Biofuel co-products as livestock feed - Opportunities and challenges

108Biofuel co-products as livestock feed – Opportunities and challengesfrom 6.4 to 40.8 percent. Buckner et al. (2011) reported arange for S content of DG from 6 ethanol plants of 0.71to 0.84 percent and a within-plant coefficient of variationranging from 2.2 to 12.9 percent. Loads of DG can be fedquickly in large feedlots, such that multiple batches couldbe fed in one day or could vary from day to day. When dietsare high in S and vary significantly in S content from day today (coefficient of variation of 15.7 percent), PEM incidencecan increase (Domby et al., 2011). Domby et al. (2011)observed that although performance and carcass characteristicswere not affected by random changes in dietary S(a switch every 1–4 days between 0.48 and 0.60 percent S;sulphuric acid added to increase dietary S), mortality dueto PEM was significantly increased (5.21 vs 0.67 percent)compared with diets that maintained a constant S concentrationof 0.48 percent.Previous research revealed a swift adaptation of sulphate-reducingbacteria to increased ruminal sulphateconcentration (Lewis, 1954; Bird and Hume, 1971; Birdand Moir, 1971). Although ruminal organisms, in general,have a greater capacity to produce sulphide (Cummings etal., 1995) and have a faster rate of sulphate reduction (deOliveira et al., 1997) after several days or weeks of highdietary S, changes in the dynamics of the ruminal microbialpopulation may actually inhibit H 2 S production andcontribute to variability in PEM incidence. Developmentof a more stable combination of assimilatory and dissimilatoryactivities of sulphate-reducing bacteria (Huisingh,McNeill and Matrone, 1974) may decrease H 2 S productionand effectively incorporate more S into bacterialprotein. Moreover, it has been suggested that dietary Sincreases propionate production by converting lactate toacryloyl-CoA, an S-containing intermediate (Russell, 2002),through the acrylate pathway (Whanger and Matrone,1967). Increasing dietary concentration of DG (and S) willincrease ruminal propionate concentrations in dry-rolledmaize-based diets (Leupp et al., 2009; Uwituze et al.,2011b), which may compete with H 2 S for H + , effectivelylowering ruminal H 2 S concentrations. Taken together,these reports are evidence that adaptive mechanisms forthe increased activity by sulphate-reducing bacteria exist.Adaptation to high dietary S by other ruminal microorganisms,however, is unclear.Thiamine and PEMThe lack of adequate dietary thiamine will inhibit thiamindependentreactions of glycolysis and the trans-carboxylicacid cycle (Brent and Bartley, 1984) and can induce PEM.This activity seems to be caused by ruminal thiaminaseproduction as a result of a shift in the ruminal environmentfrom Gram-negative to Gram-positive bacteria, which commonlywill occur during adaptation to a high-concentratediet (Brent, 1976). The link between thiamine status andPEM, and the dramatic effect that intravenous thiamineadministration can have has led to the often incorrectassumption that outbreaks of PEM are the result of alteredthiamine status (Gould, 1998). Subsequently, the additionof 100 to 200 mg of thiamine per head daily is often addedto diets of cattle perceived to be at risk of developing PEM.However, the results from efforts to treat or prevent PEMwith thiamine are mixed. Much of the confusion surroundingthiamine therapy may be attributed to the fact that highsulphate intake may induce PEM through multiple mechanisms.High sulphate intake has been shown to decreaseduodenal thiamine flow (Goetsch and Owens, 1987), andsulphite, a transient product of sulphate reduction, candestroy thiamine in the rumen resulting in thiamine deficiency(Brent and Bartley, 1984). These forms of sulphateinducedPEM may respond to thiamine therapy or may beprevented by thiamine supplementation. Olkowski et al.(1992) suggested that although sulphite is transient, it maybe a significant contributor because the sulphite producedis absorbed, oxidized to sulphate and then recycled backto the rumen and available to be reduced again. It also hasbeen suggested that sulphite could have a direct impacton the brain tissue itself, as sulphite-derived radicals havebeen postulated to cause lipid peroxidation and damage tobiological membranes (de Oliveira et al., 1996; Brent andBartley, 1984; Olkowski et al., 1992). Although ruminalthiamine status may not be affected by the occurrence ofS-induced PEM, dietary thiamine concentrations should bemonitored to ensure that adequate thiamine is available tocattle and supplemental thiamine should be considered toavoid thiaminase-induced PEM. Further, thiamine is the primarymethod of treatment for animals afflicted with PEM.An intravenous injection of thiamine (10 mg/kg of bodyweight; Cebra and Cebra, 2004) is suggested.Managing high-S dietsPossible strategies to manage high S concentrations includelimiting the amount of high-S feedstuffs or water consumed,adapting cattle to high-S feeds in the diet, or offeringfeed additives that may combat high S intakes. Use ofantibiotics that inhibit the Gram-negative bacteria responsiblefor H 2 S, and adding dietary minerals that bind sulphidein the rumen are potential strategies that have been investigated.Kung, Bracht and Tavares (2000) analysed the effectsof molybdenum, the antibiotics avoparcin, bacitracin, bambermycin,lasalocid, chlortetracycline and oxytetracycline,as well as an experimental compound, anthraquinone,on sulphide production in vitro. Anthraquinone, bambermycin,chlortetracycline, oxytetracycline and lasalocidall decreased in vitro H 2 S production, with the greatestdecreases occurring with anthraquinone, chlortetracyclineand oxytetracycline (Kung, Bracht and Tavares, 2000). Theeffect of these compounds on in vivo H 2 S production are