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.