R.D. TAYLOR
Nutrition and Dietetics,
University of Newcastle, Callaghan
Australia
The commercial wheat blend of a grower diet was changed, with or without the use of an exogenous feed enzyme. Over 48 hours the faecal excreta pH and instances of diarrhoea and excreta blood loss were recorded. At 48 h the hindgut digesta pH, plasma and hindgut digesta lactic acid and digesta short-chain fatty concentrations were recorded. Changing the wheat decreased excreta pH, irrespective of enzyme use. Lactic acid concentrations in the caecal digesta increased and blood loss in the faecal excreta and diarrhoea occurred. The feed enzyme moderated some responses. Changing the wheat blend of a grower diet results in short-term hindgut fermentation changes, diarrhoea and blood loss. This suggests that the integrity of hindgut mucosa is vulnerable to damage when modest changes to a diet are made.
Introduction
Taylor (2002; 2003ab) showed that alterations to the dietary cereals fed to growers or layers reduced excreta pH over 48-72 hours and modified the concentrations and relative proportions of short-chain fatty acids. Substantial increases in lactic acid concentrations could be produced in the ileum, caeca or colon. Lower pH and increased lactic acid concentrations were associated with fresh blood loss in the faecal excreta and histopathology indicating damage to ileal or colo-rectal mucosae. Promotion of exogenous feed enzyme use in layer diets has been aimed at the apparent benefit of improved feed conversion efficiency (Bird, 1996). Enzyme activity is influenced by pH (Marquardt and Bedford, 1996), and so a cereal change altering digesta characteristics may affect the exogenous enzyme performance. The interaction of responses to cereal change and enzyme use may alter digesta characteristics with unforeseen consequences for the bird. Previous work entailed change to the type of cereal. The following experiment examined a more subtle change; variation of the source of a single cereal type. Digesta characteristics and responses in immature birds were examined upon substitution of a commercial wheat-based diet with an alternative wheat blend, with or without application of an exogenous feed enzyme.
Methods
Aztec 101/007 growers (Bartter Enterprises, Griffith, NSW) were reared from day old and fed commercial starter - 11.94 MJ ME/kg, 198.7 g CP/kg + enzyme (Ronozyme WX) to 8 weeks, and grower (10.99 MJ ME/kg, 153.9 g CP/kg) rations (Ridley Agriproducts, Tamworth, NSW). At 15 weeks of age, the commercial diet, or one based on an alternative feed-wheat blend (Taylor, 2002; 2003ab), with or without the enzyme, was fed for 48 hours. Each 12 hours, excreta trays were cleaned and the pH of fresh faecal excreta was measured (Taylor, 2002). Subsequent excreta were scored for the presence or absence (1 or 0 respectively) of blood and diarrhoea (Taylor, 2003ab). At 48 h, the birds were bled, euthanased and digesta were collected to measure short-chain fatty, and lactic acid concentrations. Methods and data analysis were described by Taylor (2002; 2003ab). The work (Authority No. ACEC 0004, ACEC, Bartter Enterprises) complied with the NSW Animal Research Act 1985.
Results
Wheat diets reduced (P<0.05) mean excreta pH irrespective of enzyme application (7.64a, 7.26 b and 7.21 b ± 0.069 for commercial, wheat and wheat + enzyme (E) feeds respectively) but did not change (P>0.05) pH of digesta in different gut sections (Table 1). Diet did not alter (P>0.05) plasma nor ileal or colonic digesta L- and D-lactic acid concentrations (Table 2). Caecal concentrations were greater (P<0.05) when the wheat-blend was fed, moderated by enzyme-supplementation.
Use of the wheat-based diet, without enzyme, resulted in greater (P<0.05) propionic acid concentration in the caecal digesta (Table 3). Birds fed the wheat-blend diet (irrespective of enzyme inclusion), had higher mean blood scores (P=0.002) than birds maintained on the commercial diet and blood scores over time (Table 4) were lower (z = -1.724, P=0.085) from birds on the commercial diet. Diet change caused diarrhoea in most birds (z=1.976, P=0.048 and z=2.059, P=0.040; wheat and wheat + E diets respectively).
Discussion
Altering the cereal fed to growers and layers can produce rapid reductions in digesta and faecal excreta pH and increases in lactic acid concentrations in the hindgut (Taylor, 2002; 2003ab). Similar responses are associated with a fermentative or lactic acidosis found in ruminants (Allison et al., 1975), non-ruminant herbivores (Garner et al., 1975) and monogastric species (Cummings, 1981; Clayton, 1999). The present results support earlier work (Taylor 2002; 2003ab) in that a change in the source of the same cereal type used in the commercial diet can have deleterious effects. A change of diet increased total organic acid production in the caeca but the lactic acid increase was moderated when the feed enzyme was used. Bustos et al. (1994) suggested that D-lactic acidosis associated with short-bowel syndrome in humans was of concern for gut integrity and that the overproduction of D-lactate in the gut was the problem. A reducing environment favours lactate formation, lactate is not readily absorbed and does not elicit bicarbonate exchange (Newmark and Lupton, 1990). This contributes to a lower gut lumen pH. As indicated earlier (Taylor, 2002, 2003ab), the reduction in hindgut digesta pH may be transitory. The diarrhoea noted in the current work may be equated with the reduced net water transport and increased cell sloughing of rat ileum and colon found with increased H+ and lactate concentrations observed by Saunders and Sillery (1982). Hindgut mucosal damage is indicated by rapid and significant increases in blood loss (Vernia et al., 1988).
Blood loss and diarrhoea are markers used in animal models of the aetiology of inflammatory bowel disease (Okayasu et al., 1990; Clayton and Buffinton, 2000). This work adds to earlier work with growers and layers and suggests that any change in the cereal mix fed to poultry may have an immediate, adverse impact upon hindgut tissues and which may predispose the bird to enteric disease.
Acknowledgements
RDT was supported by a RIRDC (Egg Program) / AECL research grant.
References
Allison, M.J., Robinson, I.M., Dougherty, R.W. and Bucklin, J.A. (1975). American Journal of Veterinary Research, 36: 181-185.
Bird, J.N. (1996). In; Enzymes in Poultry and Swine Nutrition, Ottawa, pp 73-84.
Bustos, D., Pons, S., Pernas, J.C., Gonzalez, H., Caldarini, M.I., Ogawa, K. and De Paula, J.A. (1994). Digestive Diseases and Sciences, 39: 2315-2319.
Clayton, E.H. (1999). Ph.D. Thesis. University of New England.
Clayton, E.H. and Buffinton, G. (2000). Proceedings of the Nutrition Society of Australia, Fremantle, Western Australia; Nutrition Society of Australia 24: 114-118.
Cummings, J.H. (1981). Gut, 22: 763-779.
Garner, H.E., Coffman, J., Hahn, A.W., Hutcheson, D.P. and Tumbelson, M.E. (1975). American Journal of Veterinary Research, 36: 441-444.
Marquardt, R.R. and Bedford, M.R. (1996). In; Enzymes in Poultry and Swine Nutrition, Ottawa, pp 129-138.
Newmark, H.L. and Lupton, J.R. (1990). Nutrition and Cancer, 14: 161-171.
Okayasu, I., Hatakeyama, S., Yamada, M., Ohkusa, T., Inagaki, Y. and Nakaya, R. (1990). Gastroenterology, 98: 694-702.
Saunders, D.R. and Sillery, J. (1982). Digestive Diseases and Sciences, 27: 33-41.
Taylor, R.D. (2002). Publication No. 02/043, Project No. UNC-12A. (RIRDC), Kingston, ACT.
Taylor, R.D. (2003a). Queensland Poultry Science Symposium, Queensland University, 11:21.
Taylor, R.D. (2003b). Proceedings of the Australian Poultry Science Symposium, Sydney University, 15: 139-144.
Vernia, P., Caprilli, R., Latella, G., Barbetti, F., Magliocca, F.M. and Cittadini, M. (1988). Gastroenterology, 95: 1564-1568.
From Proceedings of the “18th Australian Poultry Science Symposium”, New South Wales, Australia.
