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Nutrition management for disease control

We have known how to prevent and reverse plant diseases with nutrition management for a long time. The information is not new, it has just been ignored or forgotten.

Fertilizers and trace minerals can be used to increase disease severity, or to reduce or eliminate disease entirely. Many fertilization practices today are known to increase disease. This knowledge should be foundational for every farmer and agronomist, but has largely been forgotten. Perhaps because it would eliminate the need for fungicide applications?

To illustrate how rich the literature is, here in as excerpt from the opening chapter of Soilborne Plant Pathogens: Management of Diseases with Macro- and Microelements published in 1989. For an up-to-date and more modern version I highly recommend Mineral Nutrition and Plant Disease.

Written by Arthur Englehard:

A large volume of literature is available on disease control affects provided by macro- and microelement amendments. Huber and Watson in 1974 in “Nitrogen Form and Plant Disease” reviewed and discussed the effects of nitrogen and/or nitrogen form on seedling disease, root rots, cortical diseases, vascular wilts, foliar diseases and others. They summarized work from the 259 references in four tables in which they list crops, diseases and citations. McNew in the 1953 USDA Yearbook of Agriculture discussed effects of fertilizers on soilborne diseases and their control. He reviewed briefly specific diseases such as take-all of wheat, Texas root rot, Fusarium wilt of cotton, club root of crucifers and common scab of potato. Many other diseases were mentioned, as well as how macro- and microelements effect host physiology and disease. Huber and Arny in “Interactions of Potassium with Plant Disease” summarized in three tables the effect of K (positive, negative, neutral) on specific diseases. They listed 267 references in the bibliography.

The Potash and Phosphate Institute is dedicated to research and education and celebrated his 50th anniversary in 1985. It is a source of information on the use of K and P in the production of plants and the effects on plant disease. The Institute promotes a systems approach to crop production; disease control is one of the factors in the system.

Leath and Ratcliffe described plant nutrition and diseases in forage crops production. They indicated that fertilizers affect pathogens in the soil and on the host, and also can affect the pathogenicity of an organism. Presley and Bird reviewed the effect of P on the reduction of disease susceptibility of cotton.

In 1983, Graham, in Australia in “Effects of Nutrient Stress on Susceptibility of Plants to Disease with Particular Reference to the Trace Elements” discussed under the heading “Macroelements,” the effect of six essential elements on disease; and under “Micronutrients,” seven essential elements and 15 others as having been reported to influence a host-parasite relationship. He gives 305 literature citations.

Another review by Huber entitled, “The Use of Fertilizers and Organic Amendments in the Control of Plant Disease” contains a wealth of information. He indicated how the severity of 157 diseases was affected by N in table 1. In table 2, a similar listing is given for nitrate and ammonium forms of N. The effects of P, K, Ca and Mg are given in tables 3, 4, 5 and 6 respectively. Tables for S, Na, Mn, Fe, Zn, B, Cu, Si and other elements are also presented.

A literature research of the CAB ABSTRACT database utilizing the DIALOG Information Retrieval Service and using some keywords: soilborne disease, macroelements, microelements, soil fungi, Fusarium, Pythium, and Phytophthora, yielded 1500 citations published during the past 14 years.

The Future

Obviously a virtual flood of literature is available regarding the effects of macro – and micro element soil amendments on the level of soilborne disease in plants. What is lacking is the correlation of the positive factors into integrated production systems. The biggest problem now is how to organize and comprehend the mountain of available and often conflicting data. We have entered an era in which computer-aided analysis and other sophisticated tools are needed to integrate information and develop systems approaches is to growing healthy, productive plants.

One of the most rewarding approaches for the successful reduction of soilborne diseases is the proper selection and utilization of macro- and microelements. Since virtually all commercially produced crops in the developed world are fertilized, it is extremely important to select macro- and microelements that decrease disease. This is an important and viable alternative or supplement to the use of pesticides which usually only gives partial disease control.

Remember, this was published in 1989. What other things have you heard about that deserve to be generally known, but aren’t?

Managing airborne diseases with nutrition

It is possible for plants to become completely resistant to disease when we manage nutrition well. On the surface, this sounds like a bold statement. When you dig deeper to understand the enzyme interactions and infection pathways of different infectious organisms, it becomes clear how nutritional imbalance is a foundational cause that allows these organisms to express themselves and produce active infections.

In this discussion, I ask Don Huber how to develop disease resistance to airborne pathogens. To dig deeper into this subject, the best reference book available is Mineral Nutrition and Plant Disease. It is a very inexpensive book for the money it can save growers.

John: You and I have spoken before about the capacity of nutritionally sound plants to become resistant to soilborne pathogens and organisms residing in the soil. We haven’t spoken about airborne pathogens, such as bacterial and fungal pathogens. How can we develop plants that are resistant to those organisms?

Don: You’ll see the same thing there. Pathogens are looking at the plant and they’re attracted to it as a food source―a nutrient source.

Also, some of them actually require specific nutrients in order to cause disease. Several of the rusts, for instance, require an exogenous source of zinc on the leaf―an available source of zinc―before the spores will germinate and produce an infection. If you don’t have exudation of those minerals on the leaf, those pathogens are much less severe because they don’t have that specific nutrient resource.

Now, some of the pathogens can change that nutrient availability. A lot of bacterial pathogens―black rot and some of those organisms that produce siderophores, which are essentially chelators to increase the solubility and availability of iron—you’ll see that those siderophores are able to actually cause a depletion or a deficiency of available iron in the infection site for plant functions―for energy relationships―that iron is involved in.

It’s important to maintain the availability for the plants, in spite of the siderophore production by the pathogen. If we can block that siderophore production, we block the disease-causing mechanism for that particular pathogen―that particular organism―whether it’s black rot or rust.

John: How do you block the siderophore production?

Don: We do that with some of the antibiotics that we use for bacterial disease control―whether it’s in humans or animals or plants. A lot of those are blocking siderophore production by the pathogen. You see that with fire blight on apples and pears and with black rot pathogens―Erwinia and Pseudomonas and Xanthomonas―that produce those siderophores.

We also block them nutritionally by compensating for the plant and keeping the plant’s metabolism and defense reactions fully active, so that in spite of what the pathogen is doing, we keep enough active and available nutrients for the plant that this doesn’t have an effect. The pathogen’s reduction is compensated for so that it can’t compromise the resistance of the plant.

John: It’s my understanding that many bacterial and fungal pathogens require a specific amino acid, or perhaps a general amino acid and carbohydrate profile, to be within the plant. When we change the amino acid profile, it’s possible to change susceptibility or resistance to some of these organisms, and that is one of the mechanisms by which different varieties are resistant or susceptible. Is that a correct understanding? Can you explain that a little bit?

Don: Yes, in part. The early fungicides that we used for apple scab, for instance, didn’t have any direct effect on the fungus. Their effect was changing the amino acid profile in the plant so that asparagine was no longer available or released onto the leaf surface. So the pathogen never had the essential amino acid it required for establishment and infection.

We see that with a number of amino acids. Certain amino acids will increase disease severity. Others will be a very strong inhibition of it. One of the techniques that I developed early on in my career was aminopeptidase profiling, where we could actually identify microorganisms just by their amino acid profile. When we had very difficult organisms to culture, all we had to do was run the aminopeptidase profile on that particular organism. Just with adding three or four amino acids to a little bit of sugar and minerals, all of those organisms that we had considered obligate, or very fastidious organisms, could be grown in a simple, well-defined culture media.

I’ve done that for the rusts and the mildew pathogens, as well as for many of the human pathogens. Wilford Lee has five patents for human pathogens―just patenting the media for their culture in the laboratory. I don’t know of any organism we have followed that system on, that we haven’t been able to culture in the laboratory so that we can do other studies. It was one of the grant proposals that Bruce Hemming and I had submitted to the Florida Citrus Foundation so that we could start getting information on control of HLB―greening disease on citrus. They could never get funding to do that.

Specific amino acids can be very inhibitory. That’s one of the things for the rusts and the mildews. Most people who have been trying to develop media for those obligate organisms want to make sure they don’t leave something out. The problem is that they throw everything in the mix except the kitchen sink, and one or two amino acids work every bit as effectively for some of those obligate pathogens in stopping their growth as any of our fungicides. That’s a very sensitive relationship.

It’s not a matter of making sure you have everything there―it’s making sure that some of those natural products and metabolites aren’t present to support the virulence mechanism of the pathogen. We see that with Fusarium and with a lot of the other pathogens―that nitrogen metabolism is very critical for them. One of the reasons you see shading controlling greening disease is that with shading you block photorespiration that provides those nitrogen intermediates for the pathogen.

2020-10-02T06:08:39-05:00October 2nd, 2020|Tags: , , , |

Insect and disease attraction to plants with reducing sugars

How is it possible for a high Brix plant to be resistant to insects and not provide them with an abundant food source when insects are attracted to sugars? The key insight is that plants contain different concentrations of different carbohydrates at various levels of plant health. The goal for optimal plant health is to have all photosynthates and soluble sugars such as glucose and fructose converted to non-reducing sugars in each 24-hour photoperiod. This means a healthy plant will have a high Brix concentration and very low levels of reducing sugars.

From the podcast interview with Don Huber.

John: Are there any negative health consequences of plants having high levels of fructose and glucose?

Don: Yes and no, depending on what other stresses there are present. If you have a deficiency of manganese, for instance, it can’t store the reducing sugars―glucose and fructose―that are being produced through photosynthesis. It can’t store them as sucrose, and so they become very attractive reducing sugars, and they become very attractive to insect pests and to a number of plant pathogens.

Manganese is a critical factor for that sucrose-phosphate synthase enzyme that converts glucose and fructose into sucrose for storage. If you’re deficient in manganese, you’ll have high reducing sugars―glucose and fructose. As insects like aphids fly over these plants, they can detect that high reducing sugar, and for them, it’s a red flag saying, “Hey, come in for dinner!” But if those sugars are converted to sucrose and stored there, you don’t see that attraction.

Reducing sugars come out of the root system―they’re the root exudates that are attracting Pythium and Phytophthora and Aphanomyces and those other oomycete pathogens―root-rotting pathogens.


John: Don, you described how the carbohydrate profile can attract aphids. Are there other insects that can be attracted by the carbohydrate profile?

Don: A lot of them are. I don’t know that all of them are, but many recognize the difference between the reducing sugars, and they don’t seem to be attracted to the non-reducing sugars nearly as much. You’ll see that association. When we get the minerals balanced for the plant, you’ll see all of those problems start to disappear or be very minor.

P.S. I appeared as a guest on The Modern Acre podcast in this episode.

The impact of soil carbon to nitrogen ratios on disease suppression

A foundational goal of regenerative agriculture management practices is to increase the volume of carbon that is cycled through soil systems. Not just statically stored in soils, but cycled through. The more volume of carbon that is cycled, the more robust the soil microbial community becomes, the more efficient plant photosynthesis becomes, and the better the entire ecosystem functions.

When more carbon is cycled in different forms, microbial balance and activity shifts to match, which results in changing the quantity of nitrogen that is sequestered, and the quantity of phosphorus, sulfur, silicon, and trace minerals that are released from the soil mineral matrix.

When abundant carbon is cycled, soil biology has the food sources required to fix all the nitrogen they require from the atmosphere, and no additional N needs to be added. This also results in a change of the dominant direction of N mineralization to be primarily nitrate or ammonium, which influences disease suppression and crop nitrogen sufficiency.

Here are some important thoughts on this topic Don Huber shared:

John: What is the impact of carbon-to-nitrogen ratios on both disease-suppressive soils and also on yield?

Don: The carbon-to-nitrogen ratio depends on the carbon source.

That got me in trouble with my first publication in plant pathology. I challenged the carbon-nitrogen ratio hypothesis. People were saying, “If you have a 12:1 versus a 40:1 ratio, you’ll always have a disease relationship.” And I demonstrated that it’s not the carbon-to-nitrogen ratio. It’s the form of nitrogen that is involved in that ratio.

You can take different crop residues or a different cropping sequence, and it’s the effect of that sequence on the form of nitrogen that determines what the disease reaction is. And, of course, the effect of that form of nitrogen quite often is an effect on manganese or zinc or copper or other nutrients, along with the form of nitrogen.

Carbon-nitrogen ratios work if you’re working with the same nutrient source or crop residue and then varying the nitrogen ratios by either harvesting plants when they’re greener or harvesting plants drier—when you have wider carbon-nitrogen ratios. But the carbon-nitrogen ratio per se isn’t the factor that’s involved there. It’s the effect of that ratio on the form of nitrogen and the other minerals that are involved—such as manganese or zinc or iron or copper—that are critical for particular physiological processes.

P.S. I had an interesting discussion with Koen van Seijen on the Investing in Regenerative Agriculture podcast that just released. Much of our discussion revolved around the question, “How would I invest a billion dollars in accelerating the adoption of regenerative ag?” You can find it here.

Nutritional integrity is needed to increase photosynthesis

We know it is possible to increase the quantity of sugars produced in each 24 hour photoperiod as much as three to four times higher than the baseline of what is considered ‘normal’ or common in most crops today. In addition, it is also possible to increase the ‘quality’ or the complexity of carbohydrates produced in each photoperiod. Plants with limited nutritional integrity produce lower volumes of simple sugars. Healthy plants produce much larger volumes of more complex sugars.

When the plant begins producing larger volumes of more complex sugars, the crop begins behaving differently. There isn’t a good way to describe this. Internode lengths become shorter, while growth is faster. Clusters of fruit or heads of grain have more kernels or fruit, and mature earlier. Very importantly, the crop begins contributing more carbon to the soil than it removes, even when 100% of the above ground biomass is removed.

Here are some thoughts Don Huber shared when I asked him about photosynthesis during our first podcast interview.

John: Don, one of the things I believe is quite important that we haven’t spoken about is the general impact of photosynthesis and the quality of photosynthesis—how photosynthesis can vary in crops and cover crops and how that influences the volume of root exudates. How can a grower increase the quantity of photosynthesis and increase the quantity of root exudates in the soil profile?

Don: You’re not going to have any photosynthesis if you don’t have manganese. Manganese is critical for splitting water; it provides the hydrogen that can then combine with carbon dioxide. You’re not going to have any photosynthesis without magnesium, which is part of the chlorophyll molecule. You’re not going to have a very efficient photosynthesis without iron and sulfur and all the other minerals, because your physiology is all tied together.

If you want to improve the efficiency of photosynthesis, the first place to look is mineral availability—having that system work. So, if you don’t have a backlog of sugar as fructose or glucose, you want that sugar to be stored as sucrose. That changes the osmotic relationship; it changes the overall physiology of the plant. You’re also not going to have any sucrose if you don’t have manganese, because manganese is responsible for your sucrose-phosphate synthase enzyme as a cofactor.

It’s a system that works together. If you don’t have sulfur, you won’t have enzymes, because most of your proteins are initiated with either cysteine or methionine—your sulfur amino acid. C4 plants have a more efficient photosynthetic pathway. They have PEP carboxylase, as well as rubisco enzymes—after the carbon dioxide from the air binds with the hydrogen that is split off of the water by manganese. So, you have C4 plants and C3 plants, and the physiology that’s involved—but all of them require the mineral nutrients. And any one of those deficiencies influences the overall efficiency of the whole process. 

Change ‘pathogens’ to ‘beneficials’ by changing the soil environment.

if the pathogens can’t bring about that compromising of the availability of manganese by converting it to an oxidized form, the fungus is essentially just a good saprophyte in the soil.

Don Huber describes for us once again that ‘disease’ organisms can only produce an infection in the correct environment. In a healthy environment, these same organisms develop symbiotic relationships with the plant. Our task as farm managers is to manage the environment properly, and crop ‘dis-ease’ vanishes.

You can listen to the entire episode here.

Don: A lot of your nutrient relationships—where you have microorganisms that are responsible for changing the valence states of various minerals so that they’re more available or less available. And you have those going on in both directions at the same time in some capacities. It’s an issue with manganese or iron or some of those things. Some of the secondary functions come into play so that all of that can take place and manifest in a very positive manner. Even though what you might be looking at—or the tests that you have—may not show the complete picture, you have to realize that it has to be going on, in order to complete the cycle.

And so, it’s a matter of either developing the techniques or understanding how all of those organisms interact—the ecological niches that make the system work. Everything isn’t just one big pool with somebody stirring the whole thing around. You really have a community of functions that are taking place at the same time, but you don’t have the same gas station at every corner or a grocery store at every corner. You have each one of those different functions taking place in its own little scheme of things. So the overall system is a very functional and very dynamic relationship relative to the plan. And it’s neat.

John: One of the pieces that you and I have discussed in the past is the challenge that we are seeing today with manganese availability. I would say that as much as 80 percent or more—perhaps even 90 percent or more of the crops that we work with today—come back showing inadequate levels of manganese. What are the major factors that contribute to that?

Don: Manganese has a very dynamic relationship with the soil, and also with many of the fungi. There are organisms—mycorrhizae—that increase the uptake of manganese, as well as zinc and phosphorus and some of the other nutrients. So, if they’re not functional, you miss that ability to absorb and to interact with a tremendous volume of the soil—where that mineral might be in short supply.

The other thing is that you have bacteria that are responsible for the valence state. You have the oxidizing groups. You have the reducing groups. The plant can utilize only the reduced form of manganese—the Mn2+ form. Mn4+ form is non-available, but we see it primarily in the soils that have high phosphate levels or high oxidative relationships—the manganese can be there and yet not be available for uptake. We see it with many of our pathogens, because the pathogens utilize manganese oxidation as a virulence factor.

We looked at several thousand isolates of Gaeumannomyces graminis, which causes take-all all over the world. We evaluated those and we found that there was one characteristic that was common in all virulent farms—manganese oxidation. If the wheat had oxidized manganese, it would never resist the disease. The same thing for rice blast. The same thing for isolates of Streptomyces scabies and a number of other pathogens. The ability to oxidize manganese to a non-available form—and to compromise the resistance of the plant to those pathogens—if the pathogens can’t bring about that compromising of the availability of manganese by converting it to an oxidized form, the fungus is essentially just a good saprophyte in the soil.

Same thing with many bacteria. So, we see these direct effects on mineral availability being involved not just in growth and quality and nutrient density, but also in susceptibility or resistance to disease. You have the virulence relationship of the pathogens with bacteria and fungi in the soil, and that’s related to those minerals that are necessary for the plant’s defenses. Those minerals are also directly related to the growth and resistance of the plants to those pathogens in their overall physiological function. It all fits together very nicely if the system is balanced—if it’s favorable.

And that’s one of the things that we can adapt to. When we’re farming, we’re really managing an ecology. It’s not a matter of a silver bullet for this problem or a stinger missile for another. It’s really a matter of having ecology work for us and support the plant. And if we don’t do that and we upset the system, then we compromise the overall quality and productivity potential we have in our soil.

John: You said that there are a number of pathogens that are dependent on manganese oxidation. And if they’re unable to oxidize manganese, they just become saprophytes in the soil profile. Are they dependent on that manganese oxidation directly—do they individually require it? Or are they just producing a manganese-deficient plant that is now susceptible to invasion?

Don: Both of those statements would be correct. They don’t necessarily need the oxidation. Some of them are also reducing organisms. In other words, if you change the environment—or if you change the association that they have with other organisms—then they may be strong reducing versus strong oxidizing organisms.

We see that especially with the Pseudomonads and a number of other organisms—you change the soil environment and they can benefit you, or they can be synergistic, or they can even be a direct pathogen, involved in compromising that resistance. The microorganisms use those minerals just like a plant does, or just like we do. Our metallo-nutrients, or strong transition elements, or electron transfer and physiological processes, are the cofactors for enzyme function. We don’t require very much of them, but if you don’t have that specific cofactor that’s involved for an enzyme, that enzyme isn’t going to do any work for you—it’s just another protein that’s sitting there. And about 80 percent of our proteins in plants are what we call metallo-proteins, where the metallo part is a cofactor. It’s a small part, but a very critical one, as far as function of that physiological pathway.

John: In essence, what you’re describing is that as long as plants have adequate availability of reduced manganese, they have resistance to all the diseases that you described.

Don: It would be very, very critical for that resistance—for the physiological functions in in the plant—without those minerals.

If you have read this far, you are welcome to join us for a webinar June 19th, at 11 AM EDT where we will discuss how to increase reduced manganese availability in soils.

2020-06-11T07:43:44-05:00June 12th, 2020|Tags: , , |

Oats, a very effective disease suppressive cover crop

Many have observed the plant performance improvements of crops being grown after oats. It is fairly common to observe not only an increase in disease resistance, but also a yield increase because of the increased manganese availability, which increases a plants (and animals) reproductive performance.

But there is another very important point hidden in this dialogue. Before crown rust was a significant challenge, oats did not have a reducing/disease suppressive effect. The plant secondary metabolite profile of oats changed once they were bred to be resistant to crown rust. This change in the metabolite profile resulted in a changed profile of root exudates, which converted a plant with a former oxidizing effect on the soil redox environment – a disease enhancer, to a reducing effect, or disease suppressive.

This means we need to consider the possibility that some plants which currently have an oxidizing effect, such as modern wheat, can be shifted to having a reducing/disease suppressive effect when we change the plant metabolite profile. We know we can change the plant metabolite profile significanly based on how we manage plant nutrition. Breeding is not the only pathway, and certainly a slower pathway, to developing crops which produce a disease suppressive microbiome.

From our interview:

John: You spoke briefly about the use of crop rotations and that 85 percent of the effect, in terms of disease suppression, happens from the prior crop or the prior cover crop. What are some particularly useful crops or cover crops that have a very strong disease-suppressive effect?

Don: Again, that’s going to depend on your disease and your overall soil biology. For instance, if you’re dealing with take-all, Gaeumannomyces graminis—the root and crown rot of cereal crops—you’ll find that brassica species have a suppressive effect. Perhaps the best cover crop overall is oats—another cereal crop. When we bred crown-rust resistance into oats, this also gave us an oat crop that provided disease control—take-all control—for our wheat and barley.

The reason is that crown-rust-resistant oats also produce a glycolcyanide root exudate that suppresses the manganese-oxidizing organisms. If you suppress the manganese-oxidizing organisms, you also suppress the manganese oxidation by the pathogen that is required for virulence. So you’ve increased the manganese availability for the plant—for its own resistance.

The shikimate pathway is a pathway that gives tolerance or resistance to take-all, because that’s where the lignotubers are formed. Lignification and callousing—all of those materials are produced through the shikimate pathway. And manganese is a very critical component in that pathway—at six or seven different steps in the pathway. If you inhibit the availability of manganese—if you have a good, strong mineral chelator that ties up manganese—you’re going to increase take-all, because you reduce the functional availability of manganese for the plant in its own defenses.

A plant like rye is very efficient in the uptake of manganese and other micronutrients. Rye takes care of itself with its resistance to take-all pathogen, but it doesn’t do anything for a subsequent crop. It does very well, with very little disease pressure, because it’s very efficient in taking up manganese and other micronutrients. If you have triticale, which is wheat-rye cross, if it doesn’t contain that section of the rye chromosome that is responsible for micronutrient uptake, then the triticale will be as susceptible to take-all as a wheat crop.

You don’t get a crop-rotation benefit out of rye like you do from oats. The root exudate of oats has a very strong antimicrobial compound against the manganese-oxidizing organisms that make manganese less available. You’ll see that effect—that change in the soil biology—carry on for two or three wheat crops after an oat crop. Subsequent crops will have very little take-all. Oats probably has the most dynamic effect in this regard.

Brassica species—canola or mustard—also produce quinolones and some other materials that have a similar ability to reduce take-all as the glycoprotein in oats. Following canola, you’ll see an increase in some of the other diseases. It’s not just influencing one particular disease. If you’re using Roundup-ready canola, genetically engineered canola—where you’re adding a very strong mineral chelator, because that’s how glyphosate works, by tying up those minerals in the physiology of the plant—if you’re growing Roundup-ready canola and applying glyphosate, it’s going to move out of the root exudates and change that soil biology. Then you may see a reduction in take-all, but you see a very dramatic increase in Fusarium root rot, as well as Fusarium head scab and the toxins of that particular plant pathogen. So, you’re changing the dynamics of the system with the particular management tools that you use. 

Managing soil borne pathogens

For soil-borne pathogens, there is no correlation between the presence of the organism in the soil and the expression of the disease in the crop. Infections severe enough to produce crop loss are correlated with the absence of suppressive organisms more than the presence of the pathogen.

Soil colonizing organisms are usually dependent on crop residue for nutrition and generally have higher nutrition requirements. Soil inhabiting organisms have much lower nutritional requirements and remain present in the soil more or less constantly.

Both groups can be effectively managed with cultural management practices to prevent any infections from occurring. From the podcast interview with Don Huber.

John: That’s a very impressive statement. We can manage disease and pathogenicity based on how we manage our soils, from a cultural perspective. That’s a very, very important perspective that I think we don’t commonly hear in agriculture.

You mentioned a number of different management tools: crop rotations, using cover crops, tillage, the impact of moisture, etc. Earlier you spoke of the differences between soil-borne pathogens and soil-inhabiting pathogens. It’s fairly well understood that we can use crop rotations to manage soil-inhabiting pathogens. Are you suggesting that it’s also possible to use these tools to manage and suppress soil-borne (colonizing) pathogens?

Don: Very definitely. Most of our soil-borne (colonizing) pathogens have very limited genetic resistance. We rely on those management techniques to control them. Sometimes we don’t recognize it as much as we need to, but soil-borne pathogens have a much more limited relationship as far as population dynamics. We may measure the population of spore load and other things for organisms like Fusarium, but the organism is there in a high-enough population that regardless of what we do—if we didn’t have the other organisms associated with it—it would take our crop.

Soil colonizers colonize only as long as they have a nutrient base to function with. So we can either extend the time between susceptible crops—which we typically do with most of our potato pathogens, for instance—we see them building up in two or three crops and we want to break that population down. Same thing with anthracnose on corn. It’s a soil colonizer. Cephalosporin on wheat. All of those organisms survive in the residue. Many of them even produce an antibiotic, so they slow down residue degradation to extend their lifetime in the soil—so that other organisms aren’t able to colonize that food base.

This is quite different from Rhizoctonia or Fusarium—many of the Basidiomycete-type pathogens are very excellent soil inhabitants. They don’t require the base of nutrients that many of our colonizers do.

We can produce enough food to feed 15 billion people with 30% less land with 1960’s tech, if we want to.

This quote from the podcast interview with Don Huber is powerful and important.

We were shooting for 400 bushels in 1979 and 1980, and now we’re struggling with 250 bushels.

John: Don, in 1979 you were producing 350-plus bushels of corn per acre in a biological soil ecosystem. Today, growers are struggling to produced 250 bushels of corn. We don’t even have a conversation about growing 350 bushels of corn on a commercial field scale. There are a few notable exceptions, but not on a large-scale production system. What happened with that knowledge? Where did it go? Why was it not adopted on a much broader scale?

Don: We started saying we had too much production. We needed to focus on different things. At our land grant universities, a lot of that research and the long-term commitments that breeding programs require for the expression of that genetic potential was closed out. Materials were just given to the private companies to develop their experiment stations.

The universities were happy to not have that long-term commitment. They could then respond to the political pressures, and their programs started being limited to three to five years—for the competitive grant programs on a federal scale. And most of our breeding programs were funded through the Hatch Program and the Smith-Lever Program, which would give the states a constant amount of money on a formula basis for those long-term agricultural developments, which are the reason why we have success in our agricultural programs. They were built on those long-term, continuous programs that were pretty much abandoned as we started looking at the bells and whistles in science rather than at the end product.

Again, we were producing more than we knew what to do with. I don’t know what we’d do with all the corn that we currently produce if we weren’t producing so much ethanol. I mean, that’s the way to use your crop: find a new market for it. Certainly, population growth is a long way from requiring our current production. We could produce enough food for about fifteen billion people with about 30 percent less land—if we wanted to really do that, if we really needed to do that—with the technology that we had in 1964.

We were shooting for 400 bushels in 1979 and 1980, and now we’re struggling with 250 bushels. But sometimes you have to reinvent the wheel. That part of the system was not considered important, and the resources were fractured. In a breeding program, you don’t just turn it on and off with each little whim or political idea that comes along. It’s a long-term program. When we turned all of that material over to the private companies, their interest was the bottom line. There’s a tremendous amount of material that could be manipulated. But as far as that long-term commitment, there hasn’t been any of that.

Genetic engineering certainly has not improved the long-term effects; you get the idea that we can do it all in a laboratory just by switching this system on or inhibiting this particular system. We forget that it’s still a system—an ecology that has to be managed—if any of it’s going to be of value to us. It’s a thought process that’s involved, as well as the necessity. But also, the desire—the innovation—drops out when you forget that you’re a part of a very dynamic, beautiful system that was all put together—when you start focusing on only one thing. Silver bullets may take care of a varmint, but they don’t provide stability in the system. 

2020-05-19T19:18:25-05:00May 20th, 2020|Tags: , , , |

How the form of nitrogen influences disease suppression

Nitrate and ammonium nitrogen have dramatically different impacts on soil biology and possible pathogens. Some pathogens are enhanced by nitrate and suppressed by ammonium. Others are the exact opposite. Most (but not all) soil-borne pathogens are enhanced by the presence of nitrate. This corresponds to the impact of reduced vs oxidized environments, since ammonium is the reduced form of nitrogen, and nitrate is the oxidized form of nitrogen. In general, reduced environments are very disease suppressive, and oxidized environments are disease enhancing.

I have had many discussion about this topic with Don Huber, inlcuding this one on a podcast interview.

John: What are the impacts of nitrogen and nitrogen applications on developing disease-suppressive soils?

Don: Most of your soil organisms are hungry for two things. One of them is nitrogen. The other is carbon. When you change either of those nutrients, you see tremendous stimulation of a lot of organisms in the soil, depending on what your source of nitrogen is.

One of their primary pathogens on a lot of vegetable crops in Florida is Fusarium oxysporum. It’s a vascular Fusarium. Growers can get pretty much complete control by using nitrate nitrogen and calcium. If they can stimulate nitrification, or if they apply nitrate nitrogen, potassium nitrate, or calcium nitrate—and also use some liming (lime = an oxidizer) to get their pH up—they have fairly effective control of Fusarium wilt diseases.

With tobacco, where we use fumigation to control some of the soil-borne diseases, you should have at least 30 percent of your nitrogen as nitrate nitrogen. If you don’t—if the plant is taking up all ammonium nitrogen—you can get into a carbon deficit because the plant detoxifies the nitrate or the ammonium nitrogen by combining with photosynthate from photosynthesis; that provides the carbon base for those amino acids. Then the nitrogen is translocated as the amino acid. If you don’t have enough nitrate nitrogen present to buffer against an ammonium source—if you’re going to get fumigation, because our soil fumigants tend to knock out nitrifying organisms—or if you don’t get nitrification there, it stabilizes in the ammonium form. It can be a drain on the carbon and the energy availability until that ammonium is detoxified and utilized by the plant.

John: I’m thinking about your description of how many soil-borne pathogens—soil-borne fungi such as Fusarium and Verticillium, for example—are dependent on oxidizing manganese and limiting manganese absorption by the plant. If that were the case, what would be the impact of adding ammonium to such an ecosystem—where you have a reduced form of nitrogen? What would the impact of the ammonium be on these soil-borne pathogens?

Don: On that group of pathogens, you will see a tremendous reduction in disease—with the ammonium nutrition. I wrote a chapter in one of the annual reviews on the impact of the form of nitrogen. You’ll see a tremendous benefit in different organisms by the form of nitrogen that the plant is predominantly supplied with. If you modify the environment so that those soil microorganisms make those conversions, you’ll see that the form of nitrogen will be available for the plant.

So, it’s important that you have both the management tools as well as the form. Most of our soil’s nitrification takes place very rapidly, so you need to do something to inhibit nitrification. We can do it biologically—we can modify the speed of that reaction so that we can increase the amount of nitrogen in nitrate or ammonium. When it’s taking ammonium nitrogen, you have a reducing environment. That reducing environment is favoring manganese-reducing organisms so that there will almost always be an increase in manganese availability for the plant—when you predominantly use an ammonium form of nitrogen. The more rapid, oxidative form is the nitrate source of nitrogen.

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