Jul 14, 2014
Today, I thought I'd share a set of photos from a herbicide symptomology demonstration that I conducted in fall 2013 for our UC Weed Science School (next scheduled for fall 2015) and more recently in spring 2014 for a training session with other UC Cooperative Extension personnel.
For those of you that work regularly with herbicides of different modes of action this may be old-hat. However, many of us who get questions about herbicide injury in the field don't get always get to see comparisons under controlled conditions.
A few definitions, caveats, and brief explanations of the attached slides:
- MOA = Mode of Action (or Mechanism of Action). Biochemical pathway or process that is affected by the herbicide. For more info go to the WSSA summary here
- PPI = preplant incorporated. Soil-applied herbicides. We sprayed the soil surface, removed the soil from the flats and mixed in a bag, returned the soil to the flats, then planted the garden seeds. Herbicides generally applied at about half of a "normal" use rate.
- POST = post emergence. Herbicide applied to the plant foliage after emergence. Generally applied at about half of a "normal" use rate.
- Please remember that this is a greenhouse demonstration conducted in very high organic matter potting media which can greatly impact the amount of herbicide binding and availability.
There were three main demonstrations plus a couple "bonus" demos.
- First, we looked at PPI (preplant incorporated) treatments. (PPI 1-10)
- Second, we looked at some of the same herbicides and some different ones applied POST (post emergence). POST 1-10)
- Third, we looked at one herbicide, chlorsulfuron, applied at a dose range from 1x down to 1/128x applied both PPI or POST to radish as an indicator species (bioassay species).
- For "bonus #1" we happened to have some hairy fleabane plants that were treated with above-label rates of glyphosate in the greenhouse. One row of plants is a resistant population and the other is susceptible to the herbicide. This set shows nicely the symptoms we often see from glyphosate drift or poorly timed applications.
- for Bonus #2, I wanted to show how herbicide dose, and route of exposure can greatly influence the severity of herbicide injury.
2014 Herbicide Symptomology WWG Demo 032514 for Blog
I don't want to belabor this too much, but here's a quick observation on each slide.
- Title slide. I've never been acknowledged for my catchy presentation titles. For good reason!
- PPI treatment setup and rates used - for you herbicide geeks. Trade names do not imply endorsement.
- PPI #1. Chlorsulfuron - mostly severe stunting and affected plants did not progress much beyond the cotyledon stage. Herbicide is registered on wheat, so that crop looks fine. Beans are also not very affected.
- PPI #2. Clopyralid is a phenoxy herbidie and shows very classic epinastic growth symptoms on most of the broadleaf plants but not the grasses. Look at the leaf cupping and stem twisting in particular.
- PPI #3. Bleaching herbicides like clomazone usually damage carotenoids which leads to chlorophyll damage and loss of color.
- PPI #4. Metolachlor symptoms are not very obvious here, mostly root stunting that is masked in this demo due to fertile soil and plenty of water.
- PPI #5. Like above, pendimethalin symptoms not particularly obvious. Would be root stunting but this is masked by the fertility and water. Also, the high OM soil probably tied up a lot of this herbicide.
- PPI #6. Trifluralin symptoms similar to pendimethalin; however you cans see how "pruned" the corn roots are on the inset.
- PPI #7. PPO inhibitors like flumioxazin would probably have had more injury applied on the surface rather than fully incorporated. However, you can see the burning of some of the affected plants as they translocate the herbicide into the foliage and excess energy from photosynthesis damages tissues.
- PPI #8 Oxyfluorfen, similar to flumioxazin, symptoms are probably weak due to incorporation and high OM soil.
- PPI #9. Bromacil is typically an "bare ground" herbicide for industrial areas for good reason! Affected plants emerge, then PSII inhibition and excess energy released from photosynthesis destroys tissues.
- PPI #10. Simazine is also a PSII inhibitor but has some selectivity on grasses (a sister compound, atrazine, is widely used in corn in some regions).
- POST treatment setup and rates.
- POST #1. Fluazifop is a grass-specific herbicide. Notice the corn plant in the foreground showing stunting and purple coloration as it dies. Hard to see, but the growing point at the base of that plant is very "mushy" and necrotic.
- POST #2. Chlorsulfuron again, this time POST. ALS inhibitors like this tend to start with chlorosis, especially of the newest leaves as this is where the greatest synthesis of new amino acids is needed.
- POST #3. Imazethapyr is another ALS inhibitor that shows similar symptoms but different selectivity to chlorsulfuron.
- POST #4. Glufosinate causing some chlorosis and necrosis of the really sensitive broadleaf species. My expectation is that the grasses would also have been injured at higher rates.
- POST #5. Trichlopyr is another phenoxy herbicide - look again for cupping, twisting and cracking. Can happened within a day or two. You could actually see the stem twisting on some plants within hours.
- POST #6. Glyphosate is pretty slow acting -7 DAT is early enough in the process that you can only see some general chlorosis in the corn in this photo.
- POST #7. Propanil is a PSII inhibitor used in rice. I think the rate or coverage was a bit low to see good symptoms here - the beans show some necrotic spots but I would have expected more burning on the margins.
- POST #8. Carfentrazone is a fast-acting, POST applied PPO inhibitor. You can see the rapid necrosis and discrete spots on most of the broadleaf plants. This herbicide is not translocated which is why coverage is so important for efficacy.
- POST #9. Paraquat is a PSI inhibitor. VERY fast acting in bright sunlight and you see the obvious necrosis on most species. Like other contact herbicide, coverage is key to control and you can imagine that many of these injured plant likely would have grown back in a few weeks because of poor coverage.
- POST #10. 2,4-D is a phenoxy and like triclopyr it causes rapid cuping and twisiting of stems and leaves in broadleaf plants with little to no activity on the grasses.
- Setup for dose-response rates and timing
- Shows the sensitivity of radish to chlorsulfuron - POST treatments injured radish at 1/128 of the field use rate (radish is super-sensitive) but the PPI treatments were less injured at the same low rates.
- Sublethal symptoms from glyphosate. Notice the leaf stunting, chlorosis, and "witches brooming" as the internodes are shortened
- Shows how herbicide dose, and route of exposure can greatly influence the severity of herbicide injury.
I like to tell people that as a college student, I learned WAY more about plant physiology after I started studying how herbicides affect and disrupt different physiological processes. Herbicides work in different ways and this can greatly impact the symptoms that you might expect to see from drift, carryover, or mis-applications. Good luck with your diagnoses of herbicide injury but remember that a lot of other biotic and abiotic problems can also cause symptoms that can be confused with herbicide injury.
Take care,
Brad