Grain Fungal Diseases & Mycotoxin Reference · fruiting bodies that form molds, mushrooms, smuts...

Grain Fungal Diseases& Mycotoxin Reference

September 2006

Preface

This manuscript is a compilation of information that has been available for some time. We will try to present this information in a way that will be helpful to non-specialists in an easy to digest manner. The nature of this information tends towards the technical and sometimes keeps needed information out of the reach of those that could use it most. We will try to keep this in mind while presenting the needed information. Also, while not being technically correct, we have kept reference citations to a minimum, and have inserted numbers, i.e.: [23], to keep the inter-ruptions to the flow ideas as few as possible.

Contents

Chapter 1: Fungi and Fungal Diseases of Plants .........................................................4

Chapter 2: What Are Mycotoxins? ..............................................................................7

Chapter 3: Mycotoxins in Grain and Feed ................................................................13

Glossary ...................................................................................................................23

References ................................................................................................................26

Fungal Disease Fact Sheets

Aflatoxin ...................................................................................................................28Black Tip ..................................................................................................................29Blue-Eye ..................................................................................................................30Ergot .........................................................................................................................31Fusarium Ear Rot ......................................................................................................32Gibberella Ear Rot ....................................................................................................33Karnal Bunt ...............................................................................................................34Scab .........................................................................................................................35TCK Smut .................................................................................................................36

Chapter 1

Fungi and Fungal Diseases of Plants

Definition and Overview. Fungi are prob-ably one of the most numerous plant familieson earth. By definition they are plants thatcontain no chlorophyll (can grow in condi-tions of little or no natural light) and rangefrom single cells to a body of branched hy-phae (tubular filaments) that often producefruiting bodies that form molds, mushrooms,smuts and yeasts. Instead of producing theirown food, fungi absorb nutrients from eithera living or dead host material. Symptoms anddisease development come about from thegrowth of the fungi through the host-parasiteinteraction. These fungi sometimes producemetabolites (by-products of growth) that aretoxic to animals and humans. Reproductionin fungi occurs through the production ofspores. These spores can then reproduce with-out coming into contact with a different plant(asexual reproduction).

The small size of the spores aid in their dis-persal. They can become airborne and moveby the action of winds and travel from field tofield. They also can become attached to in-sects and birds which then transport them fromplant to plant. Transport can also occur byuse of contaminated trucks and equipment.Fungal infection from spores can occur at anyof the various stages of crop production. Itcan begin in the fields, in or on the crop itself.It can infect healthy products during transpor-tation and storage by coming into contact withcontaminated equipment or grain products.The spores can lay dormant (inactive) in thesoil or accumulate on equipment or in storage

facilities for months or sometimes years untilthe proper conditions for growth occur andinfect generation after generation.

There are many varied environmental condi-tions that need to be in place before the sporeswill germinate or begin to grow. Generally rela-tive humidity over 70% and temperatures over30EC (86EF) for extended periods (severaldays to a week) are generally needed. Stressto the plants such as periods of drought, flood-ing, or insect infestation are also common fac-tors in the fungus growth cycle. High mois-ture content of the crops (20% or higher incorn), as at the optimal times of growth andharvest, give the spores the necessary elementsto start the growth process.

Any one of these conditions by itself will notpromote the fungal growth. It is only whenthe right conditions as a group occur, for eachparticular fungus, do the growth cycles begin.If any one optimal condition is removed, thegrowth cycle of a particular fungus will stop.But this may then promote the growth of adifferent or related fungus. Once the growthcycle begins the crop damage has alreadystarted and can not be reversed. The dryingof corn lowers the moisture content to a pointwhere growth of molds is prevented or at leaststops further damage.

Fungi and mold are normally thought of asmushrooms and the grey fuzzy stuff that growson food left in the refrigerator too long. Moldsand fungi do not necessarily have to be

visible to the naked eye to be growing anddamaging crops and foods. Many of the sporesassociated with fungi are microscopic and intheir first stages of growth are not visible with-out the aid of a microscope. Only in the laterstages or when large masses of fungi arepresent, do the fungi become visible to theunaided eye.

The presence of visual mold in grain or feedproducts does not necessarily mean that myc-otoxins are present in the sample. Moldgrowth indicates that there are some fungipresent. Many of the fungi grow under simi-lar conditions and more than one kind of fungican exist in or on the grain or feed product atthe same time. When more than one fungi ispresent at the same time on the same host, theysometimes increase the toxic effects of eachother by attacking different bodily functionswhen ingested by a human or animal. Theycan also cancel each other out by growing andattacking each other during the growth pro-cess. The lack of visual mold does not meanthat there are no mycotoxins present. Manytimes during harvest or handling the visualaspects of the mold can be brushed off, butthe toxic by-products can remain in the ker-nel.

Non-Mycotoxic Fungi

Fungi are a major cause of spoilage in storedgrain. The Food and Agriculture Associationestimates that 25% of the worlds food cropsare affected by mycotoxins (the by-productsof fungal growth) during growth and storage.The damage of fungi is second only to thatcaused by insects in stored grain products.Many of the fungi cause damage to the cropsthemselves with little or no toxic effects onhumans and animals [15].

Common Smut or Bunt. Common smut iscaused by two fungi; Tilletia tritici and Tille-tia laevis. Because it requires cool moist soilconditions, the disease is less of a problem onspring planted wheat than winter wheat. Com-mon smut reduces wheat yields and grain qual-ity. Wheat contaminated with bunt sporeshas a pungent, fishy odor and a darkened ap-pearance. Wheat that has an unmistakableodor of smut will be designated “light smutty”on official inspection certificates. In addition,bunt spores released during combining arecombustible, and have caused explosions andfires during harvesting with mechanical har-vesters. [23]

Plants may be moderately stunted but are noteasily distinguished until the heads emerge.Bunted heads are slender and maintain theirgreen color longer than healthy heads. Theglumes may spread apart exposing the smutballs they contain. Smut balls are approxi-mately the shape of normal kernels and aredull gray-brown. The small balls often rup-ture at harvest, releasing black, powderyspores. Wheat containing smut balls will bedesignated as “light smutty” (6-30 smut balls)or “smutty” (31 or more smut balls) on offi-cial inspection certificates.

Dwarf Bunt or TCK Smut . The Tilletia spe-cies of fungi cause smut or bunt diseases inwheat, rye, and barley. Tilletia controversa,commonly known as Dwarf Bunt or TCKSmut, causes dwarfing or stunting in thegrowth of the plant itself along with reducedyields. The major source of transmittal is bythe spores laying dormant in the soil until thenext crop year. These spores can lay dormantfor up to ten years retaining their infectiousproperties [23].

Karnal Bunt . Karnal Bunt is thought to haveoriginated in India (therefore the name Tille-tia indica) but has since been discovered inmany places worldwide. It is thought to be inAfghanistan, Lebanon, Mexico and now theUnited States. Karnal Bunt has spores thatare primarily wind-borne, but infection canoccur through planting in contaminated soil,use of infected seed, and coming into contactwith contaminated equipment and machinery.The spores attack the developing kernelswithin the seed head with little or no outwardsign of infection. The infected kernels areshrunken at the germ end and are covered withsori (small hairlike filaments) that will discolorflour made from infected kernels. These ker-nels will also impart a fishy odor and taste toflour making their commercial use impracti-cal [10, 23].

Black Tip / Black Point. Black Tip fungusis another non-mycotoxic fungus that attackswheat and barley. The name Black Tip orBlack Point can generally refer to any of anumber molds that form dark brown to blacksooty mold. The principal species of infec-tion are Alternia, Fusarium, andHelminthosporium, with the speciesHelminthosporium generally being the causalagent in infections associated with wheat [23].The mold generally occurs when seeds aresown in infected soils, but can also occur whenthe seeds themselves are infected. The mostcommon forms of Helminthosporium are gen-erally associated with dry, warm soils. Mois-ture in the form of rain or extended periods ofhigh humidity (over 90% relative humidity)then start the disease on the maturing kernels.If the mold begins early in kernel growth ste-rility and germ death occur, often accompa-nied with a shriveled germ resulting in de-creased yields. If the mold attacks in the later

stages of kernel development the seed is dis-colored and often carries an odor causingmarket discounts.These molds are also associated with seedlingblight and root rot which will effect the over-all health of the plant leading to increased sus-ceptibility of other plant diseases and molds.

Blue-Eye Rot. Blue-eye mold occurs instored corn with high moisture content. Blue-eye damage is caused by species of Penicil-lium and is characterized by a blue-green dis-coloration in the germ area. The discolora-tion results when Penicillium fungi invade thegerm area through the tip of the kernel. Somecorn varieties have a purple colored plumulewhich can be mistaken for the presence ofPenicillium fungi in the germ area.

Corn Smut. Smut is caused by Ustilagemaydis and is always present in field corn. Noharmful effects have been noted from feedingsilage made from smutty corn to livestock.

Background. In the previous chapter the prin-cipal damage caused by the fungi was themold. There were little or no toxic affects fromby-products of the mold. The molds were alsolimited as to the hosts they attacked. Mycotox-ins on the other hand are metabolites (by-prod-ucts) of the growth of the molds. They havevery real toxic side effects to other plants, ani-mals, and humans. They are also generallyless selective of the hosts they attack and cancross plant species.

The species Fusarium can and will attack bothcorn and wheat with different effects in eachplant. In wheat, they cause scab damage tothe kernels and produce deoxynivalenol(DON). In corn, they create Gibberella EarRot and produce DON, zearalenone (ZEN) andT-2 toxins. Both DON and ZEN have toxiceffects on animals and humans, with differ-ences depending on the species.

Mycotoxin contamination of crops has beena world wide problem for thousands of years.Only in the last thirty or forty years has tech-nology allowed researchers to isolate the fun-gal mycotoxins and study the effects on feedcrops, livestock, and their affects on humans.The study of mycotoxins is a narrow part ofthe research into naturally occurring toxins andtheir effects on plants, animals, and humans.Much of the information in print becomesquickly dated as the field expands and grows.With recent improvements in testing methodsmore research is now being done, and ingreater detail, with lower costs than was pre-

viously possible. Many of the newest researchpapers are now posted on the Internet allow-ing new information to reach more peoplefaster and more efficiently than was possiblebefore. Information that was published only20 to 25 years ago is now considered datedand questionable. But with the limited natureof the end usefulness of the information allinformation must be considered.

The problems associated with mycotoxin con-tamination of grains are world wide and areuncontained by national borders. A look at amap of North America shows that the impor-tant grain producing areas stretch from northcentral Canada to the southern reaches of theUnited States. These areas in turn export theirproducts to countries in Asia, the Pacific is-lands, South and Central America, Europe, theMiddle East, India and Africa [15].

Scientists estimate that there are 300 to 400mycotoxins presently identified with morebeing isolated as new techniques and processesevolve. The most frequently found mycotox-ins are aflatoxin, deoxynivalenol (DON),zearalenone (ZEN), fumonisin, and T-2 as faras grain crops are concerned. In surveys con-ducted by the North Carolina CooperativeExtension service in 1990 some amount ofaflatoxin, DON, or fumonisin was found inover 70% of the samples tested [20].

Mycotoxic molds generally attack the kernelsof grain robbing the nutrients and lower thefat, protein, and vitamin content of the grain.

Chapter 2

What Are Mycotoxins?

The mold also often changes the color of thekernels, the consistency (texture), and oftenimparts an odor that causes feed refusal inanimals. These effects lead to economic lossesdue to impaired health in animals and humans,reduced productivity (reduced production ofeggs, milk, and weight gain), and in severecases death to animals and humans. Whenthe grain is processed into final products likeflour or feed, the visible mold may be removed,but the majority of toxins are not and can stillcause poisoning.

Economic effects. The economic effects at-tributed to mycotoxin infection are widely feltin all sectors of the production and consump-tion of grain products. Grain producers areaffected by limited yields, restricted end mar-kets, and price discounts. Grain handlers areaffected by restricted storage options, cost oftesting grain lots, and loss of end markets.Grain processors incur higher costs to due tohigher product losses, monitoring costs, andrestricted end markets. Consumers end uppaying higher end product prices due to in-creased monitoring at all levels of handling,and in extreme cases health problems due toconsumption of contaminated products. So-cieties as a whole end up paying higher costsdue to increased regulations, needed research,lower export costs, and higher import costs.

While these costs are found at every level ofthe grain production system, it is almost im-possible to put a dollar figure on the losses.Estimates of losses to small portions of thegrain and related industries are the best thatcan be accomplished. The North CarolinaCooperative Extension Service published anestimate for 1992 that the losses to the animalproduction industry in North Carolina were$20 million for poultry, $10 million for swine,

$5 million for dairy, $1 million for beef andsheep, and $1 million for horses. In 1990 avomitoxin (DON) outbreak in New York andother Northeastern states, the NorthcentralU.S., and Eastern Canada had widespread eco-nomic affect. The New York Corn Growersestimated, conservatively, that $12 milliondollars was lost by the corn farmers due tolost markets, decreased crop value, and costsassociated with testing for the 1990-91 cropyear [15,20].

Health Hazards. The health hazards associ-ated with mycotoxin contamination in humansare rarely seen in North America and Europe.This is generally attributed to a higher levelof general health than is seen in underdevel-oped countries and better control of food andfeed storage.

The levels of intake of affected products thatare necessary to bring about poisoning inhealthy individuals are actually quite high. Inthe rare cases that humans have been reportedto be poisoned by mycotoxins, the populationswere consuming limited quantities of othernon-tainted foods and lived in areas of eco-nomic and environmental stress. The great-est threat of health hazards to humans comesfrom long term exposures of tainted food prod-ucts, either from spoilage or from consumingmilk or meat from animals that have been fedcontaminated feed [6, 12].

One possible avenue of concern to humans isthe suspected link between aflatoxin and can-cer. While the International Agency for Re-search on Cancer (IARC) has listed aflatoxinB

1 as having a definite link to cancer in ani-

mals, it is listed as having a probable link tocancer in humans. The studies that have beendone on the cancer link to humans have been

done in Africa and Asia and show anassociation between aflatoxin and cancer butno definitive cause and effect relationship hasyet been documented [21].

Mycotoxicoses (poisoning due to mycotoxins)have several common symptoms that areshared from species to species and toxin totoxin. These symptoms include:

1. Drugs and antibiotics are not effective intreatment.

2. The symptoms can be traced (associated)to food or feedstuffs.

3. Testing of food/feedstuffs reveals fungalactivity. [12]

4. The symptoms are not transmissible tocontrol subjects.

5. The degree of toxicity in subjects isinfluenced by age, sex, and the nutritionalstatus of the host.

6. Outbreak of symptoms is seasonal.

Mycotoxins have been linked to birth defectsin many animals, nervous system problems(tremors, limb weakness, staggering, and sei-zures), and tumors of the liver, kidneys, uri-nary tract, digestive tract, and the lungs [6].

Aflatoxin primarily attacks the liver, with sec-ondary effects shown in decreased production,and immune system suppression. Thetrichothecene group of mycotoxins (DON andT-2) cause necrosis and hemorrhage of the di-gestive tract with decreased blood productionin the bone marrow and spleen along withchanges to the reproductive system as the sec-ondary sites of attack.

Zearalenone has affects different from othermycotoxins in that it mimics the bodies pro-duction of estrogen causing feminization of

male animals and interference with concep-tion, ovulation, and fetal development infemale animals [6].

One of the primary similarities in mycotoxi-cosis is the health status of the host beforeinfection, which will to a large extent deter-mine the degree to which the host is attacked.In both animals and humans if the host ishealthy the final prognosis is generally verygood except in cases of acute poisoning wherevery large doses of toxin are eaten over a veryshort period of time.

Many variables affect the degree of suscepti-bility of various hosts. These include:

General health. A healthy individual is moreable to fight the toxins than a one that startsout malnourished or diseased.

Age. The very young and very old have weak-ened immune systems that are less able to fightthe effects of toxicoses.

Sex. In general female animals, and to a de-gree female humans, seem to be more suscep-tible to the effects of mycotoxicoses.

Environment. Hosts exposed to harsh livingconditions of neglect or squalor have an addedburden on their systems.

Adequate food storage. If grain is left in openstorage to the effects of weather the grain isfurther weakened allowing for continued fun-gal growth. If the grain is also not adequatelydried, the conditions for fungal growth con-tinue to persist.

Exposure Level. Very high doses of aflatoxinattack the host quicker than lower doses.

Exposure duration. A very short time of ex-posure (a single dose) allows the host time tofight the infection where a continued expo-sure tends to have cumulative effects.

Other food sources. If contaminated grainis the only or main source of nourishment, thehost has less nutrients available to feed theirsystem.

Lack of Regulatory and Monitoring sys-tems. Areas that lack the means to regulateand monitor the presence of mycotoxins ingeneral, and aflatoxin in particular, leave theirinhabitants open to unknown poisonings thatcan continue over long periods of time un-checked. [21]

Although the mycotoxins have been greatlyresearched over the course of the last fortyyears, little research has been done on the in-teractions of the mycotoxins and their com-bined effects. Almost all research has been indetermining the effects of pure strains devel-oped in the laboratory. Animal feed can con-tain several different grains and grain in stor-age can contain several different strains of thevarious mycotoxins.

Studies done with natural field contaminatedDON and ZEN have produced results thathave varied from those that have been carriedout in the laboratory. This leads researchersto believe that there are unknown strains oftoxins in the field or that the toxins interactwith each other to produce effects greater thanor different from what laboratory tests havepredicted would occur [15].

Regulatory Control. In 1965, the Food andDrug Administration (FDA) established actionlimits of 20 parts per billion (ppb) of aflatoxin

in all food and feeds to limit the inclusion ofthis contaminate into the food chain. But sinceaflatoxin can occur both in raw products andin finished by-products, this has necessitatedthe testing for aflatoxin and other mycotoxinsat many points in the food chain. As technol-ogy has progressed in recent years testing hasbecome simplified, faster, and cheaper (us-ing ELISA methods) allowing more testing tobe accomplished in all phases of food han-dling.

The Grain Inspection; Packers and StockyardsAdministration (GIPSA) tests all corn that isexported for aflatoxin with an action level of20 ppb. If a sample tests above 20 ppb, theFDA must be notified. Testing for vomitoxinis done as a service to customers with no FDAaction level set. FGIS will institute new test-ing services as the tests are certified for reli-ability and repeatability, and as customer de-mand requires.

Aspergillus Toxins

Aspergillus is an important genus in foodswith most species occurring as spoilage orbiodeterioration fungi. Aspergillus is a largegenus containing more than 100 recognizedspecies, several of which are capable of pro-ducing mycotoxins.

Nearly 50 species of Aspergillus have beenlisted as producing toxic metabolites. Thoseof greatest significance in feed and foods in-clude: aflatoxin, ochratoxin A, sterigmato-cystin, cyclopiazonic acid, citrinin, patulin,and tremorgenic toxins.

Aspergillus species produce toxins that ex-hibit a wide range of toxicities, with the most

significant effects being long term. AflatoxinB

1 is a potent liver carcinogen. Ochratoxin A

and citrinin both affect kidney function.Cytopiazonic acid has a wide range of effectsand tremorgenic toxins affect the nervous sys-tem.

While there is a known link between aflatoxinand cancer in animals, it should also be notedthat the Aspergillus species of fungi also havemany beneficial uses. One of the largest com-mercial uses of Aspergillus fungi is in the pro-duction of soft drinks. The extraction of purecitric acid from fruits and vegetables hasproved to be to expensive, so the manufactur-ers have developed a way to use large vats toferment Aspergillus niger to form artificialcitric acid [22].

The Japanese have developed methods of fer-menting rice with strains of Aspergillus flavus(aflatoxin) to cause the enzymes in the ker-nels to breakdown the carbohydrates intosimple sugars, to produce a sweetened ricedrink. These drinks or Koji, are marketedunder many different brand names [7].

The family of products that includes miso, soysauce, and sake also use strains of Aspergil-lus oryzae to ferment grain products into us-able food and drink products [22].

Penicillium Toxins

Penicillium is a large genus with over 150 spe-cies recognized and at least 50 species of com-mon occurance. The discovery of penicillinin 1929 gave impetus to a search for otherPenicillium metabolites with antibiotic prop-erties. This search led to the recognition of“toxic antibiotics” or mycotoxins.

Nearly 100 Penicillium species have been re-ported as toxin producers. Of these the fol-lowing nine mycotoxins produced by 17 Peni-cillium species are potentially significant tohuman health: citreoviridin, citrinin,cyclopiazonic acid, ochratoxin A, patulin,penitrem A, PR toxin, Roquefortine C, andSecalonic acid D.

The toxins produced by Penicillium speciescan be placed in two general groups: those thataffect the liver and kidney function, and thosethat are neurotoxic. The Penicillium toxinsthat affect liver or kidney function are asymp-tomatic or cause generalized debility in hu-mans or animals while the neurotoxins arecharacterized by sustained trembling.

Fusarium Toxins

Fusarium species are the most importantgroup of mycotoxigenic molds other than As-pergillus and Penicillium. Many Fusariumspecies are plant pathogens and most can befound in the soil.

Fusarium species are most often encounteredas contaminants of cereal grains, oilseeds, andbeans. Corn, wheat, barley and products madefrom these grains are most commonly con-taminated although rye, triticale, millet, andoats can also be contaminated.

F. graminearum is a plant pathogen foundworldwide in the soil and is the most widelydistributed toxigenic Fusarium species. Itcauses various diseases of cereal grains suchas gibberella ear rot in corn and head blight orscab in wheat and barley. The mycotoxinsproduced by F. graminearum include:

deoxynivalenol, zearalenone, 3-acetyldeoxy-nivalenol, 15-acetyldeoxynivalenol,diacetyldeoxynivalenol, nivalenol, T-2,neosolaniol, and diacetoxyscirpenol.

F. moniliforme is a soilborne plant pathogenthat is found in corn growing in all regions ofthe world. It is the most prevalent mold asso-ciated with corn. It has also been found inrice, sorghum, yams, hazelnuts, pecans, andcheeses.

F. moniliforme has long been suspected ofbeing involved in animal and human diseases.Animal diseases associated withF. moniliforme include equine leukoencephal-omalacia (ELEM) a liquefactive necrosis ofthe brain of horses, pulmonary edema andhydrothorax in swine, liver cancer in rats, andabnormal bone development in chicks andpigs.

The main human disease associated with F.moniliforme is esophageal cancer. Severalstudies have linked the presence of F.moniliforme and fumonisins in corn to highincidences of esophageal cancer in humans incertain regions of the world including an areaaround Charleston S.C. Mycotoxins that havebeen associated with F. moniliforme includefumonisins, fusaric acid, fusarins, andfusariocins.

Alternaria Toxins

Alternaria species may be significant as po-tential contaminants of food. Alternaria in-fects the plant in the field and may contami-nate wheat, sorghum, and barley. Alternariaspecies also infect various fruits and veg-

etables and can cause spoilage of these foodsin refrigerated storage.

Alternaria toxins include: alternariol,alternariol monomethyl ether, altenuene,tenuazonic acid, and the alertoxins. Little isknown about the toxicity of these toxins; how-ever, cultures of Alternaria that have beengrown on corn or rice and fed to rats, chicks,turkey poults, and ducklings have been shownto be quite toxic.

Claviceps Toxins

The ergot mold, Claviceps purpurea, is thecause of the earliest recognized human myc-otoxicosis, ergotism. Ergot has been reportedin sporadic outbreaks in Europe since 857,with near epidemic outbreaks in the MiddleAges.

Ergot is a disease of cereal grains such as ryeand wheat in which the grains are replaced byergot sclerotia that contain toxic alkaloids.The main ergot alkaloid, ergotamine, has vaso-constrictive properties that can cause swollenlimbs, and alternating burning and cold sen-sations in the fingers, hands, and feet (St.Anthony’s Fire).

AflatoxinPathogen. The name aflatoxin comes fromA(Aspergillus) + FLA(flavus) + toxin. Mod-ern research into aflatoxin had its beginningsin 1961, looking into what caused the deathsof 100,000 young turkey poults in England.The research traced the poison to contaminatedBrazilian peanut meal that had been used asfeed. When the feed was given to ducks andpheasants, the same outcome was produced.

Research found that there were four differentmetabolites formed from aflatoxin. When thecontaminated grain in question was viewedunder a black light, the metabolites glowedeither blue (B metabolite) or green-yellow (Gmetabolites). Of the two distinct color variet-ies there were isolated two distinct toxins (B

1,

B2, G

1, G

2). The subscripts refer to their sepa-

ration patterns on TLC plates. Of the fourmetabolites B

1 was the most predominate and

the most toxic [17].

Further research in the years since has foundother metabolites, with two found in the milk(M

1 and M

2) and urine of lactating mammals.

Aflatoxins M1 and M

2 are produced from their

respective B aflatoxins by hydroxylation inlactating animals and are excreted in milk atthe rate of approximately 1.5% of the rate ofingested B aflatoxins. Research has alsofound that aflatoxin is most commonly foundin tree nuts, peanuts, and oilseeds includingcorn and cottonseed.

Ecology. The greatest problems associatedwith aflatoxin are in corn production and food-stuffs. These problems occur for two reasons.Corn is grown in climatic areas that give thefungi/mold the greatest opportunity for growthand dispersal, and the areas that grow cornconsume it as a main part of the diets of bothanimals and humans [17].

Aflatoxin grows best at temperatures of 80Eto 90E F, but can survive at temperatures aslow 40E F. The mold also needs a high mois-ture content in the host, either through kernelmoisture or in the form of rainfall. Kernelmoisture of 20% or greater is optimal, but thefungus can survive and grow in grain withmoisture content as low as 15% [17]. In corn,insect damage to developing kernels allowsentry of aflatoxigenic molds, but invasion canalso occur through the silks of developing ears.

Research conducted into the growth of afla-toxin has indicated that the fungus needs someform of associated stress in the plants for thefungus to invade. The stress may be in theform of drought that weakens the plant sys-tem, extended periods of high temperature,damage from insects or birds, high crop den-sity, or competition from weeds. All of theseconditions weaken the host or provide a meansof entry to the spores to establish a footholdin/on the host [17].

As was indicated in Chapter One, the sporesneed a means of transmittal to spread andgrow. Insects and birds can carry spores on

Chapter 3

Mycotoxins in Grain and Feed

their bodies and when moving through a fieldcontaminate many plants. Raindrops hittinginfected plants and splashing to another planthave also been shown to be a means of trans-mittal. Poor field management in cleaningaway contaminated residual crop debris leavesthe spores in the fields to further continue thegrowth cycle in later crops.

Infection of harvested crops also occurs oncethe grain reaches storage. If corn is not cleanedand dried to adequate levels (moisture con-tent of less than 15%), the fungus will growand contaminate healthy clean grain. “Hotspots” containing spores and moisture canoccur in storage bins that create a self-sus-taining environment of moisture (respiration)and heat (decaying grain) that provide primegrowing conditions for the aflatoxin fungi [1].

Figure 1. Aspergillus flavus Infection of Corn(Wicklow and Donahue, 1984)

Health Effects. Aflatoxins are both acutelyand chronically toxic in animals and humans.The disease primarily attacks the liver caus-ing necrosis, cirrhosis, and carcinomas. Noanimal has been found to be totally resistantto the effects of aflatoxin, although suscepti-bility differs from species to species. Afla-toxin B

1 has been shown through research to

be the most potent naturally occurring carcino-gen in animals, with a very strong link to hu-man cancer incidence [21].

Scientists have conducted studies that haveshown a positive correlation between con-sumption and the level of intake of contami-nated food and feed, to liver cancer in Kenya,Mozambique, Uganda, and Swaziland in Af-rica, and China and Thailand in Asia. Studiesconducted in the Southeastern United Stateswhere foods that possibly contain aflatoxin aregrown also show an increase in liver cancers.While this increased incidence of cancer isstatistically apparent, there is no confirmedlaboratory link of cancer to humans, only ani-mals [11].

Aflatoxicosis refers to poisoning from the in-gestion of aflatoxins in contaminated food orfeed. It can occur from acute exposure of veryhigh doses of contaminated grain over a shortperiod of time, or from the chronic ingestionof low levels of aflatoxin over longer periodsof time [21].

Acute aflatoxicosis in humans is rare; how-ever, several outbreaks have been reported. In1967, twenty-six people in two farming com-munities in Taiwan became ill with apparentfood poisoning. Nineteen were children, threeof whom died. Rice from affected householdscontained about 200 ppb of aflatoxin whichwas probably responsible for the outbreak.

An outbreak of hepatitis in India in 1974 af-fected four hundred people, one-hundred ofwhom died. The outbreak was traced to corncontaining up to 15,000 ppb. It was calcu-lated the affected adults may have consumed2 to 6 mg on a single day, implying that thelethal dose for adult humans is on the order of10 mg.

Perhaps of greater significance to humanhealth are the immunosuppressive effects ofaflatoxins. Immunosuppression can increasesusceptibility to infectious diseases, particu-larly in populations where aflatoxin ingestionis chronic, and can interfere with productionof antibodies in response to immunization inanimals and perhaps also in children.

As stated before aflatoxicosis primarily attacksthe liver but does cause other health effects.Acute symptoms include vomiting, abdomi-nal pain, pulmonary edema, convulsions,coma, and cerebral edema. Many of theseconditions can only be treated with medicalcare which is beyond that available to devel-oping or third world areas, leaving their popu-lations at great risk.

Research has shown that animals that developaflatoxin poisoning have compounding effectsthat can effect the human population aroundthem. Cows’ reduced milk and meat produc-tion limits the variety of diet in third worldcultures. The milk products can also havemetabolites that are passed on through the milkand milk end products including nonfat drymilk, cheese, and yogurt. In poultry, chick-ens lay fewer eggs, and can pass on aflatoxinin the yolks of their eggs further adding to theproblem. Both the animal and human popula-tions can develop secondary immune systemproblems that leave them susceptible to fur-

ther unassociated diseases and viruses [17].

Tolerance Levels. The Food and Drug Ad-ministration (FDA) has established action lev-els for aflatoxin present in food or feed. Theselimits are established by the Agency to pro-vide an adequate margin of safety to protecthuman and animal health.

seicepS ytidommoCnoitcAleveL

snamuH kliMbpp5.0

M(1)

snamuHtpecxedoofynA

klimbpp02

slaminaerutammI,)yrtluopgnidulcni(

ro,slaminayriadtonsiesudnenehw

.nwonk

rehtodnanroCsniarg

bpp02

seicepSllArehtodeeflaminAnottocronrocnaht

laemdeesbpp02

feebgnideerBgnideerb,elttacerutamro,eniws

yrtluop

rehtodnanroCsniarg

bpp001

foeniwsgnihsiniFretaergro.sbl001

rehtodnanroCsniarg

bpp002

elttacfeebgnihsiniFrehtodnanroC

sniargbpp003

,eniws,elttacfeeByrtluop

laemdeesnottoC bpp003

Table 1. FDA Action Levels for Aflatoxin

Detoxification. Many companies and re-searchers have tried to find a means of detoxi-fying aflatoxin contaminated grains. Most ofthe treatments have been found to be eithertoo expensive to use in storage facilities or tohave side effects on the end products thatcancel the benefits of detoxification.

Dietary supplements to strengthen the generalhealth of affected animals and humans haveshown the most promise. The addition of vi-tamins, proteins, and trace elements, alongwith inorganic absorbents added to feed, havethe most positive effects. The absorbents bindand immobilize the toxins holding them in theintestinal tract, allowing them to be eliminatedin urine and fecal matter [17].

Occupational Risks. It must be emphasizedthat there have been no definitive links be-tween aflatoxin and cancer in humans, butstudies have shown associative risks in grainhandling and processing occupations. Re-search conducted in Holland and the UnitedStates showed elevated risk of respiratory andliver cancer to those exposed to dust associ-ated with grain and flour production. Thegreatest risk appeared in flour baggers andemployees working at dump pits unloadinggrain into storage facilities. Accordingly careshould be taken when handling raw grain prod-ucts or fine end products to avoid inhalationof fine particulates [12].

Ergot

Pathogen. Ergot is another fungi that attackswheat, rye, barley, and oats. Clavicepspurpurea, or ergot, is the cause of the earliestrecognized human mycotoxicosis, ergotism.

Ecology. C. purpurea has three differentmeans of transmittal. Windborne ascosporescan attack the immature kernels and grow intosclerotium, purple-black hornlike structures,that replace kernels on the heads of grain. Ifthese sclerotium mature on the stalk, they ripenand grow small club like stromata that in turngrow and release more ascospores. As the

sclerotium mature they release a substancecalled honeydew (sugary dew-like liquid) thatencourages insects to feed. This liquid con-tains small conidiophores that will attack theimmature grain heads and start the processover and therefore spread the spores from plantto plant. The sclerotium, what are commonlycalled ergot, must be exposed to cold (36 -37E F) for several weeks before they can ger-minate. The sclerotium can overwinter in thesoil or stay dormant in storage until the properconditions exist to again start the process overagain [9].

The damage of ergot is two fold. It decreasesthe yields of infected crops by replacinghealthy kernels and robbing the host plant ofneeded nutrients. The sclerotium contain al-kaloids that can have adverse health affectson humans and animals. The grains are alsodiscounted in market value if the sclerotiumare present after harvest.

Health Effects. Animals can suffer severeblood vessel constriction that can result in drygangrene. Internal bleeding, vomiting, con-stipation, diarrhea, and intestinal inflamma-tion are also common problems in livestock.Swine that are fed ergoty feed may abort anyfetuses that they hold.

Humans can suffer gastrointestinal distressand convulsions, abortion of fetuses, or a ne-crotic gangrenous condition of the extremi-ties if the ergot is ingested in sufficient quan-tities. Ergotism was known as St. Anthony’sfire during the Middle Ages because it wasbelieved that pilgrimages to a shrine of St.Anthony could lead to a cure of the disease.It is likely that as pilgrims traveled to theshrine, they left areas where bread wascontaminated with ergot and traveled to areas

where ergot was not a problem. The main er-got alkaloid, ergotamine, has vasoconstrictiveproperties that cause swollen limbs and alter-nating burning and cold sensations in fingershands and feet, hence the term “fire” in St.Anthony’s fire. Convulsive ergotism may alsohave been the reason for the Salem witchcrafttrials of 1692. In recent history, outbreaks ofergotism have occurred in Russia in 1926, Ire-land in 1929, France in 1953, India in 1958,and Ethiopia in 1973.

The ancient Chinese and Europeans used er-got alkaloid compounds to reduce bleedingafter childbirth and to induce abortions whenneeded. Modern science has found ways tocontrol these alkaloids. Several useful medi-cations have been developed to treat bleed-ing, muscle spasms, and migraine headaches.Two alkaloid compounds of ergot have shownremarkable effectiveness in treating migraineheadaches. Research is continuing to findmore and varied medical uses for these ergotalkaloids [23].

Trichothecenes

Pathogen. The trichothecenes are a chemi-cally related family of compounds that areproduced by fungi such as Fusarium, Tricho-derma, Myrothecium, and Stachybotrys. Thetrichothecene mycotoxins have been isolatedand found in Canada, England, Japan, SouthAfrica, and the United States. The most com-mon mycotoxins in the trichothecene familyfound in grain are DON and T-2, with ZENand Fumonisin also commonly found [12].Fusarium gramminearum, the parent fungithat produces DON, causes both GibberellaEar Rot in corn, and head scab in wheat.

Over a ten year period the Mycotoxin Labo-ratory at North Carolina State Universityfound Fusarium species of fungi in almostevery lot of corn tested. DON was detected inover 60 percent of poultry and dairy feedtested, and ZEN was found in 15 to 20 per-cent of feeds tested.

The Fusarium species of fungi are capable ofproducing 70 different mycotoxins, with somespecies producing as many as 17 strains ofmycotoxins simultaneously. Research is find-ing new strains of previously unknown myc-otoxins as testing methods improve and moreresearch is conducted. Fumonisin is a recentdiscovery that research indicates is very toxicto horses, but little is known of its incidenceor range [20].

Health Hazards. The trichothecene familyof mycotoxins affects each species of animalsin different ways. Testing done so far indi-cates that poultry has the highest resistance tothese toxins. Cattle, sheep, and goats havesome level of resistance due to their multipledigestive process, while animals of the mo-nogastric digestive process seem to have theleast resistance to the toxins. Swine seem tobe the most sensitive, partly due to their in-creased sense of smell which leads to feed re-fusal [15].

The greatest problems associated with thesetoxins are from prolonged feed intake at lowcontamination levels. The effects depend onthe specific toxin, the duration of exposure,and the type of animal involved. All animalspecies suffering from chronic toxicoses showvery good to excellent signs of improvementwhen the contaminated feed is removed. Fewlong term side effects remain with most of thisgroup of toxins if diagnosis is made quickly

before the general health of the affectedanimals is compromised [12].

The processing of grain with toxins in thetrichothecene group generally does little to re-move the toxin. Milling, baking or boilinghas only a slight effect in removing the tox-ins. Tests conducted on finished products con-taminated with these mycotoxins have shownthat 50 to 60 percent of the toxins are trans-mitted to the finished product. In some cases,such as the tempering of grain to reach a de-sired moisture level, the toxins have actuallyincreased due to the proper environmentalconditions needed for toxin production. Thetoxins can be transmitted to final productssuch as flour, bread, crackers, and cereal [12].

Deoxynivalenol (DON)

Pathogen. Fusarium graminearum is the par-ent fungi of deoxynivalenol (DON) orvomitoxin. Wheat and barley are the mostcommonly effected grain crops but the samefungus does infect corn. In the field, it showsup as a brown discoloration at the base of bar-ley glumes, a pink to reddish mold on theglumes and kernels of the wheat heads andthe tips of the ears of corn. Spores from themold stage of the fungi can stay dormant oninfected residues left on or in the soil. Con-tamination is most severe in fields where cornfollows corn, or where corn follows wheat,especially if the previous crop was infected[24].

Ecology. The optimal temperature range forthe DON mold is 70 to 85 F with moisturelevels preferred to be greater than 20 percent.There are exceptions to be noted. The moldcan survive temperatures as low as 0 F for short

periods of time. This particular fungi has twodistinct growth cycles, with the mold grow-ing during the warm temperatures of daytime,while the toxins are produced during the coolertemperatures of the night [2].

Health Effects. The symptoms associatedwith DON poisoning are many and variedwhich sometimes leads to its misdiagnosis asa problem. At low levels of toxicoses thesymptoms may include behavioral and skinirritations, feed refusal, lack of appetite, andvomiting. In later stages, symptoms may in-clude hemorrhage and necrosis of the diges-tive tract, neural problems, suppression of theimmune system, lack of blood production inthe bone marrow and spleen, and possible re-productive problems including birth defectsand abortion [15, 20].

Table 2. FDA Advisory Levels for DON

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mpp5

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As stated earlier, DON stays in end feed prod-ucts even after processing. In 1995, 16,000tons of dog food was produced using wheatby-products (most probably dust). After itreached the consumer level it was found tocontain DON in excess of 30 ppm. The prod-ucts were recalled costing the company inquestion a loss of approximately $20 million[16].

Tolerance Levels. Canada has set action lev-els for DON in grain and finished products,while the United States has set only advisorylevels. Canada’s tolerance levels are set at lessthan 2 ppm in wheat for human consumption,and less than 1 ppm for wheat destined foruse in infant food products.

The United States has set their advisory lev-els at less than 1 ppm for finished wheat pro-ducts for human consumption, and less than5 ppm for most animal feed products [12].

Zearalenone (ZEN)

Pathogen. Zearalenone is very similar todeoxynivalenol (DON) in most aspects with afew exceptions.

Ecology. The growing conditions of ZEN arevery comparable to DON, with the optimaltemperature range of 65E to 85E F. A drop intemperature during growth also stimulates theproduction of toxins [2].

The moisture content required by ZEN is alsosimilar to DON at 20 percent or greater. Butif the moisture content during growth dropsbelow 15 percent the production of toxins ishalted. This is one of the reasons that corn

for storage must be dried to moisture levelsless than 15 percent [24].

Health Effects. The greatest difference be-tween ZEN and DON is the way the toxin actsin animals. ZEN mimics the hormone estro-gen in the way it effects animal tissue. Swineare the most sensitive to its effects with levelsof 1 ppm causing feed refusal. Continued con-sumption of contaminated grain will causeestrogenism (health problems related to thereproductive system). These effects includeswelling of the reproductive organs includingthe genital and mammary glands, interruptionof the reproductive cycles, birth defects, andatrophy of the ovaries and testes. In male ani-mals, feminization occurs with enlargementof the mammary glands and loss of sex drive[20, 2].

Poultry show little or no effects from ZEN con-sumption. Cattle also show very little effectexcept in cases of prolonged consumption ofhigh levels (greater than 15 ppm) of ZEN. Theeffects produced are reduced milk production,swollen reproductive organs, and in somecases infertility. The ZEN is passed throughthe system with very little absorption shownin milk, urine, or body tissues [2].

Tolerance Levels. The FDA has issued noadvisory levels for zearalenone recommend-ing only that the levels of concern for DONbe observed (See above). Levels of as little as0.1 ppm to 5 ppm have been shown to causereproductive problems in swine so great careshould be used when feeding wheat that ispossibly contaminated to pigs [24].

Fumonisin

Pathogen. Fumonisin moniliforme is the par-ent fungi species of fumonisin. This funguscauses Fusarium Ear Rot in corn which is themost common disease of corn in the UnitedStates Midwest region. Testing of corn fieldshas shown that over 90 percent of fields areaffected by this fungi in one of its variousstrains [24].

The mold appears on the corn ears as a cot-tony white to light grey filaments between thecorn kernels. As the mold progresses the ker-nels will turn grey to light brown.

The fumonisin toxin can grow in the kernelseven with no apparent outward signs of mold.Testing of the grain is the only positive meansof verifying whether fumonisin is present ornot [24].

Ecology. Growing conditions vary widely.The temperature and moisture ranges are sowide spread as to include most of the North-ern and Southern Hemispheres. The one com-mon factor associated with fumonisin is thathigher incidence of infections seem to occurafter periods of drought which stress the plantsimmune system [24].

Fumonisin causes the corn kernels to becomebrittle and crack more frequently than is nor-mal. The more the grain is handled the morecracking and breaking occurs, giving the fungimore host material to grow on. For this rea-son corn screenings should be very suspectwhen used as feed, especially in horses. Test-ing has shown that screenings contain a higherlevel of fumonisin toxin (and mycotoxins ingeneral) than the whole grain product [24].

Health Effects. Fumonisin is one of the my-cotoxins that has only recently been discov-ered and has been little studied. The relatedhealth effects have shown few effects in hu-mans and most animals other than swine andhorses. While in depth research is lacking,fumonisin has shown a high degree of toxic-ity in preliminary studies conducted in horses.Swine have shown little or no effects with theonly preliminary symptoms to be possible res-piratory problems and possible links to theliver and kidneys. [20].

Toxin levels of as low as 5 ppm have showndirect links in horses with symptoms whichinclude: disorientation, walking/agitation, de-rangement, colic, head pressing, blindness,and death. The toxin seems to attack the liverand kidneys, which is similar to other myc-otoxins except in the severity. Fumonisin hasalso been linked to equine leukoencephal-omalicia, also known as “Blind Staggers” (acomplete breakdown of the neural system inthe brain) which has a high mortality rate [20].

Tolerance Levels. Currently there are no ac-tion or advisory levels in place by the FDAbecause so little is known about the effects.Industry levels have recommended levels tobe no higher than 5 ppm in horses, 10 ppmfor swine, and 50 ppm for cattle [24].

Nivalenol (NIV)

Pathogen. Nivalenol is produced by theFusarium nivale fungi and has also only re-cently been isolated. Little is known of itsgrowth cycle or habitat range. Studies haveshown it to be much rarer in occurrence andhas only been found in a few samples of bar-ley, wheat, wheat flour, and rice [12].

Health Effects. Though little actual test datahas been produced, the results so far cause sci-entists to be extremely cautious. Preliminarytesting shows that NIV is thought to be 10times more potent than DON. If the advisorylevel for Don is used as a guide for toxicity,NIV would have an advisory level of only 0.2ppm [12].

Ochratoxin

Pathogen. Ochratoxins were initially associ-ated with Aspergillus ochraceus but are pro-duced primarily by Penicillium verrucosum.

Ecology. A. ochraceus is widely distributedin dried foods such as peanuts, pecans, beans,dried fruit, and dried fish. Ochratoxin con-tamination of foods is of greatest concern inScandinavia and the Baltic states where it isproduced by Penicillium verrucosum. It isfound in barley and wheat crops infected inthe field or in storage crops used for both breadmaking and animal feeds.

Health Effects. Ochratoxin is the most im-portant toxin produced by a Penicillium spe-cies. It can cause listlessness, huddling, diar-rhea, tremors, and other neural abnormalitiesin poultry and has been associated with kid-ney disease in swine in Scandinavia and north-ern Europe.

Because ochratoxin A is fat soluble and notreadily excreted, it accumulates in the fat ofaffected animals and from there is ingestedby humans eating pork. A second source isbread made from infected barley or wheat.

T-2

Pathogen. Fusarium tricinctum and somestrains of F. roseum produce T-2 . T-2 hasbeen found in corn in the field, silage, andprepared feeds made with corn.

Health Effects. During WWII, a very severehuman disease occurred in the former SovietUnion. Alimentary toxic aleukia (ATA) is be-lieved to have been caused by T-2 and HT-2in grain left to overwinter in the field. Whenthis grain was consumed, severe mycotoxico-sis occurred. ATA results in a burning sensa-tion in the mouth, tongue, esophagus, andstomach. Eventually the blood making capac-ity of the bone marrow is destroyed and ane-mia develops. In the final stages hemorrhag-ing of the nose, gums, stomach, and intestinesdevelops and the mortality rate is high. In poul-try, T-2 may produce lesions at the edges ofthe beaks, abnormal feathering, reduced eggproduction, eggs with thin shells, reducedbody weight gain, and mortality.

Cyclopiazonic Acid (CPA)

Pathogen. CPA is produced by A. flavus andseveral Penicillium species. It has been foundin corn and peanuts in Georgia. The principlePenicillium species producing CPA, P. com-mune, is a cause of cheese spoilage aroundthe world.

Health Effects. CPA is a highly toxic com-pound that causes fatty degeneration and he-patic cell necrosis in the liver and kidneys ofdomestic animals. Chickens are particularlysusceptible. When the compound is injectedinto experimental animals, central nervous

dysfunction occurs and high doses can resultin death. CPA and aflatoxin may act syner-gistically when consumed together by animals.

CitrininPathogen. Citrinin is primarily a metaboliteof Penicillium citrinum but is also producedby P. expansum and P. verrucosum. Thesethree species are the most commonly occur-ring penicillia, and so citrinin is probably themost widely produced Penicillium toxin.

Ecology. Citrinin has been isolated from al-most every kind of food surveyed for fungi.The most common sources are cereals suchas rice, wheat, and corn, milled grains, andflour.

Health Effects. Citrinin is a kidney toxinwhich has been associated with mycotoxicosesin swine, horses, dogs, and poultry. No toxiceffects to humans have been noted when cit-rinin is ingested in the absence of other tox-ins, however, there is a possibility of syner-gism if ingested with other toxins.

Aflatoxicosis A poisoning that results from ingestion of aflatoxins in contaminated foodor feed.

Ascospores A sexual spore formed in an ascus.

Ascus Saclike structure in which ascospores are borne.

Blight General term for sudden, severe, and extensive spotting, discoloration,wilting, or destruction of leaves, flowers, stems, or the entire plant.

Carcinogen A substance or agent producing or inciting cancer.

Carcinoma A new growth or malignant tumor enclosing cells in connective tissue.

Cirrhosis A chronic disease of the liver characterized by progressive destruction andregeneration of liver cells, ultimately resulting in liver failure and death.

Coleoptiles Ephemeral, nonpigmented tissue sheathing the first true leaf of a grass(maize) seedling.

Clums Stem of a grass plant.

Cultivars Cultivated variety.

Embryo Seed “germ”; the rudimentary plant within a seed.

Florets Small flower enclosed in a spikelet.

Fungicide Chemical or physical agent that kills or inhibits the growth of fungi.

Fungus (fungi) Organism having no chlorophyll, reproduces by sexual or asexual sporesand not by fission, and, generally, a mycelium with well-marked nuclei.

Germination Begin growth as of a seed, spore, sclerotium, or other reproductive body.

Glumes Empty bract at the base of a spikelet.

Glossary(Derived from underlined words in text)

Host Living plant attacked by (or harboring) a living parasite and from whichthe invader is obtaining part or all of its nourishment.

Hybrids Offspring of two individuals of different genetic character.

Hyphae A tubular, threadlike filament of fungal mycelium.

Inoculum Spores or other diseased material that may cause infection.

Lesions Well-marked but localized diseased area; a wound.

Metabolite A product of the chemical changes in living cells by which energy isprovided for vital activities and processes and new material is assimilated.

Mycelium Mass of hyphae constituting the body (thallus) of a fungus.

Mycotoxicoses Literally, fungus poisonings; current usage limited to poisoning of peopleand animals by various food and feed products contaminated (and sometimes rendered carcinogenic) by toxin-producing fungi.

Necrosis Death of plant or animal cells, usually resulting in tissue turning dark;commonly a symptom of fungus, nematode, virus, or bacterial infection.

Pathogen Organism or agent that causes disease in another organism.

Pericarp Outer layer of a seed or fruit.

Perithecia A small fruiting body in certain fungi, containing ascospores.

Sclerotia Hard, frequently rounded, and usually darkly pigmented resting body of afungus composed of a mass of special hyphae cells. The structure mayremain dormant for long periods. Sclerotia germinate upon return offavorable conditions to produce stroma, fruiting bodies and mycelium.

Sori Compact fruiting structure of rust and smut fungi.

Spikelet Spike appendage comprised of glumes and florets; unit of inflorescencesin grasses.

Spore One-to-many-celled reproductive body in fungi and lower plants that candevelop into a new plant.

Subcrowninternode Short, culm-like connection between the crown and seed roots of wheat.

Teliospores Thick-walled resting spore of rust and smut fungi that germinates to forma basidium.

Toxin A poisonous substance, having a protein structure, that is secreted bycertain organisms and is capable of causing toxicosis when introducedinto the body tissue. Toxins are also capable of inducing an antitoxin.

Trichothecene A group of chemically related compounds produced by fungi such asFusarium.

1. Black, Kevin. “Aflatoxins in Corn” (Dec. 1996): 2 pag. Online. Internet. 20, Feb. 1997

2. Cheeke, Peter R., Lee R. Shull. ed. Natural Toxicants in Feeds and Poisonous Plants.Westport: AVI Publishing 1985.

3. Chen, Yuan-Kuo. “Zearalenone” CU Toxic Plant Pages (nd): 2 pag. Online. Internet.

4. Christensen, CM., C.J. Mirocha, R.A. Meronuck. “Molds, Mycotoxins, and Mycotoxi-coses” Cereal Foods World Vol. 22 No. 10 (Oct 1977): 513-520.

5. Cook, James R., Roger J. Veseth. Wheat Health Management St. Paul: APS Press 1991.

6. Council For Agricultural Science and Technology. Mycotoxins: Economic and HealthRisks. Iowa: Task Force Report No. 116, 1989.

7. Grainaissance, Inc. “What is Amazake” (nd): 4 pag. Online. Internet. 19, Feb. 1997.

8. Hart, L.P. “Variability of Vomitoxin in Truckloads of Wheat in a Wheat ScabEpidemicYear”Plant Disease Volume 82 No.6 June 1998

9. Karow, Russ. “Ergot in Cereal Grains - Cause, Hazards and Control” OSU ExtensionService (nd): 2 pag. Online. Internet 19, Feb. 1997.

10.Karow, Russ., Dick Smiley. “Karnal Bunt” Wheat Diseases” (nd) 3 pag. Online. Internet.4, Feb. 1997.

11. “Known Carcinogen: Aflatoxin” [Cas. No. 1402-68-2] (nd): 2 pag. Online. Internet.20, Feb. 1997.

12.Krogh, Palle. ed. Mycotoxins in Food. San Diego: Academic Press Limited 1987.

13.Mathre, D.E. ed. Compendium of Barley Diseases St. Paul: APS Press 1991.

14.McMullen, Marcia P., Robert W. Stack. “Head Blight (Scab) of Small Grains” NDSUExtension Service pp-804, (nd): 6 pag. Online. Internet. 6, Feb. 1997.

15.Miller, J.D., H.L. Trenholm ed. Mycotoxins in grain: Compounds Other Than Aflatoxin.St. Paul: Eagan Press 1994.

References

16.“Mycotoxins in Feed Grains” Dept. of Botany & Plant Pathology, Purdue University(July 1996)

17.Saad, Nabil., “Aflatoxins: Occurrence and Health Risks” (nd): 7 pag. Online. Internet.20, Feb. 1997.

18.Shurtleff, Malcom C. ed. Compendium of Corn Diseases 2ndedition. St. Paul: APS Press1992.

19.Trucksess, Mary W., John L. Richard. Labortory Safety Considerations in the Handlingof Natural Toxins. Fort Collins: Alaken, Inc. 1992.

20. “Understanding and Coping With Effects of Mycotoxins in Livestock Feed and For-age” North Carolina Extension Service (nd)

21.US Food and Drug Administration Center for Food Safety and Applied Nutrition.“ Aflatoxin” Foodborne Pathogenic Microorganisms and Natural Toxins [Bad Bug Book](1992): 2 pag. Online. Internet. 4, Feb. 1997.

22.Volk, Tom. “Fungus of the month of February 1997” (Feb. 1997): 3 pag. Online. Internet.26, Feb. 1997.

23.Wiese, M.V. ed. Compedium of Wheat Diseases. 2nd edition. St. Paul: APS Press 1991.

24.Woloshuk, Charles P. Dept. of Botany & Plant Pathology, Purdue University “Mycotoxinsand Mycotoxin Test Kits”, Cooperative Extension Service, Corn Diseases BP-47 (July 1994):12 pag. Online. Internet. 10, Feb. 1997.

25.Woloshuk, Charles P. Dept. of Botany & Plant Pathology, Purdue University “Vomitoxin inFeed Wheat For Hogs” Grain Quality Task Force No. 26 (July, 1996): 2 pag. Online.Internet. 6, Feb. 1997.

26.Woloshuk, Charles P., Dirk Smiley . Dept. of Botany & Plant Pathology, Purdue University.“Blue Eye in Corn” Grain Quality Task Force No. 18 (Sept, 1994): 2 pag. Online. Internet.6, Feb. 1997.

Fungal Disease Fact Sheet

Disease Name: Aspergillus Ear Rot

Grain Affected: Primarily Corn/Corn products, Peanuts/Peanut products;Secondarily Pecans, Walnuts, Almonds, Cottonseed meal,Sorghum, Barley and Oats.

Mycotoxin: Aflatoxin

Pathogen: Aspergillus flavus, A. parasiticus, A. nomius, A. niger, A. glaucus.

Synptom: Yellow-Green mold found on ears of corn in the field or on kernelsin storage.

Conditions: Preharvest moisture >18%, Temperature 12 -40 C (54 -104 F),Humidity >85%, Severe drought stress, nitrogen deficiency, andsignificand insect damage. Stored grain should be dried and stabil-ized to <14% moisture.

Inoculumn Waterborne via rain, splashing water, airborne and also transmittedDispersal: through insect and bird damage.

Inoculumn Overwinters on or near soil surface on decaying host plant debris.Survival:

Effect on Crop: Decreased yeilds, grain quality

Management: Minimize crop stress from drought and insect damage, harvestearly, and reduce storage moisture levels to <15%.

FDA Action 20 parts per billion (ppb) for grain and feed products, and 0.5 ppbLevel: for milk. Recommended limits in feed are: 20ppb for dairy cattle;

100ppb for breeding cattle, breeding swine, and mature poultry;and 300 ppb for finishing cattle and swine.

Livestock No animal species is resistant to the acute toxic effects of aflatoxinsAffected: according to FDA literature.

Livestock Liver damage, decreased reproductive performance, reduced milkSymptoms: or egg production, embryonic death, birth defects,

tumors,suppressed immune system functions. Aflatoxin is a verypotent carcinogen.

Human Historical outbreaks of aflatoxicosis where contaminated corn wasSymptoms: he major dietary food 397 persons were affected and 108 persons

died. The patients experienced high fever, rapid progressivejaundice, edema of the limbs, pain, vomiting, and swollen livers.Histopathological examination of humans showed extensive bileduct proliferation and peripirtal fibrosis of the liver and gastrointes-tinal hemorrhages. A 10-year follow up of the outbreak found thesurvivors fully recovered

Photo 1. Aspergillus sp.growing on corn kernel(R. Friedrich)

Photo 2. A. flavus oninsect damaged ear ofcorn (J.L.Richard)

Photo 3. Ear of corninfected with A. flavus.(G. Munkvold)


Disease Name: Black Tip / Black Point

Grain Affected: Wheat, Barley

Mycotoxin: None

Pathogen: Cochliobolus sativus,Helminthosporium sativum (asexual stage)

Synptom: Brown lesion on coleoptiles, subcrown internodes, roots, andculmsof seedlings. Black-brown leaf lesions on maturing plants.

Conditions: Seedlings: warm, dry seedbeds. Maturing heads: humidity >90%,Rainfall during seed maturation, seed moisture >20%

Inoculumn Almost exclusively by planting infected seeds. OccasionallyDispersal: soilborne.

Inoculumn Primarily through storage of infected seed grain. Can overwinter inSurvival: soil.

Effect on Crop: Discolored grain is discounted in value due to undesirable colorand odor. Possible decrease in yield, test weight, and germinability.Causes seedling blight, root rot, and spot blotch. Barley may beunacceptable for malting.

Management: Plant non-diseased seed. Deep soil tillage.

FDA Action NoneLevel:

Livestock NoneAffected:

Livestock NoneSymptoms:

Human NoneSymptoms:

Photo 4. Wheat kernelsinfected with black tipfungus (FGIS)

Photo 5. Black tipdamage (FGIS W-1.0)

Photo 6. Barley kernelsseverely infected withblack tip (E. Banttari)

Photo 7. Wheat kernelsseverely infected withblack tip (APS)


Disease Name: Blue-Eye Mold

Grain Affected: Corn

Mycotoxin: None

Pathogen: Penicillium oxalicum

Synptom: Powery green or blue-green mold on and/orbetween kernels usually at the ear tips. Discoloration of germindicates kernel death.

Conditions: Primarily a storage mold. Enhanced by prolonged wet-holdingperiods, especially on cob stored corn in cribs. Moisture/Temp.>14%, 25 C (75 F) for A. glaucus and >18%, 5 C(40 F) forP. oxalicum. Humidity >70%. Can occur in field if introducedthrough insect/bird damage.

InoculumnDispersal: Soil and airborne, insects, birds, equiptment and storage facilities.

Inoculumn Overwinters on/near soil surface in host residues. Equiptment andSurvival: storage facilities.

Effect on Crop: Decreased feed and market value.

Management: Early harvest, areation and drying to reduce moisture <15%




Human NoneSymptoms:

Photo 8. Blue-eye molddamage (FGIS C-1.0)

Photo 9. Purple plumule;not damage (FGIS C-1.1)

Photo 11. Conidia andconidiphores of Penicil-lium sp. (M. Brown &H. Brotzman)

Photo 10. Penicillium earrot (APS)


Disease Name: Ergot

Grain Affected: Wheat, Rye, Triticale, Barley, Oats, Cultivated & Wild Oats

Mycotoxin: Ergot Alkaloids - Ergotamine, Ergotpeptide pyrroloidine andLysergic Acid Alkaloids.

Pathogen: Claviceps purpurea, Claviceps paspalli and Claviceps fusiformis.

Synptom: Purple-black, hornlike sclerotia (ergot bodies) that replace one ormore seeds in the head, up to 10 times larger that normal seeds.Infected florets exude a sugary slime in sticky yellow droplets.

Conditions: Ergot is favored by wet, cool weather that accompanies and prolongs flowering periods. Germinates during spring and earlysummer.

Inoculumn Airborne, splashing rain and insects.Dispersal:

Inoculumn Sclerotia remain viable for approximately 1 year in soil and Survival: longer for grain in storage.

Effect on Crop: Decreased yields, discounted market value.

Management: Deep soil tillage, crop rotation clean seeds, use of modern graincleaning equipment, clean cultivation, and eliminate potentialergot sources by mowing headlands and roadways, before grassesmature.


Livestock Cattle and SheepAffected:

Livestock Blood vessel constriction of extremities followed by dry gangrene.Symptoms: Digestive tract inflammations, internal bleeding, vomiting,

constipation or diarrhea. Abortion may occur in swine.

Human Historical accounts indicate gangrene, convulsions and gastro-Symptoms: intestinal disorders were common with approximately 50%

resulting in death. Modern cultivation techniques along witheducation have virtually eliminated this threat.

Photo 12. Ergot sclerotia(FGIS OF-12.0)

Photo 13. Wheat headwith ergots (F.J. Zilinsky)

Photo 14. Barley headwith honeydew and ergots(APS)

Photo 15. Ergot sclerotia(APS)


Disease Name: Fusarium Ear Rot


Mycotoxin: Fumonism

Pathogen: Fusarium moniliforme

Synptom: Salmon-pink to reddish-brown spore mass starting at the ear tip oron groups of kernels scattered thoughout the ear, progressing to apowdery or cottony-pink mold. Has also been found in seeminglyhealthy corn.

Conditions: Infection tends to follow injury by insects or birds. Diseasedevelopment favors dry, warm weather. High kernel moisture attime of harvest. Affects as much as 90% of midwest corn crops.

Inoculumn Soil and airborne, insects, birds, corn borers and earworms. Con-Dispersal: taminated storage facilties and equipment.

Inoculumn Overwinters on/near soil surface in host plant debris. ContaminatedSurvival: storage facilties and equipment.

Effect on Crop: Decreased feed and market value. Reduced yield, test weights, andbaking qualities.

Management: Crop rotation, deep soil tillage, resistant hybrids, reduce nitrogenlevels in fields, and use of clean equipment and storage facilities.

FDA Action None; Advisory levels are 5ppm for horses, 10ppm for swine, andLevel: 50ppm for cattle.

Livestock Horses, donkeys, mules, swine and cattle.Affected:

Livestock Equine leukoencelhalomalacia (blind staggers). Loss of appetite.Symptoms:

Human On going research indicates potential for adverse health problemsSymptoms: (cancer).

Photo 16. Corn infectedby Fusarium sp.(G. Munkvold)

Photo 17. Fusarium earrot (APS)


Disease Name: Gibberella Ear Rot


Mycotoxin: Deoxynivalenol (Vomitoxin, DON), Zearalenone, T-2

Pathogen: Fusarium graminarum, Fusarium roseum (sexual stage),Gibberella zeae

Synptom: Pink to reddish mold beginning at the ear tip. Occasional blue-black specks (perithecia) found on husk and ear shank.

Conditions: Enhanced by cool wet periods within 3 weeks after silking.Moisture >20%, Temperature DON 21 -29 C (70 -85 F),Temperature ZEA, T-2 <15 C (59 F), Humidity High

Inoculumn Waterborne via rain, splashing water, airborne and also transmittedDispersal: through insect and bird damage.

Inoculumn Overwinters on / near soil surface in host residues such as grasses,Survival: corn, and wheat stubble.

Effect on Crop: Decreased yields, grain quality and lower test weights.

Management: Crop rotation, deep soil tillage to bury crop residues. Post harvestdrying to <18% moisture for whole ear storage, <15% for shelledcorn. Early harvest and resistant hybrids.

FDA Action No Action Level; FDA has issued DON advisory levelsLevel: 1ppm finished wheat products,

5ppm grain/ grain by-products for swine (<20% of diet),10ppm grain/ grain by products for cattle/poultry (<50% of diet).5ppm grain/ grain by-products all other animals (<40% of diet),

Livestock Predominately swine with concentrations as low as 1ppm.Affected:

Livestock DON-Vomiting, decreased weight gain, diarrhea, lethargy,Symptoms: blanched skin color, dermal irritation, hypothermia, intestinal

hemorrhage, and ultimately feed refusal.

ZEA-Infertility, abortion and other breeding problems.

Human None shown to date. On going research.Symptoms:

Photo 18. Gibberella earrot (G. Munkvold)

Photo 20. Gibberella earrot (APS)

Photo 19. Kernelsinfected with Gibberellazeae (APS)


Disease Name: Karnal Bunt

Grain Affected: Wheat, Triticales and Rye

Mycotoxin: None

Pathogen: Tilletia indica

Synptom: Dark brown teliospores affect only a few seeds per head andusually at their embryo end. Larger sori may extend along thecrease and occasionally envelope the whole kernel. Spores mayimpart a fishy odor to the grain.

Conditions: Wet conditions required for teliospores germination. Furrowirrigation or rainfall, followed by 3-4 days of cool, humid weatherare required for sporidia penetration.

Inoculumn Primarily airborne during harvest when the pericarp of buntedDispersal: kernels is broken. Also through use of contaminated equipment.

Inoculumn Spores overwinter in soil then germinate at or near surface inSurvival: response to favorable conditions. Spores can survive in the soil up

to 5 years.

Effect on Crop: Reduced crop yield and quality. Flour made from bunted kernelsare discolored with an unpleasant odor and taste.

Management: Chemical seed treatments can inhibit the germination of seedborneteliospores. Some fungicides applied at heading protect againstinfection.




Human None, though wheat containing >3% bunted kernels is consideredSymptoms: unfit for human consumption.

Photo 21. Wheat infectedwith karnal bunt (F.J. Zilinski)

Photo 22. Seed infectedwith karnal bunt (APS)

Photo 23. Teliospore ofT. indica (APS)

Photo 24. Infectionbegins at the embreyo andprogresses along thecrease. (APHIS)


Disease Name: Scab (Head Blight)

Grain Affected: Wheat, Barley

Mycotoxin: Deoxynivalenol (Vomitoxin, DON)

Pathogen: Fusarium graminarum, Gibberella zeae, Zearalenone

Synptom: Wheat-Spikes appear bleached with brown / purplish discolorationof stem. Pink to salmon-orange spore mass appears on glumes andkernelsBarley-The first indication of infection is a small water-soaked,somewhat brownish spot at the base of middle of the glume or onthe rachis. Water soaking and discoleration then spread in alldirections.

Conditions: Moist periods, Moisture >20%, Temperature 21 -30 C (70 -86 F),Humidity high. Also infection can occur at temperatures as low as15 C (59 F) if humidity remains high for up to 72 hours.

Inoculumn Airborne. During rainy seasons spores can be splashed onto otherDispersal: heads of cereal crops or windblown. Soil borne spores overwinter

from previous host crops. Also insect and bird damage.

Inoculumn Overwinters on / near soil surface in host residues such as grasses,Survival: wheat and barley stubble.

Effect on Crop: Decreased yields, grain quality and lower test weights. Adverselyaffects flavor and baking qualities.

Management: Crop rotation, deep soil tillage to bury crop residues. Post harvestdrying to <15% moisture, <13% for scabby grain going into storage.

FDA Action None: DON advisory levels are 1ppm finished wheat products,Level: 5ppm grain/ grain by-products for swine (<20% of diet), 5ppm

grain/ grain by-products all other animals (<40% of diet), 10ppmgrain/ grain by products for cattle and poultry (<50% of diet).

Livestock Predominately swine with concentrations as low as 1ppm.Affected: DON can also cause problems in horses, breeding and

lactating animals, but only at high concentrations. Cattle andpoultry are more tolerant of vomitoxin and zearalenone.

Livestock DON Vomiting, decreased weight gain, diarrhea, lethargy,Symptoms: blanched skin color, dermal irritation, hypothermia, intestinal

hemorrhage, and feed refusal.ZEA-Enlargement or swelling of vulva. Severe reproductive andinfertility problems. Decreased milk yield in cattle.

Human Induced muscle spasms and vomitingSymptoms:

Photo 27. Wheat spikletwith orange spore mass(C.R. Luzzard)

Photo 28. Scab damage (FGIS W-2.0)

Photo 25. Plants infectedwith scab (APS)

Photo 29. Barley kernelsinfected with G. Zeae (APS)

Photo 26. Spikes infectedwith scab (APS)


Disease Name: TCK Smut (Dwarf Bunt)

Grain Affected: Wheat, Rye, Barley, Wild & Cultivated Grasses

Mycotoxin: None

Pathogen: Tilletia controversa

Synptom: Plants infected are ¼ to ½ the normal size. The glumes areconspicuously spread apart exposing plump bunt (smut) balls.

Conditions: Temp. 3 - 8 C (38 - 46 F). Limited to areas where winter issubject to prolonged snow cover.

Inoculumn Primarily soilborne, then germinates under snow or at soil surface.Dispersal:

Inoculumn Can persist in soil up to 10 yrs.Survival:

Effect on Crop: Reduced yield and grain quality. Imparts pungent, fishy odor anddarkened appearance. Bunt spores released during threshing arecombustible, occasionally resulting in fires sparked by harvesters.

Management: Resistant wheat varities, apply fungicides to soil surface afterseeding.




Human NoneSymptoms:

Photo 30. head infectedwith dwarf bunt (APS)

Photo 31. Teliospores ofT. controversa (APS)

Photo 32. Teliosporecloud during harves ofdwarf bunt infected wheat(APS)

Grain Fungal Diseases & Mycotoxin Reference · fruiting bodies that form molds, mushrooms, smuts...

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Transcript of Grain Fungal Diseases & Mycotoxin Reference · fruiting bodies that form molds, mushrooms, smuts...