Vomitoxin deoynivalenol (DON) is a pervasive pathogen that infects large portions of our common cereal grains. The presence of the toxin is a chronic threat to crop, human, and animal health throughout the world.
When consumed by livestock, vomitoxin DON causes the animals to refuse feed (especially swine). Vomitoxin makes pigs throw up! Even low levels of DON produce irritation in the GI tracts (of animals and humans alike) which reduces feed intake and efficiency, reflected in reduced animal performance.
Vomitoxin appear to affect via the nervous system. Vomitoxin is a class of mycotoxins (trichothecenes) which is a low-molecular-weight inhibitor of protein synthesis with a broad spectrum of toxigenicity against animals. Ingestion of contaminated grain or by-products of exposed animals has severe long-term consequences, including immunosuppression, neurotoxicity, and nutrient uptake alteration. It is reported that vomitoxins cause the brain to increase its uptake of tryptophan, in turn increasing serotonin. It is the serotonin that is likely responsible for the anorexic effects of DON and other trichothecenes. Of the trichothecenes, and there are nearly 200 of them, its cousin T-2 is responsible for tens of thousands of deaths and has been used as a biological weapon. Glyphosate is also a T-2 toxin.
Vomitoxin toxicity also destroys the intestinal barrier functions which are the body’s largest and most important barrier. The intestinal barrier facilitates the transport of nutrients into the body while keeping toxins out. The selective barrier is made of protein-protein networks that link adjacent cells, and are known as tight junctions. When these tight junctions are destroyed it allows antigens and other toxins to enter the body and blood stream. The breakdown of tight junctions is associated with the onset and recurrence of chronic intestinal inflammation (which is a result of a triggered immune response). The diseases that follow this pattern are inflammatory bowel disease (IBD), food allergies and celiac disease. Ref: Demeo, Mark T., Ece A. Mutlu, Ali Keshavarzian, and Mary C. Tobin. "Intestinal Permeation and Gastrointestinal Disease" Journal of Clinical Gastroenterology 34.4 (2002) 385-96.
Fusarium graminear (Gibberella zeae) and F. culmorum are the pathogens that produce vomitoxin deoynivalenol (DON) which infects the various plants, mostly corn and cereal grains. It is the gibberella or fusarium ear blight in corn or maize. Head blight in wheat and other grains is caused by Fusarium culmorum and F. graminearum.
Trichothecene mycotoxins are stable to baking processes so they are also stable to ensiling or fermentation process where heat is concerned. The concern is that these mycotoxin / vomitoxin components are in so much of the grains that are the fundamental building blocks in the human / livestock diet.
Certainly there are beneficial microorganisms that are able to reduce the living presence of these fungal pathogens and decompose the mycotoxins in the fermenting forages, but this is a secondary approach. The primary approach should be to protect the plants from these and other pathogenic organisms before they are infected. You can do this by increasing the plant’s natural defenses through balanced nutrition and the proper minerals to prevent the formation of the mycotoxins and vomitoxins.
Trace minerals (70+ of them) in general are essential to this approach. There are numerous trace elements that have a major impact on the pathogens directly and the prevention of the vomitoxins. These same trace minerals also control indirect pathways where these and other minerals strengthen the plant's natural defense systems so they can resist these pathogens. The major trace elements in these processes are: Molybdenum, Manganese, Zinc, Copper, Boron, and Potassium. We discuss each of them below.
Mo is required for nitrate reductase (NO3 -> NO2) with Mg which is the co-factor for nitrite reductase (NO2 -> NH2). Nitrate-N can’t be utilized by plants without Mo. In legumes, ureides are the most prevalent form of N and Mo is the co-enzyme in their metabolism (in and out of nodules). Mo deficiency leads to nitrogen deficiency. Mo is also involved in sulfur oxidation. In HLB, there appears to be an N-intermediate, formed during the nitrate metabolism, which inhibits this disease and blocks the vomitoxin formation (Huber 2015).
Mo appears to possess a suite of mechanisms, acting outside the host plant, by which Mo can function in influencing host-pathogen balance. These are related to the known effects of heavy metals on biologically important macromolecules, notably in denaturing them. All known cases have favored the host plant by suppressing the pathogen or otherwise deactivating its toxin or exoenzyme. Mo, like other heavy metals, deactivates viruses by denaturing their protein coat (Verma and Verma 1967)
Mo demonstrates a suppressive effect on zoospores of Phytophthora sp. (Halsall 1977) and the inhibition of nematodes (Haque and Makhopadhyaya 1983).
Mo plays a role in the suppression of pre- and postharvest sprouting (Cairns and Kritzinger 1992). This is biochemically novel in that it involves Mo in hormone synthesis or regulation. Sprouting of grain, especially preharvest, is due to untimely rain on the mature crop. The role of Mo is apparently in stimulating hormonal biosynthetic pathways that may have no direct link to pathways leading to disease resistance. Even so, the greater resistance to sprouting in Mo-sufficient plants may be expected to be associated with less postharvest losses from pathogens while in storage.
Fungal and, to a large extent, bacterial diseases are often reduced with increased Mn availability (Huber and Wilhelm 1988). The presence of the glyphosate-resistant gene in corn and soybeans reduces the uptake and utilization efficiency of Mn and may predispose plants to disease (Dodds et al.2002).
There are several potential mechanisms of disease control with Mn. The involvement of Mn in carbohydrate, nitrogen, and secondary metabolism provides multiple opportunities for both direct and indirect effects of Mn on disease (Graham 1983; Huber 1989, 1991; Huber and McCay-Buis 1993). Direct effects on the pathogens include inhibition of growth, sporulation, replication, enzyme production, and toxin production. The effect of Mn on enhanced host resistance may be indirect, through root exudates that modify the rhizosphere environment or by modification of metabolic constituents required for pathogenic activity. Direct effects include enhanced production of inhibitory compounds (phenolics, phytoalexins) and physical defenses (callus formations, lignification). Mn activates important biochemical reactions in the host defense, such as production of phenylalanine ammonium lyase and the deposition of recalcitrant lignin and wall barrier materials (Burnell 1988).
Plants use Mn in the reduced form (Mn2+) which is available for plant and microbial uptake and internal transport. The presence of Mn-oxidizing fungi and bacteria in the soil or rhizosphere can increase disease, while Mn-reducing bacteria can decrease disease. Mn-oxidation is highly correlated with fungal virulence and disease.
Glyphosate even at minimal application rates has a devastating effect on Mn-reducing bacteria while at the same time has a stimulating effect, as high as a 500 fold increase, in fungal pathogens such as fusarium species that oxidize Mn. Mn-oxidizing microbes increase Mn oxidation rates in the soils by up to five orders of magnitude (Brouwers et al. 2000; Tebo et al. 1997). The function of Mn oxidation in fungi is thought to primarily involve the depolymerization of lignin, with chelated Mn(III) serving as the final redox mediator in the breakup of randomly assembled, enzyme-resistant polyphenolic structures that inhibit pathogen penetration.
In addition, Glyphosate chelates and immobilizes MN in the soil as well as in the plant to make it unavailable for use by the beneficial microorganisms and the plant physiological and enzymatic systems. Mn functions primarily as an enzyme activator including dehydrogenases, transferases, hydroxylases, and decarboxylases (Burnell 1988; Romheld and Marschner 1991). Many of these enzymes are involved in C and N metabolism. Fundamentally, Mn serves as an activator of several enzymes in the synthesis of important secondary metabolites that lead to the production of phenolics, cyanogenic glycosides, and lignin plant defense compounds (Burnell 1988).
Mn deficiency adversely affects yield, photosynthesis, and root growth and alters soluble levels of N, soluble carbohydrates, hormonal regulation, and the synthesis of secondary compounds such as phenols, lignin, chlorophyll, gibberellic acid, sterols, and quinines.
Mn is a crucial nutrient element in host resistance to disease and in disease interactions (Rengel et al. 1994).
Zn is required for the multiplication of every cell in animals, plants and microorganisms. Zn deficiency is the most common and widespread of the micronutrient deficiencies in plants (Cakmak et al. 1996; Crewal 2001). Zn plays a critical role as the catalytic center in hundreds of enzymes and other proteins (Coleman 1992; Rhodes and Klug 1993; Berg and Shi 1996; Auld 2001; Maret 2001; Thiele 1992; Gomis-Ruth 2003). Zn is the most prevalent metal in microbial enzymes, followed by Fe, Cu, Mo, Mn, Co, and Ni (Wackett et al. 2004). Zn enzymes are critical in the cycling of most major elements, such as H, O, C, N and S (Vignais et al. 2001).
Zn nutrition modulates growth, dimorphism, infectivity, and phytotoxin and mycotoxin production in pathogenic microorganisms. Zinc finger proteins are at the heart of the regulatory cascade for biosynthesis of the major trichothecene mycotoxins of F. sporotrichioides Sherb. and F. graminearum (Protor et al.1995; Matsumoto et al. 1999; Alexander et al. 2004).
There are by far more reported effects of zinc on fungi and fungal diseases than on any other group of pathogens. Zn has direct effects on fungal growth and secondary metabolism and indirect effects on host susceptibility. Zn deficiency impairs superoxide production, which is involved in a cascade of plant defense pathways against fungi and bacterial phytopathogens (Adams et al. 1995; Doke et al. 1996; Kawano et al. 2002).
Zn inhibits the production of the mycototoxin fusarium C by fusarium moniliforme. Mg2+ competes with Zn2+ and reduces uptake; Zn is primarily taken up as Zn2+.(Marschner 1985).
Combining a mixture of zinc and other heavy metals (Cu, Fe, and Mn) greatly increased the microbicidal activity of chlorine dioxide, used for the disinfectation of water, and improved control of F. oxysporum and Thieaviopsis basicola (Berk. & Broome) Ferraris (Cope et al. 2004).
Copper-based polyphenoloxidases catalyze oxidation reactions of plant phenols in cell walls involved in the biosynthesis of lignin and the formation of brown, melanotic substances (Marschner 1995). Copper deficiency results in a failure of lignin and secondary cell wall formation, which leads to severe or unexpected lodging in wheat and barley (Bussler 1981; Marschner1995). Reduced lignin and secondary wall formation leads to increased disease. Copper is a regulator of or an essential cofactor in various enzyme systems involved in the plant defense against infection, the production of antimicrobial compounds, and general disease resistance (Graham 1983: Graham and Webb 1991: Lebeda et al. 2001).
Only recently has a structural role in the cell wall been more formally established, which in itself identifies B as an essential element in the plant-pathogen interaction. B can also affect carbohydrate transport through the sieve tubes of phloem vessels, thereby acting in a somewhat nonspecific role in regulating carbon supply to both plant tissues and the pathogen. B plays a role in the regulation of phenols and lignification, quinines, and free radical production. With such wide-ranging effects on structural and metabolic defense mechanisms, one can easily see that B is essential in the host-pathogen interaction.
For pathogens able to penetrate the vascular system of the plant, a common symptom is a lower nutrient concentration in the shoot, which leads to deficiency. Fusarium and Verticillium are pathogens that invade vascular tissue and are generally confined to the xylem (Mai and Abawi 1987). B in the cell wall is structural, in forming borate cross-links to RG-II Monomers (Matoh et al. 1993) Boron's role of keeping Ca within the wall is equally important for maintenance of cell wall integrity and therefore reduced pathogenesis. According to Corden and Edgington (1960), calcium pectates do not form in the absence of B, and the pectic materials that form part of the cell wall and middle lamella are susceptible to hydrolysis by fungal pectic enzymes. If these pectic compounds are bound to calcium ions, cell wall materials are relatively resistant to maceration by fungal enzymes. B has long been associated with lignin biosynthesis. B deficiency may impair the polymerization of the monomeric precursors to lignin.
A role for B is in callose and lignin formation; plant response to pathogen challenge includes the strengthening of the invaded tissue by callose and lignin deposition, the production of phytoalexins, and the induction of the expression of defense-related genes (Osbourn 2001).
In B deficiency are seen an increased production of oxygen free radicals, such as the superoxide radical and hydrogen peroxide (Cakmak et al. 1995; Cakmak and Romheld 1997).
Also, the major nutrient of potassium (K) expresses resistance both to the pathogen(s) and also by assisting plants functions.
Maize stalk rots caused by Gibberella zeae disease were reduced by K application. Disease increased with high levels of N and low levels of K. (Warren et al. 1975). K-deficient plants are more susceptible than plants with adequate levels of K (Huber 1980) This indicates that K affects the host resistance more than it directly affects the pathogens.
While we address some specific minerals in this discussion, the real issue is the desperate need to remineralize our soils with ALL the required minerals ( at least 80 plus of them). We also need to get those minerals into balance one to another in the right ratios so that biology and plants have the vital resources to flourish and produce nutrient rich foods for higher organisms. Minerals drive physiological processes in all biology, all plants, all animals and humans. Disease in all forms and in all places is merely a natural manifestation that the required minerals and microbes are missing and life in whatever form is not healthy in that environment. Disease occurs due to a lack of mineral nutrition. Overpopulation of pathogens occurs because there are too few beneficial microorganisms in that environment to keep them in check.
We have depleted our soil minerals through centuries of poor farming practices. Our soils lack mineral content, balance and biological life. How can our soils give us health and life when they no longer possess them?
Current practices focus on only a few macro minerals. To compensate for the lack of trace minerals, an emphasis is placed on toxic chemical applications to kill pathogens on unhealthy, nutrient deficient crops. That lack of nutrition and chemical toxicity is what we harvest, what we feed our animals, and what we eat. There is your explanation for our poor production, failing health and escalating diseases. This system has been expressing signs of failure for well over 100 years, yet the companies that perpetuate this ‘failure’ philosophy say we need more N, P, K and stronger, more toxic chemistry to win the war on plant, animal and human diseases. That is a profitable industry, designed to expand on perpetual dependency and increasing revenue streams. The damages to soils, the biology, the minerals, plants, animals and humankind are not a factor in their quest for money.
The processes involved in reversing and eliminating the pathogens such as Fusarium graminear (Gibberella zeae) and F. culmorum that produce vomitoxin deoynivalenol (DON) in our cereal grains and corn are very much the same for other pathogens and toxins produced in other crops causing other problems in livestock and humans. Other minerals may take a more dominant role and promote other plant functions through different enzyme systems but the process is all the same. It is NEVER about one mineral being the ‘silver bullet.’ Every mineral relies on multiple other minerals to function and work properly. All minerals are interactive, so for life to be healthy and vibrant requires ALL the minerals in totality; not just a few. The same factors apply to biology.
Balancing ALL the minerals of the soil, aided by the proper biology in the right balances, is the only sustainable method for agriculture to provide healthy nutrient rich foods that sustain livestock and human populations into future productive healthy generations.
YOU WILL NEVER FIX BROKEN SYSTEMS USING THE VERY FACTORS THAT CAUSED THEM TO BREAK.
Do you need help controlling Vomitoxin in your crops? Call us, we can show you how!