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Instant Insights: Metabolic disorders in dairy cattle

Instant Insights: Metabolic disorders in dairy cattle

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Instant Insights: Metabolic disorders in dairy cattle

Länge:
244 Seiten
3 Stunden
Freigegeben:
Dec 8, 2020
ISBN:
9781786769329
Format:
Buch

Beschreibung

This specially curated collection features four reviews of current and key research on metabolic disorders in dairy cattle.

The first chapter reviews the prevalence, etiology and effects of ruminal acidosis, as well as ways to counteract it through regulation of ruminal pH. The chapter includes a case study on subacute rumen acidosis (SARA) in the post-partum phase of the transition period.

The second chapter assesses the main pathways for rumen fermentation which is a major factor in efficient transformation of nutrients. It discusses factors influencing the efficiency of microbial growth as well as the interactions between rumen energy and nitrogen metabolism in ensuring efficient digestion and avoiding metabolic disorders.

The third chapter investigates the genetics of improving feed intake efficiency which has significant potential in reducing metabolic disorders. The chapter reviews key challenges in developing genomic selection indices for feed intake, including recording feed intake, pooling genetic data and establishing genomic breeding values for feed efficiency.

The fourth chapter discusses how cereal grains impact feed efficiency in cattle. It reviews how cereal grains can be used to improve feed efficiency and the microbiology of cereal grain fermentation. The chapter also discusses ways of avoiding acidosis and other negative feed effects.
Freigegeben:
Dec 8, 2020
ISBN:
9781786769329
Format:
Buch

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Instant Insights - Dr Gregory B. Penner

BURLEIGH DODDS SCIENCE: INSTANT INSIGHTS

NUMBER 06

Metabolic disorders in dairy cattle

Published by Burleigh Dodds Science Publishing Limited

82 High Street, Sawston, Cambridge CB22 3HJ, UK

www.bdspublishing.com

Burleigh Dodds Science Publishing, 1518 Walnut Street, Suite 900, Philadelphia, PA 19102-3406, USA

First published 2021 by Burleigh Dodds Science Publishing Limited

© Burleigh Dodds Science Publishing, 2021. All rights reserved.

This book contains information obtained from authentic and highly regarded sources. Reprinted material is quoted with permission and sources are indicated. Reasonable efforts have been made to publish reliable data and information but the authors and the publisher cannot assume responsibility for the validity of all materials. Neither the authors nor the publisher, nor anyone else associated with this publication shall be liable for any loss, damage or liability directly or indirectly caused or alleged to be caused by this book.

No part of this publication may be reproduced, stored in a retrieval system or transmitted in any form or by any means electronic, mechanical, photocopying, recording or otherwise without the prior written permission of the publisher.

The consent of Burleigh Dodds Science Publishing Limited does not extend to copying for general distribution, for promotion, for creating new works, or for resale. Specific permission must be obtained in writing from Burleigh Dodds Science Publishing Limited for such copying.

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Notice

No responsibility is assumed by the publisher for any injury and/or damage to persons or property as a matter of product liability, negligence or otherwise, or from any use or operation of any methods, products, instructions or ideas contained in the material herein.

British Library Cataloguing in Publication Data

A catalogue record for this book is available from the British Library

ISBN 978-1-78676-931-2 (Print)

ISBN 978-1-78676-932-9 (ePub)

DOI 10.19103/9781786769329

Typeset by Deanta Global Publishing Services, Dublin, Ireland

Contents

1 Disorder of digestion and metabolism in dairy cattle: the case of subacute rumen acidosis

Gregory B. Penner, University of Saskatchewan, Canada

1 Introduction

2 Prevalence, aetiology, and biological consequences of ruminal acidosis

3 Regulation of ruminal pH

4 The dogma of ruminal acidosis

5 Case study: SARA risk in the post-partum phase of the transition period

6 Other examples SARA risk induced by low feed intake

7 Conclusion and future trends

8 Where to look for further information

9 References

2 Factors influencing the efficiency of rumen energy metabolism

Emilio M. Ungerfeld, Instituto de Investigaciones Agropecuarias (INIA), Chile; and Timothy J. Hackmann, University of California-Davis, USA

1 Introduction

2 Main pathways of rumen fermentation

3 Methane

4 Factors influencing the efficiency of microbial growth

5 Interactions between rumen energy and nitrogen metabolism

6 Conclusion and future trends

7 Where to look for further information

8 Where to look for further information

3 Advances in dairy cattle breeding to incorporate feed conversion efficiency in national genetic evaluations

Mike Coffey, Scotland’s Rural College (SRUC), UK

1 Introduction

2 The importance of feed efficiency as a target for breeding

3 Recording feed intake

4 Pooling genetic data on feed intake

5 Establishing genomic breeding values for feed efficiency

6 Future trends

7 Conclusion

8 Where to look for further information

9 References

4 The use of feedlot/cereal grains in improving feed efficiency and reducing by-products such as methane in ruminants

Kristian Hales, US Meat Animal Research Center – USDA-ARS, USA; Jeferson Lourenco, Darren S. Seidel, Osman Yasir Koyun, Dylan Davis and Christina Welch, University of Georgia, USA; James E. Wells, US Meat Animal Research Center – USDA-ARS, USA; and Todd R. Callaway, University of Georgia, USA

1 Introduction

2 Types of cereal grains fed to cattle

3 Cereal grain production

4 Dietary factors affecting methane production by ruminants

5 The role of starch and forage in methane formation

6 H2 sinks in the rumen and methane production

7 Using cereal grains to improve feed efficiency and reduce methane production

8 Microbiology of cereal grain fermentation

9 Bacteria and archaea involved in fermentation

10 Feed retention time

11 Acidosis and other negative feed effects

12 Summary

13 Where to look for further information

14 References

Chapter 1

Disorder of digestion and metabolism in dairy cattle: the case of subacute rumen acidosis

Gregory B. Penner, University of Saskatchewan, Canada

1 Introduction

2 Prevalence, aetiology, and biological consequences of ruminal acidosis

3 Regulation of ruminal pH

4 The dogma of ruminal acidosis

5 Case study: SARA risk in the post-partum phase of the transition period

6 Other examples SARA risk induced by low feed intake

7 Conclusion and future trends

8 Where to look for further information

9 References

1 Introduction

Given the high milk and milk component yield of current dairy cattle, feeding energy-dense diets is necessary to meet nutrient requirements. Typically, this entails the use of diets that are highly fermentable. While these diets are necessary to meet nutrient demand, excessive fermentation in the rumen decreases ruminal pH and leads to a digestive disorder called ruminal acidosis. Ruminal acidosis has been investigated extensively and has been reported, on an individual cow basis, to be associated with reduced milk production (Stone, 2004), reduced milk fat yield (Gao and Oba, 2016), laminitis (Nocek, 1997) and liver abscesses. Additional responses to ruminal acidosis include variable feed intake and altered feed sorting. Ruminal acidosis also decreases NDF digestibility (Calsamiglia et al., 2002), demonstrating a direct effect of pH on microbial activity. Others have also shown that exposing rumen tissue to low pH (pH 5.2) reduces nutrient absorption (Gaebel and Martens, 1988; Wilson et al., 2012; Schwaiger et al., 2014), and increases permeability of the tissue allowing non-desired compounds to cross (Aschenbach et al., 2000; Penner et al., 2010). Correspondingly, induction of ruminal acidosis induces a systemic inflammatory response as indicated by elevated serum amyloid A, haptoglobin and lipopolysaccharide (LPS)-binding protein (Plaizier et al., 2012), indicating that ruminal acidosis can have detrimental effects extending beyond those observed in the rumen. Thus, there is a dilemma – how to balance the need for highly fermentable diets while minimizing the risk for ruminal acidosis.

2 Prevalence, aetiology and biological consequences of ruminal acidosis

Ruminal acidosis is arguably the most common digestive disorder in conventional dairy production (Penner and Beauchemin, 2010). Data obtained, using ruminocentesis, in lactating dairy cattle in the United States suggest that prevalence rates range between 19 and 40%, depending on the stage of lactation (Krause and Oetzel, 2006). More recent data using continuous ruminal pH measurement have indicated that the prevalence may be higher than those previously reported. In fact, during the post-partum phase of the transition period prevalence rates may exceed 60% (Penner et al., 2007, 2009). While intensive feeding management is often implicated with ruminal acidosis, there is considerable evidence to suggest that ruminal acidosis can occur on pasture when cattle are fed high-quality fresh forages, especially when supplemental silage or grain is provided (Bargo et al., 2002; Kolver and de Veth, 2002; O’Grady et al., 2008). Moreover, Holstein calves at the time of weaning also have ruminal pH profiles indicative of ruminal acidosis (Suarez et al., 2006; Laarman et al., 2012; Wood et al., 2015), suggesting that ruminal acidosis is not limited to lactating cows.

Ruminal acidosis can be classified as acute or subacute (SARA). The most common form of ruminal acidosis in dairy cattle is thought to be SARA, whereas lactic acidosis or acute acidosis is thought to be the primary form in beef cattle fed high-concentrate diets (Schwaiger et al., 2013a,b). Subacute ruminal acidosis (SARA) (pH < 5.8) is caused by a rapid rate of short-chain fatty acid (SCFA) production while, for acute acidosis (pH < 5.2), the pH depression is often associated with an increase in lactic acid (Owens et al., 1998). For SARA, the resulting low pH is caused by rates of SCFA production and subsequent dissociation that exceeds the capability of cattle to remove acid from the rumen. While thresholds are used to characterize ruminal acidosis, the actual pH value that induces damage to the ruminal epithelium, alters the microbial community structure and activity, and results in depressed feed intake likely varies among animals. This sequence of events associated with low ruminal pH is demonstrated in Fig. 1. In Fig. 1, although concrete pH thresholds are shown, it should be noted that pH is on a continuum and that absolute values are from a point of reference rather than quantitative in nature.

Figure 1 Cascade of events associated with ruminal acidosis. Corresponding with rapid fermentation, bacterial growth and activity in the rumen increases leading to greater production of short-chain fatty acids (SCFA). Under normal situations, a mild reduction in ruminal pH can be observed followed by recovery of ruminal pH as the quantity of fermentable carbohydrate decreases and consequently, bacterial growth rates decrease. However, if bacterial fermentation rates do not decline, SCFA production drives an increase in ruminal fluid osmolarity and a decrease in ruminal pH. The red arrows show the consequential impacts of ruminal acidosis leading to inflammation. For example, low ruminal pH and high osmolarity cause a reduction in both absorptive and barrier function of the ruminal epithelium. Low pH causes acid-sensitive bacteria to lyse and when combined with decreased barrier function it increases the risk for pathogen and antigen translocation leading to systemic inflammation and secondary diseases such as liver abscesses and laminitis. However, ruminal pH can recover thereby resuming normal ruminal fermentation and pH profiles (based on Owens et al., 1988).

Simply stated, ruminal acidosis occurs when the rate of acid production exceeds the rate of acid removal from the rumen. Ruminal acidosis has been characterized based on the extent of ruminal pH depression with mild reductions (pH < 5.8) referred to as SARA, and more severe reductions defined as acute ruminal acidosis (<5.2). It should be noted that there is substantial variation in ruminal pH among cows within a herd, and for individuals within a day (Penner et al., 2007). Some cattle are also more tolerant of low ruminal pH than others (Penner et al., 2007, 2009a). Thus, the ruminal pH thresholds used to characterize SARA and acute ruminal acidosis are used as a guideline rather than true biological threshold. Nevertheless, as fermentation proceeds, microbial activity is stimulated resulting in the production of SCFAs and an increase in osmolality. The decrease in ruminal pH has received most attention and is a causative factor, in isolation, for many of the observed consequences. For example, inducing low pH (5.6) in in vitro culture systems has been reported to decrease NDF digestibility (Calsamiglia et al., 2002) demonstrating a direct effect of pH on microbial activity. Others have also shown that exposing ruminal tissue to low pH (pH 5.2) ex vivo reduces nutrient absorption (Gaebel and Martens, 1988; Wilson et al., 2012; Schwaiger et al., 2014), and increases permeability of the tissue allowing non-desired compounds to cross (Aschenbach et al., 2000; Penner et al., 2010). Thus, clearly low pH can have detrimental effects. That said, osmolality also increases in association with increased rates of fermentation. Osmolality refers to the concentration of dissolved solutes, and in the rumen, SCFAs are the primary dissolved solutes. Very little research has evaluated the effect of osmolality, but it is clear that high osmolality increases permeability of rumen tissue (Schwiegel et al., 2005; Lodemann and Martens, 2006). More recently, Penner et al. (2010) compared the effects of low pH and hyperosmolality on permeability of ruminal tissue. In that study, they exposed tissues to control conditions of pH 6.2 and an osmolality of 300 mOsmol/kg (similar to that in the rumen). Osmolality was then increased to 450 mOsmol/kg for one treatment and pH was reduced to 5.2 for another treatment. Those conditions were held for 1 h and then the tissues were exposed to the control conditions. That study demonstrated that high osmolality has an acute effect and increase tissue permeability, whereas the effect of low pH did not occur until tissues were returned to control conditions. This suggests that with conditions that occur with ruminal acidosis, high osmolality will immediately increase tissue permeability with low pH having more persistent effects even after the pH has recovered. Only one study has combined the effects of low ruminal pH and high osmolality (Wilson et al., 2012) and they noted a strong reduction for SCFA absorption and increased tissue permeability ex vivo. It should also be noted that induction of ruminal acidosis causes a reduction in pH in more distal regions of the gastrointestinal tract (Fig. 2) where not only was ruminal and omasal pH reduced, but also pH of the large intestinal regions was also reduced. While this is known to occur, the relevance of reduced pH in the large intestine is still not fully understood.

Figure 2 Effect of inducing ruminal acidosis on the pH of rumen, duodenum, jejunum, ileum, caecum, and proximal and distal colon in sheep. Data adapted from Pederzolli (2016).

SCFA production and their subsequent dissociation drive the reduction in ruminal pH (Fig. 1; Aschenbach et al., 2011). It should be noted that this process is normal and is not indicative of ruminal acidosis. However, under normal scenarios, the relative rate of acid production subsequently declines and that of acid removal (via neutralization and passage) increases allowing for stabilization and recovery of ruminal pH. However, in some cases, ruminal pH continues to decline leading to ruminal pH values that can compromise barrier function of the ruminal epithelium. In addition, as pH declines, ruminal concentration of antigens such as LPS increase, thereby heightening the risk of antigen translocation. If the ruminal epithelium is damaged, pathogen translocation may also occur. The translocation of antigens and pathogens can serve to stimulate a systemic immune response leading to increased acute phase proteins in venous circulation (Plaizier et al., 2012). The magnitude of the previously mentioned response is multi-factorial and includes dietary composition (Khafipour et al., 2009), the magnitude and extent of pH depression, and host factors such as tolerance to low ruminal pH.

As a consequence of rapid fermentation, microbial growth increases. Some researchers have suggested that with rapid growth, microbes may shed components of their cell while others may die and lyse, thereby releasing cell wall components (Plaizier et al., 2012). As such, an increase in LPS (an endotoxin) concentration in the rumen (Gohzo et al., 2005; Ametaj et al., 2010) is commonly observed with ruminal acidosis. This increase in LPS has also been observed to occur in other regions of the gastrointestinal tract (Plaizier et al., 2014). While LPS has been investigated extensively, it is likely that other compounds (components of bacteria) that can stimulate a pro-inflammatory response also increase including lipoteichoic acid, flagellin, leucotoxin and bacterial DNA. Others have also noted increased histamine in ruminal fluid in association with ruminal acidosis and increased permeability of the ruminal epithelium when exposed to ruminal acidosis-like conditions (pH 5.2) ex vivo (Gabel and Aschenbach, 2002). It is hypothesized that these compounds enter cells lining the gastrointestinal tract

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