Use of different levels of ground endophyte-infected tall fescue seed during heat stress to separate characteristics of fescue toxicosis.

Studies of fescue toxicosis using whole seed diets show reduced feed intake and thermoregulatory ability, but much of the seed passes undigested through the animal. Cattle were fed ground tall fescue seed at different levels to potentially facilitate digestion and absorption of toxins and identify toxin sensitivity for major characteristics of the condition [i.e., hyperthermia, reduced feed intake (FI), reduced blood prolactin]. Steers (n = 18; 350 kg BW) were housed in the Brody Climatology Laboratory at thermoneutrality (TN; 19°C) and randomly assigned to daily diet treatments with either ground endophyte-infected [E+; low and high doses at 20 and 40 µg ergovaline/(kg BW/d), respectively] or endophyte-free [E-; control at 0 µg ergovaline/(kg BW/d)] tall fescue seed. After 12 d at TN, animals received 2 d of transition to heat stress (HS; 36°C daytime, 25°C nighttime) and maintained for 14 more days. Cattle were fed twice daily at 0800 and 1600 h, with water ad libitum. Feed intake was measured at 0700 h, with skin and rectal temperatures, and respiration rate at 0600, 1100, 1600, and 2100 h. Blood was sampled on selected days for prolactin and leptin determinations. Steers fed ground E+ diet decreased (P ≤ 0.0001) FI below controls at TN, with no dose effect. Maximum FI reduction with E+ treatment was 25% at TN, with an additional 46% decrease during HS (P ≤ 0.05). By the end of HS, E+ FI increased (P > 0.05) to that of E-, suggesting recovery. Prolactin was reduced (P ≤ 0.05) in high E+ cattle below controls at study end. Leptin blood concentrations were unaffected by E+ treatment (P > 0.05) but was reduced (P ≤ 0.05) by the end of HS. Pattern of rectal temperature response to HS showed a more rapid initial increase and decline for both E+ groups compared with controls (P ≤ 0.05). Skin temperature was the only variable that identified E+ dose differences. Although there were no treatment differences at TN, skin temperature was lower (P ≤ 0.05) for high E+ steers compared with controls during HS when air temperature was reduced each day. In general, FI was more responsive to E+ toxins than body temperature or blood prolactin, declining even at TN and exhibiting dynamic activity during HS. Although body temperature response to E+ toxins appears to stabilize during HS, this is misleading as rapid change in air temperature exposes effects on skin temperature.

Regional differences in sweat rate response of steers to short-term heat stress.

Six Angus steers (319 +/- 8.5 kg) were assigned to one of two groups (hot or cold exposure) of three steers each, and placed into two environmental chambers initially maintained at 16.5-18.8 degrees C air temperature (Ta). Cold chamber Ta was lowered to 8.4 degrees C, while Ta within the hot chamber was increased to 32.7 degrees C over a 24-h time period. Measurements included respiration rate, and air and body (rectal and skin) temperatures. Skin temperature was measured at shoulder and rump locations, with determination of sweat rate using a calibrated moisture sensor. Rectal temperature did not change in cold or hot chambers. However, respiration rate nearly doubled in the heat (P < 0.05), increasing when Ta was above 24 degrees C. Skin temperatures at the two locations were highly correlated (P < 0.05) with each other and with Ta. In contrast, sweat rate showed differences at rump and shoulder sites. Sweat rate of the rump exhibited only a small increase with Ta. However, sweat rate at the shoulder increased more than four-fold with increasing Ta. Increased sweat rate in this region is supported by an earlier report of a higher density of sweat glands in the shoulder compared to rump regions. Sweat rate was correlated with several thermal measurements to determine the best predictor. Fourth-order polynomial expressions of short-term rectal and skin temperature responses to hot and cold exposures produced r values of 0.60, 0.84, and 0.98, respectively. These results suggest that thermal inputs other than just rectal or skin temperature drive the sweat response in cattle.