Abstract
Three experiments were performed to examine for causes of poor growth of young Merino sheep. Weekly testing of animals 42 weeks of age for 10 weeks revealed that 90% of clinically poor animals were excreting high levels of thiaminase in their faeces; low levels of activity were present in 20% of clinically normal animals. There were significant differences in the mean erythrocyte transketolase activity of the thiaminase excreting poor animals and the thiaminase free normal animals. Other known causes of poor growth could not be demonstrated. Weekly monitoring of thiaminase activity in the faeces from 80 lambs 6 weeks of age showed 23% to be excreting significant levels of enzyme (>3mUg−1 DM) throughtut a 10 week test period. Mean growth rates of these lambs were significantly below those of lambs not excreting thiaminase or excreting low levels intermittently. Supplementation of thiaminase excreting lambs with intra-muscular injections of thiamine HCl was associated with a statistically significant improved growth rate (P<0.01) compared to unsupplemented sheep excreting thiaminase. Mean growth rates of lambs not excreting thiaminase on a continuous basis (sampled weekly) were the same with or without thiamine HCl supplementation. High thiaminase levels were found in the ruminal fluids of trial animals excreting the enzyme in their faeces, confirming this previously established association.Bacillus thiaminolyticus was isolated from faeces and ruminal fluids from clinically poor animals and is the most likely source of the thiaminase. Subclinical thiamine deficiency was indicated by low erythrocyte transketolase activities and elevated TPP effects and is proposed as the cause of the poor growth by the young sheep.
This is a preview of subscription content, log in via an institution to check access.
Similar content being viewed by others
Bibliography
Bakker, H.J., Dickson, J., Steel, P. and Nottle, M.C., 1980. Experimental induction of ovine polioencephalomalacia. Vet. Rec.107: 464–466.
Bauer, J.D., Ackerman, P.G. and Toro, G., 1974. Clinical Laboratory Methods, (8th ed.), C.V. Mosby, Saint Louis, pp. 402–403.
Beliveau, G.P. and Freedland, R.A., 1980. Effect of thiamine deficiency on gluconeogenesis and transketolase activity in isolated hepatocytes. Proc. Soc. Exptl. Biol. Med.164: 514–518
Berrett, S. and Hebert, C.N., 1979. A semi-quantitative spot test for glutathione peroxidase in blood of cattle and sheep for the assessment of biological selenium status. Vet. Rec.105: 145–146.
Brook, P.J., 1959. A volumetric spore trap for sampling pastures. N.Z. J. Agric. Res.2: 690–693.
Connor Johnson, B., Hamilton, T.S., Nevens, W.B. and Boley, L.E., 1948. Thiamine deficiency in the calf. J. Nutr.35: 137–145.
Cushnie, G.H., Richardson, A.J., Lawson, W.J. and Sharman, G.A.M., 1979. Cerebrocortical necrosis in ruminants: Effects of thiaminase type 1 — producingClostridium sporogenes in lambs. Vet. Rec.105: 480–482
Dacie, J.V. and Lewis, S.M., 1975. Practical Haematology (5th Ed), Churchill Livingstone, Edinburgh, pp. 30–34.
Davis, E.T., Pill, A.H., Collings, D.F., Venn, J.A.J. and Bridges, G.D., 1965. Cerebrocortical necrosis in calves. Vet. Rec.77: 290
Draper, H.H. and Connor Johnson, B., 1951. Thiamine deficiency in the lamb. J. Nutr.43: 413–422.
Edwin, E.E., Hebert, N.C. and Masterman, S., 1976. Thiamine requirement of young ruminants. J. Agric. Sci. Camb.87: 679–688.
Edwin, E.E. and Jackman, R., 1970. Thiaminase I in the development of cerebrocortical necrosis in sheep and cattle. Nature, Lond.228: 772–774.
Edwin, E.E. and Jackman, R., 1973. Ruminal thiaminase and tissue thiamine in cerebrocortical necrosis. Vet. Rec.92: 640–641.
Edwin, E.E. and Jackman, R., 1974. A rapid radioactive method for determination of thiaminase activity and its use in the diagnosis of cerebrocortical necrosis in sheep and cattle. J. Sci. Fd. Agric.25: 357–368.
Edwin, E.E., Lewis, G. and Allcroft, R., 1968a. Cerebrocortical necrosis: A hypothesis for the possible role of thiaminases in its pathogenesis. Vet. Rec.83: 176–178.
Edwin, E.E., Spence, J.B. and Woods, A.J., 1968b. Thiaminases and cerebrocortical necrosis. Vet. Rec.83: 417.
Evans, W.C., Evans, A., Thomas, A.J., Watkins, J.E. and Chamberlain, A.G., 1958. Studies on bracken poisoning in cattle. Part IV. Brit. Vet. J.114: 180–198.
Fujita, A., 1954. Thiaminase. Advan, Enzymol.15: 389–421.
Gibson, T.T. and Gordon, R.E., 1974. Endospore forming rods and cocci. In R.E. Buchanan and N.E. Gibsons (co-editors), Bergys manual of determinative bacteriology. Williams and Wilkins, Baltimore, Part 15.
Guggenheim, K. and Buechler, E., 1946. Thiamine deficiency and susceptibility of rats and mice to infection withSalmonella typi murium. Proc. Soc. Exp. Med. Biol.61: 413–416.
Jensen, R., Griner, L.A. and Adams, O.R., 1956. Polioencephalomalacia of cattle and sheep. J. Amer. Vet. Med. Assoc.129: 311–321.
Kubiatowicz, D.O., Ithakissios, D.S. and Windorski, D.C., 1977. Vitamin B12 radioassay with oyster toadfish (Opsanus tau) serum as binder. Clin. Chem.23: 1037–1045.
Lewis, G., Terlecki, S., Markson, L.M. and Allcroft, R., 1967. Thiamine status of lambs in relation to cerebrocortical necrosis. Proc. Nutr. Soc.26: xiii-xiv.
Linklater, K.A., Dyson, D.A. and Morgan, K.T., 1977. Faecal thiaminase in clinically normal sheep associated with outbreaks of polioencephalomalacia. Res. Vet. Sci.22: 308–312.
Morgan, K.T. and Lawson, G.H.K., 1974. Thiaminase type 1 — producing bacilli and ovine polioencephalomalacia. Vet. Rec.95: 361–363.
Pill, A.H., 1967. Evidence of thiamine deficiency in calves affected with cerebrocortical necrosis. Vet. Rec.81: 178–181.
Prasad, R., Rao, Y.V.B.G., Mehta, K. and Subrahmanyam, D., 1980. Effect of thiamine deficiency on the filarial infection of albino rats withLitomosoides carinii. Int. J. Parasitol.10: 93–96.
Read, D.H. and Harrington, D.D., 1981. Experimentally induced thiamine deficiency in beagle dogs: Clinical observations. Amer. J. Vet. Res.42: 984–991.
Roberts, G.W. and Boyd, J.W., 1974. Cerebrocortical necrosis in ruminants. Occurrence of thiaminase in the gut of normal and affected animals and its effect on thiamine status. J. Comp. Path.84: 365–374.
Sauberlich, H.E., 1967. Biochemical alterations in thiamine deficiency — their interpretation. Amer. J. Clin. Nutr.20: 528–542.
Schouten, H., Statius van Eps, L.W. and Struyker Boudier, A.M., 1964. Transketolase in blood. Clin. Chim. Acta.10: 474–476.
Shreeve, J.E. and Edwin, E.E., 1974. Thiaminase- producing strains ofCl. sporogenesassociated with outbreaks of cerebrocortical necrosis. Vet. Rec.94: 330.
Singh, M., 1982. Effect of thiamin deficiency on pancreatic acinar cell function. Amer. J. Clin. Nutr.36: 500–504.
Smeyers-Verbeke, J., Massart, D.L., Versieck, J. and Speecke, A., 1973. The determination of copper and zinc in biological materials. A comparison of atomic absorption with spectrophotometry and neutron activation. Clin. Chim. Acta.44: 243–248.
Spicer, E.M. and Horton, B.J., 1981. Biochemistry of natural and amprolium-induced polioencephalomalacia in sheep. Aust. Vet. J.57: 230–235.
Spicer, E.M., Horton, B.J. and Thomas, K,W., 1980. Studies on poliocephalomalacia in sheep. Vic. Vet. Proc.38: 45.
Steele, P. and Lambe, W.J., 1979. Ruminal thiaminase type 1 activity associated with outbreaks of polioencephalomalacia in sheep. Proc. Nutr. Soc. Aust.4: 130.
Street, H.R., Zimmerman, H.M., Cowgill, G.R., Hoff, H.E. and Fox, J.C. Jr., 1941. Some effects produced by long-continued subminimal intakes of vitamin B1. Yale. J. Biol. Med.13: 293–308.
Thornber, E.J., Dunlop, R.H., Gawthorne, J.M. and Huxtable, C.R., 1979. Polioencephalomalacia (cerebrocortical necrosis) induced by experimental thiamine deficiency in lambs. Res. Vet. Sci.26: 378–380.
Trinder, P., 1969. The determination of glucose in blood using glucose oxidase with an alternative oxygen acceptor. Ann. Clin. Biochem.6: 24–27.
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Thomas, K.W. The effect of thiaminase-induced subclinical thiamine deficiency on growth of weaner sheep. Vet Res Commun 10, 125–141 (1986). https://doi.org/10.1007/BF02213975
Accepted:
Issue Date:
DOI: https://doi.org/10.1007/BF02213975