Calf intestinal health: assessment and dietary interventions for its improvement

Castro Marquez, Juan

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Description

Title

Calf intestinal health: assessment and dietary interventions for its improvement

Author(s)

Castro Marquez, Juan

Issue Date

2014-09-16

Director of Research (if dissertation) or Advisor (if thesis)

Drackley, James K.

Doctoral Committee Chair(s)

Drackley, James K.

Committee Member(s)

• Swanson, Kelly S.
• Murphy, Michael R.
• Aldridge, Brian
• Pettigrew, James E.

Department of Study

Animal Sciences

Discipline

Animal Sciences

Degree Granting Institution

University of Illinois at Urbana-Champaign

Degree Name

Ph.D.

Degree Level

Dissertation

Keyword(s)

• Intestinal health
• Assesment
• Prebiotics
• Microbiome
• Glucagon like peptide 2

Abstract

Digestive problems are common in calves between birth and weaning, and about 25% of pre-weaned heifer population in the US commonly presents diarrhea. Moreover, about 57% of the mortality in pre-weaned heifers is due to diarrheal disease. Costs associated with high mortality and reduced productivity exceed $200 million annually. Part of the problem is that methods to assess gut health in pre-weaning dairy calves at the farm level are not well defined. Aside from sound facility hygiene protocols, there is a lack of effective preventive gut health schemes and mostly ex-post therapeutic schemes are available. Development of complementary ex-ante quantitative models based on gut health measures at the calf and tissue level could help prevent disease. Here, results from analysis of calf level data are reported, where quantitative changes in calf gut health throughout the first month of life as measured by fecal scores, and their relationship with thermal variability, blood protein and bodyweight at birth, are described. We also assessed the changes in calf gut health as measured by intestinal paracellular permeability in response to age, failure of passive transfer, and intestinal location. Analysis of fecal score data indicated that risk for intestinal disease changed hyperbolically from 5 to 35 days with a risk peak around 13 days of age (~0.7), which agrees with previous reports in the literature. The variations in time, however, depended on the calf-specific features noted above, suggesting that variables related to thermal homeostasis, passive immunity obtained by the calf, and variables related to fetal maturity in early life might influence the risk of diarrheal episodes. However, the direction and size of such effects were not consistent and seem to be dependent upon other unknown variables that evolve over time. On the other hand, gut health as measured by paracellular permeability in Ussing chambers appeared not to be intrinsically related with time but colon appeared to be the tissue having the largest changes in permeability compared to other GIT regions. Also, failure of passive transfer appeared to have no influence on gut health at the tissue level even though it reduced the odds (0.84/day) of scour episodes at the calf level. More data on intestinal permeability should be collected in response to key predictor variables. Furthermore, indicators of gut health other than just permeability need to be evaluated for development and implementation of quantitative models to be feasible. Specific areas of search for risk factors, including calf immune, intestinal pathogen load and metabolomic/metabonomic profiling appear to be promissing for development of calf and tissue level empirical prediction models that support individual calf preventive care protocols. Another portion of this research related to the assessment of the effect of age and gastrointestinal location (rumen vs colon) on microbiota diversity and composition, and short-chain fatty acid profiles of Holstein pre-ruminant calves. Compared to rumen, higher lactic acid bacteria abundance (e.g. Lactobacillus: 51 vs 2 %, p < 0.001) and high concentrations of lactate (0.1 vs 1.5 mmol/mL, p<0.05) and butyrate (0.4 vs 2.3 mmol/mL, p<0.05) were observed in the colon at 2 and 4 weeks of age. Comparatively, ruminal microbiota was not stable and varied more between animals by 4 weeks of age. Such microbiota and fermentation profiles in the hind gut could help prevent diarrheal infections. In addition, the prebiotic potential of enzymatically treated whey permeate rich in galactooligosacharides was evaluated. Galactooligosacharide (GOS) supplementation at 3.4% of dietary dry matter caused a dramatic increase in the lactobacillus (Control: 39, GOS: 63%) and bifidobacterium (Control: 2.3, GOS: 5.6%) populations along with more developed intestinal epithelial structures. Nevertheless, greater odds (2.36, p<0.001) of higher fecal scores, indicative of diarrhea, were observed as a result of prebiotic supplementation. Because epithelium barrier function was unaffected, we hypothesize that a laxative effect from prebiotic overdosing caused the diarrhea like condition observed in these animals. Definition of the galactooligosacharide dose response curves and its dependence on milk feeding rates is crucial to optimize use of this prebiotic in terms of calf health. Lastly, another experiment was conducted to test the hypothesis that glucose, non-metabolizable glucose, stevioside and a glutamate source could enhance GLP-2 secretion and thereby increase gut growth or health of newborn Holstein calves. No effect of any treatment on intestinal growth and development, as measured by epithelium histomorphological dimensions, cellular proliferation, gastrointestinal organ size or the mRNA expression of the GLP2 signaling pathway, was observed. Such lack of response was perhaps due to consideration of one single fixed food intake rate and failure to identify supplementation levels that could stimulate incretin release, even though previously published and non-published work with models such as lambs and pigs, respectively, had detected responses at these concentrations. Species-specific sensitivity to sweet flavor or glutamate may render direct dose extrapolation between species inappropriate. Species-specific dose response surfaces, likely in interaction with food intake levels, may provide a better approach to optimize the incretin release response.

Graduation Semester

2014-08

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Copyright and License Information

Copyright 2014 Juan Castro Marquez

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