Abstract:
SPECIES DIFFERENCES BETWEEN RUMINANTS IN SUSCEPTIBILITY TO MOLASSES TOXICITY F. CALDERON CORTES, H. PEIRIS, LINDA BLINKS and R. ELLIOTT SUMMARY Rumen thiaminase activities were found to be unimportant in the Molasses-based diets development of molasses toxicity in beef cattle. produced elevated concentrations of propionic acid in both sheep and goats but not in cattle which exhibited high butyric acid concentrations. The importance of glucose supply to animals fed molasses diets is discussed. INTROIXICTION The role of molasses as a feed for livestock has changed in recent yearsfrom that of a carrier for urea and minerals to the realization that it could provide most of the dietary energy intake of animals (Gulbransen 1984) l * * * * Although ad lib diets of molasses/urea or fortified molasses diets (8% urea plus Eozn meals) are of high dry matter content, such diets Rumen provide little in the way of physical stimulation to the rumen. contractions in animals fed molasses/urea diets are both weak and infrequent (Peron and Preston 1971). Adequate forage supplementation of cattle fed such diets is important in order to stimulate intake of molasses. In practice this is achieved by either offering limited amounts of cut forage daily, or by 9 system of restricted grazing of pasture or Elias et al (1969) recommended that in order to obtain legume banks. maximum intakes of molassey the daily intake of fresh forage should not exceed 3.5% of the animal's liveweight or 0.500.7% of liveweight on a dry Adequate forage supplementation is also important in matter basis. preventing the nutritional disorder known as molasses toxicity. MOLASSES TOXICITY Molasses toxicity was first noted in Cuba with the introduction of large scale feed lotting of cattle using molasses (Preston and Willis In such situations it was observed that the toxicity was quickly 1974). corrected by increasing the level of forage in the diet. Animals given forage under conditions of restricted grazing also showed a much lower incidence of the disease than those given cut forage in troughs where perhaps difficulty of access occurs for individual animals. The encephalopathy of the disorder is indistinguishable from cerebra-cortical necrosis (CCN) or polioencephalmalacia which is caused by a deficiency of thiamin (Edwin et al 1979). Experimentally, symptoms of molasses toxicity usually appeardto 8 days after removal of forage (Loscada et al, 1971; Rowe et a. 1979). At' first there is refusal to eat molasses and an increase inthe shivering reflex. Subsequently, excessive salivation occurs and a tendency to wander around in circles. If untreated the animal becomes comatose and quickly dies. The cause of the necrosis in the central nervous system has been attributed to a decrease in energy supply to the tissues (caused by a deficiency of thiamine, (Edwin et aJ.1979) or by an absolute deficiency of glucose (Losada and Preston 19z). One central feature associated with the disorder however is the need for adequate fibre intake. The reduced rmen turnover rate exhibited by animals fed molasses, would be exacerbated by insufficient fibre intakes (Rowe et al. 1979) and thus causes a reduction in flm of protein and the micronutrients to the *Department of Agriculture, University of Queensland, St. Lucia, Qld. 4067 99 It has also been suggested that the extremely slow post-ruminal tract. rumen turnover rate may favour the growth of micro-organisms which produce However, evidence for their thiaminase enzymes (Mella et al. 1976). involvement is still inconcluxF(Rowe et al. 1980). wIn a recent experiment a total of 32 steers (ca. 300 + 10 kg liveweight) were housed in pens (2 animals/pen) under feedlot cozitione and fed a diet of ad lib molasses/urea (3% w/w) with varying amounts of chaffed pangola (Di&zia decumbens) hay or barley straw. Each pair of steers received daily either the pangola or barley straw at one of the following treatment levels, 0.2, 0.4, 0.6 or 0.8% of bodyweight. The steers were fed their respective diets for 6 weeks after which time samples of rumen liquor were ranoved by stanach tube for immediate assay of thiaminase activity (Boyd 1985), and volatile fatty acid analysis. Rumen thiaminase activities were not significantly different between treatments (Table l), but two of the steers fed the lowest quantities of pangola hay (0.2% of bodyweight) developed symptans of molasses toxicity and one animal died. However, rumen thiaminase activities in these animals were 4.42 x loo6 and 3.29 x loo6 umol of thiazole formed/ml/min respectively similar to levels recorded in steer fed the highest levels of forage supplements.. TABLE 1 Effects of increasing levels of roughage on thiaminase activity and VFA concentrations and proportions in the rumen liquor of steers fed molasses/urea based diets. GLUCOSE REQUIREMENT OF RUMINANTS FED MOLASSES DIETS On grain based diets (particularly sorghum and maize) a substantial proportion of dietary starch may escape microbial degradation (Armstrong 1974) and in animals fed such diets the rumen fermentation and propionic acid is characterised by high concentrations of propionic acid. The sugars in molasses however are readily fermented in the rumen, leaving no' glucose available to the animal fran post ruminal carbohydrate digestion and propionic acid concentrations in the ruxnen of molasses fed animals are usually low (Table 1) which exacerbates any glucose insufficiency. 100 Gaytan et aA. (1977) successfully prevented molasses toxicity in cattle by orally supplying glycerol (400 g/l/d) and attributed the protective response to the additional availability of glucose from post rminal digestion of the glycerol. However, Rawe et al. (1979) found that glucose entry rates in cattle fed molasses dietFw;re not affected by removal of forage, yet symptoms of molasses toxicity were evident in the Rumen fermentation patterns in the animals used by Rowe et al. animals. (1979) were somewhat atypical of those normally observed in molasses-fed animals showing elevated proportion of acetic acid (0.68) and very low butyric acid levels (0.15). Although cattle easily succumb to molasses toxicity, the condition has not been recorded in small ruminants fed ad lib molasses. In a recent experiment (Peiris unpublished information) 3 cattle, sheep and goats (4 animals/treatment) were offered feed lot diets based on cereal grain (cracked sorghum) or molasses/urea with restricted amounts of forage (0.6% of bodyweight) for 4 weeks, after which time, samples of rmen liquid were removed by stanach tube. El evated concentrations of propionic acid were recorded in the rumen liquid f ran sheep and goats fed the molasses diets, whereas cattle exhibited high levels of butyric acid Both sheep and goats fed the grain-based diets, produced (Table 2). fermentation patterns with low butyrate concentrations whereas cattle exhibited relatively high levels of butyrate. In a second experiment (Blinks 1985) f our rumen fistulated goats were fed the following sequence of dietary regimes: (i) pangola grass (ii) molasses/urea plus 1OOg of (iii) molasses/urea hay (ad lib) -w (ad lib) panzgrass daily (ad lib) without any forage supplements. TABLE 2 Intakes of molasses and differences in rumen VFA proportions in cattle, sheep and goats fed ad lib diets of sorghum grain or molasses/urea plus restricted forage supplements. Each dietary regime lasted 21 days, and during the final three days of each period rumen thiaminase activities and rumen volatile fatty acid concentrations were determined in each animal. 101 The results presented in Table 3 show that rumen thiaminase activities were not different between dietary treatments and unlike the situation in cattle, `the levels of propionic acid in rumen fluid were significantly elevated by the molasses diet. Butyric acid concentrations At no time during the last remained low throughout the experiment. treatment (21 days on molasses/urea without forage supplements) did the goats present symptoms of molasses toxicity. TABLE 3 Rumen parameters in goats fed an ad lib forage diet on an ad lib w -s molasses diet with or without forage. Interestingly, in an experiment comparing the effects of molasses and sucrose solutions on rumen metabolism in sheep, Godoy-Montanez et al. (1984) found that the rate of sugar intake significantly affected;&& fermentation patterns. Rapid intake of sucrose solutions produced elevated butyric acid concentrations whereas the slow rate of molasses consumption produced propionate-rich fermentations. It would seem therefore that glucose deficiency is the main cause of molasses toxicity. The greater quantities of rumen propionic acid produced in small ruminants (perhaps as a direct result of slower intake of the molasses) renders these animals less susceptible to molasses toxicity. In the absence of high rumen propionate levels in cattle fed molasses diets, there is a greater need to maintain adequate rumen turnover rates in order to supply sufficient quantities of gluconeoginic amino acids. In this regard Preston (1972) reported that supplements of ground dried lucerne significantly reduced the incidence of molasses toxicity in cattle and the presence of supplemental protein of low rumen degradability in fortified molasses mixtures may also protect the animal from toxicity. Gulbransen c 1984) reported feeding beef cows up to 6 kg of fortified molasses for 26 weeks without forage with no signs of molasses toxicity occurring. The reduced intake of fortified molasses caused by the high levels of urea (8%) incorporated into such mixtures may also result in high rumen propionic acid levels. 102 'Nutritional considerations in the feeding of Armstrong, D.G. (L974) Technical cereals to ruminant0 In Cereal Supply and Utilisation. Publication of London Office of U.S. Feed Grains Council. Honours Thesis Dept of Agriculture, University of Blinks, L. J. (1984) Queensland. Boyd, J.W. (1985) 3. Agric. Sci. (Camb) 104, 637. Edwin, E.E., Markson, L.M., Shreeve, J.J8ckman, R. and Carroll, P.J. (1979) Vet. Rec. 104, 4. Elias, A., Preston, T.Rxnd Willis, D.B. (1%8) Cuban J. Agric. Sci. 2, Gaytan,'T., Zamora, F. and Shimada, A.S. (1977) C u b a n J. Anric. Sci. 11, 29 Godoy-Pdntanez, R.H., Parker, D.S. and Armstrong, D.G. (1984) Proc, Nut0 Soc. 42, 33A. Gulbrzen, G. 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