Effects of alkaloid exposure and environment on digestion, nutrient balance, and immune function in beef cattle
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Fescue toxicosis is a complex condition in cattle caused by the consumption of ergot alkaloids produced by the endophyte (Epichloe coenophiala) that infects tall fescue [Lolium arundinaceum (Schreb.) Darbysh.]. Observable symptoms of fescue toxicosis include decreased weight gains and impaired health status in growing cattle. These symptoms are the result of changes that take place at the physiological level in the animal. Endocrine imbalance, vasoconstriction, improper thermoregulation, metabolism regulation, and immune activity all reduce productivity and burden producers with reduced revenue. Multiple strategies have been implemented to combat fescue toxicosis with varying degrees of success. However, better understanding the biology behind fescue toxicosis is crucial for developing more effective solutions. Chapters 2 and 3 address the interaction of alkaloid exposure, via the use of a synthetic alkaloid (bromocriptine), and heat stress on the immune function, nutrient digestion, and energy balance of beef cattle. Cattle received injections of bromocriptine mesylate (Bromo) or saline (Con) and were housed in climate-controlled chambers at thermoneutral (TN; 19.5[plus or minus]0.26 [degrees] C; 10-d) before transitioning (2-d) to heat stress (HS; 27.2[plus or minus]0.26 [degrees] C nighttime, 34.5[plus or minus]0.26 [degrees] C daytime; 10-d). Respiration rate (RR) and rectal temperature (RT) served as key variables to measure changes in thermoregulation. Bromocriptine decreased (P [less than or equal] 0.01) serum prolactin levels and increased (P [less than or equal] 0.04) RR and RT in during TN and HS. Pro-inflammatory cytokine (TNF-[alpha], IFN-[alpha], IFN-[gamma], IL-1[alpha], IL-1[beta], and IL-17) concentrations increased to a greater extent during heat stress in BROMO steers (P [less than or equal] 0.03) than CON steers. Chemokine (MIP-1[beta], IP-10, MIG, RANTES) were greatest (P [less than or equal] 0.01) in BROMO steers during HS. Anti-inflammatory cytokines (IFN-[beta] and IL-13) were greater for Con steers during HS (P [less than or equal] 0.01) whereas IL-21 was greater for Bromo during HS (P = 0.01). Bromocriptine decreased (P = 0.01) the concentrations of IL-1-F5. Concentrations of IL-10 and LIF increased (P [less than or equal] 0.02) during HS. Digestion of OM was greater (P = 0.05) in Bromo steers and tended (P = 0.09) to increase for both treatments during HS. Digestion of NDF tended to increase (P = 0.07) in Bromo steers. Heat stress increased (P = 0.04) the digestion of NDF and tended to increase (P = 0.08) digestion of ADF. Nitrogen balance was reduced (P = 0.02) during HS. Oxygen consumption, CO2 production, or CH4 production were not altered (P [greater than or equal to] 0.36). Estimate of DE intake tended to increase in Bromo steers (P = 0.09). Similarly, ME intake was greatest (P = 0.02) for Bromo steers. The conversion of DE to ME was not different affected (P = 0.71) by treatment and was reduced (P = 0.05) during HS. Retained energy was not affected by bromocriptine or heat stress (P [greater than or equal to] 0.19). Bromocriptine mesylate and heat stress influenced immune response in beef cattle potentially affecting immune competency. Energy metabolism was minimally affected by bromocriptine and heat stress. Chapter 4 evaluates the effectiveness of an enhanced zeolite-based flow agent to bind ergot alkaloids and mitigate symptoms of fescue toxicosis. Digestion and N balance were not affected (P [greater than or equal to] 0.16) by treatment. Zeolite numerically (P = 0.16) increased fecal recovery of ergovaline. Serum prolactin declined over time (P [less than] 0.01). Serum prolactin was greater (P = 0.01) in steers fed E+Z. Following TRH infusion, prolactin was numerically greater (P = 0.11) for E+Z. Rectal temperatures and respiration rates were not affected (P [greater than or equal to] 0.89) by E+Z. Addition of zeolite-based feed additives had minimal impact on ergot alkaloid recovery and physiological markers associated with fescue toxicosis.
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Ph. D.