by Jesse Bussard

Now that you have a basic understanding of the origins of tall fescue and the endophyte which infects it from last week’s post, we can move onto the next part of my thesis: the mechanism of how this endophyte-grass relationship causes the declines in animal performance typically seen in grazing livestock.

Cattle grazing endophyte-infected (E+) tall fescue that are suffering from fescue toxicosis exhibit a number of symptioms including reduced growth or milk production, decreased feed intake, rough hair coat, elevated body temperature, increased respiratory rate, lower serum prolactin levels, excessive salivation, and reduced reproductive performance. Other noticeable behavioral changes include reduced grazing time and extended times in shade, mud holes, ponds, or streams.

The main driver behind this multitude of symptoms is compromised cardiovascular function linked to the presence of ergot alkaloids in the diet. Ergot alkaloids have been found to cause constriction of blood vessels in both extremities and interior tissues of animal’s grazing E+ tall fescue. This altered cardiovascular function leads to an inability to regulate body temperature and consequently a higher risk of heat stress during the summer months.

Research has also proven a reduction in blood flow to the gastrointestinal tract, which likely impede’s the animals ability to absorb nutrients, in turn causing the reduction in growth commonly seen in cattle suffering from fescue toxicosis.

As said previously, ergot alkaloids are the favored primary compound that induces the cardiovascular dysfunction. Vascular tissues contain receptors on the membranes of endothelial cells that line the inside of the vessel. These receptors act to moderate blood pressure and flow through the vessels in response to different hormone and neurotransmitter signals from biological chemicals such as norepinephrine (adrenaline), dopamine, and serotonin. Ergot alkaloids are structurally similar to these compounds allowing them to also interact with these receptors impairing vascular function through agonistic and antagonistic activity. Responses to ergot alkaloids vary across the body as the population of receptor sites changes across tissues and organs.

To put it simply, chronic, long-term exposure to ergot alkaloids in cattle grazing E+ tall fescue causes a sustained contraction in bovine blood vessels.  A majority of ergot alkaloids are metabolized and excreted in urine within 48 hours after cattle are removed from E+ tall fescue. Speculation would assert that with this rapid excretion of ergot alkaloids it could be expected that cattle finished in the feedyard after coming off of E+ tall fescue would not exhibit any carryover effects of fescue toxicosis in the final finishing period.

However, recent research has also found that over time ergot alkaloids can bioaccumulate in both vascular and fat tissues. Accounts from producers and researchers alike have also suggested a residual effect, noticing what seemingly looked like symptoms of fescue toxicosis, days after removal from E+ pastures.

To determine whether or not this occurs, to what severity, and what time length is necessary for ergot alkaloids to dissipate from receptors for normal vascular activity to resume, several methods have been developed to evaluate cardiovascular function and blood flow in cattle. Next week, I’ll discuss the two methods that I looked at in my graduate research and the pros and cons of each.

As always, if you have any questions or comments, feel free to leave a comment below or email me (pearlsnapsponderings@gmail.com). I’ll do my best to get you the right answer. Thanks for reading!