Behavioral and Physiological Alterations in Angus Steers Grazing Endophyte-Infected Toxic Fescue during Late Fall

Toxins (Basel). 2023 May 18;15(5):343. doi: 10.3390/toxins15050343.

Abstract

Fescue toxicosis is caused by grazing ergot alkaloid-producing endophyte (Epichloë coenophiala)-infected tall fescue (E+). Summer grazing of E+ leads to decreased productivity, associated impaired thermoregulation, and altered behavior. The goal of this study was to determine the role of E+ grazing-climate interaction on animal behavior and thermoregulation during late fall. Eighteen Angus steers were placed on nontoxic (NT), toxic (E+) and endophyte-free (E-) fescue pastures for 28 days. Physiological parameters, such as rectal temperature (RT), respiration rate (RR), ear and ankle surface temperature (ET, AT), and body weights, were measured. Skin surface temperature (SST) and animal activity were recorded continuously with temperature and behavioral activity sensors, respectively. Environmental conditions were collected using paddocks-placed data loggers. Across the trial, steers on E+ gained about 60% less weight than the other two groups. E+ steers also had higher RT than E- and NT, and lower SST than NT post-pasture placement. Importantly, animals grazing E+ spent more time lying, less time standing, and took more steps. These data suggest that late fall E+ grazing impairs core and surface temperature regulation and increases non-productive lying time, which may be partly responsible for the observed decreased weight gains.

Keywords: Epichloë coenophiala; fescue toxicosis; pasture behavior; tall fescue; thermoregulation.

Publication types

  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Animal Feed / analysis
  • Animal Feed / toxicity
  • Animals
  • Behavior, Animal
  • Endophytes
  • Ergot Alkaloids* / toxicity
  • Festuca*
  • Lolium*

Substances

  • Ergot Alkaloids

Grants and funding

This research was funded by a grant from the USDA, National Institute of Food and Agriculture (NIFA). Grant #67015-31301 to NMF.