Pesticides (insecticides, miticides, fungicides and bactericides) are still the primary means of managing arthropod (insect and mite) pests and diseases (fungi and bacteria) in greenhouse production systems because they are easy and convenient to apply, and generally very effective. Many facets of greenhouses favor pest and disease population growth, including environment (e.g. temperature, relative humidity and photoperiod), cultural practices (e.g., watering and fertility) and a continuous food source (lots of plants in the greenhouse that are spaced close together). Consequently, greenhouse producers apply pesticides to prevent or minimize plant damage. However, the continual reliance on pesticides promotes the development of pesticide resistance in insect/mite pest and disease populations.
This is the third article in a series of six scheduled for publication in 2019 and 2020 associated with pesticide resistance and resistance management of arthropod pests and diseases. In this article, we discuss the arthropod pests and plant pathogens that are more predisposed to develop resistance to pesticides.
Resistance develops at the population level and is an inherited trait with surviving individuals passing traits (genetically) to their offspring (young) or next generation, thus enriching the gene pool with resistant genes. Selection pressure for resistance increases as application frequency increases (number of times a pesticide is applied), and this is especially the case when pesticides with the same mode of action are applied in succession. Resistance can vary from one greenhouse to another based on pesticide use patterns. In addition, the prevalent movement of plant material globally can also impact resistance by exposing pest populations to pesticides with similar modes of action and transporting insects that have already acquired resistant traits.
In general, arthropod pests of greenhouse-grown horticultural crops are not predisposed to develop resistance, but the intense selection pressure placed upon pest populations as a consequence of the frequency of applying pesticides exacerbates the potential for the development of resistance. Most arthropod pests, including aphids, thrips, whiteflies and spider mites, have developed resistance to a wide range of pesticides in various chemical classes (organophosphates, carbamates, pyrethroids, macrocyclic lactones and spinosyns). In fact, more than 550 insect pest species have developed resistance to one or more insecticides over the past 50 years.
Many insect and mite pests encountered in greenhouse production systems have short developmental times and females have high reproductive rates, which can foster the likelihood of pest populations developing resistance. Below are the biological factors responsible for promoting resistance in insect and mite pest populations:
- short generation time
- multiple generations during the growing season
- high reproductive rate of females
- broad range of plants fed upon, which increases exposure to pesticide applications
- haplo-diploid breeding system. The male only has one set of chromosomes (haploid), so resistance genes are directly exposed to selection from pesticide applications. Consequently, this increases the potential for resistance developing
Insect and mite pests within greenhouse production systems can breed year-around, with many generations being produced and generations occurring simultaneously, which increases exposure to pesticides due to more frequent applications.
Furthermore, insect and mite pests within greenhouse production systems can breed year-around, with many generations being produced and generations occurring simultaneously, which increases exposure to pesticides due to more frequent applications. Pesticides are typically applied at short intervals, although this depends on the pesticide and residual activity (persistence), and a certain number of individuals may not be exposed to a pesticide application. These surviving individuals are likely to be resistant and will breed with other surviving resistant individuals resulting in the production of a population of highly resistant individuals — consequently, a pesticide-resistant population has been selected.
Another problem is that localized or isolated insect or mite pest populations may develop resistance faster than mobile arthropod pests. The reason is that the intense selection pressure associated with the frequency of applying pesticides reduces the number of susceptible individuals that can breed with resistant individuals. This is especially true in most greenhouse situations where there is not a continuous influx of susceptible individuals entering greenhouses from outside throughout the growing season.
Plant pathogens, like fungi and bacteria, can become resistant to fungicides and bactericides. They differ in some ways from insects and mites in that they cannot move on their own. That means that when a population becomes resistant to a fungicide, the population will not spread from a single crop within a greenhouse or between greenhouses, or especially from state-to-state. However, we make up for that lack of mobility by obtaining propagative materials from many sources worldwide and then selling our plants all over the world. This means of spread of resistant populations is the main way we create a resistance incident in one operation a worldwide problem in short order. We are a very effective vector in our own right.
The pathogens that are most likely to become resistant have certain characteristics like short reproduction times (for bacteria it can be 20 minutes). Thus, many generations are created quickly, making the chance of a genetic change higher, leading to the development of resistance. Another characteristic of fungi that makes resistance to fungicides possible, is the production of many, many, many spores. One good example is Botrytis blight. Resistance in some populations of Botrytis to SDHI fungicides (Fungicide Resistance Action Committee (FRAC) 7 — like those containing boscalid) have been reported on many crops including fruit trees, strawberries and most recently cut flowers. Other plant pathogens that can develop resistance very quickly include the downy and powdery mildews because they also produce lots of spores.
Sometimes resistance develops because there are very few effective products that can be used for a specific disease and the products represent only a few FRAC groups. The bacterial pathogens are primarily controlled with copper-based products (FRAC M01) and historically antibiotics like streptomycin. When a crop is sprayed with copper or an antibiotic consistently and without alternation, resistance in the bacterial population can develop very quickly — sometimes in one season. This has been shown in Florida on a number of ornamental crops starting in the 1960s. Luckily, we have more choices today and can alternate copper with some of the biopesticides that contain Bacillus and certain plant extracts. These compounds are very effective and are often equal to copper bactericides, and also make excellent rotational partners.
At other times, the product works well and is relatively inexpensive, leading to its overuse. I believe this is what has happened with the FRAC 4 product containing mefenoxam (originally metalaxyl) and Pythium resistance. So many greenhouse producers relied exclusively on this active ingredient that resistance developed over 25 years ago. However, mefenoxam is still a viable choice for Pythium control when proper rotations are employed using multiple FRAC groups including FRAC 14 (etridiazole), FRAC 21 (cyazofamid) and FRAC 11 (strobilurins like fenamidone).
The nature of the products we employ currently for fungi makes resistance development more likely than when we primarily used broad-spectrum fungicides (sometimes referred to as a “shotgun approach”). For instance, products containing the active ingredients: chlorothalonil and mancozeb had multiple means of controlling the fungus by interfering with many different systems in the plant pathogen. It is still rare to see resistance to these active ingredients even though they have been used for more than 40 years. The narrow targeted products of today, like the strobilurins, sterol inhibitors (FRAC 3) and SDHI fungicides are predisposed to have fungi develop resistance since fewer changes or alterations in the fungal genetics are required. These products are better for the environment due to limited non-target effects but are also more susceptible to the development of resistance by plant pathogens.