Ergopeptine alkaloid toxicosis in horses Ergopeptine alkaloids (EPAs) are toxic compounds produced by fungal organisms including Epichloë coenophiala and Claviceps purpurea.
Mare with new newly-born foal.
A microscopic fungus that lives on certain types of tall fescue grass can cause various reproductive problems in horses, especially late-gestation mares.
© 2016 by Sarah Ahrens
The first is an endophyte, a microscopic fungus that lives within the intercellular spaces of leaf sheaths, stems and seeds of certain types of tall fescue grass (Schedonorus arundinaceus (Schreb.) (Dumort.)), especially the infamous variety Kentucky-31. Endophyte-infected tall fescue is indistinguishable from endophyte-free varieties without microscopic examination and special staining.
The tall fescue endophyte produces primarily ergovaline and much smaller amounts of other EPAs. The highest concentrations are typically in the seedheads and the bottom- most parts of the plant. The alkaloids confer increased vigor to the plant by increasing resistance to drought, insects and other plant stressors.
In return, the plant provides nutrients to the endophyte. Claviceps purpurea (ergot fungus) is a plant pathogen and can infect the seeds and grains of a wide variety of small-grain forages (including oats, barley, wheat, rye and triticale) and grasses, including tall fescue grass.
Other commonly affected pasture grasses include bluegrasses, bentgrasses and redtops, bromegrasses, canary grasses, cocksfoot and orchard grasses, June grasses, love grasses, quackgrasses and wheatgrasses, ryegrasses, timothy and wild barleys, oats and ryes. Ergot-infected (ergotized) seeds form dark brown/black ergot bodies – also called sclerotia – in place of individual seeds.
Affected plants are easily identified by direct examination of the seedheads. Ergot fungus produces a wide variety of EPAs, predominately ergotamine, ergocristine, ergosine, ergocornine and ergocryptine. Ergot bodies/sclerotia generally contain much higher EPA concentrations than toxigenic endophyte-infected tall fescue.
Horses and other livestock can be exposed to EPAs via contaminated pastures or hay, processed feeds (especially pelleted formulations) and screenings from ergotized grains. It is important to note that although most mammals are susceptible to EPAs, the effects vary dramatically depending on the species.
Effects in horses (and probably other equids) are dose dependent and primarily affect reproduction. The most consistent signs are lactation abnormalities in late-term pregnant mares. Markedly decreased or absent mammary development and milk production can occur at relatively low EPA doses and may be the only clinical signs observed.
Common indicators of impending foaling, including rapid udder development (“bagging up”), colostrum accumulation at teat orifices (“waxing”) and increasing calcium concentrations of mammary secretions, are often absent or minimal with EPA exposure. This can lead to unexpected/unattended deliveries and consequently higher foal morbidity and mortality. Additionally, the lack of colostrum production can lead to failure of passive transfer and potentially sepsis in these foals.
At higher EPA doses, other effects can include prolonged gestation, placental thickening and edema, premature placental separation (“red bag”), dystocia, retained placenta, metritis and other reproductive abnormalities.
Foals continue to grow during prolonged gestation but fail to develop normally. They are typically large and gangly, with poorly developed muscle mass, an abnormally long, fine haircoat, overgrown hooves and sometimes prematurely erupted central incisors. The suckling reflex is often decreased or absent.
Nonpregnant mares exposed to sufficient concentrations of EPAs may not respond normally to seasonal photoperiod changes, leading to long spring transitional periods. These mares can experience irregular or prolonged estrus without ovulation. Increased incidence of early embryonic death has been reported following experimental EPA exposures. Therefore, it is recommended to withdraw any potential EPA sources from the diet of mares with a history of abnormalities in seasonal cyclicity, early embryonic loss and/or other reproductive abnormalities.
Unfortunately, there are no blood, urine, tissue or other tests in horses to diagnose excessive EPA exposure. Currently, the only reliable diagnostic test for EPA toxicosis is measurement of dietary concentrations.
Feeds and forages can be analyzed for ergopeptine alkaloids; however, “safe” or “nontoxic” concentrations have not been established in mares. Additionally, EPAs can have effects long after dietary exposure has ceased, and ergovaline concentrations in toxigenic endophyte-infected tall fescue can fluctuate week-to-week; therefore, by the time a problem is identified and samples are collected, measured concentrations may not truly reflect exposures.
Also, different laboratories use different analytical methods and may report in different units, which makes comparisons between results from different labs impossible. The same is true for interpreting “relevant” concentrations reported in the literature. Finally, some mares appear more sensitive than others. Lactation abnormalities have been reported in individual mares at relatively low dietary EPA concentrations.
There are very few other causes of lactation abnormalities; EPA toxicosis should always be considered in these cases and the diet evaluated carefully. If tall fescue is not a component of the diet, particular attention should be paid to potential sources of ergot fungus.
Ergopeptine alkaloids, regardless of source, can cause various reproductive problems in horses, especially late-gestation mares. Dietary EPA concentrations in these animals should be kept as low as possible by minimizing exposure to potential sources including toxigenic endophyte- infected tall fescue and ergotized pasture grasses, hay and grain.
Press release by Megan C. Romano, Dip. ABVT Clinical Veterinary Toxicologist UK Veterinary Diagnostic Laboratory Department of Veterinary Science