a peanut (groundnut) meal contaminated with secondary metabolites from Aspergillus flavus (aflatoxins), scientists started working on them and found several mycotoxins that can cause diseases in both humans and animals.

Dietary, respiratory, dermal, and other exposures to toxic fungal metabolites produce the diseases collectively called mycotoxicoses. Mycotoxicoses are examples of “poisoning by natural means”. The symptoms of a mycotoxicosis depend on the type of mycotoxin, the amount and duration of the exposure, the age, health, and sex of the exposed individual, and many poorly understood synergistic effects involving genetics, dietary status, and interactions with other toxic materials. Thus, the severity of mycotoxin poisoning can be compounded by factors such as vitamin deficiency, caloric deprivation, alcohol abuse, and infectious disease status. In turn, mycotoxicoses can heighten vulnerability to microbial diseases, worsen the effects of malnutrition, and interact synergistically with other toxins. These fungal metabolites constitute a toxigenically and chemically heterogeneous assemblage that are grouped together only because the members can cause disease and death in human beings and other vertebrates. Some 300 to 400 compounds are now recognized as mycotoxins, of which approximately a dozen groups regularly receive attention as threats to human and animal health. Mycotoxicoses are the animal diseases caused by mycotoxins and mycotoxicology is the study of mycotoxins.

Mycotoxin exposure is more likely to occur in parts of the world where poor methods of food handling and storage are common, where malnutrition is a problem, and where few regulations exist to protect exposed populations. However, even in developed countries, specific subgroups may be vulnerable to mycotoxin exposure, where the fungi grow in dark, moist buildings, when food is contaminated by mycotoxin -producing fungi, mycotoxicosis can occur.

Now let us learn more about individual mycotoxins and what harm they can cause to us.


These are toxins produced mainly by a fungus called Aspertgillus flavus. Others that produce this toxins are A. parasiticus , plus related species, A. nomius and A. niger.

Aflatoxins have been associated with various diseases, such as aflatoxicosis. There are four major aflatoxins called B1, B2, G1, and G2 based on their fluorescence under UV light (blue or green) and relative chromatographic mobility during thin-layer chromatography. Over a dozen other aflatoxins (e.g., P1. Q1, B2a, and G2a) have also been identified by mycologists. Two additional metabolic products, M1 and M2, that are of significance as direct contaminants of foods and feeds. The aflatoxins M1 and M2 were first isolated from milk of lactating animals fed aflatoxin preparations; hence, the M designation.

Aflatoxins are detected occasionally in milk, cheese, corn, peanuts, cottonseed, copra, nuts, almonds, figs, spices, and a variety of other foods and feeds . Milk, eggs, and meat products are sometimes contaminated because of the animal consumption of aflatoxin-contaminated feed . However, the commodities with the highest risk of aflatoxin contamination are corn, peanuts, copra and cottonseed.

Aflatoxins often occur in crops in the field prior to harvest. Postharvest contamination can occur if crop drying is delayed and during storage of the crop if water is allowed to exceed critical values for the mould growth. Insect or rodent infestations facilitate mould invasion of some stored commodities.

Aflatoxin B1 is the most potent natural carcinogen (cancer - causing) known and is usually the major aflatoxin produced by toxigenic strains.

Aflatoxicosis is primarily a hepatic (liver) disease. Aflatoxins cause liver damage, decreased milk and egg production by animals, recurrent infection as a result of immunity suppression (eg. salmonellosis), in addition to embryo toxicity in animals consuming low dietary concentrations. While the young of a species are most susceptible, all ages are affected but in different degrees for different species. Clinical signs of aflatoxicosis in animals include gastrointestinal dysfunction, reduced reproductivity, reduced feed utilization and efficiency, anemia, and jaundice. Nursing animals may be affected as a result of the conversion of aflatoxin B1 to the metabolite aflatoxin M1 excreted in milk of dairy cattle.

The induction of cancer by aflatoxins has been extensively studied. Aflatoxin B1, aflatoxin M1, and aflatoxin G1 have been shown to cause various types of cancer in different animal species. However, only aflatoxin B1 is considered by the International Agency for Research on Cancer (IARC) as having produced sufficient evidence of carcinogenicity in experimental animals to be identified as a carcinogen.

People are exposed to aflatoxins by consuming foods contaminated with products of fungal growth. Such exposure is difficult to avoid because fungal growth in foods is not easy to prevent. Even though heavily contaminated food supplies are not permitted in the market place in several countries, concern still remains for the possible adverse effects resulting from long-term exposure to low levels of aflatoxins in the food supply.
Evidence of acute aflatoxicosis in humans has been reported from many parts of the world, namely the Third World Countries, like Taiwan, Uganda, India, and many others. The syndrome is characterized by vomiting, abdominal pain, pulmonary edema, convulsions, coma, and death with cerebral edema and fatty involvment of the liver, kidneys, and heart.

There are established specific guidelines on acceptable levels of aflatoxins in human food and animal feed. They are: 20 ppb (parts per billion) total aflatoxins, with the exception of milk which has an action level of 0.5 ppb for aflatoxin M1. The action level for most feeds is also 20 ppb.

Now how can you avoid aflatoxin contamination? Keep the moisture level of the food products low so that fungus doesn't grow on them. Keep them near light, sunlight is the most promising inhibitor of mycotoxins. If you find any fungus growing on any food item, just throw it away. Never consume any fungus - infested food product. Even if you scrape the superficial fungus and wash the material, the metabolites already produced and are present inside the food can cause severe health conditions.


This toxin was first isolated from Penicillium citrinum prior to World War II. Subsequently, it was identified in over a dozen species of Penicillium and several species of Aspergillus (e.g., Aspergillus terreus and Aspergillus niveus), including certain strains of Penicillium camemberti (used to produce cheese) and Aspergillus oryzae (used to produce sake, miso, and soy sauce). More recently, citrinin has also been isolated from Monascus ruber and Monascus purpureus, industrial species used to produce red pigments.

Citrinin causes different toxic effects, like nephrotoxic (Kidney -related toxicity), hepatotoxic (liver-related toxicity) and cytotoxic (toxic to living cells) effects. Citrinin induced micronuclei ( small nucleus of cells when compared to normal ones), aneuploidy (presence of an abnormal number of chromosomes in cells) and chromosomal aberrations ( a chromosome anomaly, abnormality, aberration, or mutation is a missing, extra, or irregular portion of chromosomal DNA).

Citrinin is mainly found in stored grains, but sometimes also in fruits and other plant products. Citrinin often occurs together with other mycotoxins like ochratoxin A or aflatoxin B1, because they are produced by the same fungi species ( I myself have first reported citrinin and ochratoxin A in coconut products). The combination which is observed most often is citrinin with ochratoxin A and this is also the most studied combination.

Citrinin has been associated with yellow rice disease in Japan. It has also been implicated as a contributor to porcine nephropathy ( kidney disease in pigs). Citrinin acts as a nephrotoxin in all animal species tested, but its acute toxicity varies in different species. The 50% lethal dose for ducks is 57 mg/kg; for chickens it is 95 mg/kg; and for rabbits it is 134 mg/kg. Citrinin can act synergistically with ochratoxin A to depress RNA synthesis in murine (mice) kidneys .

Wheat, oats, rye, corn, barley, and rice have all been reported to contain citrinin. With immunoassays, citrinin was detected in certain vegetarian foods colored with Monascuspigments . Citrinin has also been found in naturally fermented sausages from Italy . I have reported this toxin in coconut products too.


These are are a group of mycotoxins produced by some Aspergillus and Penicillium species. Ochratoxin A was discovered as a metabolite of Aspergillus ochraceus in 1965 during a large screen of fungal metabolites that was designed specifically to identify new mycotoxins.

Ochratoxin A is recognized as a potent nephrotoxin (kidney-related toxicity). Members of the ochratoxin family have been found as metabolites of many different species of Aspergillus, including Aspergillus alliaceus, Aspergillus auricomus, Aspergillus carbonarius, Aspergillus glaucus, Aspergillus melleus, and Aspergillus niger. Because Aspergillus niger is used widely in the production of enzymes and citric acid for human consumption, it is important to ensure that industrial strains are nonproducers of this toxin.

As with other mycotoxins, the substrate on which the molds grow as well as the moisture level, temperature, and presence of competitive microflora interact to influence the level of toxin produced. Ochratoxin A has been found in barley, oats, rye, wheat, coffee beans, and other plant products, with barley having a particularly high likelihood of contamination. There is also concern that ochratoxin may be present in certain wines, especially those from grapes contaminated with Aspergillus carbonarius . Again, I have reported this toxin in copra for the first time. It was produced by a Penicillium species in the product.

The kidney is the primary target organ of this toxin. Ochratoxin A is a nephrotoxin to all animal species studied to date and is most likely toxic to humans as well, who have the longest half-life for its elimination of any of the species examined. In addition to being a nephrotoxin, animal studies indicate that ochratoxin A is a liver toxin, an immune suppressant, a potent teratogen (an agent or factor which causes malformation of an embryo), and a carcinogen ( cancer-causing).

Ochratoxin has been detected in blood and other animal tissues and in milk, including human milk . It is frequently found in pork intended for human consumption.

There has been speculation that ochratoxins are involved in a human disease called endemic Balkan nephropathy . This condition is a progressive chronic nephritis that occurs in populations who live in areas bordering the Danube River in parts of Romania, Bulgaria, and the former Yugoslavia. In one Bulgarian study, ochratoxin contamination of food and the presence of ochratoxin in human serum were more common in families with endemic Balkan nephropathy and urinary tract tumors than in unaffected families. In addition to ochratoxin poisoning, this curious disease has been attributed to genetic factors, heavy metals, and possible occult infectious agents.


The trichothecenes constitute a family of more than sixty sesquiterpenoid metabolites produced by a number of fungal genera, including Fusarium, Myrothecium, Phomopsis, Stachybotrys, Trichoderma, Trichothecium, and others. The term trichothecene is derived from trichothecin, which was the one of the first members of the family identified. They are commonly found as food and feed contaminants, and consumption of these mycotoxins can result in alimentary hemorrhage and vomiting; direct contact causes dermatitis.

The trichothecenes are extremely potent inhibitors of eukaryotic (membrane -bound complex-celled or single-celled complex organisms) protein synthesis; different trichothecenes interfere with initiation, elongation, and termination stages. There is a long history of mouldy grain “intoxications” in Japan, where disease in both human beings and farm animals has been attributed to Fusarium mycotoxicoses. Fusarium graminearum (Gibberella zeae), regularly found on barley, oats, rye, and wheat, is considered the most important plant pathogen in Japan and is believed to be the cause of red mould disease (Akakabi toxicosis). As with all mycotoxins, depending on weather conditions, the growth of trichothecene-producing fungi and subsequent production of toxins vary considerably from year to year and from place to place.

The symptoms produced by various trichothecenes include effects on almost every major system of the vertebrate body. Many of these effects are due to secondary processes that are initiated by often poorly understood metabolic mechanisms related to the inhibition of protein synthesis.

Zearalenone is a secondary metabolite from Fusarium graminearum ( Gibberella zeae)

Others that produce this toxin are Fusarium culmorum, Fusarium equiseti, and Fusarium crookwellense. All these species are regular contaminants of cereal crops worldwide. An association between mouldy grain consumption and hyperestrogenism ( excess production of the hormone estrogen that results in adverse health conditions) in swine has been observed since the 1920s; modern work shows that dietary concentrations of zearalenone as low as 1.0 ppm (parts per million) may lead to hyperestrogenic syndromes in pigs; higher concentrations can lead to disrupted conception, abortion, and other problems. Reproductive problems have also been observed in cattle and sheep because of this toxin.


The fumonisins are a group of mycotoxins derived from Fusarium species. At least 15 different fumonisins have so far been reported. Fumonisins affect animals in different ways by interfering with sphingolipid ( a class of fats) metabolism . They cause leukoencephalomalacia (hole in the head syndrome) in equines and rabbits, pulmonary edema and hydrothorax ( a type of pleural effusion in which serous fluid accumulates in the pleural cavity) in swine (pigs) and hepatotoxic and carcinogenic effects and apoptosis ( programmed cell death) in the liver of rats. In humans, there is a probable link with esophageal cancer. The occurrence of fumonisin B1 is correlated with the occurrence of a higher incidence of esophageal cancer in regions of Transkei (South Africa), China, US, and northeast Italy. Acute exposure to fumonisin B1 involved 27 villages in India, where consumption of unleavened bread made from mouldy sorghum or corn caused transient abdominal pain, borborygmus (a rumbling or gurgling noise made by the movement of fluid and gas in the intestines), and diarrhea.

Patulin is a mycotoxin produced by a variety of moulds, in particular, Aspergillus, Penicillium and Byssochlamys.

It is most commonly found in rotting apples, pears, cherries, and other fruits. In addition, patulin has been found in other foods such as grains, fruits, and vegetables.

A number of studies have shown patulin to be genotoxic (agents that damages the genetic information within a cell causing mutations, which may lead to cancer), which has led some to theorize that it may be a carcinogen, although animal studies have remained inconclusive.

Ergot Alkaloids
The ergot alkaloids are among the most fascinating of fungal metabolites. The most prominent member of this group is Claviceps purpurea ("rye ergot fungus"). This fungus grows on rye and related plants, and produces alkaloids that can cause ergot poisoning in humans and other mammals who consume grains contaminated with its fruiting structure. Two forms of ergotism are usually recognized, gangrenous and convulsive. The gangrenous form affects the blood supply to the extremities, while convulsive ergotism affects the central nervous system. Clinical symptoms of ergotism in animals include gangrene, abortion, convulsions, suppression of lactation, hypersensitivity, and ataxia ( the loss of full control of bodily movements).

Other Mycotoxins

Penicillium roqueforti and Penicillium camemberti , species used to manufacture mould-ripened cheeses, produce a number of toxic metabolites, including penicillin acid, roquefortine, isoflumigaclavines A and B, PR toxin, and cyclopiazonic acid .

Several mycotoxins induce tremors as a neurological response in farm animals; most of these fungal tremorgens contain a modified indole moiety and are produced by certain species of Aspergillus, Penicillium, and Claviceps. The tremorgenic mycotoxins include the penitrems, janthitrems, lolitrems, aflatrem, paxilline, paspaline, paspalicine, paspalinine, and paspalitrem A and B. Penicillium crustosum produces penitrem A, a compound implicated in several cases of canine intoxication and one case of human tremor, vomiting, and bloody diarrhea.

Originally isolated from Penicillium cyclopium (Penicillium aurantiogriseum), cyclopiazonic acid is an indole tetramic acid. This mycotoxin is a specific inhibitor of calcium-dependent ATPase and induces alterations in ion transport across cell membranes. It is produced by many other species of Penicillium as well as several species of Aspergillus, including Aspergillus flavus. Cyclopiazonic acid was isolated from a sample of the ground nut meal that had been implicated in the original turkey X disease and may have contributed to the severity of that early aflatoxicosis. Furthermore, consumption of a kodo millet that was heavily contaminated with moulds and contained detectable levels of cyclopiazonic acid produced kuduo poisoning, characterized by giddiness and nausea. Some strains of Penicillium camembertii involved in the production of gourmet cheese produce cyclopiazonic acid.

The yellow rice toxins (citrinin, citreoviridin, luteoskyrin, rugulosin, rubroskyrin, and related compounds) are believed to have exacerbated Shoshin-kakke, a particularly malignant form of beriberi seen in Japan in the early 20th century .

A number of rare and obscure diseases have also been hypothesized to be possible mycotoxicoses. The research work is still going on and several of these fungal metabolites have identified with definite adverse health conditions.

These beautiful, innocent-looking fungi can cause so much havoc when they make our food their home and when the conditions are right.

Now that you know enough about the harmful effects of mycotoxins  you can become wise.  So, never ever use fungi-infested products as food. Don't give them to animals too because when you consume various animal-derived foods like milk, eggs and meat you too will fall sick as these animal products also get contaminated when animals producing them consume these harmful fungal metabolites.

And most importantly,  share this knowledge with everybody around.

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Replies to This Discussion


Varied diet repels poisoned fungus

  • Maize is popular in parts of Africa but is prone to fungal contamination

  • Switching to sorghum, millet and cassava would lower toxin exposure

  • Checking harvested crops and improving storage would also help

Food contamination with fungal toxins is best prevented by improving post-harvest processing and diversifying crops, according to a World Health Organization agency report.
Four out of 15 interventions to prevent the toxins’ health effects are ripe for implementation in low-income countries.
“The intervention for which the strongest evidence of improvement of health exists, but which is also the most difficult to achieve, is to increase dietary diversity,” they write.

In the 1950s, sorghum, millet and cassava were a large source of starch calories in Sub-Saharan Africa, Miller says, but their consumption has dropped in favour of maize, which is more prone to fungus. The study calls for more investment in appropriate crops for the target region, both in terms of climatic and cultural suitability.

“There are a whole bunch of interesting crops that have suffered a reduction in use globally,” says Miller. Diversification is not easy, but is “not an impossible dream” either, he adds. “It’s one of the things we know will work.”

Another possible intervention is better food processing, says the report. This includes sorting crops early to exclude contaminated food and improving storage conditions to lower humidity, which the fungus needs to grow.

“The solutions mentioned in the report are good to implement in developing countries,” says Anitha Seetha, a food safety researcher at the International Crops Research Institute for the Semi-Arid Tropics in Malawi. “For example, post-harvest management methods like drying and storing grains appropriately are very simple with no involvement of chemicals.”

In Latin America, another method called nixtamalization reduces mycotoxins in maize by cooking the grain in an alkaline solution. But this requires lots of water and has not been adopted in Africa and Asia, the report says.

On 23-24 March a meeting in Ethiopia of the Partnership for Aflatoxin Control in Africa discussed the report’s findings and interventions to reduce the health risks from aflatoxin exposure.

The health impact of mycotoxin contamination “has been neglected for too long”, Christopher Wild, director of the International Agency for Research on Cancer, said in a statement. “We have the tools to make a difference. Now we must find the political will.”


Mycotoxin control in low- and middle-income countries (International Agency for Research on Cancer, 2015)

Corn genetically engineered to make ninjalike molecules can launch an attack on invading fungi, stopping the production of carcinogenic toxins.

These specialized RNA molecules lie in wait until they detect Aspergillus, a mold that can turn grains and beans into health hazards. Then the molecules pounce, stopping the mold from producing a key protein responsible for making aflatoxins, researchers report March 10 in Science Advances. With aflatoxins and other fungal toxins affecting up to 25 percent of crops worldwide, the finding could help boost global food safety, the researchers conclude.

“If there’s no protein, no toxin,” says study coauthor Monica Schmidt, a plant geneticist at the University of Arizona in Tucson.

Schmidt and colleagues used a technique called RNA interference, which takes advantage of a natural defense mechanism organisms use to protect against viruses. The researchers modified corn to make it produce short pieces of RNA that match up to sections of an RNA in the fungus made from the aflC gene. That gene encodes a key step of a biochemical pathway that the fungus uses to make the toxins. When the corn’s modified RNAs match up with those of the fungus, that triggers Aspergillus to chop up its own RNA, preventing a key protein, and thus the toxin, from being made.

Then, the team infected both engineered and not-tweaked corn with A. flavus, an Aspergillus species that releases the most potent aflatoxins. After allowing the corn — and fungus — to grow for a month, the researchers were unable to detect aflatoxins in the engineered corn. But they consistently measured more than 1,000 parts per billion of aflatoxin in the unmodified corn, and sometimes as much as 200,000 ppb, Schmidt says. 


D. Thakare et al. Aflatoxin-free transgenic maize using host-induced gene silencing. Science Advances. Published online March 10, 2017. doi: 10.1126/sciadv.1602382.

L. Beil. I, MoldScience News. Vol. 177, May 22, 2010, p. 26.

T.H. Saey. Corn genome a maze of unusual diversityScience News. Vol. 176, December 19, 2009, p. 9.

J. Raloff. Putting the pressure on poisons. Science News Online, April 11, 2006.

J. Raloff. Carcinogens in the diet. Science News Online, February 14, 2005.




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