2012 Annual Report
1a.Objectives (from AD-416):
The overall objective of this research is to minimize economic losses from fescue toxicosis. Specific objectives include:.
1)development of plant germplasm that is both non-toxic and persistent, which could involve germplasm infected with novel endophytes or germplasm that is endophyte-free;.
2)development of management practices that improve animal performance and reduce effects of heat stress associated with fescue toxicosis in animals;.
3)further evaluation of fescue toxicosis effects on animal physiology and recovery from this condition; and.
4)identification of markers of animal sensitivity to heat stress and fescue toxicosis.
1b.Approach (from AD-416):
Tall fescue, infected with endophytes that do not produce animal toxic alkaloids, will be tested for animal toxicosis in feeding and grazing trials. Persistence of new germplasms will be measured in grazed pastures. Forage management practices will be developed to control and reduce toxicity of tall fescue. Endophyte-free germplasm with increased concentrations of plant proteins associated with nematode resistance will be tested for persistence. New approaches to monitor body temperature will be established and used to evaluate techniques for reducing heat stress. Treatments that promote healthy immune systems, like antioxidant activity and body temperature regulation, will be assessed for effects on severity of fescue toxicosis under field and in climate-controlled environmental chambers. Genetic and physiological markers of animal sensitivity to heat stress and fescue toxicosis will be identified to improve selection of animals that are more resistant to these problems.
Consequences of cattle consuming tall fescue infected with the endophyte (Neotyphodium coenophialum) are well known, including a reduction in feed intake and weight gain. In addition, the body temperature of cattle increases during summer months with exposure to heat stress. Less information is available about "real-world" adaptation to stressors such as heat stress and fescue toxicosis. Several studies were conducted using cattle in field and heat chambers to identify the components of physiological adaptation to heat stress and fescue toxicosis. Both heat-sensitive and –tolerant breeds were tested on uninfected pastures during summer months to look at heat adaptation. Interestingly, even the heat-tolerant animals showed increased respiration rate due to heat stress during mid-summer, albeit at a lower level than the heat-sensitive animals. Both groups showed signs of heat adaptation by the end of the week.
A study was conducted on exposure of Angus cattle to heat stress in environmental chambers. There was an increase in respiration rate in heat-stressed compared with non-stress cattle that remained elevated and unchanged for up to two weeks. In contrast, there was an initial increase in rectal temperature followed by an even greater rise under constant heat stress cycling similar to day/night temperatures. There was an initial heat-induced rise in sweat rate that decreased with time.
In another study, Angus cattle were maintained on endophyte-infected (E+) and uninfected (E-) tall fescue pastures for two months into mid-summer, then tested in environmental chambers, followed by return to identical pastures for another two months (late-summer) and retesting after this time. Feed intake and sweat rate were depressed in E+ treated cattle exposed to heat stress in the chambers with no change from mid- to late-summer periods, showing no signs of adaptation. In contrast, rectal temperature of E+ animals exhibited a progressively greater heat stress response from mid- to late-summer periods. However, this hyperthermia was similar to control cattle after a few days of heat stress. Likewise, respiration rate of E+ animals increased, and then quickly returned to that of control cattle after several days of heat stress, to suggest adaptation occurred. Despite evidence of thermoregulatory adjustment or an adaptation by the animal to these stressors, some thermal responses characteristic of fescue toxicosis (i.e., skin temperature) still showed increased sensitivity to a change in air temperature. Ultimately, the results of these studies identified changes in animal response to fescue toxicosis and heat stress that did not show signs of adaptation. They include depressed feed intake and sweat rate. Likewise, night core body temperature did not drop as low in stressed as control cattle, suggesting that the mechanism to dissipate heat was changed. In contrast, night skin temperature was lower in stressed than unstressed cattle, and was reduced even further with a reduction in ambient temperature to support the idea of persistent peripheral vasoconstriction and reduced blood flow. These results demonstrate that thermoregulatory and non-thermoregulatory responses to the combined stressors of heat stress and fescue toxicosis exhibit different long-term patterns of change. The development of genetic markers to identify animal sensitivity to these environmental stressors would be useful to producers to maximize production on tall fescue.