Tall Fescue Revisited: Establishing Novel Endophyte Tall Fescue as a solution to Fescue Toxicosis

Dr. Matt Poore

Tall Fescue.  

It performs better than any other cool season perennial grass over most of the Mid-atlantic and Mid-South of the USA.   It can be stockpiled to provide winter grazing that can nearly eliminate the winter hay feeding season with good planning and help from mother nature.  While it is not well adapted to sandy soils, it is very well adapted to the loamy and clay soils that dominate the region.  It stands heavy grazing, is tolerant of drought conditions, and yields more than most other cool season grasses.  It also persists for longer than any other perennial cool-season grass, with many stands lasting indefinitely.   The fescue pastures at our place were planted in the 50s and persist today.  Long stand life is a serious economic advantage.  Within a few years of development at the University of Kentucky, KY-31 tall fescue was declared to be the “wonder grass” and promoted as the solution to forage problems in the south. 

So what‘s the trouble?   

The trouble is that Kentucky-31 tall fescue, the variety that was released in 1943 and that took the southeast by storm, is infected with a fungus that gives it this incredible advantage over any other plant it competes with.  The fungus that lives between the plant cells produces toxins known as “ergot alkaloids” that cause severe health and reproduction problems, and reduced growth in livestock.  Some cows, especially those from “heat tolerant breeds” tolerate the toxins pretty well, but never the less suffer from many of the same problems temperate cattle experience.  Some individuals within temperate breeds are clearly “intolerant” of toxic fescue as evidenced by very poor body condition, long hair, and generally poor health.  It is important to get bulls that are tolerant to fescue when you buy bulls, but where can you find bulls selected on toxic fescue? 

It is unfortunate that fescue was planted on so many acres before the discovery of  toxic fungus or “endophyte”.  We now know that this little fungus causes many of our most severe production problems.  The plant is so aggressive and successful that it now covers 35-40 million acres in the Eastern US and there are very good stands even on land that was never planted to fescue.  Droughts in recent years have increased the dominance of fescue in our region, and also increased the infection rate of individual plants in a pasture which increases the toxin levels.  The warming climate has resulted in fescue moving up the mountains to higher elevations, and also into more northern states that never had problems with it before. 

All said and done, fescue is now estimated to cost the beef industry $1 billion a year.  That is not a typo folks, it costs us $1 billion a year!  Let’s put that into perspective.  Another major problem in the beef industry is shipping fever more correctly called “BRD” (bovine respiratory disease).   BRD costs us $1 billion a year too, but BRD is considered by most to be a much more important problem than fescue is.  Why do you think that is?  I think it is because the losses from fescue come as money that never gets into your pocket (and the pockets of a hundred thousand other producers).  Your cows may “tolerate” fescue and still give you a 500 lb calf.  Also, your breeding rate might be 85%, and your incidence of weak calves, no milk, etc. may only cost you a few calves a year.  The truth is that those calves could weigh 600 lbs, your breeding rate could be 90%+, and you should have almost no losses due to weak calves or lack of milk.  The difference between the fescue problems and BRD is the lost value is something you really don’t realize you lost.  With BRD, a feedlot owner is looking down at a dead calf that they paid a lot for, and it is real obvious to them that the value of that calf was a cash loss.   

As we deal with our fescue problems across the entire region called the Fescue Belt we need to be aware of what it is costing us.  There are a number of ways we may significantly reduce the problems we have, but they all will take a lot more research and education to get them in place.  I am really excited about where we are in our studies with fescue, and both Clemson and NC State can claim to be making serious progress into figuring out the problem which will lead to real solutions 

How do these toxins work? 

Our current understanding is that fescue works through at least two major mechanisms.  The first is the effect on the brain through the hypothalamic and pituitary system, and then through the ovary where some of the hormones from the pituitary work.  We know that fescue toxins bind to dopamine receptors in the pituitary and inhibit the release of the important hormone prolactin.  Prolactin is important for the initiation of milk production, and may also be important for weight gain and hair coat shedding and growth.  The effects of fescue on the secretion of prolactin is quickly reversed when the toxins are removed from the diet.  Ergot alkaloids also appear to cause problems with the reproductive hormones including progesterone that is produced by the ovary in pregnant cows.  This system that is not understood nearly as well and is under investigation. 

The other major mechanism elicited by fescue is through the adrenergic system where the ergot alkaloids bind the beta receptors and cause constriction of blood vessels in the peripheral circulatory system.  This leads to the heat stress, the sloughing of tail switches and the loss of ear tips due to freezing.  The effect on the circulation is not quickly reversed and it takes several months off fescue before the blood vessels return to normal. 

One of the biggest negative effects of fescue is on the feed intake of the animal.  Growth rate and reproduction is directly influenced by intake, so many of the problems we see may be caused by that.  We don’t understand the decrease intake very well because there is not a clear reason to explain the large reduction in intake we see.  Recent work in Kentucky suggests that motility of the gut may be reduced by ergot alkaloids which may directly cause the reduction in intake.  Much more work is needed to understand that, but the more we know about the fescue the worse it looks. 

So, why not just kill the fescue off and replace it?  That does make sense in many situations, and on almost all farms in the fescue belt there should be a substantial percentage of acres in something other than infected toxic tall fescue.  Novel Endophyte Infected Tall Fescue (including Jesup-MaxQ, Bar Optima, Martin 2, Texoma, Lacefield, Tower, and Estancia) or warm season grasses (like bermudagrass, big bluestem, indiangrass, switchgrass, etc.)  make sense even without the toxin issue, so certainly we all should look at our forage system and diversify it away from fescue.  But, fescue has become established in many environments where we can’t possibly do away with it, or where producers just don’t have the ability or desire to fight it.  There is some terrain so difficult to traverse that killing and reseeding are just not options.  Also, it is a great grass for stockpiling, and the toxin levels decline a lot about Christmas time.   

The real solution to this problem is going to take replacement of toxic fescue with other forages on some acreage, improved genetic tolerance to toxic fescue in the cattle, and supplements and/or remedies that will  help alleviate symptoms of the toxins.  The good news is that currently the community of researchers and extension personnel working with fescue around the country have started working together to create a cohesive strategy for dealing with the problem.    

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