Postgraze assessment of toxicosis symptoms for steers grazed on toxic endophyte-infected tall fescue pasture.

A 2-yr pen experiment was conducted using 12 different crossbred Angus steers each year to determine if short-term changes in prolactin concentrations, body temperature, and vasoconstriction reflect recovery from fescue toxicosis after steers that previously grazed toxic endophyte (Neotyphodium coenophialum)-infected Kentucky 31 tall fescue [Lolium arundinaceum (Schreb.) Darbysh] are placed on nontoxic feed. Groups of 6 steers from toxic endophyte-infected and endophyte-free tall fescue grazing treatments were blocked by BW for assignment to pens as a randomized complete block design with 2 replications. Two environments were implemented by initiating the experiment on 18 August in yr 1 and on 8 September in yr 2 for durations of 30 and 21 d, respectively. Rectal temperatures were recorded, jugular blood was collected for assaying serum prolactin, and cross sections of the caudal artery were ultrasonically imaged at selected time points to evaluate temporal changes in the response variables. Rectal temperatures in steers on the toxic endophyte pasture treatment declined (P < 0.05) linearly over time in yr 1 and 2 and were similar (P > 0.10) to those on endophyte-free treatment on d 30 in yr 1 and by d 15 in yr 2. Prolactin concentrations in steers on the toxic endophyte pasture treatment showed curvilinear increases (P < 0.05) over time and were similar (P > 0.10) to steers on the endophyte-free treatment by d 15 in yr 1 and by d 10 in yr 2. Luminal areas of the caudal artery in toxic endophyte steers were less (P < 0.05) than those in endophyte-free steers across all dates in both years. Results indicated that rectal temperatures in steers after they are removed from toxic fescue may decrease over time, but temporal changes in rectal temperatures could be affected more by prevailing ambient temperatures than by actual mitigation of fescue toxicosis. Prolactin concentrations in steers after they are removed from toxic endophyte tall fescue can increase and stabilize in less than 2 wk, but alkaloid-induced vasoconstriction that causes a vulnerability to severe heat stress is not alleviated within 30 d.

Steer and pasture responses for a novel endophyte tall fescue developed for the upper transition zone.

A 2-yr grazing experiment was conducted with crossbred steers (8 to 10 mo and with initial BW of 304 kg ± 34 kg in 2008 and 277 kg ± 24 in 2009) to evaluate animal performance and pasture responses of a late maturing tall fescue [Lolium arundinaceum (Schreb.) Darbysh; KYFA9301] population infected with the AR584 novel, non-toxic endophyte (Neotyphodium coenophialum; NE9301) as compared with Kentucky 31 fescue infected with the common toxic endophyte strain (KY31), 'Jesup' MaxQ fescue infected with the AR542 endophyte (MaxQ), and endophyte-free KYFA9301 (EF9301). Treatments were assigned for seeding in 1.0-ha pastures in a randomized complete block design with 3 replications. Pastures were grazed from 6 May to 23 July in 2008 (76 d) and 2 April to 25 June in 2009 (84 d). Each pasture was grazed with 4 tester steers and put-and-take steers were used to maintain forage mass at 2,500 ± 250 kg DM/ha. Shrunk BW was taken at initiation and termination of grazing each year. Rectal and skin temperatures were recorded, and jugular blood was collected each year at approximately d 28, 56, and study completion. Forage samples were collected at 2-wk intervals for analyzing CP, IVDMD, ADF, and NDF. Responses were analyzed with mixed models, and preplanned orthogonal contrasts were used to compare KY31 with non-toxic fescues, EF9301 vs. novel endophyte fescues, and NE9301 vs. MaxQ. All steer responses were similar (P > 0.10) among the non-toxic fescues. Average daily gains and total BW gain/ha for the 3 non-toxic fescues were greater (P < 0.001) than for KY31. Rectal/skin temperatures for the 3 non-toxic fescues were less (P < 0.001) and serum prolactin concentrations were greater (P < 0.01) than for KY-31. Pasture carrying capacity was greater (P = 0.003) for KY31 than the 3 non-toxic fescues and was greater for EF9301 (P = 0.017) than the 2 novel endophyte fescues. However, stocking rates (kg BW/ha) at the initial and midpoint days of grazing were similar (P > 0.40) among endophyte-fescue combinations, but by the end of the grazing season, stocking rate was greater (P < 0.001) for KY31 than for the non-toxic fescues and was greater (P = 0.053) for NE9301 than for MaxQ. Results indicated that NE9301 is as effective as EF9301 and MaxQ in improving BW gain and alleviating fescue toxicosis and that NE9301 can provide greater carrying capacities than MaxQ in late June and July.

Assessment of vasoconstrictive potential of D-lysergic acid using an isolated bovine lateral saphenous vein bioassay.

Vasoconstriction has been associated with several symptoms of fescue toxicosis thought to be alkaloid induced. Lysergic acid, an ergot alkaloid, has been proposed as a toxic component of endophyte-infected tall fescue. The objective of this study was to examine the vasoconstrictive potential of D-lysergic acid using a bovine lateral (cranial branch) saphenous vein bioassay. Before testing lysergic acid, validation of the bovine lateral saphenous vein bioassay for use with a multimyograph apparatus was conducted using a dose-response to norepinephrine to evaluate the effects of limb of origin (right vs. left) and overnight storage on vessel contractile response. Segments (2 to 3 cm) of the cranial branch of the lateral saphenous vein were collected from healthy mixed breed cattle (n = 12 and n = 7 for the lysergic acid and norepinephrine experiments, respectively) at local abattoirs. Tissue was placed in modified Krebs-Henseleit, oxygenated buffer and kept on ice or stored at 2 to 8 degrees C until used. Veins were trimmed of excess fat and connective tissue, sliced into 2- to 3-mm sections, and suspended in a myograph chamber containing 5 mL of oxygenated Krebs-Henseleit buffer (95% O2, 5% CO2; pH = 7.4; 37 degrees C). Tissue was allowed to equilibrate at 1 g of tension for 90 min before initiation of treatment additions. Increasing doses of norepinephrine (1 x 10(-8) to 5 x 10(-4) M) or lysergic acid (1 x 10(-11) to 1 x 10(-4) M) were administered every 15 min after buffer replacement. Data were normalized as a percentage of the contractile response induced by a reference dose of norepinephrine. Veins from both left and right limbs demonstrated contractions in a dose-dependent manner (P < 0.01) but did not differ between limbs. There were no differences in dose-response to norepinephrine between tissue tested the day of dissection and tissue tested 24 h later. Exposure of vein segments to increasing concentrations of lysergic acid did not result in an appreciable contractile response until the addition of 1 x 10(-4) M lysergic acid (15.6 +/- 2.3% of the 1 x 10(-4) M norepinephrine response). These data indicate that only highly elevated concentrations of lysergic acid result in vasoconstriction. Thus, in relation to the symptoms associated with vasoconstriction, lysergic acid may only play a minor role in the manifestation of fescue toxicosis.