Diseases
Researchers led by Ahmad Fakhoury, associate professor of plant pathology and fungal genetics at Southern Illinois University Carbondale analyzed soil samples from 45 soybean fields in Illinois, Iowa and Minnesota. They collected samples from symptomatic patches in fields and from adjacent areas where soybean sudden death syndrome (SDS) foliar symptoms did not develop. Fakhoury’s team compared microbial populations in the “healthy” and “diseased” soil to correlate the presence incidence and severity of SDS. 
Resistant soybean varieties have helped farmers manage soybean cyst nematodes (SCN) for decades. Almost all SCN-resistant soybean varieties possess the same resistance genes, from a soybean breeding line called PI88788.

Recently, Iowa State researchers analyzed 25 years of data, from tens of thousands of four-row variety evaluation research plots, to look for long-term trends. The results, published in the scientific journal Plant Health Progress, showed a breakdown of resistance in SCN-resistant varieties. 

“This is an alarming trend and sets the stage for even greater yield loss from SCN in the future,” Gred Tylka, Iowa State University nematologist said. | READ MORE
Wheat is an important crop in Canada, representing nine per cent of total farm cash receipts in 2015, and averaging 16 per cent of crop receipts in Canada from 2011 to 2015, according to Statistics Canada. And Fusarium head blight caused by Fusarium graminearum is the most important wheat disease. Fusarium head blight also infects barley and is a problem in malt barley production. With increasing corn acreage in Manitoba, there is a greater incidence of ear rot caused by F. graminearum as well.

The first and worst epidemic in Manitoba was in 1993. Since then, Fusarium has slowly spread to new areas across the Prairies, and by 2008, it was commonly found in the Dark Brown and Black soil zones in all three Prairie provinces.

There has been an emergence of new Fusarium populations and shifts in existing populations since 2000. A possible cause is the accidental introduction of isolates from one area to another, or one country to another.

Fusarium head blight is a concern because of the mycotoxins that can be produced by the pathogens. Fusarium graminearum produces two toxicologically relevant groups of mycotoxins. These mycotoxins have major impacts on swine feeding, resulting in poor feed intake and poor growth. Swine feed intake is reduced 7.5 per cent for every one part per million (ppm) of deoxynivalenol (DON) found in the diet.

The first mycotoxin group is the Trichothercens, which includes DON and the acetylated derivatives such as 15-ADON and 3-ADON. The DON mycotoxin is very stable during storage, milling, processing and cooking and doesn’t degrade at high temperatures. The other mycotoxin group in the Trichothercens is Nivalenol (NIV) caused by F. cerealis. It is not a virulent but is 10 times more toxic than DON. This group could become a concern and we don’t have a good monitoring system for NIV.

The second major mycotoxin group is Zearalenone and its derivatives.

The current issues with Fusarium mycotoxins in the Canadian feed supply is that Fusarium pressure in Canada is widespread and may be increasing because of wet seasons that promote the disease. There is also the additional risk of mycotoxin exposure from new feed ingredients such as distiller’s dried grains with solubles (DDGS) that are corn or wheat based. There is an increased risk in livestock feed with DDGS, since DON concentrates in in DDGS by approximately three times.

There appears to be a shift in the pathogen population with 3-ADON becoming more prevalent. This is a concern since 3-ADON makes significantly more toxin that is also more toxic. The LD50 for swine with 15-ADON is 113 milligrams per kilogram (mg/kg) while it is 49 mg/kg for 3-ADON. Analysis conducted by Ward et al in 2008 found that 3-ADON was found in six per cent of Alberta samples tested, 11 per cent of Saskatchewan samples, and 39 per cent of Manitoba samples.

We have looked at genetic chemotyping of DON isolates. On winter wheat, we found 3-ADON accounted for 82.4 per cent of F. graminearum isolates in Winnipeg and 84.6 per cent in Carman, Man. At Melfort, Sask., 3-ADON accounted for 100 per cent of the DON population. Canadian Grain Commission samples of CWRS wheat in 2015 indicated a shift to 3-ADON in the Black and Dark Brown soils zones.

This shift to a greater prevalence of 3-ADON brings new issues in managing the disease because of the increased virulence of 3-ADON. And because of the higher toxin production, there will be new issues at the elevator, in DDGS feeding and at the trade level because of potential downgrading.

The accidental discovery of NIV producing isolates in winter wheat at Carman by Chami Amarasinghe at the University of Manitoba is also a concern. Five of 132 Fusarium isolates were found to be NIV. In these isolates, 65 per cent were identified as 3-ADON, 31 per cent 15-ADON, and four per cent NIV. The presence of NIV is a concern, since it is 10 times more toxic to livestock than DON.

The identification of NIV is a concern because F. cerealis and F. graminearum are very similar and difficult to distinguish from each other. Until 2012, NIV had only been detected in a few barley samples in Canadian grain. However, testing for NIV in Canada is not routinely conducted at grain mills or elevators.

Amarasinghe also investigated the possibility of masked mycotoxins in our grains. These mycotoxins are masked because their structure has been changed in the plant. This process occurs when plants detoxify DON by converting it to DON-3-Glucosides (D3G). Masked mycotoxins are also known as modified mycotoxins and can’t be detected by conventional chemical analysis. However the danger is that gut microbes in livestock digestive systems may be able to convert D3G back to DON.

Findings from Amarasinghe’s research showed Canadian spring wheat cultivars produced D3G upon Fusarium infection, and there were significant differences among wheat cultivars. The susceptible cultivars showed a lower D3G to DON ratio (less D3G content) compared to the moderately resistant/intermediate cultivars. She found the level of resistance might have an effect on the production of D3G during the infection.

Looking into the future, Canadian wheat production may be at greater risk of Fusarium infections. An increase of 3-ADON, the potential for NIV to establish, and masked mycotoxins in our grain may be food safety issues. Additionally, with climate change, there is a possible threat of an increase in mycotoxins or having new mycotoxins such as the new NX-2 population establish.

Historically, in Canada we have seen shifts in the past. In the Great Lakes area, we saw a shift from ZEN to DON in the mid-70s, similar to the shift from 15-ADON to 3-ADON on the Prairies in the 2000s.

There are now some wheat varieties that have resistance to Fusarium in winter wheat and Canadian Spring wheat. Other classes also have varieties that are moderately resistant to Fusarium as well. These are important and should be considered as management tools.

This article is a summary of the presentation "War of the titans: The battle for supremacy in wheat-fusarium interactions," delivered by Dr. Dilantha Fernando, University of Manitoba, at the Field Crop Disease Summit, Feb. 21-22 in Saskatoon. Click here to download the full presentation.

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I work in Manitoba and we’ve been dealing with Fusarium head blight (FHB) for the last 25 years. In the 1990s, Manitoba started seeing severe infections. Those of you who are from Saskatchewan and Alberta, over the last two to three years, have definitely seen what it can be like when conditions are correct for Fusarium head blight infection.
Syama Chatterton discusses the incidence of Aphanomyces and Fusarium in Western Canada. 

Click here for the full summary of Chatterton's presentation.

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Mary Burrows discusses the emerging pulse crop diseases she has seen in her home state of Montana, and what this could mean for western Canadian growers. Burrows also discusses the important of seed treatment in fighting these diseases. 

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In 2016, we conducted field surveys for root rot of pea and lentil in Alberta and Saskatchewan. In Alberta we surveyed 27 lentil and 89 pea fields during flowering, and 67 lentil and 68 pea fields in Saskatchewan.
Montana has seen a spike in pulse crop acres in the last 10 to 20 years. When I started 10 years ago, my crop responsibilities included spring wheat, winter wheat, durum, and maybe a little barley. Now wheat is becoming a rotational crop for pulse production.
What I’d like to give you is a view from my previous careers working in Europe, New Zealand, and now Australia with regards to disease management. I’d like to give you a flavour of some of my impressions of disease management over the last 35 years with reference to getting the balance right with regard to the disease triangle and integrated disease management. 

Where are we in terms of integrated disease management (IDM)? What is IDM all about? Principally it’s about trying to make sure we use all the tools in the toolbox, integrating genetic resistance with chemical fungicides, cultural control and overall crop agronomy. When we sow the crop and how we look after it with nitrogen can profoundly affect how much disease pressure we’re under.

Getting it just right is never going to be easy. What’s happened in Australia? Before 2002, there wasn’t a huge amount of fungicide usage because it’s a much less responsive environment. Then we had an “exotic incursion.” Stripe rust came in from North America, probably on a grower’s boots. That changed the pendulum, from a dependence on genetic resistance to a reliance on fungicides, because, overnight, a huge proportion of all of the germplasm in Australia became susceptible to stripe rust.

Meanwhile in Europe, there was a totally different swing of the pendulum. It was inspired by a new set of varieties, in this case semi-dwarf varieties. With the new cultivars and more nitrogen, crops stayed greener for longer. Suddenly yields increased enormously in the ’70s. Higher yields and longer growing seasons in Europe drove growers to apply more and more fungicide. If you go to Europe now, it’s all about T1, T2 and T3 – Timing 1, Timing 2, Timing 3 with fungicides as a fixed part of crop agronomy. Up until 2005 in Europe, the pendulum had swung very much to the fungicide side of the IDM pendulum.

Slide 6
However, that’s all changed. In Europe, the profound driver for change has been fungicide resistance. Fungicide resistance influences everything that a European grower now does with fungicides. If there’s one thing that I think is really important to take on, it is that fungicide resistance – if it’s not affecting you now, it will be shortly unless you can moderate your use of fungicides.

What’s gradually happened over time is that we’ve got better products with greater activity, but at the same time fewer products based on limited modes of action. There are fewer products that are more and more environmentally benign, but at the same time at greater risk of resistance development. In other words, we’ve moved from multi-site fungicides that killed the fungus in many different ways to single-site fungicides that do less damage in the environment but actually are much more vulnerable to resistance.

Fungicide insensitivity and resistance
Fungicide insensitivity and resistance has occurred principally in two ways. In Europe in the late 1990s and early 2000s, strobilurins, such as pyraclostrobin and azoxystrobin, came along with the biggest media hype since glyphosate. However, after only three to four years, the pathogen causing powdery mildew and then Septoria tritici (now Zymoseptoria tritici) in wheat developed resistance to stobilurins, and that’s been a real challenge ever since. In two to three years, the strobilurins went from being the best products to control foliar diseases in broad acre cereals to products that wouldn’t work against Septoria, a disease that is widespread in northwest Europe. I think that’s when attitudes really changed and people started asking the question, “Is there a different way to control disease?”

Slide 16
We’re in our infancy with fungicide resistance issues in Australia. We can see it in the field with powdery mildew in barley. Our triazole fungicides such as Tilt (propiconazole), Folicur (tebuconazole), Proline (prothioconazole), Prosaro (prothioconazole and tebuconazole co-formulated) don’t work as effectively to control powdery mildew. With Septoria, we’re not yet seeing reduced activity in the field, but the samples are showing insensitivity in the laboratory, so there is increasing threat that we will see resistance to fungicides in the field. 

Europe and triazole use
What has happened in Europe with the triazoles over the last 20 years is that triazole fungicides have gradually become less effective against key diseases, firstly not working as effectively in the lab and then gradually being noted to be less effective in the field. That’s why with triazoles I think it’s important to talk about “fungicide insensitivity” and not “fungicide resistance.”

For example, it’s taken 20 years of exposing the Septoria pathogen population to the triazoles for them to become less effective. They still have activity but are now only 60 to 70 per cent effective when it used to be 90 to 100 per cent. So in Europe the triazoles and the strobilurins become less effective and ineffective for key diseases in a similar time period, but the triazoles had been gradually degrading in their effectiveness over time. 

Therefore with the terminology we use, I think it’s important to recognize we really have three basic modes of action that we use in broad acre cereal disease control – triazoles, strobilurins, and the new SDHIs [succinate dehydrogenase inhibitors].

With the triazoles I think it is probably more appropriate to call it “insensitivity” rather than resistance, since if you say to a grower, “It’s resistant,” the tendency is to think that it won’t work when in reality it is still partially effective.

With regard to the SDHIs, they’re not actually that new since the family of chemistry has been around for 40 years. But a new branch of SDHI chemistry is now taking Europe by storm, as the strobilurins now have less application because of resistance in key pathogens. But after only three years of commercial use with these new SDHIs, resistance is developing quickly in the net blotch and Septoria pathogens.

It’s really important to recognize that fungicide resistance is changing the way in which growers and advisors elsewhere in the world manage their cereal crops. In Australia, growers and advisors are just beginning on that resistance journey. You’ve already had some exposure in Canada to the fact that the strobilurins are at high risk of resistance development in the pathogen.  It begs the question, “What can you do about it?”

Click here for part two: The importance of multiple modes of action and linking pathology with crop physiology.
Nick Poole discusses what lessons farmers in Canada can learn about fungicide use from Europe, Australia and New Zealand, and what we can do to avoid fungicide resistance.  

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[Miss part one? Click here]
Importance of multiple modes of action

I’m horrified to hear that you can apply straight strobilurin fungicide to your crops, since there’s no other mode of action in the application to protect you from pathogen mutants that might be strobilurin resistant. If you went back to when the strobilurins were breaking down to Ascochyta in some of your pulse crops, it’s worth asking yourself, wouldn’t it have been better to have been using them in combination with other older multi-site fungicides in order to give the strobilurins a degree of protection? 

What’s now happening in Europe is that there’s a lot of dependence on the triazole fungicides since there is widespread resistance amongst a number of pathogens to strobilurins and increasingly to SDHIs. However it’s not the same with all pathogens. For example, the rusts – stripe rust, leaf rust – seem particularly stable. But with the necrotrophic diseases such as Septoria, such as net blotch, such as scald, populations are shifting. That stated, the triazoles remain the backbone of disease management programs all over the world.

It’s actually becoming more complicated for advisors in Europe. What’s happening is that different regions in Europe have different pathogen populations that are differentially susceptible to triazoles. What researchers are finding is that the triazole that works best in one area of Europe might not be the triazole that works best in another.

Now I know what you’re thinking: aren’t triazoles all from the same family of chemistry with the same mode of action? That’s where the resistance to these molecules is more complicated. For example, in one region, Folicur might not work very well on the Septoria pathogen, but a Tilt still does a reasonable job, depending on the history of fungicide use. Somewhere else in Europe, the exact reverse might be happening.

In Europe, they’ve set up a project called EuroWheat with 26 trials all across Europe examining triazole fungicides and their activity against key diseases, looking at not only what’s happening in the field in terms of foliar control, but then taking samples for lab analysis. It’s revealing that the pathogen is adapting in different regions differently, depending on what fungicides have been used, particularly the Septoria population. 

We are now beginning to see the same thing with Septoria in Australia. Some products that are effective on the mainland of Australia don’t work well in Tasmania. 

What can we do to protect fungicides going forward? We can minimize our use of them. Pick the best adapted, highest yielding, and most resistant varieties we can use. Such a choice might enable you to use just one fungicide application instead of two applications. In some parts of the world, there are guidelines advising using that active ingredient just once in a growing season. But probably the strongest message that comes out around the different regions of the world is the one about mixing different modes of action in cereal crops. 

So think about fungicides as part of that integrated disease management package – use them, but don’t overuse them. 

Across Europe at the moment, the new SDHIs are entering the market already mixed and formulated with a triazole in order to ensure the use of two modes of action in a fungicide application. “Make sure that you’re mixing different modes of action” is the strongest message that comes out of the scientific studies on fungicide resistance and it’s the one key take-home that I can give you. If you’re not mixing, ask why not.

There is one area that is important to clarify and that is with regard to fungicide rate and resistance. I don’t believe that there’s a lot of scientific evidence in the literature that suggests keeping fungicide rates high is a good anti-resistance strategy. Generally it is with herbicides, but I’m not sure that evidence exists for fungicides. Frank van den Bosch from Rothamsted in the U.K. did a literature search on 46 different fungicide studies and found there were more studies showing that increasing fungicide rate increased resistance selection pressure than the reverse. I think it’s more appropriate that we consider fungicide rate as an efficacy message, not a resistance message: i.e. what rate of fungicide is appropriate to obtain the best economic outcome. There are other things, like mixing our active ingredients with different modes of action, which are far more important in resistance management than considering fungicide rates.

Linking pathology with crop physiology
The other factor that is really important is linking our knowledge of pathology with crop physiology. Fungicides don’t only kill a disease, they keep plant leaves greener for longer, providing soil water is available to express the benefit of the disease free leaves. The upper leaves of the cereal crop canopy, particularly the top four, affect the ability of a plant to produce yield. In Australia, disease management strategies based on fungicides are particularly dependent on the presence of soil water to express the benefit of a fungicide both in terms of yield response and economic return. 

One of the things from Europe that I think they have right is that they talk all the time about “What are the key parts of the plant to protect from disease?” If you’re growing a cereal crop, what do the individual leaves on that cereal crop contribute to yield? That’s an incredibly important part of any strategy using a fungicide. We use fungicides to make money, not just control disease, and what’s been really good in Europe is actually characterizing which parts of the plant are best to protect from disease.

When it comes to thinking about fungicides, don’t only think about the disease. The time of disease onset in the crop will determine to which leaves fungicides are applied. In Europe, set development timings trigger the questions. “Do we have the disease? Are the conditions conducive for the disease? What’s this crop going to yield?” These are key questions that link the effect of the disease with the physiology of the crop.

Slide 29
slide 30
I think the key message when it comes to thinking about using fungicides as part of an integrated disease management package is to recognize that they’re not very effective at protecting tissue that’s not emerged at the time of application. Other than reducing overall inoculum in the crop, fungicides only directly protect the leaves and plant structures that are emerged at the time of application, so you need to target the most important leaves that contribute to yield.

The interaction of crop disease development and crop physiology is now a target for an Australian modelling team. In summary, it’s important to look at disease development and crop development together. 

I’d like to finish off with a reference to future developments. The Magnetic Induction Cycler (MIC) is about the size of a four-litre pail. From leaf samples using MIC, you can determine the genetic makeup of the pathogen population, determining not only the presence of genetic mutations that might affect fungicide performance but also the frequency of the population with that mutation. In the future this technology will assist the advisor in making the right product choice for individual paddocks. That technology moving forward could be linked with automated spore traps informing us when pathogen spores are moving into the paddock, their genetic makeup and how that’s going to affect product choice.

Lastly, I believe RNA interference technology has the potential to produce the next phase of environmentally-friendly fungicides. The technology is based on short segments of nucleotide that are absorbed into the plant and pathogen, and which can switch off the RNA messenger before it can synthesize the proteins for fungal development in that plant. It is very specific technology and offers some great potential for disease management in the future.
Dr. Gary Peng discusses the key management strategies for blackleg in canola and how farmers will benefit from the new resistant gene labelling. 

Click here for the full summary of Dr. Peng's presentation. 

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Blackleg is caused by two species of the pathogen. The major one is called Leptosphaeria maculans. The other one is a much less virulent species called Leptosphaeria biglobosa. For control of the disease, pathologists look at some of the weak links where we can apply most of the impact on the disease. The pathogen only survives on residues. If you don’t have a residue, it doesn’t survive well in the soil. That’s why rotation is important.

The pathogen produces a fruiting body in the spring called a pseudothecium or another type called a pycnidium. They produce spores that land on the cotyledons of canola. If you have insect damage from pests like flea beetles, the infection can be worse. With wounding, the pathogen can get into the cotyledon tissue even without moisture. From there the infection develops and you see the cankers at the base of the stem later on in the growing season.
Slide 4
Photo courtesy of Gary Peng.

There are three important things that can lead to an infection:
·      there’s residue to harbour the pathogen inoculum
·      you need to have early infection to get into the stem
·      insect damage may help the infection to occur more severely. 

The disease was very prevalent in the late ’80s, early ’90s. Then we introduced some resistant varieties in the early ’90s, which brought down the occurrence for many years. Partially that was resistance bred into varieties, but we also had three- or four-year rotations. That was a big part of the whole management effectiveness.

In the last five to six years, the disease incidence has been creeping back up to 20 to 25 per cent in Alberta and Manitoba, and about 10 per cent in Saskatchewan. However, the average severity remained below level 1 (light). Research by Sheau-Fang Hwang in Alberta indicates that in most years, this level of severity could result in a yield loss of about two to eight per cent on a susceptible variety. But from a trade perspective, our trading partners want to see the disease level trend going down.

Why the upward trend?
The first reason for an increase in blackleg incidence is likely the change of the pathogen population, which is adapting to the resistant varieties. The pathogen population may be becoming more virulent or with a greater proportion of virulent isolates in it. 

Plant breeders have used major gene resistance to control the disease. The resistant gene blocks the infection by the pathogen carrying the corresponding avirulence gene. For example, an Rlm3 resistant gene would block the pathogen with avirulence AvrLm3 gene (abbreviated to Av3). It might be like a lock-and-key, but for some reason, over time, the Av gene may change and the resistant gene may not be able to recognize it.

My colleague, Randy Kutcher, looked at the change in pathogen populations in 2007 when he looked at the avirulent gene prevalence on the Prairies. In his work looking at 800 isolates of L. maculans, the percentage of Av2 and Av6 genes were very high in the population, and the others at more moderate to low levels. Further work in 2010 and 2011 with Dilantha Fernando at the University of Manitoba found the picture had changed quite a bit. The presence of the Av3 and Av9 genes had decreased quite a bit, but at the same time Av7 seemed to be increasing quite a bit. That means the Rlm3 gene would be less likely to be effective across the Prairies because the Av3 gene had changed mostly to the virulent type. The Rlm3 gene was first introduced back in early 1990s and has been used for over 20 years.

Other research in Fernando’s lab also looked at what resistant genes are present in 206 varieties/breeding lines in Western Canada. The resistance gene that was predominantly found was Rlm3 in around 70 per cent of the varieties/breeding lines. There was also a bit of Rlm1 detected as well. Overall, the diversity of R genes is still quite limited in the germplasm tested. The important message is that Rlm3 is not going to remain effective on the Prairies because the corresponding Av3 gene is already fairly low in the pathogen population. 

However, when we looked at field data in Alberta and Manitoba, while the occurrence of other Av genes was high, disease levels ranged widely. This told us there was something else going on, which we called non-specific resistance in our varieties, although the effect was definitely less than the major gene resistance.

We further investigated this non-specific resistance in our varieties. We tested commercial varieties with a pathogen without a corresponding Av gene so any resistance observed would be due to non-specific gene resistance. Almost all the varieties had a slightly smaller amount of the disease on inoculated cotyledons than the susceptible Westar. At the same time, it’s a totally different kind of resistance reaction as opposed to the major gene resistance. It would not stop the infection completely – it just slowed it down a little bit, and on some varieties, substantially.

A further look at three of those varieties found the progress of plant mortality originated from cotyledon or petiole inoculation was somehow reduced, but varied between the varieties. Using a fluorescent protein gene labeled isolate, photography was able to show the reduced spread of the pathogen in the cotyledon compared to the susceptible Westar variety.

If you can slow down the movement from the cotyledon via the petiole into the stem, there may not be enough of the pathogen getting into the stem before the cotyledons drop off. This is one of the reasons that non-race-specific resistance works in some of those varieties we have.
SLIDE 22
Photo courtesy of Gary Peng.
Click here for part two: management strategies

This article is a summary of the presentation “Managing blackleg of canola in Western Canada,” delivered by Dr. Gary Peng, Agriculture and Agri-Food Canada, Saskatoon, at the Field Crop Disease Summit, Feb. 21-22, 2017. Click here to download the full presentation.

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Management strategies
The Canola Council of Canada is proposing a risk assessment chart. If you have a four-year rotation, likely your risk of having blackleg is very low. We know it’s effective, but I realize it isn’t always easy to implement. [Miss part one? Click here]

Scouting is important because it gives you a sense of your risk situation. There is an easy procedure that can be used to assess risk. After swathing, pull 50 plants, cut the stems at the base of the plant where blackleg develops and assess the damage to the stem. Use the pictorial guide I developed to assess the level of disease. If you don’t have any disease or very light disease, your variety might still be holding fairly well as long as you continue with longer crop rotation. But if you have an R-rated variety with a much higher disease level than you expected, your variety may not be holding up.

If you do want to switch varieties, try to rotate to another major resistance gene. We currently don’t have enough public information from seed companies to know what their resistance sources are. The Canola Council of Canada has proposed a new resistance labelling system to show the resistance gene labelling. It is voluntary and may start in 2018.   
Slide 25
Photo courtesy of Gary Peng.

If you don’t have any issues or major blackleg damage, there’s no urgency for you to switch between resistance groups right away, but it’s always a good practice to rotate them if you know the R genes. We understand 90 per cent of growers would rotate among the different varieties today mostly for weed management options. There is a similar principle in rotating varieties for disease management.

I want to also stress that we have quite a diverse pathogen population on the Prairies. In reality, over 90 races have been detected. That means with every known resistance gene, there is a different virulent isolate out there that would be able to overcome the resistance right away. We really need to consider, if we have different R genes available, rotation of those R genes. And we also need to maintain the non-race-specific resistance, which has been serving us relatively well.

What about fungicides?
Research on various fungicide products and application timings has been conducted. One involved 17 station years across the Prairies. We used four fungicide products, mostly the strobilurins and a triazole, and a combination of both active ingredients. We looked at applications at the two- to four-leaf stage, the bolting stage, and an application at both stages.  We also compared a susceptible variety with a resistant and a moderately resistant variety.

When we put all the data from 17 station years together, the early application of a strobilurin fungicide reduced the disease severity and also increased yield quite significantly compared to the non-treated check. The average disease severity was around about 1.5. The later application did not work, which makes sense because the key stage of infection is the cotyledon. 

We further looked at the data and divided it into two scenarios: those fields with much lower disease levels of around a 0.5 severity rating, and those with a disease severity of about 2.5. In the fields with low disease severity, the fungicide application did not provide any yield benefit. Where disease severity was about 2.5, a fungicide application at the two- to four-leaf stage reduced the disease severity significantly and also increased yield by seven bushels per acre compared to the non-treated check. 

However, these results were on Westar – a susceptible variety that was used to show the worst case when an R/MR variety is losing resistance. We looked at R/MR canola varieties at the 17 site years and found none of the fungicide applications were effective in providing a yield advantage (also indicating that the R/MR varieties have stronger tolerance to blackleg impact). That means if you have a certain level of resistance in your variety, in most cases the fungicide application would not provide a substantial yield benefit.

Where a fungicide treatment might come in is if the varieties you have been using are starting to show signs of an increased amount of blackleg. You should scout crops and assess the level of disease development over time. Also consider the length of the crop rotation and other risk factors outlined by the Canola Council of Canada. If you feel you are at high risk, an early application at the two- to four-leaf stage may be warranted.
Risk chart


This article is a summary of the presentation “Managing blackleg of canola in Western Canada,” delivered by Dr. Gary Peng, Agriculture and Agri-Food Canada, Saskatoon, at the Field Crop Disease Summit, Feb. 21-22, 2017. Click here to download the full presentation.

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Dr. Kelly Turkington discusses considerations to spray a fungicide, recommendations for Fusarium head blight in cereals and how to get the most out of your cereal fungicide applications. 

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