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Dried distillers grains with solubles (DDGS) have been used in production animal diets; however, overuse of DDGS can cause toxic concentrations of ruminal hydrogen sulfide gas (HS), resulting in polioencephalomalacia, a deleterious brain disease. Because HS gas requires an acidic rumen environment and diet can influence ruminal pH, it has been postulated that dietary manipulation could help mitigate HS production. The objective of this study was to assess the effect of dietary roughage and sulfur concentrations on HS production and rumen fermentation. In Exp. 1, 7 dual-flow continuous culture fermenters were used in 4 consecutive 9-d periods consisting of 6 d of adaptation followed by 3 d of sampling. At the conclusion of each 9-d continuous culture period, adapted rumen fluid was used for inoculation of 24-h batch culture incubations for Exp. 2. For both experiments, 6 dietary treatments were formulated to consist of 0.3%, 0.4%, or 0.5% dietary sulfur (LS, MS, and HS, respectively) and 3% or 9% dietary roughage (LR and MR, respectively), using grass hay as the roughage source. A corn-based diet without DDGS was used as a control diet. Headspace gas was sampled to determine HS production and concentration. In Exp. 1, greater dietary roughage had no effect ( = 0.14) on HS production but did create a less acidic environment because of an increase ( < 0.01) in the in vitro pH. In Exp. 2, an increase in dietary sulfur caused an increase ( = 0.04) in ruminal HS production, but there was no direct effect ( = 0.25) of dietary roughage on HS production. Greater dietary roughage resulted in a less ( = 0.01) acidic final batch culture pH but a lower ( < 0.01) total VFA concentration. Further investigation is needed to determine a more effective way to mitigate ruminal HS production using dietary manipulation, which could include greater inclusion of dietary roughage or the use of different roughage sources.

Twenty-four steers (initial BW = 385 ± 1.1 kg) were blocked by BW and randomly assigned to 3 dietary treatments (0, 30, or 60% wet distillers grains with solubles [WDGS]; DM basis) and were fed individually to determine the effect of WDGS on live growth and carcass performance, visceral organ mass, trace mineral status, and polioencephalomalacia biomarkers. Steers were slaughtered at 125, 150, 164, and 192 d (2 blocks/slaughter date) when external fat depth was approximately 1.3 cm based on visual appraisal. Steers fed 30% WDGS had greater DMI than those fed 0 or 60% WDGS (P 0.41) on either live or carcass-adjusted basis. Steers fed 30% WDGS had greater liver S and Mn concentrations (DM basis) and lower liver Fe concentrations than control steers (P < 0.10; initial values used as a covariate), and feeding 60% WDGS decreased liver Cu and increased liver Fe (P < 0.10) compared with feeding 30% WDGS. Cytochrome c oxidase (COX) activity in brain tissue tended to be decreased with 60 vs. 30% WDGS (P = 0.12), and COX activity decreased linearly (P = 0.06) in lung tissue as dietary WDGS concentration increased. Likewise, gut fill linearly increased (P = 0.01) with increasing WDGS concentration. Feeding 30% WDGS increased fractional mass (g/kg of empty BW) of the small intestine (P < 0.10) compared with controls, whereas 60% WDGS increased fractional kidney mass (P < 0.10) compared with 30% WDGS. Overall, results suggest that gut fill, Cu status, and COX activity seem to be compromised by WDGS when fed at 60% of diet DM in diets based on steam-flaked corn, which suggests a greater susceptibility to polioencephalomalacia.

Poor performance and S-induced polioencephalomalacia (sPEM) have been observed in ruminant livestock in high-S drinking water regions. No gainful method of removing S from drinking water is available and therefore a feed supplement that negates the effects of high-S water is needed. Our objective was to determine if supplementing Mo improves health and performance of steers administered a high-fiber diet and high-S drinking water. We hypothesized that if the supplemental Mo adequately bound excess S in the rumen, it would not be available at toxic concentrations. Yearling steers (n = 96; 260.0 ± 1.3 kg BW) were stratified by pretrial BW into 12 feedlot pens (n = 8 steers per pen). One of 3 treatments, low-S water (LS; 375 mg SO(4)/L), high-S water (HS; 2,218 mg SO(4)/L), or high-S water plus Mo (HSMO; 2,218 mg SO(4)/L; 187.5 mg Mo/kg DM), were randomly assigned to pens within 4 blocks for a 56-d trial. Body weights were recorded on d -2, -1, 29, 56, and 57, ruminal H(2)S concentrations were measured by rumenocentesis on d -1, 29, and 57, and liver biopsies were performed on d -1 and 57. Performance data were analyzed over the 56-d trial period (overall) as well as over 2 periods: Period 1 (d 0 to d 28) and Period 2 (d 29 to d 56). One case of sPEM was confirmed by the presence of cortical lesions in the HS treatment group. Daily DMI and ADG were affected by treatment and period (P < 0.001) main effects. The LS steers had the greatest (P < 0.05) DMI followed by HS and HSMO steers, respectively. Similar results were observed for ADG. Daily water intake was affected (P < 0.001) by period only, with greater daily water intake in Period 2 than Period 1. Change in hepatic concentrations of Cu, Fe, and Mo over the course of the trial were all affected (P < 0.001) by treatment. Hepatic Cu increased from d 1 to 57 in LS and HS steers but was depleted in HSMO steers. Hepatic Fe and Mo increased in HSMO steers only. Ruminal H(2)S concentrations were affected by treatment (P < 0.021), with greater H(2)S concentrations in HSMO compared with LS and HS steers. Signs of Mo toxicity such as severe diarrhea, loss of body condition, anorexia, changes in hair color, and stiffness in joints were observed in the Mo supplemented steers. These results indicate that added dietary Mo does not adequately bind excess S in the rumen, causing aggravated toxic effects from potentially both the high dietary S and Mo.

Limited data are available regarding the influence of thiamine supplementation on the incidence of polioencephalomalacia (PEM) in lambs fed diets containing increased concentrations of S in the diet (>0.7%). Therefore, our objective was to evaluate the influence of thiamine supplementation on feedlot performance, carcass quality, ruminal hydrogen sulfide gas concentrations, and incidence of PEM in lambs fed a finishing diet containing 60% distillers dried grains with solubles (DDGS; DM basis). Two studies were conducted using completely randomized designs to evaluate the influence of concentration of thiamine supplementation. Study 1 used 240 lambs fed in 16 pens, whereas study 2 used 55 individually fed lambs. Lamb finishing diets contained 60% DDGS, which resulted in a dietary S concentration of 0.73% (DM basis). Treatments diets were based on the amount of supplemental thiamine provided: 1) no supplemental thiamine (CON), 2) 50 mg/animal per day (LO), 3) 100 mg/animal per day (MED), or 4) 150 mg/animal per day (HI). Additionally, in study 2, a fifth treatment was included, which contained 0.87% S (DM basis; increased S provided by addition of dilute sulfuric acid) and provided 150 mg of thiamine/animal per day (HI+S). In study 1, ADG decreased quadratically (P = 0.04), with lambs fed the CON, LO, and MED diets gaining BW at a greater rate than lambs fed the HI diet. In study 1, DMI responded quadratically (P or = 0.17) in lamb performance were observed in study 2. In both studies, most carcass characteristics were unaffected, with the exception of a tendency for decreased carcass conformation (study 1; P = 0.09) and greater flank streaking (study 2; P = 0.03). No differences in ruminal hydrogen sulfide concentration (P > 0.05) among treatments were apparent until d 10, at which point lambs fed the LO diet had less hydrogen sulfide concentrations than all other treatments. Lambs fed HI had the greatest concentrations of hydrogen sulfide on d 31 (1.07 g of hydrogen sulfide /m(3); P < 0.009). Ruminal pH did not differ (P = 0.13) and averaged 5.6 +/- 0.06. No clinical cases of PEM were observed during the course of either study. The use of thiamine as a dietary additive to aid in the prevention of PEM in finishing lambs does not appear to be necessary under the conditions of this study.

Sulfur-induced polioencephalomalacia (sPEM), a neurological disorder affecting ruminants, is associated with consumption of diets with increased S (high-S). High-S water is commonly found in many western states and is a major source of dietary S for grazing cattle. Consumption of high-S water has been associated with sPEM and decreased performance. Identification of a feed supplement that would counteract the negative effects of high-S water would decrease the incidence of sPEM and prevent performance reductions in regions with problematic water sources. The objectives of this study were to 1) determine the effects of administering high-S drinking water to forage-fed feedlot steers on health and performance, and 2) determine the effectiveness of clinoptilolite, a clay mineral with increased cation-exchange capacity, in negating the effects of high-S drinking water. Yearling steers (n = 96; 318.2 +/- 2.1 kg of BW) were randomly assigned to 1 of 4 treatments for a 77-d trial period: control with low-S water (566 mg of SO(4)/L), high-S water (3,651 mg of SO(4)/L), or high-S water plus clinoptilolite supplemented at 2.5 or 5.0% of the diet DM. Feed and water consumption were measured daily, and all steers were weighed on d -2, -1, 29, 53, 76, and 77. Plasma samples were collected on d 0, 58, and 77, and liver samples on d 0 and 77. There was a greater (P or= 0.546) in ADG or G:F were observed. Plasma Cu decreased (P = 0.029) to a greater magnitude in high-S water steers than the control steers over the 77-d trial period. Mineral analyses of hepatic tissue from randomly selected healthy steers from each treatment group (n = 10 per treatment) showed an interaction (P

Acute and subacute ruminal acidosis, bloat, liver abscesses, and polioencephalomalacia (PEM) were reviewed with respect to contributions published in the Journal of Animal Science (JAS) regarding these metabolic and digestive disorders in beef cattle. Increased grain feeding and expansion of the feedlot industry in the 1960s led to considerable research on acidosis, and early publications defined ruminal changes with acute acidosis. The concept of subacute acidosis was developed in the 1970s. Significant research was published during the 1980s and 1990s on adaptation to high-grain diets, effects of ionophores, and the development of model systems to study ruminal and metabolic changes in acidosis. Since 2000, JAS publications on acidosis have largely focused on individual animal variability in response to acid loads and the role of management strategies in controlling acidosis. Increased grain feeding also was associated with an increase in the incidence of liver abscesses, which were quickly linked to insults to the ruminal epithelium associated with acidosis. The role of antibiotics, particularly tylosin, in decreasing the incidence and severity of liver abscesses was a significant contribution of JAS publications during the 1970s and 1980s. Papers on bloat were among the earliest published in JAS related to metabolic and digestive disorders in cattle. Noteworthy accomplishments in bloat research chronicled in JAS include the nature of ruminal contents in legume and feedlot bloat, the role of plant fractions and microbial populations in the development of bloat, and the efficacy of poloxalene, ionophores, and, more recently, condensed tannins in decreasing the incidence and severity of bloat. Although less research has been published on PEM in JAS, early publications highlighting the association between PEM and ruminal acidity and the role of thiaminase in certain forms of the disorder, as well as more recent publications related to the role of sulfur in the development of PEM, are noteworthy contributions. Since the 1940s, outstanding and often-cited review articles have made JAS a highly visible source of information on these disorders. Thus, JAS has played a significant role as a repository for information pertaining to metabolic and digestive disorders in cattle and other ruminants, and it will no doubt continue to be a premier resource for information on these conditions during the second century of the American Society of Animal Science.

PANTER, K. E., HARTLEY, W. J., JAMES, L. F., MAYLAND, H. F., STEGELMEIER, B. L., AND KECHELE, P. O. (1996). Fundam. Appl. Toxicol. 32, 217-223. Selenium is an essential micronutrient, although ingestion in excess in pigs can cause disease conditions including neurological dysfunction and chronic skin and hoof lesions. Controlled feeding trials in growing swine, using the same Se content in feed sources, resulted in higher concentrations (p =£ 0.05) of Se in blood and organs of pigs fed seleno-DL-methionine compared with those receiving Astragalus bisulcatus or sodium selenate. Clinical signs of Se toxicity including neurological signs of paralysis were more severe and occurred sooner in the A. bisulcatus group than in the sodium selenate or seleno-DL-met hionine groups. All five pigs fed A. bisulcatus developed neurological signs of paralysis, and in four the signs occurred within 5 days of the start of treatment. Four of five pigs fed sodium selenate also developed paralysis, but this occurred 4 to 21 days after treatment began. The fifth pig in the group developed signs of chronic selenosis. Two of five pigs fed seleno-DL-methionine developed paralysis on 9 and 24 days, respectively, and the remaining three developed chronic selenosis. Selenium fed to pigs in three forms [plant (A. bisulcatus), sodium selenate, or seleno-DL-methionine] resulted in neurological dysfunction and lesions of symmetrical poliomyelomalacia. These were most severe in the A. bisulcatus group, which also had polioencephalomalacia. Although seleno-DL-methionine caused the greater increase in tissue and blood Se concentrations, this did not correlate with severity of pathological changes, since animals fed A. bisulcatus developed more severe and disseminated lesions. Field observation and experimental trials in the United States have shown a great variety of syndromes and pathology resulting from ingestion of certain species of Astragalus by livestock. The syndromes include disease conditions induced by the nitro-containing Astragalus (A. miser), the swainsonine-containing Astragalus (A. lentiginosus, locoweeds), and the selenium-containing Astragalus (A. bisulcatus). These syndromes have been reviewed by James et al. (1981). Two Se-accumulating plants (A. bisulcatus and A. praelongus) and inorganic Se compounds have been shown to produce neurological signs and microscopic lesions of focal symmetrical polioencephalomalacia and poliomyelomalacia when fed to young pigs (Hartley et al., 1984). Both plant species also contain small amounts of swainsonine, an amannosidase inhibitor that causes the lesions and clinical syndrome known as locoism. This toxin might contribute to the development of lesions when animals are poisoned eating these plants. In previous studies of Se intoxication, organic Se was fed to growing pigs in the form of selenocystine . The animals failed to thrive and had varying degrees of hepatic fibrosis, but neither neurological signs nor histological lesions were seen in the central nervous system (Hartley et al., 1984). The biochemical parameters of some of these pigs have been reported (Baker et al., 1989). This report details additional trials including dosing with seleno-DL-methionine (organic form of Se) and a comparison of the resulting tissue Se and histological lesions with those seen in animals treated with sodium selenate (inorganic form of Se) or A. bisulcatus (nonprotein, water-soluble plant forms of Se) at the same Se dose.

Thiamin analogs, produced in the rumen by thiaminase I, in the presence of a cosubstrate appear to be responsible for the central nervous system disorder, polioencephalomalacia (PEM). For PEM to occur, an analog must be produced that inhibits an essential thiamin-requiring reaction, and results from a cosubstrate present in the rumen. In high concentrate diets, thiaminase I is produced by rumen microbes. However, PEM can also be caused by thiaminase I of plant origin. Based on physical characteristics and cosubstrate specificity, the thiaminase I enzymes produced by Bacillus thiaminolyticus and Clostridium sporogenes appear to be different from the enzyme produced by the rumen. Because niacin and certain antihelmentics are thiaminase I cosubstrates, they should be used cautiously. Supplementary niacin increased microbial protein synthesis in vitro and in vivo, and was more effective with urea than soybean meal. Supplementary niacin (5 to 6 g X cow-1 X d-1) increased milk production in postpartum cows but not in those in mid-lactation, and in cows fed soybean meal but not in those fed urea. We believe the heating of soybean meal during commercial processing decreased the availability of niacin for rumen protozoa. Supplementary niacin for postpartum cows increased blood glucose, decreased blood ketones and reduced the incidence of ketosis. Niacin flow to the small intestine and its absorption from the small intestine increased with niacin supplementation. Supplemental niacin prevented the postpartum decrease in red blood cell niacin observed in control cows.