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DUNCAN & PRASSE’S VETERINARY LABORATORY MEDICINE: CLINICAL PATHOLOGY Fifth Edition Companion website This book is accompanied by a companion website: www.wiley.com/go/latimer The website includes: • All images from the book for downloading in PowerPoint • All references hyperlinked to PubMed DU...

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DUNCAN & PRASSE’S VETERINARY LABORATORY MEDICINE: CLINICAL PATHOLOGY Fifth Edition

Companion website This book is accompanied by a companion website: www.wiley.com/go/latimer The website includes: • All images from the book for downloading in PowerPoint • All references hyperlinked to PubMed

DUNCAN & PRASSE’S

VETERINARY LABORATORY MEDICINE:

CLINICAL PATHOLOGY Fifth Edition

KENNETH S. LATIMER

A John Wiley & Sons, Inc., Publication

This edition irst published 2011 © 2011 by John Wiley & Sons, Inc. Previous editions © 1977, 1986, 1994, 2003 Iowa State University Press Wiley-Blackwell is an imprint of John Wiley & Sons, formed by the merger of Wiley’s global Scientiic, Technical and Medical business with Blackwell Publishing. Registered ofice:

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For details of our global editorial ofices, for customer services and for information about how to apply for permission to reuse the copyright material in this book please see our website at www.wiley.com/wiley-blackwell. Authorization to photocopy items for internal or personal use, or the internal or personal use of speciic clients, is granted by Blackwell Publishing, provided that the base fee is paid directly to the Copyright Clearance Center, 222 Rosewood Drive, Danvers, MA 01923. For those organizations that have been granted a photocopy license by CCC, a separate system of payments has been arranged. The fee codes for users of the Transactional Reporting Service are ISBN-13: 978-0-8138-2014-9/2011. Designations used by companies to distinguish their products are often claimed as trademarks. All brand names and product names used in this book are trade names, service marks, trademarks or registered trademarks of their respective owners. The publisher is not associated with any product or vendor mentioned in this book. This publication is designed to provide accurate and authoritative information in regard to the subject matter covered. It is sold on the understanding that the publisher is not engaged in rendering professional services. If professional advice or other expert assistance is required, the services of a competent professional should be sought. Library of Congress Cataloging-in-Publication Data Duncan & Prasse’s veterinary laboratory medicine : clinical pathology / [edited by] Kenneth S. Latimer. – 5th ed. p. ; cm. Duncan and Prasse’s veterinary laboratory medicine Veterinary laboratory medicine Rev. ed. of: Duncan & Prasse’s veterinary laboratory medicine / Kenneth S. Latimer, Edward a. Mahaffey, Keith W. Prasse. 4th ed. 2003. Includes bibliographical references and index. ISBN 978-0-8138-2014-9 (hardcover : alk. paper) 1. Veterinary clinical pathology. I. Latimer, Kenneth S. II. Duncan, J. Robert. III. Latimer, Kenneth S. Duncan & Prasse’s veterinary laboratory medicine. IV. Title: Duncan and Prasse’s veterinary laboratory medicine. V. Title: Veterinary laboratory medicine. [DNLM: 1. Pathology, Veterinary–Outlines. 2. Pathology, Clinical–Outlines. SF 772.6] SF772.6.D86 2011 636.089'607–dc22 2010049553 A catalogue record for this book is available from the British Library. Set in 9.5/11.5 pt Berkeley by Toppan Best-set Premedia Limited

Disclaimer The publisher and the author make no representations or warranties with respect to the accuracy or completeness of the contents of this work and speciically disclaim all warranties, including without limitation warranties of itness for a particular purpose. No warranty may be created or extended by sales or promotional materials. The advice and strategies contained herein may not be suitable for every situation. This work is sold with the understanding that the publisher is not engaged in rendering legal, accounting, or other professional services. If professional assistance is required, the services of a competent professional person should be sought. Neither the publisher nor the author shall be liable for damages arising herefrom. The fact that an organization or Website is referred to in this work as a citation and/or a potential source of further information does not mean that the author or the publisher endorses the information the organization or Website may provide or recommendations it may make. Further, readers should be aware that Internet Websites listed in this work may have changed or disappeared between when this work was written and when it is read. 1

2011

TABLE OF CONTENTS

Contributing Authors PrefACe

vii

ix

ACknowledgments

xi

ChAPter 1.

erythroCytes 3

ChAPter 2.

leukoCytes 45

ChAPter 3.

hemAtoPoietiC neoPlAsiA 83

ChAPter 4.

hemostAsis 107

ChAPter 5.

wAter, eleCtrolytes,

And

ChAPter 6.

Proteins, liPids,

CArbohydrAtes 173

ChAPter 7.

liver 211

ChAPter 8.

digestive system 231

ChAPter 9.

urinAry system 253

ChAPter 10.

musCle 283

ChAPter 11.

endoCrine system 295

ChAPter 12.

Cytology 331

ChAPter 13.

generAting And interPreting test results: test vAlidity, QuAlity Control, referenCe vAlues, And bAsiC ePidemiology 365

And

ACid bAse 145

CAse studies 383 index 475

Companion website This book is accompanied by a companion website: www.wiley.com/go/latimer The website includes: • All images from the book for downloading in PowerPoint • All references hyperlinked to PubMed v

CONTRIBUTING AUTHORS

Perry J. Bain, DVM, PhD Diplomate, American College of Veterinary Pathologists Assistant Professor Department of Biomedical Sciences Large Animal Hospital Cummings School of Veterinary Medicine at Tufts University North Grafton, MA 01536 Holly S. Bender, DVM, PhD Diplomate, American College of Veterinary Pathologists Professor Department of Veterinary Pathology College of Veterinary Medicine Iowa State University Ames, IA 50011 Dorothee Bienzle, DVM, MSc, PhD Diplomate, American College of Veterinary Pathologists Professor and Canada Research Chair in Veterinary Pathology Department of Pathobiology Ontario Veterinary College University of Guelph Guelph, Ontario, Canada N1G 2W1 Mary K. Boudreaux, DVM, PhD Professor Department of Pathobiology College of Veterinary Medicine Auburn University, AL 36849 Denise I. Bounous, DVM, PhD Medical Technologist (American Society of Clinical Pathologists) Diplomate, American College of Veterinary Pathologists Group Director, Drug Safety Evaluation Bristol-Myers Squibb Princeton, NJ 08543

Charles W. Brockus, DVM, PhD Diplomate, American College of Veterinary Internal Medicine Diplomate, American College of Veterinary Pathologists Charles River Reno, NV 89511 Ellen W. Evans, DVM, PhD Diplomate, American College of Veterinary Pathologists Senior Director, Immunotoxicology Center of Emphasis Pizer, Inc. Groton, CT 06340 Duncan C. Ferguson, VMD, PhD Diplomate, American College of Veterinary Internal Medicine Diplomate, American College of Veterinary Clinical Pharmacology Professor and Head Department of Veterinary Biosciences College of Veterinary Medicine University of Illinois at Urbana-Champaign Urbana, IL 61802 Jeanne W. George, DVM, PhD Diplomate, American College of Veterinary Pathologists Professor Emeritus Department of Pathology, Microbiology and Immunology School of Veterinary Medicine University of California-Davis Davis, CA 95616

vii

viii

CONTRIBUTING AUTHORS

Christopher R. Gregory, DVM, PhD Medical Technologist (American Society of Clinical Pathologists) Associate Research Scientist Department of Small Animal Medicine College of Veterinary Medicine The University of Georgia Athens, GA 30602 Robert L. Hall, DVM, PhD Diplomate, American College of Veterinary Pathologists Covance Laboratories, Inc. Madison, WI 53704

Elizabeth A. Spangler, DVM, PhD Diplomate, American College of Veterinary Pathologists Diplomate, American College of Veterinary Internal Medicine Assistant Professor Department of Pathobiology College of Veterinary Medicine Auburn University, AL 36849 Heather L. Tarpley, DVM Diplomate, American College of Veterinary Pathologists Chestatee Animal Hospital Dahlonega, GA 30533

Margarethe Hoenig, Dr med vet, PhD Professor Department of Veterinary Clinical Medicine College of Veterinary Medicine University of Illinois at Urbana-Champaign Urbana, IL 61802

Niraj K. Tripathi, BVScAH, MVSc, PhD Diplomate, American College of Veterinary Pathologists Covance Laboratories, Inc. Madison, WI 53704

Paula M. Krimer, DVM, DVSc Diplomate, American College of Veterinary Pathologists Assistant Professor Athens Veterinary Diagnostic Laboratory College of Veterinary Medicine The University of Georgia Athens, GA 30602

Julie L. Webb, DVM Diplomate, American College of Veterinary Pathologists Instructor Department of Pathobiological Sciences College of Veterinary Medicine University of Wisconsin Madison, WI 53706

Kenneth S. Latimer, DVM, PhD Diplomate, American College of Veterinary Pathologists Covance Laboratories, Inc. Vienna, VA 22182 and Professor Emeritus Department of Pathology College of Veterinary Medicine The University of Georgia Athens, GA 30602

Elizabeth G. Welles, DVM, PhD Diplomate, American College of Veterinary Pathologists Professor Department of Pathobiology College of Veterinary Medicine Auburn University Auburn, AL 36849

Pauline M. Rakich, DVM, PhD Diplomate, American College of Veterinary Pathologists Professor Athens Veterinary Diagnostic Laboratory College of Veterinary Medicine The University of Georgia Athens, GA 30602

Shanon M. Zabolotzky, DVM Diplomate, American College of Veterinary Pathologists Clinical Pathologist IDEXX Laboratories, Inc. West Sacramento, CA 95605

PREFACE

The publication of the ifth edition of Duncan & Prasse’s Veterinary Laboratory Medicine: Clinical Pathology represents a collation and distillation of educational information about veterinary clinical pathology that spans almost 40 years. Prior to retirement, Drs. Duncan and Prasse (Figure 1) established a legacy of excellence in teaching, diagnostic service, and applied research in veterinary clinical pathology that endures to the present day. This textbook has evolved along with the specialty of veterinary clinical pathology. Since the initial American College of Veterinary Pathologists (ACVP) certiication of Drs. Duncan and Prasse in clinical pathology, some of the new authors of this text now represent the third generation of veterinary clinical pathologists. General authorship also has continued to expand and the expertise of all coauthors has added a new dimension and considerable depth to the ifth edition of this textbook. Hopefully, a new editor will continue this legacy in the future to educate another generation of veterinary students, interns, residents, clinicians, and practitioners in the science, art, and practice of interpreting laboratory data.

Dr. J. Robert Duncan, Professor Emeritus (left), and Dr. Keith W. Prasse, Retired Dean (right), The University of Georgia College of Veterinary Medicine.

ix

ACKNOWLEDGMENTS

This ifth edition of edition of Duncan & Prasse’s Veterinary Laboratory Medicine: Clinical Pathology would not have been possible without the assistance of several new and many repeat authors. Their professional contributions to this textbook are gratefully acknowledged and will have a positive impact on patient diagnostics and care. I would also like to recognize colleagues, clinical and anatomic pathology residents, veterinary students, and practicing veterinarians who have continued to provide the professional feedback that has improved the revision of this textbook. Kip Carter, MS, CMI, at The University of Georgia College of Veterinary Medicine again revised several line drawings. Erica Judisch, Nancy Turner, and the production staff at Wiley-Blackwell provided the professional assistance that was essential for the timely printing of this new edition. With the completion of this project, I can once again enjoy life with the whippets at home, in the show ring, and on the lure coursing ield.

Cody (FC Longlesson Private Conversation) on the ield and looking for action. Image courtesy of Julie Poole Photography, Knoxville, TN.

xi

DUNCAN & PRASSE’S VETERINARY LABORATORY MEDICINE: CLINICAL PATHOLOGY Fifth Edition

CHAPTER 1

ERYTHROCYTES Charles W. Brockus, DVM, PhD

BASIC CONCEPTS OF ERYTHROCYTE FUNCTION, METABOLISM, PRODUCTION, AND BREAKDOWN I. THE ERYTHRON

A. This widely dispersed mass of erythroid cells includes circulating erythrocytes and bone marrow precursor, progenitor, and stem cells. B. Its function is oxygen transport, which is mediated by hemoglobin. C. Hemoglobin is transported in erythrocytes whose membrane, shape, cytoskeleton, and metabolic processes ensure survival of the cell against the stresses of circulation and various injurious substances. D. Hemoglobin consists of heme and globin, and each complete hemoglobin molecule is a tetramer. 1. Each heme moiety contains an iron atom in the 2+ valence state (Fe2+). 2. A globin chain of speciic amino acid sequence is attached to each heme group. 3. The complete hemoglobin molecule is a tetramer, containing four heme units and four globin chains. The globin chains are identical pairs (dimers), designated as α-chains or δ-chains.

II. HEME SYNTHESIS

A. Heme synthesis is unidirectional and irreversible. It is controlled at the irst step by the enzyme δ-aminolevulinic acid synthase, whose synthesis is controlled by negative feedback from heme concentration within the erythrocyte. 1. Lead inhibits most of the steps in heme synthesis to some degree. Lead also inhibits the delivery of iron to the site of ferrochelatase activity. 2. Chloramphenicol may inhibit heme synthesis. B. Porphyrins and their precursors are the intermediates of heme biosynthesis. 1. Certain enzyme deiciencies in the synthetic pathway can lead to excessive accumulation of porphyrins and their precursors. 2. These excesses of porphyrins and their precursors are called porphyrias. 3. Porphyrias vary in the intermediate products that accumulate and in their clinical manifestations. 4. These excess porphyrins escape the erythrocyte and may be deposited in the tissues or excreted in the urine and other body luids. C. After formation of protoporphyrin, iron is inserted into the molecule by ferrochelatase, and heme is formed. 3

4

CHAPTER 1

III. GLOBIN SYNTHESIS

A. Each hemoglobin molecule is comprised of four globin chains, each of which binds to a heme group. 1. The hemoglobin type depends on the type of globin chains, which are determined by amino acid sequences. a. Embryonic, fetal, and adult hemoglobins are found in various animals. b. The presence and number of each hemoglobin type vary with the species. 2. Heme and globin synthesis are balanced (increase in one results in an increase in the other). B. Abnormalities in globin synthesis (i.e., hemoglobinopathies) have not been described in domestic animals.

IV. IRON METABOLISM

Body iron metabolism/content is based on an extremely eficient system of conservation and recycling that is regulated by the rate of duodenal absorption rather than excretion. Hepcidin is a recently identiied 25 amino acid peptide (bioactive form) produced within the liver and transported within the blood by α-2-macroglobulin. It has been found to play a key role in mediation of iron metabolism. In short, increased hepcidin is accompanied by a decrease in iron availability, whereas decreased Hepcidin is associated with an increase in iron availability. Hepcidin is a component of the type II acute phase response induced by interleukin-6 and controls plasma iron concentration by inhibiting iron export by ferroportin from enterocytes and macrophages. Absorption is regulated by the amount of storage iron (large iron stores decrease absorption) and rate of erythropoiesis (accelerated erythropoiesis increases absorption). Less than 0.05% of the total body iron is acquired or lost each day. A. Iron is transported in blood bound to the δ-globulin, transferrin. 1. Iron bound to transferrin is measured as serum iron (SI). This is an unreliable measure of total body iron stores. a. Conditions with decreased SI (1) Iron deiciency (2) Acute and chronic inlammation or disease (including anemia of inlammatory disease) (3) Hypoproteinemia (4) Hypothyroidism (5) Renal disease b. Conditions with increased SI (1) Hemolytic anemia (2) Accidental lysis of erythrocytes during sampling (hemolysis) (3) Glucocorticoid excess in the dog and horse. In contrast, SI is decreased in cattle with glucocorticoid excess. (4) Iron overload, which may be an acquired (e.g., iron toxicity) or hereditary (e.g., hemochromatosis in Salers cattle) condition. Iron overload in some birds (e.g., mynahs and toucans) also may be hereditary. (5) Nonregenerative anemia c. SI can be expressed as a percentage of total iron-binding capacity (TIBC, see below) and reported as the percent saturation. 2. TIBC is an indirect measurement of the amount of iron that transferrin will bind. An immunologic method is available to quantitate transferrin, but is not used commonly. a. Only one-third of transferrin binding sites usually are occupied by iron. This is expressed as percent saturation. b. TIBC is increased in iron deiciency in most species except the dog.

ERYTHROCYTES

5

3. Transferrin can bind more iron than is normally present. Therefore, the numeric difference between TIBC and SI is the amount of iron-binding capacity remaining on transferrin or the unbound iron-binding capacity (UIBC). B. Hepcidin has been found to be the main regulator of iron homeostasis; it is produced in the liver and acts systemically in iron overloading (increased) or in response to anemia or hypoxia (decreased). Hephaestin (an intestinal ceruloplasmin analog) and ceruloplasmin (synthesized in the liver) are both copper-containing proteins involved in iron transport. Ceruloplasmin also is an acute phase inlammatory reactant. Ferroportin 1 and divalent metal transporter 1 (DMT1) are necessary for transfer of iron from intestinal epithelium and macrophages to serum transferrin. Hepcidin induces the internalization and degradation of ferroportin, thereby inhibiting iron transport. C. Iron is incorporated into hemoglobin during the last step of heme synthesis. Lack of intracellular iron causes an increase in erythrocyte protoporphyrin concentration. D. Iron is stored in macrophages as ferritin and hemosiderin. E. Ferritin is a water-soluble iron-protein complex. 1. Ferritin is the more labile storage form of iron. 2. Small amounts circulate that can be measured as serum ferritin, which is an indirect measurement of the storage iron pool. A species-speciic immunoassay is required. a. Serum ferritin concentration is decreased in iron deiciency. b. Serum ferritin concentration is increased in the following: (1) Hemolytic anemia (2) Iron overload (3) Acute and chronic inlammation (4) Liver disease (5) Some neoplastic disorders (e.g., lymphoma, malignant histiocytosis) (6) Malnutrition (cattle) F. Hemosiderin is a more stable, but less available, storage form of iron that is comprised of native and denatured ferritin and protein. It is not water-soluble and is stainable within tissues by Perl’s or Prussian blue techniques. G. Abnormalities in serum iron are re...