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How Do Pecan Biofungicides Work?

We have made it through another winter, and the pecan trees are growing catkins and nut clusters as we impatiently wait to see who will be happy with their crop and who will wish they had more. The first crop estimate will take place this month. It has been a typical spring, with questions on pruning, training trees, grafting, fertilizer options, and of course, insects and diseases. Over the years, getting questions on pecan diseases in the spring is definitely more consistent than the weather.

When discussing plant disease management with growers, we generally discuss practices such as selecting the most disease-tolerant or disease-resistant pecan cultivars to plant in the orchard, level of fertilization, micro-climate modification, sanitation, and selection of the most appropriate fungicides to use in the orchard. Fungicides are typically considered a vital part of disease management because let’s face it, we often don’t perform cultural practices often enough or consistently to adequately control diseases. Resistant cultivars may not have been available at the time we chose to establish the orchard, or we chose susceptible cultivars based on their nut quality instead of their disease resistance, and it is easier to cover up our mistakes because proper fungicide use will control most diseases satisfactorily. Proper use means that we don’t treat our trees like they’re human (we typically wait until we are sick before someone drags us to the doctor to get medicine to cure the disease). Unlike human medicines, plant fungicides need to be applied before the disease infection occurs to be most effective. Fungicides are applied to protect new uninfected growth from attacking diseases. Relatively few fungicides are effective after pathogens have infected a plant. And those with “curative” properties are only effective a few hours to a few days after the pathogen has infected the tree.

Before we continue, let’s think about a native pecan grove before we started trying to manage the trees to maximize production. For decades and centuries, the pecans and diseases would be considered to be in equilibrium. Some years the disease is more prevalent and causes more damage, and other years the pecan matures a good crop with little disease damage.

Consider the endgame for the host and pathogen. The pathogen wants to infect the pecan enough to complete its reproductive cycle, but can’t wipe the host out of existence or it is over for the pathogen too. For the host pecan, it wants to expend only enough energy to keep the disease at bay, but still use the bulk of its energy to complete its life cycle and produce good seed for the next generation. For this example, the native pecans will sacrifice some crop to the disease, as long as they can maintain the capacity to reproduce. However, from a grower’s perspective, our goal is to maximize the trees’ yield and quality, while minimizing losses to the pathogen. We accomplish this by using elite cultivars, maximizing fertility, and altering the micro-climate to maximize plant growth while minimizing disease prevalence, often with the aid of pesticides.

We know that diseases and plants have co-evolved and history has recorded many serious disease outbreaks. From the Bible to other manuscripts, records show that rusts, mildews, and blights caused famine across large expanses of land. Everyone learns about the Irish Potato Famine (An Gorta Mór) in the mid-1800s and its impact on Ireland’s demographics, politics, and cultural landscape. Other commodities with severe disease issues over the years include powdery and downy mildew of grape, Panama disease of banana, coffee rust, southern bacterial wilt of tobacco, and black stem rust of wheat—to name a few. We know that diseases are a common occurrence in all crops, but before man got involved, how did plants protect themselves against pathogens?

Plants have evolved a variety of perception systems (special signaling pathways) to recognize the initial attack by a pathogen. Upon recognition of the threat, plants establish a broad-spectrum and long-lasting resistance, generally referred to as systemic acquired resistance (SAR), to protect themselves from the pathogenic invaders (Ryals et al., 1996).

Volumes have been published on SAR, so I will only provide an abbreviated overview. Working with tobacco mosaic virus, Ross (1961) coined the SAR term in reference to uninfected systemic plant parts becoming more resistant to a pathogen after a localized infection occurred on another part of the plant. While initial work on SAR was with pathogens, it has been proven that SAR can also be induced by avirulent pathogens, leading to resistance to a wide range of normally virulent pathogens, including bacterial, fungal, and viral pathogens. This SAR response is characterized by increased levels of the phytohormone salicylic acid (SA). SA controls plant defense responses through its receptor protein, NPR1. Upon binding with SA, NPR1 undergoes a conformational change allowing it to act as a transcriptional co-activator and to activate the transcription of pathogenesis-related genes, which play a role in plant immunity. Although several hormones are involved in modulating SAR, the presence of SA and the NPR1 protein are two absolute requirements for the induction of SAR in plants (Ward et al., 1991; Pieterse et al., 2009; We et al., 2012).

Another type of resistance (discovered in 1991), induced by beneficial (nonpathogenic) microbes, is termed Induced Systemic Resistance (ISR). Basically, ISR is an induced state of resistance in plants triggered by either a biological or chemical inducer, which results in the nonexposed plant parts being protected against pathogen attack in the future. Induced resistance is expressed not only locally at the site of induction but also systemically in plant parts that are spatially separated from the inducer. Generally, induced resistance confers an enhanced level of protection against a broad spectrum of attackers. The induced state of resistance is characterized by the activation of latent defense mechanisms that are expressed upon a subsequent challenge from a pathogen. Induced resistance is regulated by a network of interconnected signaling pathways in which plant hormones play a major regulatory role. The signaling pathways that regulate induced resistance elicited by beneficial microbes, pathogens, and insects share signaling components (Pieterse et al., 2014).

In Pecan South’s May 2020 issue, I discussed the eight FRAC groups of fungicides that are typically used in pecan orchards to control diseases. Those would include:

  • Group 1 – MBC fungicides,
  • Group 3 – DMI fungicides,
  • Group 7 – SDHI fungicides,
  • Group 11 – QoI fungicides,
  • Group 30 – Organo tin fungicides,
  • Group M3 – Dithiocarbamates,
  • Group P 07 – Phosphonate fungicides, and
  • Group U12 – Guanidine fungicides.

However, I did not discuss the fungicide groups that are classified with the following Modes of Action (MOA): P 01 – P 08: host plant defense induction, and BM 01 – BM 02: Microbial disrupters of pathogen cell membranes. Most of the fungicides in these groups are OMRI certified and often serve as the backbone of disease protection in organic production (Table 1). Since I had provided an example of a conventional spray schedule, I thought I should include an example of an organic schedule for disease control in a pecan orchard (Table 2) as well.

Table 1. Examples of fungicide products with classified Modes of Action (MOA) as host plant defense induction (P 01 – P 08) or Microbial disrupters of pathogen cell membranes (BM 01 and BM 02).
Trade Name


OMRI Approved


Target Site FRAC



Vacciplant Yes


Polysaccharide elicitors P 04
Regalia, Yes


Anthraquinone elicitors P 05
LifeGard WG Yes Microbial elicitors P 06
Agri-Fos, Confine Extra, Fosphite, Fungi-Phite DF, Kphyte 7LP, Plant Doctor, ProPhyt, Reliant, Resist 57 No Phosphonates P 07
Timorex ACT Yes cell membrane disruption, cell wall, induced plant defense mechanisms BM 01
Double Nickel 55, PlantShield HC, Serenade ASO, Serenade MAX, Serenade OPTI, Serifel, Tenet WP, Yes Competition, mycoparasitism, antibiosis, membrane disruption by fungicidal lipopeptides, lytic enzymes, induced plant defense BM 02

Adapted from the FRAC Code List, 2022.

What are Biofungicides?

Biofungicides are formulations of living organisms that are used to control the activity of plant pathogenic fungi and bacteria. Biocontrol microorganisms are free-living fungi, bacteria, or actinomycetes that are active in root, soil, and foliar environments. Depending on the microorganism, several modes of action are utilized including production of antibiotic substances, parasitization of other fungi, competition for resources with other fungi, and induced localized or systemic resistance in plants. The ISR response is initiated within minutes after application, but it will generally take several days to maximize the response.

Table 2. Example of a Fungicide Spray Schedule for an organic pecan orchard, all chemicals are OMRI certified.

Time Of Application 

Pesticide* (active ingredient) rate/100 gal water Group RATE/REI 
First Pre-pollination Spray: When leaves of disease susceptible cultivars are about 1 inch in length. Double Nickel 55
Bacillus amyloliquefaciens strain D747
BM 02


0.25-3.0 lbs./A
REI = 4 hours
Second Pre-pollination Spray: About two weeks after 1st spray if weather is warm and leaves are growing rapidly. Regalia
Extract of Reynoutria sachalinensis
P 05 1.0-4.0 quarts/A
REI = 4 hours
First Leaf and Nut Cover Spray: Two to three weeks after last spray. Often in early May. Serenade
Bacillus subtilis strain QST 713
BM 02 2.0-4.0 quarts/A
REI = 4 hours 
Second Cover Spray:
Cover sprays should be made at 2- to 4-week intervals. Two-week intervals are used during periods of frequent rainfall in orchards with very scab susceptible cultivars.
Timorex ACT
Tea Tree OilOrLifeGard WG
Bacillus mycoides
BM 01


P 06

13-35 fluid ounces/A
REI = 4 hours
4.5 oz/100 gal/A
Third Cover Sprays Regalia
Extract of Reynoutria sachalinensis
P 05


1.0-4.0 quarts/A
REI = 4 hours
Fourth Cover Sprays Serenade
Bacillus subtilis strain
QST 713
BM 02 2.0-4.0 quarts/A
REI = 4 hours
Fifth Cover Spray:
The last two cover sprays often made from late July through August can be eliminated if there is little scab on the nuts and rainfall is sparse
Extract of Reynoutria sachalinensis
P 05 1.0-4.0 quarts/A
REI = 4 hours

Sixth Cover Spray

Timorex ACT
Tea Tree Oil

BM 01

13-35 fluid ounces/A
REI = 4 hours

*Any reference to commercial products, trade or brand names is for information only, and no endorsement or approval is intended. Inclusion of a product here does not imply approval of that product to the exclusion of others which may be available. All agrochemicals/pesticides listed are registered for suggested uses in accordance with federal laws and regulations as of the date of printing. State regulations may vary. If the information does not agree with the current labeling, follow the label instructions. The label is the law.

Biofungicides will not cure a plant that is already infected by a pathogen and should be applied before a pathogen attacks the plant. Some cultural practices will help mitigate disease, such as the use of composts and suppressive growing medium, both of which contain beneficial microorganisms that can aid the plant in avoiding disease infection. Let’s look more closely at some of the ways that biofungicides work:

  • Rhizosphere Competence – The ability to colonize and grow in association with plant roots. Here they effectively compete with plant pathogens for nutrients, infection sites, and space. Competition for glucose in the soil is involved in disease suppression. Biofungicide organisms also metabolize seed and root exudates that normally stimulate pathogen germination or zoospore attraction. A commercial example is Double Nickel 55®, which is a strain (D747) of the beneficial rhizobacterium Bacillus amyloliquefaciens. D747 rapidly colonizes plant root hairs, leaves, and other surfaces, preventing the establishment of disease-causing fungi and bacteria.
  • Mycoparasitism – Parasitism is a relationship between two organisms in which one directly gains nutrients from the other. Mycoparasitism of biocontrol microorganisms includes directed growth, contact and binding, coiling of hyphae around the host fungus, penetration, and degradation. Production of cell wall degrading enzymes is almost always part of the process. A commercial example would be Tenet® WP, which uses multiple modes of action to suppress and destroy soilborne disease-causing fungi.
  • Antibiosis – Antibiosis occurs when one microorganism is negatively affected by secondary metabolites produced by another microorganism. The antagonism can be direct toxicity or inhibitors of growth or metabolism. One of the most common would be the production of antibiotics, such as streptomycin, produced by the actinomycete Streptomyces species. These antimicrobial products are produced at very low concentrations, and they are only locally distributed and have a short life span; therefore, their toxicological risks to humans are low. Actinovate® AG would be an example that is commercially available and labeled for both soil and foliar diseases.
  • Membrane disruption by fungicidal lipopeptides – Lipopeptides have been described to have (among others) surfactant, antibacterial, antifungal, antiviral, and cytotoxic properties. They often affect the integrity of membranes, and some can inhibit cell wall biosynthetic enzymes of fungi. These are the main compounds produced by Bacillus subtilis and are responsible for its biocontrol effect. Serenade® would be a commercial formulation to control plant pathogens.
  • Inducing Metabolic Changes – An important mechanism of biocontrol microorganisms is the ability to induce metabolic changes in plants that increase their resistance to a wide range of plant pathogenic fungi and bacteria. There are two main reported types of induced resistance: systemic acquired resistance (SAR) and induced systemic resistance (ISR). Both provide long-lasting resistance against plant pathogens but differ in the signaling molecules and pathways that result in such an increased state of alertness. As such, the induction of SAR is usually activated by pathogen infection and requires the signaling molecule salicylic acid to accumulate pathogenesis-related proteins. In contrast, ISR is triggered by beneficial microorganisms and usually does not rely on salicylic acid but is dependent on pathways regulated by jasmonate and ethylene (Pieterse et al., 2014).
  • Plant Growth Promotion – A final way in which these organisms act is through plant growth promotion. Beneficial root-colonizing microorganisms promote plant growth and productivity. Plant growth is improved by the microbes enhancing soil nutrient availability, supplying phytohormones, as well as triggering ISR. Many resistance-inducing fungi and bacteria promote both root and shoot growth in the absence of plant pathogens. They often play a critical role in organic matter recycling.

While researchers have found much information over the past couple of decades, there are still many unanswered questions concerning the proper use of biopesticides. Greenhouse research needs to be moved to the field to look at effectiveness in different soil conditions, environmental conditions, the impact of different agricultural practices, and selection of the optimum formulation, especially regarding long-term storage. What impact will regenerative soil practices such as increasing plant diversity of cover crops in orchards or high stock density livestock grazing in silvopasture have on soil microbial diversity and functioning? And consequently, what impact will that have on disease resistance and crop production? Can cultural management practices be used to customize the microbiome around a pecan tree, supplanting the need to use biopesticides in a native grove? While these are intriguing questions, there is a great deal of research to conduct before the answers will be revealed. Stay tuned.

Pieterse, C.M., Leon-Reyes, A., Van der Ent, S., Van Wees, S.C.M. 2009. Networking by small-molecule hormones in plant immunity. Nat. Chem. Biol. 5:308-316.
Pieterse, C. M., Zamioudis, C., Berendsen, R. L., Weller, D. M., Van Wees, S. C., and Bakker, P. A. 2014. Induced systemic resistance by beneficial microbes. Annu. Rev. Phytopathol. 52:347–375.
Ross AF. 1961. Systemic acquired resistance induced by localized virus infections in plants. Virology 14:340–58.
Ryals, J. A., Neuenschwander, U. H., Willits, M. G., Molina, A., Steiner, H. Y., and Hunt, M. D. (1996). Systemic acquired resistance. Plant Cell 8:1809–1819.
Ward, E. R., Uknes, S. J., Williams, S. C., Dincher, S. S., Wiederhold, D. L., Alexander, D. C., et al. (1991). Coordinate gene activity in response to agents that induce systemic acquired resistance. Plant Cell 3:1085–1094.
Wu, Y., Zhang, D., Chu, J. Y., Boyle, P., Wang, Y., Brindle, I. D., et al. (2012). The Arabidopsis NPR1 protein is a receptor for the plant defense hormone salicylic acid. Cell Rep. 1:639–647.
Author Photo

Charlie Graham

Charles J. Graham is the Senior Pecan Specialist at the Noble Research Institute. Noble Research Institute, 2510 Sam Noble Parkway, Ardmore, OK 73401; E-MAIL: