The Feline Patient, 4th Edition

The Feline Patient Fourth Edition

The Feline Patient Fourth Edition

Editor

Gary D. Norsworthy, DVM, DABVP (Feline)

Founding Authors

Gary D. Norsworthy, DVM, DABVP (Feline) Mitchell A. Crystal, DVM, DACVIM (Internal Medicine) Sharon Fooshee Grace, MAgric, MS, DVM, DABVP (Canine-Feline), DACVIM (Internal Medicine) Larry P. Tilley, DVM, DACVIM (Internal Medicine)

A John Wiley & Sons, Inc., Publication

Edition first published 2011 © 2011 Blackwell Publishing Ltd. Blackwell Publishing was acquired by John Wiley & Sons in February 2007. Blackwell’s publishing program has been merged with Wiley’s global Scientific, Technical, and Medical business to form Wiley-Blackwell. Editorial Office 2121 State Avenue, Ames, Iowa 50014-8300, USA For details of our global editorial offices, 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 specific 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 code for users of the Transactional Reporting Service is ISBN-13: 978-0-8138-1848-1/2011. 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 The feline patient / editor, Gary D. Norsworthy. – 4th ed. p. ; cm. Includes bibliographical references and index. ISBN 978-0-8138-1848-1 (hardback : alk. paper) 1. Cats–Diseases. I. Norsworthy, Gary D. [DNLM: 1. Cat Diseases–diagnosis. 2. Cat Diseases–therapy. SF985.F46 2011 636.8′0896–dc22

SF 985 F3156 2011]

2010020439 A catalog record for this book is available from the U.S. Library of Congress. Set in 8/10pt Palatino by Toppan Best-set Premedia Limited Printed in Singapore 1

2011

Dedications Gary D. Norsworthy The previous editions of this book have been dedicated to my family members who have stood behind me in this effort, to primary care practitioners who are the first deliver care to feline patients, to secondary care practitioners who deliver the next level of care, to researchers who discover the future level of care, and to veterinary students who will deliver the future level of care. For this edition I would like to repeat my appreciation to each of those groups and add to them the externs who have spent time in my practice. You keep me rejuvenated and refreshed with your enthusiasm for the future of feline medicine. I would also like to express appreciation to my staff: Drs. Anderson and Macdonald, Amanda, Linda, Emily, Stephanie, Rachel, Lorenzo, Lewis, Stacey, Veronica, Laura, Melody, and Kelsey. Each of you has contributed to this in ways you may not realize.

Sharon Fooshee Grace Dedicated to: My Lord and Savior, Jesus Christ; My family, Pete, Branion, and Mary; The memory of my parents, Joel and Janie Fooshee; and And Cleopatra, the kitten who continues to inspire me.

Mitchell A. Crystal I dedicate this book to all those who make up the veterinary profession who have treated me so kindly and allowed me to achieve so much. I hope in this book I have given something back to you. I dedicate this book to my family, Sue, Samantha, Matthew, Bunny, Kacy and Heidi, thanks for teaching me to have fun, to try my best, and to be a good sport. I dedicate this book to Gary Norsworthy who keeps all of us on track and on time, who dots all the i’s and crosses all the t’s, and who is the face, heart, and soul of The Feline Patient.

Larry P. Tilley To my wife, Jeri, and my son, Kyle, in honor of that secret correspondence within our hearts; To Tucker, our new grandson who represents the purity of life.

Contents Founding Authors / xiii Contributors / xiv Preface / xvii

Section 1: Diseases and Conditions 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52

Acetaminophen Toxicosis Sharon Fooshee Grace / 5 Acne Christine A. Rees / 7 Acromegaly Sharon Fooshee Grace / 8 Actinomycosis Sharon Fooshee Grace / 10 Adenocarcinoma and Carcinoma Mark Robson / 12 Amyloidosis Andrew Sparkes / 14 Anal Sac Disease Gary D. Norsworthy / 16 Anaplasmosis Sharon Fooshee Grace / 18 Anemia Sharon Fooshee Grace / 19 Anorexia Mitchell A. Crystal / 22 Aortic Stenosis Larry P. Tilley / 24 Arrhythmias Larry P. Tilley and Francis W. K. Smith, Jr. / 26 Ascites Larry P. Tilley / 28 Aspergillosis Sharon Fooshee Grace / 30 Aspirin Toxicosis Sharon Fooshee Grace / 32 Atopic Dermatitis Christine A. Rees / 33 Bartonellosis Mark Robson and Mitchell A. Crystal / 35 Basal Cell Tumor Bradley R. Schmidt and Mitchell A. Crystal / 37 Biliary Cysts Michele Fradin-Fermé / 39 Bite Wounds: Canine Gary D. Norsworthy / 41 Bite Wounds: Feline Gary D. Norsworthy / 44 Blastomycosis Sharon Fooshee Grace / 46 Blindness Karen R. Brantman and Harriet J. Davidson / 48 Bordetella Infection Teija Kaarina Viita-aho / 50 Brachial Plexus Neuropathy Gary D. Norsworthy / 52 Brachycephalic Syndrome Mac Maxwell and Gary D. Norsworthy / 53 Bronchial Disease, Chronic Philip Padrid / 58 Calicivirus Infection Gary D. Norsworthy / 62 Carcinomatosis Bradley R. Schmidt / 65 Cardiopulmonary Arrest Larry P. Tilley / 67 Cataracts Shelby L. Reinstein and Harriet J. Davidson / 70 Ceruminous Gland Disease Mark Robson / 72 Cervical Ventroflexion Mitchell A. Crystal and Paula B. Levine / 74 Chemotherapy for Lymphoma Mitchell A. Crystal and Bradley R. Schmidt / 76 Chlamydophila Infection Teija Kaarina Viita-aho / 81 Chylothorax Gary D. Norsworthy / 83 Cobalamin Deficiency Jörg M. Steiner / 85 Coccidiomycosis Sharon Fooshee Grace / 87 Coccidiosis Mark Robson and Mitchell A. Crystal / 89 Constipation and Obstipation Sharon Fooshee Grace and Mitchell A. Crystal / 91 Corneal Ulcers Gwen H. Sila and Harriet J. Davidson / 93 Coughing Gary D. Norsworthy / 96 Cryptococcosis Sharon Fooshee Grace / 97 Cryptosporidiosis Mark Robson and Mitchell A. Crystal / 100 Cutaneous Markers of Internal Disease Christine A. Rees / 102 Cuterebra Sharon Fooshee Grace / 104 Cytauxzoonosis Mark Robson and Mitchell A. Crystal / 106 Dermatophytosis Christine A. Rees / 108 Diabetes Insipidus Andrew Sparkes / 111 Diabetes Mellitus: Chronic Complications Gary D. Norsworthy / 113 Diabetes Mellitus: Ketoacidosis Jacquie Rand / 115 Diabetes Mellitus: Uncomplicated Jacquie Rand / 118

vii

Contents

53 54 55 56 57 58 59 60 61 62 63 64 65 66 67 68 69 70 71 72 73 74 75 76 77 78 79 80 81 82 83 84 85 86 87 88 89 90 91 92 93 94 95 96 97 98 99 100 101 102 103 104 105 106 107 108 109 110 111 112 113 114 115 116 117 118

viii

Diaphragmatic Hernia Gary D. Norsworthy / 121 Diarrhea Mitchell A. Crystal and Mark C. Walker / 124 Digital Diseases Mitchell A. Crystal and Paula B. Levine / 126 Dilated Cardiomyopathy Larry P. Tilley / 129 Draining Tracts and Nodules Christine A. Rees / 131 Dysautonomia Karen M. Lovelace / 134 Dyspnea Gary D. Norsworthy / 136 Dystocia Gary D. Norsworthy / 138 Dysuria, Pollakiuria, and Stranguria Gary D. Norsworthy / 140 Ear Mites Sharon Fooshee Grace / 143 Envenomization: Arachnids Tatiana Weissova / 145 Envenomization: Insects Tatiana Weissova / 148 Envenomization: Snakes Tatiana Weissova / 151 Eosinophilic Granuloma Complex Christine A. Rees / 154 Eosinophilic Keratitis Gwen H Sila and Harriet J. Davidson / 157 Epilepsy Teija Kaarina Viita-aho / 159 Esophageal Disease Andrew Sparkes / 162 Ethylene Glycol Toxicity Tatiana Weissova and Gary D. Norsworthy / 167 Exocrine Pancreatic Insufficiency Jörg M. Steiner / 169 Eyelid Diseases and Surgery Gwen H. Sila and Harriet J. Davidson / 171 Feline Enteric Coronavirus Infection Amanda L. Lumsden and Gary D. Norsworthy / 175 Feline Idiopathic Cystitis Tatiana Weissova and Gary D. Norsworthy / 176 Feline Immunodeficiency Virus Infection Sharon Fooshee Grace / 179 Feline Infectious Peritonitis Gary D. Norsworthy / 181 Feline Leukemia Virus Diseases Fernanda Vieira Amorim da Costa and Gary D. Norsworthy / 184 Fever Mitchell A. Crystal and Paula B. Levine / 187 Flea Allergy Dermatitis Christine A. Rees / 189 Fleas Sharon Fooshee Grace / 191 Flukes: Liver, Biliary, and Pancreatic Gary D. Norsworthy / 193 Food Reaction Christine A. Rees / 195 Giardiasis Mark Robson and Mitchell A. Crystal / 197 Gingivitis-Stomatitis-Pharyngitis Mark Robson and Mitchell A. Crystal / 199 Glaucoma Shelby L. Reinstein and Harriet J. Davidson / 202 Glomerulonephritis Gary D. Norsworthy / 205 Granulosa Cell Tumor Fernanda Vieira Amorim da Costa and Heloisa Justen Moreira de Souza / 207 Heartworm Disease Jane E. Brunt / 208 Heinz Body and Methemoglobinemia Anemia Sharon Fooshee Grace / 211 Helicobacter Mark Robson and Mitchell A. Crystal / 213 Hemangiosarcoma Bradley R. Schmidt / 215 Hemoplasmosis Sharon Fooshee Grace and Gary D. Norsworthy / 218 Hepatic Lipidosis Gary D. Norsworthy / 220 Hepatitis, Inflammatory Sharon Fooshee Grace / 222 Herpesvirus Infection Sharon Fooshee Grace / 225 High-Rise Syndrome Mitchell A. Crystal / 228 Histoplasmosis Sharon Fooshee Grace / 231 Hookworms Mitchell A. Crystal and Mark C. Walker / 234 Horner’s Syndrome Sharon Fooshee Grace / 235 Hydronephrosis Gary D. Norsworthy / 237 Hyperadrenocorticism Karen M. Lovelace / 239 Hyperaldosteronism Andrew Sparkes / 241 Hypercalcemia Michele Fradin-Fermé / 243 Hypereosinophilic Syndrome Sharon Fooshee Grace / 245 Hyperesthesia Syndrome Amanda L. Lumsden / 246 Hyperkalemia Michele Fradin-Fermé / 247 Hypertension, Systemic Beate Egner / 250 Hypertensive Cardiomyopathy Beate Egner / 254 Hyperthyroidism Mitchell A. Crystal and Gary D. Norsworthy / 256 Hypertrophic Cardiomyopathy Larry P. Tilley / 261 Hypoadrenocorticism Karen M. Lovelace / 265 Hypoalbuminemia Sharon Fooshee Grace / 267 Hypocalcemia Karen M. Lovelace / 270 Hypokalemia Mark Robson and Mitchell A. Crystal / 272 Hypomagnesemia Michele Fradin-Fermé / 274 Hypophosphatemia Stephanie G. Gandy-Moody / 275 Icterus Sharon Fooshee Grace / 277 Idiopathic Ulcerative Dermatitis Christine A. Rees / 280

Contents

119 120 121 122 123 124 125 126 127 128 129 130 131 132 133 134 135 136 137 138 139 140 141 142 143 144 145 146 147 148 149 150 151 152 153 154 155 156 157 158 159 160 161 162 163 164 165 166 167 168 169 170 171 172 173 174 175 176 177 178 179 180 181 182 183 184

Immune-Mediated Hemolytic Anemia Anthony P. Carr / 282 Inflammatory Bowel Disease Mark Robson and Mitchell A. Crystal / 284 Inflammatory Polyps and Masses Gary D. Norsworthy / 287 Intraocular Tumors Karen R. Brantman and Harriet J. Davidson / 290 Ischemic Encephalopathy Sharon Fooshee Grace / 292 Keratitis and Conjunctivitis Shelby L. Reinstein and Harriet J. Davidson / 294 Kidneys, Abnormal Size Gary D. Norsworthy / 297 Laryngeal Disease Andrew Sparkes / 298 Leprosy Syndrome Sharon Fooshee Grace / 302 Linear Foreign Body Gary D. Norsworthy / 304 Lung Parasites Gary D. Norsworthy / 306 Lymphoma Bradley R. Schmidt and Mitchell A. Crystal / 308 Malassezia Dermatitis Christine A. Rees / 313 Mammary Gland Neoplasia Bradley R. Schmidt and Mitchell A. Crystal / 314 Mammary Hyperplasia Gary D. Norsworthy / 317 Manx Syndrome Vanessa Pimentel de Faria / 318 Mast Cell Tumors Bradley R. Schmidt and Mitchell A. Crystal / 320 Megacolon Mitchell A. Crystal / 323 Meningioma Sharon Fooshee Grace / 326 Mesothelioma Fernanda Vieira Amorim da Costa / 328 Metaldehyde Toxicity Tatiana Weissova / 330 Miliary Dermatitis Christine A. Rees / 332 Mitral Valve Dysplasia Larry P. Tilley / 333 Murmurs Larry P. Tilley and Francis W. K. Smith, Jr. / 334 Myasthenia Gravis Paula Schuerer and Sharon Fooshee Grace / 336 Mycobacterial Diseases, Rapidly Growing Sharon Fooshee Grace / 338 Myiasis Elizabeth Macdonald / 340 Nasal Discharge Gary D. Norsworthy / 342 Nasal-Frontal Sinus Infection Gary D. Norsworthy / 344 Nasal Myiasis Sarah M. Webb / 347 Nasopharyngeal Disease Arnold Plotnick / 349 Neonatal Isoerythrolysis Sharon Fooshee Grace / 352 Neurogenic Bladder Sharon Fooshee Grace / 354 Nocardiosis Sharon Fooshee Grace / 356 Obesity Mark Robson, Mitchell A. Crystal, and Debra L. Zoran / 358 Oral Neoplasia Bradley R. Schmidt and Mitchell A. Crystal / 361 Organophosphate and Carbamate Toxicosis Gary D. Norsworthy / 364 Osteoarthritis Andrew Sparkes / 366 Otitis Externa Gary D. Norsworthy / 369 Otitis Media and Interna Sharon Fooshee Grace / 374 Pancreatitis, Acute Jörg M. Steiner / 377 Pancreatitis, Chronic Jörg M. Steiner / 380 Panleukopenia (Feline Parvovirus Infection) Sharon Fooshee Grace / 382 Panniculitis Mark Robson and Mitchell A. Crystal / 384 Paraneoplastic Syndromes Mark Robson / 386 Patent Ductus Arteriosis Larry P. Tilley / 388 Pectus Excavatum Sharon Fooshee Grace / 390 Pemphigus Foliaceus Christine A. Rees / 392 Perinephric Pseudocysts Fernanda Vieira Amorim da Costa / 394 Peritonitis, Septic Sharon Fooshee Grace / 397 Plague (Yersiniosis) Sharon Fooshee Grace / 400 Plant Toxicities Karen M. Lovelace / 402 Pleural Effusion Gary D. Norsworthy / 412 Pneumothorax Gary D. Norsworthy / 414 Pododermatitis: Lymphoplasmacytic Richard Malik and Gary D. Norsworthy / 416 Polycystic Kidney Disease Gary D. Norsworthy / 418 Polydactylism Sharon Fooshee Grace / 420 Polyphagic Weight Loss Mitchell A. Crystal and Paula B. Levine / 422 Polyuria and Polydipsia Mark Robson and Mitchell A. Crystal / 424 Portosystemic Shunt Mark Robson and Mitchell A. Crystal / 426 Pulmonary Fibrosis Sharon Fooshee Grace / 428 Pulmonic Stenosis Larry P. Tilley / 430 Pyelonephritis Gary D. Norsworthy / 432 Pyometra and Mucometra Gary D. Norsworthy / 434 Pyothorax Gary D. Norsworthy / 436 Pyrethrin and Pyrethroid Toxicosis Gary D. Norsworthy / 439

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Contents

185 186 187 188 189 190 191 192 193 194 195 196 197 198 199 200 201 202 203 204 205 206 207 208 209 210 211 212 213 214 215 216 217 218 219 220 221 222 223 224 225 226 227 228 229 230

Rabies Mark Robson and Mitchell A. Crystal / 440 Recreational Drug Toxicosis Tatiana Weissova / 442 Rectal Disease Heloisa Justen Moreira de Souza / 446 Refeeding Syndrome Karen M. Lovelace / 449 Renal Failure, Acute Sharon Fooshee Grace / 452 Renal Failure, Chronic Gary D. Norsworthy / 455 Renal Insufficiency Gary D. Norsworthy / 457 Restrictive Cardiomyopathy Larry P. Tilley / 460 Retinal Disease Karen R. Brantman and Harriet J. Davidson / 462 Rodenticide Toxicosis Mitchell A. Crystal / 466 Roundworms Mitchell A. Crystal and Mark C. Walker / 468 Salmonellosis Mark Robson and Mitchell A. Crystal / 470 Sarcomas, Injection Site Sharon Fooshee Grace / 472 Sarcomas, Other Mark Robson / 475 Scottish Fold Osteochondrodysplasia Sharon Fooshee Grace / 478 Seizures Sharon Fooshee Grace / 480 Skin Parasites Christine A. Rees / 483 Sporotrichosis Vanessa Pimentel de Faria / 487 Squamous Cell Carcinoma, Cutaneous Bradley R. Schmidt and Mitchell A. Crystal / 489 Stomach Worms Mitchell A. Crystal and Mark C. Walker / 492 Stud Tail Christine A. Rees / 493 Tail Injuries Sharon Fooshee Grace / 494 Tapeworm Infections Mitchell A. Crystal and Mark C. Walker / 496 Tetanus Sharon Fooshee Grace / 498 Tetralogy of Fallot Larry P. Tilley / 500 Thiamine Deficiency Gary D. Norsworthy / 502 Third Eyelid Diseases Gwen H. Sila and Harriet J. Davidson / 503 Thromboembolic Disease Larry P. Tilley / 506 Thymoma Bradley R. Schmidt / 509 Toxoplasmosis Gary D. Norsworthy and Sharon Fooshee Grace / 512 Tracheal Disease Andrew Sparkes / 515 Triad Disease Anthony P. Carr / 519 Trichobezoars Mitchell A. Crystal / 521 Tritrichomoniasis Mark Robson and Mitchell A. Crystal / 523 Ureteral Obstruction Rhett Marshall / 526 Urethral Obstruction Rhett Marshall / 530 Urinary Bladder Tumors Bradley R. Schmidt / 535 Urolithiasis Gary D. Norsworthy / 538 Uveitis Gwen H. Sila and Harriet J. Davidson / 543 Ventricular Septal Defect Larry P. Tilley / 546 Vestibular Syndrome Mitchell A. Crystal / 548 Viral Dermatitis Christine A. Rees / 550 Vitamin A Toxicosis Gary D. Norsworthy / 552 Vitamin D Toxicosis Gary D. Norsworthy / 553 Vomiting Mitchell A. Crystal and Paula B. Levine / 555 Weight Loss Mitchell A. Crystal and Mark C. Walker / 558

Section 2: Behavior 231 232 233 234 235 236 237 238 239

Aggression towards Humans Debra F. Horwitz / 563 Catnip Effects Sharon Fooshee Grace / 566 Environmental Enrichment in the Home Debra F. Horwitz / 567 Environmental Enrichment in the Hospital Gary D. Norsworthy and Linda Schmeltzer / 571 Housesoiling Debra F. Horwitz / 577 Intercat Aggression Debra F. Horwitz / 581 Marking Debra F. Horwitz / 584 Psychogenic Alopecia Debra F. Horwitz / 587 Behavioral Pharmaceuticals Debra F. Horwitz / 591

Section 3: Dentistry 240 241 242 243

x

Dental Examination R. B. Wiggs and B. C. Bloom / 597 Dental Prophylaxis R. B. Wiggs, S. L. Ruth, and B. C. Bloom / 599 Endodontics and Restorations R. B. Wiggs, S. L. Ruth, and B. C. Bloom / 602 Extractions R. B. Wiggs, B. C. Bloom, and S. L. Ruth / 606

Contents

244 245

Dental Resorption R. B. Wiggs, B. C. Bloom, and S. L. Ruth / 608 Oral and Dental Radiography R. B. Wiggs, B. C. Bloom, and S. L. Ruth / 610

Section 4: Surgery 246 247 248 249 250 251 252 253 254 255 256 257 258 259 260 261 262 263 264 265 266 267 268 269 270 271 272 273 274 275 276 277 278

Anesthesia: Local Ludovic Pelligand / 617 Anesthesia: Sedation and General Ludovic Pelligand / 620 Bulla Osteotomy: Ventral Approach Don R. Waldron / 626 Colectomy Don R. Waldron / 631 Corneal Surgery Gwen H. Sila / 636 Cranial Cruciate Ligament Rupture Mac Maxwell / 638 Cryptorchidism Surgery Mac Maxwell / 640 Esophagostomy Tube Placement Gary D. Norsworthy / 642 Frontal Sinus Obliteration Gary D. Norsworthy / 646 Gastrostomy Tube Placement Don R. Waldron / 649 Jejunostomy Tube Placement Don R. Waldron / 651 Laser Surgery, CO2 John C. Godbold, Jr. / 655 Lip Avulsion Replacement Gary D. Norsworthy / 660 Luxating Patella Otto Lanz / 662 Mandibular Symphyseal Separation Don R. Waldron / 664 Mastectomy Don R. Waldron / 666 Nasopharyngeal Polyp or Mass Removal Gary D. Norsworthy / 667 Nephrolith Removal Don R. Waldron / 670 Onychectomy Don R. Waldron / 673 Oronasal Fistula Repair Heloisa Justen Moreira de Souza / 676 Pain Management Sabine Tacke / 682 Perivulvar Skin Fold Removal Gary D. Norsworthy / 685 Physical Therapy and Rehabilitation Barbara Bockstahler and David Levine / 687 Rhinotomy Gary D. Norsworthy / 691 Sliding Skin Flaps Mac Maxwell / 693 Subcutaneous Fluid Catheter Placement Gary D. Norsworthy / 696 Thoracostomy Tube Placement Don R. Waldron / 698 Thyroidectomy Gary D. Norsworthy / 701 Total Ear Canal Ablation and Lateral Bulla Osteotomy Don R. Waldron / 704 Ureterolith Removal Don R. Waldron / 707 Urethrostomy, Perineal Don R. Waldron / 709 Urethrostomy, Prepubic Don R. Waldron / 712 Urinary Bladder Marsupialization Gary D. Norsworthy / 715

Section 5: Cytology 279 280 281 282 283 284 285 286 287 288 289 290

Sample Staining Amy C. Valenciano, Rick L. Cowell, and Tara P. Arndt / 719 Inflammation versus Neoplasia: Differentiation Tara P. Arndt, Rick L. Cowell, and Amy C. Valenciano / 721 Adenocarcinoma Amy C. Valenciano, Rick L. Cowell, and Tara P. Arndt / 728 Atypical Bacterial Infections Tara P. Arndt, Rick L. Cowell, and Amy C. Valenciano / 730 Fibrosarcoma Amy C. Valenciano, Rick L. Cowell, and Tara P. Arndt / 732 Hepatic Lipidosis Tara P. Arndt, Rick L. Cowell, and Amy C. Valenciano / 734 Lymph Node Disease Tara P. Arndt, Rick L. Cowell, and Amy C. Valenciano / 736 Lymphoma Amy C. Valenciano, Rick L. Cowell, and Tara P. Arndt / 738 Mast Cell Tumors Amy C. Valenciano, Rick L. Cowell, and Tara P. Arndt / 740 Pleural Effusions Amy C. Valenciano, Rick L. Cowell, and Tara P. Arndt / 742 Systemic Fungal Disease Tara P. Arndt, Rick L. Cowell, and Amy C. Valenciano / 746 Transtracheal Wash Hemosiderosis Tara P. Arndt, Rick L. Cowell, and Amy C. Valenciano / 749

Section 6: Imaging 291 292 293 294

Imaging: The Thorax Merrilee Holland and Judith Hudson / 753 Imaging: The Abdomen Merrilee Holland and Judith Hudson / 784 Imaging: The Head and Spine Merrilee Holland and Judith Hudson / 828 Imaging: Cardiovascular Disease Merrilee Holland and Judith Hudson / 849

Section 7: Clinical Procedures 295 296

Blood Transfusion Sharon Fooshee Grace / 879 Bone Marrow Aspiration Mitchell A. Crystal / 882

xi

Contents

297 298 299 300 301 302 303 304 305 306 307 308 309 310 311 312

Central Venous Catheter Placement Mitchell A. Crystal / 885 Cerebrospinal Fluid Collection Mitchell A. Crystal / 888 Eye Examination Karen R. Brantman and Harriet J. Davidson / 890 Euthanasia Amanda L. Lumsden and Gary D. Norsworthy / 893 Fine-Needle Biopsy Mitchell A. Crystal / 896 Fluid Therapy Sharon Fooshee Grace / 898 Jugular Blood Collection Gary D. Norsworthy / 902 Lung Aspiration Karen M. Lovelace / 904 Nasal Sampling Gary D. Norsworthy / 906 Necropsy of Kittens Michele Fradin-Fermé / 908 Neurologic Examination Stephanie G. Gandy-Moody / 910 Orogastric Tube Feeding Gary D. Norsworthy / 913 Polymerase Chain Reaction Testing Christian M. Leutenegger / 915 Restraint Devices and Techniques Gary D. Norsworthy / 920 Testing Procedures Mitchell A. Crystal and Gary D. Norsworthy / 924 Therapeutic Laser Applications Ronald J. Riegel / 928

Section 8: Appendices 313 314 315 316 317 318 319 320 321 322 323 324 325 326 327 328 329

Age Approximation Karen M. Lovelace / 933 Anatomical Differences in Cats and Dogs Clay Anderson and James E. Smallwood / 937 Body Surface Area Conversion Gary D. Norsworthy / 939 Breed Specific Diseases James K. Olson / 940 Cattery Hygiene Suvi Pohjola-Stenroos / 943 Echocardiographic Tables Larry P. Tilley and Francis W. K. Smith, Jr. / 945 Electrocardiographic Tables Larry P. Tilley and Francis W. K. Smith, Jr. / 947 Feral and Free-Roaming Cats Christine L. Wilford / 948 Grief Response by Cat Owners Larry A. Norsworthy, Kacee Junco, and Brooke Woodrow / 954 Hospital Hygiene Suvi Pohjola-Stenroos / 957 Life Stage Guidelines AAFP/AAHA / 960 Normal Laboratory Values Gary D. Norsworthy and Teija Kaarina Viita-aho / 977 Pregnancy, Parturition, and Lactation Teija Kaarina Viita-aho / 979 Purring Sharon Fooshee Grace / 982 Renal Transplantation Daniel A. Degner / 984 Vibrissae Sharon Fooshee Grace / 987 Zoonotic Diseases Suvi Pohjola-Stenroos / 989

Section 9: Formulary 330

Drug Formulary Gary D. Norsworthy, Linda Schmeltzer, Sharon Fooshee Grace, and Mitchell A. Crystal / 999

Index / 1034

xii

Founding Authors Gary D. Norsworthy, DVM, DABVP (Feline) Chief of Staff Alamo Feline Health Center San Antonio, TX Adjunct Professor College of Veterinary Medicine Mississippi State University

Mitchell A. Crystal, DVM, DACVIM (Internal Medicine) North Florida Veterinary Specialists, P.A. Jacksonville, FL Larry P. Tilley, DVM, DACVIM (Internal Medicine) President, VetMed Consultants Consultant, New Mexico Veterinary Referral Center Santa Fe, NM

Sharon Fooshee Grace, MAgric, MS, DVM, DABVP (Canine-Feline), DACVIM (Internal Medicine) Mississippi State University College of Veterinary Medicine Mississippi State, MS

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Contributors Fernanda Vieira Amorim da Costa, DVM, MSc, PhD Founder and President, Brazilian Academy of Feline Practice Florianopolis, Brazil Clay Anderson, DVM Alamo Feline Health Center San Antonio, TX Tara Arndt, DVM, DACVP Ontario Veterinary College Department of Pathobiology Guelph, ON, Canada Bonnie. C. Bloom, DVM Fellow, Academy of Veterinary Dentistry Dallas Dental Service Animal Clinic Dallas, TX Barbara Bockstahler, DVM, CCRP Specialized Veterinarian in Physiotherapy and Rehabilitation University of Veterinary Medicine Vienna, Austria Karen R. Brantman, DVM Michigan Veterinary Specialists Grand Rapids, MI Jane E. Brunt, DVM Owner and Founder Cat Hospital at Towson Cat Hospital Eastern Shore Baltimore, MD Anthony P. Carr, DVM, DACVIM (Internal Medicine) Professor Small Animal Clinical Sciences Western College of Veterinary Medicine University of Saskatchewan Saskatoon, SK, Canada Rick L. Cowell, DVM, MS, MRCVS, DACVP IDEXX Laboratories Stillwater, OK Harriet J. Davidson, DVM, DACVO Michigan Veterinary Specialists Grand Rapids, MI Daniel A. Degner, DVM, DACVS Michigan Veterinary Specialists Auburn Hills, MI Beate Inge Egner, Doctor med. vet., Board Certified Freelance specialist for cardiovascular disease Kleintierzentrum Hörstein (Clinical Center for Small Animals) Hoerstein, Germany

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Michele Fradin-Fermé, DVM Vincennes, France Stephanie G. Gandy-Moody, DVM The Cat Hospital of Madison Madison, AL John C. Godbold, Jr. DVM Stonehaven Park Veterinary Hospital Laser Surgery Center Jackson, TN Merrilee Holland, DVM, DACVR Associate Professor, Radiology Section Department of Clinical Science College of Veterinary Medicine Auburn University Auburn, AL Debra F. Horwitz, DVM, Diplomate, ACVB Owner, Veterinary Behavior Consultations St. Louis, MO Judith Hudson, DVM, DACVR Professor, Radiology Section Department of Clinical Sciences College of Veterinary Medicine Auburn University Auburn, AL Kacee Junco, BS QMHP-CS, M.S., LPC-I Texana Center Brookshire, TX Heloisa Justen Moreira de Souza, DVM, PhD Professor Feline Medicine and Surgery Department of Medicine and Surgery Institute of Veterinary Medicine University Federal Rural of Rio de Janeiro Rio de Janeiro, RJ, Brazil Otto Lanz, DVM, DACVS Associate Professor, Surgery Department of Small Animal Clinical Sciences Virginia-Maryland Regional College of Veterinary Medicine Virginia Tech Blacksburg, VA Christian M. Leutenegger, Dr. Vet. Med., PhD, FVH Regional Head of Molecular Diagnostics (MDx) IDEXX Reference Laboratories West Sacramento, CA

Contributors

David Levine, PT, PhD, DPT, OCS, CCRP Walter M. Cline Chair of Excellence in Physical Therapy Department of Physical Therapy The University of Tennessee at Chattanooga Chattanooga, TN Paula B. Levine, DVM, DACVIM (Internal Medicine) North Florida Veterinary Specialists, P.A. Jacksonville, FL Karen M. Lovelace, DVM The Cat Doctor (Thousand Oaks) Thousand Oaks, CA Amanda L. Lumsden, DVM Cat and Bird Clinic Santa Barbara, CA Elizabeth Macdonald, DVM Alamo Feline Health Center San Antonio, TX Richard Malik, DVSc DipVetAn, MVetClinStud, PhD, FACVSc, FASM Centre for Veterinary Education Veterinary Science Conference Centre The University of Sydney Sydney, NSW, Australia Rhett Marshall, BVSc, MACVSc (Small Animal Surgery) Member, Australian College of Veterinary Scientists in Small Animal Surgery Senior Feline Practitioner and Principle The Cat Clinic, Mt. Gravatt, QLD, Australia Mac Maxwell, DVM, DACVS Medvet Veterinary Specialists Cordova, TN Larry A. Norsworthy, PhD Professor of Psychology Licensed Clinical Psychologist Department of Psychology Abilene Christian University Abilene, TX James K. Olson, DVM, DABVP (Feline) Cat Specialist, PC Castle Rock, CO

Vanessa Pimentel de Faria, DVM, MSc Specialized in Feline Medicine Owner, Só Gatos Brasilia-DF, Brazil Arnold Plotnick MS, DVM, DACVIM (IM) Manhattan Cat Specialists New York, NY Suvi Pohjola-Stenroos, DVM, PhD, DABVP (Feline) Clinivet Oy, Cat Clinic Felina Founder, Practitioner Helsinki, Finland Jacquie Rand, BVSc, DVSc, Diplomate ACVIM (Internal Medicine) Professor of Companion Animal Health Director, Centre for Companion Animal Health School of Veterinary Science The University of Queensland St. Lucia, QLD, Australia Christine A. Rees, DVM, DACVD Veterinary Specialists of North Texas Dallas, TX Shelby L. Reinstein, DVM, MS Research Veterinarian Retinal Disease Studies Facility School of Veterinary Medicine University of Pennsylvania/NBC Kennett Square, PA Ronald J. Riegel, DVM Independent Consultant, Author, Manufacturer Marysville, OH Mark Robson, BVSc (Distinction), DACVIM, Registered Veterinary Specialist Veterinary Specialist Group Auckland, New Zealand Sunny L. Ruth, DVM Dallas Dental Service Animal Clinic Dallas, TX Linda Schmeltzer, RVT Head Technician Alamo Feline Health Center San Antonio, TX

Philip Padrid, DVM Southwest Regional Medical Director VCA Associate Professor of Molecular Medicine (Adjunct) University of Chicago Pritzker School of Medicine Associate Professor of Small Animal Medicine (Adjunct) The Ohio State University School of Veterinary Medicine Corrales, NM

Bradley R. Schmidt, DVM, Diplomate ACVIM (Oncology) Staff Oncologist North Florida Veterinary Specialists, P.A. Jacksonville, FL

Ludovic Pelligand, Dr. Med. Vet., MRCVS, Dipl. ECVAA Royal Veterinary College North Mymms, Hatfield Hertfordshire, UK (England)

Gwen H. Sila, DVM Michigan Veterinary Specialists Southfield, MI

Paula A. Schuerer, DVM, MBA Animal Ark Animal Hospital, LLC Franklin, TN

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Contributors

Andrew H. Sparkes, BVetMed, PhD, DECVIM, MRCVS Head of Small Animal Studies Animal Health Trust Lanwades Park Kentford Newmarket Suffolk United Kingdom (England) James E. Smallwood, DVM, MS Alumni Distinguished Professor of Anatomy Director of CVM Alumni Relations Department of Molecular Biomedical Sciences North Carolina State College of Veterinary Medicine Raleigh, NC Francis W.K. Smith, Jr., DVM, DACVIM (Cardiology and Small Animal Internal Medicine) Lexington, MA Vice-President, VetMed Consultants, Inc. Clinical Assistant Professor Tufts University Cummings School of Veterinary Medicine North Grafton, MA Jörg M. Steiner, DVM, PhD, Dipl. ACVIM, Dipl. ECVIM-CA Associate Professor and Director of Gastrointestinal Laboratory Department of Small Animal Clinical Sciences College of Veterinary Medicine and Biomedical Sciences Texas A&M University College Station, TX PD Dr. Sabine Tacke Anesthesia, Pain Therapy, Perioperative Intensive Care Animal Protection Officer of the Department of Veterinary Clinical Sciences Consultant Veterinary Anesthetist Consultant Veterinary Surgeon Treasurer EVECCS Department of Veterinary Clinical Sciences Clinic for Small Animals, Surgery Justus-Liebig-University Giessen Giessen, Germany Amy C. Valenciano, DVM, MS, DACVP IDEXX Reference Laboratories Veterinary Clinical Pathologist Dallas, TX

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Teija Kaarina Viita-aho, DVM Helsinki, Finland Don Waldron, DVM, DACVS Director of Specialty Services VCA Veterinary Care Animal Hospital and Referral Center Albuquerque, NM Mark C. Walker, BVSc, DACVIM (Internal Medicine) North Florida Veterinary Specialists, P.A. Jacksonville, FL Sarah M. Webb, BVSc, MACVSc Specialist Small Animal Surgeon Surgical Referral Services Gungahlin, ACT Australia Tatiana Weissova, DVM, PhD The Small Animal Clinic Department of Internal Diseases University of Veterinary Medicine Slovak Republic R. B. Wiggs, DVM, DAVDC, deceased Fellow, Academy of Veterinary Dentistry Adjunct Professor, Baylor College of Dentistry Texas A&M University Systems Dallas Dental Service Animal Clinic Dallas, TX Christine L. Wilford, DVM Cats Exclusive Veterinary Center Shoreline, WA Brooke Woodrow, M.S., LPC-I Academic Counselor Academic Development Center Abilene Christian University Abilene, TX Debra L. Zoran, DVM, PhD, DACVIM-SAIM Associate Professor and Chief of Medicine Department of Small Animal Clinical Sciences College of Veterinary Medicine and Biomedical Sciences Texas A&M University College Station, TX

Preface In the real world of veterinary practice, diagnosis and treatment of feline diseases are usually done at a rapid pace. The primary goal of this book is to resolve the conflict between the need for accurate and relevant information and the urgency demanded by a patient on your examination table while others are waiting for your care. I have designed this book like I would want it for my use in the primary care setting. Knowing that primary care practitioners are the ones who will use it most, I hope

that The Feline Patient, Fourth Edition, will prove itself to be a valuable resource for thousands of veterinary practitioners around the world to the betterment of feline health. Gary D. Norsworthy, DVM, Diplomate, ABVP (Feline) Alamo Feline Health Center, San Antonio, Texas

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The Feline Patient Fourth Edition

SECTION

1 Diseases and Conditions

CHAPTER 1

Acetaminophen Toxicosis Sharon Fooshee Grace

Overview Acetaminophen toxicosis usually occurs when well-intentioned owners, unaware of the significant toxicity of this drug in cats, administer the drug for a variety of reasons. Most case reports indicate that owners give acetaminophen to individual cats as a pain reliever. Ingestion of as little as 10 mg/kg of acetaminophen may be fatal for cats. This amounts to less than one regular-strength tablet (325 mg) for a 4- to 5-kilogram (8.8to 11-pound) cat. One case report described fatal toxicosis in a kitten that had played with an empty acetaminophen bottle. Acetaminophen attacks several metabolic peculiarities of the feline species. Once the cat’s limited ability to produce nontoxic drug metabolites via sulfate and glucuronide conjugation has been exceeded, the hepatic cytochrome P450 oxidase system converts acetaminophen to the reactive electrophilic intermediate N-acetyl-para-benzoquinoneimine (NAPQ1). The toxic effects of acetaminophen are a direct result of formation of NAPQ1 and its assault on cellular macromolecules. Following depletion of glucuronide and sulfate, supplies of the next available line of defense—the cellular antioxidant, glutathione—become exhausted by rising levels of NAPQ1. As NAPQ1 continues to accumulate, hemoglobin is oxidized from its normal ferrous state (+2) to a ferric state (methemoglobin, +3) and becomes unable to effectively deliver oxygen to tissues, with catastrophic consequences for the patient. Notably, even under normal circumstances, the feline erythrocyte is always vulnerable to oxidative stress because of the relatively large number of sulfhydryl groups present in cat hemoglobin. Further, precipitation of damaged hemoglobin on the erythrocyte membrane leads to the second significant event: development of Heinz body hemolytic anemia. The feline spleen is relatively ineffective at removing Heinz bodies from erythrocyte membranes so they persist, with the net effect of increased erythrocyte membrane fragility, decreased deformability, and development of hemolytic anemia. Whereas methemoglobinemia is potentially reversible, Heinz body formation (and damage to the red blood cell membrane) is not. Finally, acetaminophen toxicosis may cause liver necrosis in cats via oxidative damage to hepatocyte membranes and reaction with hepatocellular proteins, but hepatic damage is usually minimal when compared with that typically seen in dogs. Earliest signs of toxicosis include anorexia, vomiting, and ptyalism. The appearance of cyanotic or brown-colored mucous membranes (usually within 24 hours of drug ingestion) heralds the onset of significant methemoglobinemia. Edema of the face and paws is common, though the precise cause for these findings remains unclear. As Heinz body hemolytic anemia develops within hours to a few days of drug ingestion, the mucous membranes become pale and sometimes icteric.

• Clinical Signs: The appearance of cyanotic or brown-colored mucous membranes and facial and paw edema are noteworthy. Other findings may include vocalization, tachycardia, dyspnea, depression, and weakness. Icterus may occur 24 to 48 hours after drug ingestion. • Complete Blood Count (CBC): Submitted blood will often have a dark brown color (see Diagnostic Notes for more information). Typical findings include anemia and the appearance of Heinz bodies on the red cell membrane. See Figure 1-1. Reticulocytes may appear several days later if the cat survives. Heinz bodies and reticulocytes are more easily recognized if a drop of new methylene blue stain is applied to an air-dried blood smear, which is then coverslipped and examined microscopically. See Figure 89-2 and Chapter 311. • Chemistry Profile: Hepatocellular leakage enzymes (serum alanine aminotransferase and serum aspartate aminotransferase) may be mildly to severely elevated. Because acetaminophen does not commonly cause significant hepatic necrosis in cats, these elevations could be due to hepatocyte hypoxia. Serum bilirubin is sometimes increased. • Urinalysis: Chocolate- or red-colored urine may be seen due to methemoglobinuria or hematuria.

Diagnostic Notes • In healthy, nonanemic cats up to 5% of erythrocytes may contain Heinz bodies. As such, detection of occasional Heinz bodies should be considered normal in cats. • Methemoglobinemia is the usual cause of death. It appears when more than 20 to 30% of hemoglobin is in the form of methemoglobin. • Methemoglobinemia is sometimes difficult to discern in a blood sample because venous blood is normally dark. As a clinical screening test, one drop of patient blood can be placed on a white paper towel or filter paper next to a drop of normal “control” blood. If the methemoglobin content is greater than 10%, the patient’s blood

Diagnosis Primary Diagnostics • History: Because the clinical signs are not always distinctive, a history of acetaminophen administration or potential exposure to the drug is critical to help confirm a diagnosis.

The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.

Figure 1-1 Heinz body formation (arrow) on the red blood cells is one of the diagnostic features of acetaminophen toxicity.

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SECTION 1: Diseases and Conditions

is expected to be noticeably brown when compared to the brighter red of the control blood. • Acetaminophen serum concentration may be measured and is maximally increased 2 to 3 hours post-ingestion. In most cases, it is unnecessary and impractical to measure blood levels of the drug.

Treatment Primary Therapeutics • Removal of the toxin: Acetaminophen is rapidly absorbed from the gastrointestinal tract so emesis should be induced only if drug ingestion has occurred within the previous 1 to 2 hours. Emesis may be induced by apomorphine or xylazine. Use of activated charcoal is controversial; it should be given only if acetaminophen ingestion has occurred within the preceding 2 hours. Because of the risk for aspiration pneumonia, activated charcoal should be used cautiously if the cat is vomiting or if emesis has been induced. If acetylcysteine is given orally, charcoal may bind the drug. • Acetylcysteine (Mucomyst®): This drug is recommended as a specific antidote. It supplies precursors for replenishment of glutathione stores. The available solutions are in 10 and 20% concentrations and should be appropriately diluted to a 5% solution with 5% dextrose. An initial oral or intravenous dose of 130 to 140 mg/kg should be followed by 70 mg/kg q6h PO, IV for five to seven treatments. It is recommended that intravenous treatments be administered through a 0.2-µm Millipore filter over 60 minutes. Some have suggested that oral administration may be superior to the intravenous route because of the higher concentration of drug available to the liver via portal circulation. It has been shown that therapy is less effective when started more than 8 hours after ingestion of acetaminophen, though there may still be some benefit appreciated when treating up to 80 hours post-ingestion.

Secondary Therapeutics • Cimetidine: This drug may have an additive effect with Nacetylcysteine because of its ability to inhibit the cytochrome P450 oxidase system and thus limit formation of toxic metabolites and limit hepatotoxicity. It should be used as adjunctive therapy only. The true efficacy of cimetidine in the setting of acetaminophen toxicosis remains unknown. The dose is 5 mg/kg q6 to 8 h IV for 48 hours. • Ascorbic acid (vitamin C): Vitamin C is an antioxidant which, through nonenzymatic means, is proposed to assist in reduction of methemoglobin back to hemoglobin, though the process is slow. This is an adjunctive therapy and should not be substituted for acetylcysteine administration. Give 30 mg/kg q6h IV until methemoglobinemia resolves. Consult a formulary before mixing ascorbic acid with other solutions due to a high likelihood of incompatibility. If intravenous ascorbic acid is not available, an oral formulation may be given at 125 mg/kg q6h for six treatments. • S-Adenosylmethionine (SAMe): SAMe, currently marketed as Denosyl® and Denamarin®, demonstrates hepatoprotective and

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systemic antioxidant properties. SAMe has been shown to increase the cat’s resistance to oxidative stress and thus appears beneficial as an adjunct therapy for acetaminophen toxicity. In one placebocontrolled feline study evaluating oxidant injury caused by acetaminophen, SAMe-treated cats had reduced Heinz body formation and erythrocyte destruction as compared to cats receiving only acetaminophen. However, additional studies need to be done, especially with regard to its effect on methemoglobinemia, which did not appear to improve with SAMe therapy in the aforementioned study. At this time, it should be considered an adjunctive treatment because N-acetylcysteine is a proven therapy. • Transfusion with blood or hemoglobin solutions: Administration of whole blood or Oxyglobin® (5–15 ml/kg IV) may be useful in cats with severe hemolytic anemia and should be considered if the hematocrit falls below 20%. Signs of hypoxemia would also warrant a transfusion, even with a normal hematocrit because the hematocrit is not a true reflection of the oxygen-carrying capacity of the blood. Oxyglobin is currently limited in availability and its use is controversial in this setting. It has the potential to cause volume overload in cats so slow infusion rates of 0.5 to 5 ml/kg per hour are recommended. • Supportive therapy: This may include intravenous fluids, electrolytes, and limited handling of the patient.

Therapeutic Notes • Corticosteroids are of no value in treating acetaminophen toxicosis. • The literature contains varied opinions about the benefit of oxygen therapy because methemoglobin is unable to bind oxygen. However, it is reasonable to consider oxygen support, being mindful that oxygen administration may further stress the patient. • Though opinions vary, most consider that methylene blue is contraindicated in treatment of this disorder because of the potential to worsen the hemolytic anemia. • A positive response to therapy is indicated by improvement within 48 hours.

Prognosis A grave prognosis is indicated when methemoglobinemia and Heinz body hemolytic anemia are severe and unresponsive to appropriate therapy. For cats that recover, no long-term effects have been reported.

Suggested Readings Allen AL. 2003. The diagnosis of acetaminophen toxicosis in a cat. Can Vet J. 44(6):509–510. El Bahri L, Lariviere N. 2003. Pharm profile: N-Acetylcysteine. Compend Contin Educ Pract Vet. 25(4):276–278. Savigny M, Macintire DK. 2005. Acetaminophen toxicity in cats. Compend Contin Educ Pract Vet. 7(3):8–11. Webb CB, Twedt DC, Fettman MJ, et al. 2003. S-adenosylmethionine (SAMe) in a feline acetaminophen model of oxidative injury. J Fel Med Surg. 5(2):69–75.

CHAPTER 2

Acne Christine A. Rees

Overview Acne is a common dermatologic condition in cats. Feline acne is a follicular keratinization and glandular proliferation of tissue and glands of the chin area. Other areas that can also be affected include the lower and upper lips. The usual age of onset is 6 months to 14 years of age (median age 4 years old). One study evaluating 22 cats with acne found that a variety of skin lesions are present with feline acne. The most common skin lesions noted with acne are comedones (73%), alopecia (68%), crusts (55%) papule (45%), and erythema (41%). In severe cases edema, cysts, and scars can be present. The most common body location is the chin. Pruritus is infrequent (35% of 22 cats). Malassezia pachydermatitis is uncommon (18%) of affected cats. Bacteria is present almost half of the patients (45%). The bacteria that are isolated include coagulase-positive staphylococci and alpha-hemolytic streptococci. Histopathologic findings in cats with acne include lymphoplasmacytic periductal inflammation, sebaceous gland duct dilatation, follicular keratosis with plugging and dilatation, folliculitis, pyogranulomatous adenitis, and furunculosis. See Figures 2-1 and 2-2.

Diagnosis Primary Diagnostics • History and Clinical Signs: These are so distinct that they are usually used to formulate the diagnosis. • Histopathology: Histologic signs for feline acne are classic (see description).

Figure 2-2 Advanced acne can result in severe folliculitis, pyogranulomatous adenitis, and furunculosis. At this stage, aggressive cleansing under anesthesia and antibiotic therapy are indicated. Image courtesy Dr. Gary D. Norsworthy.

Treatment Primary Therapeutics • Secondary infections should be treated with systemic antibiotics for 3 weeks or 1 week beyond when the skin appears normal. • Topical medications are useful for treating feline acne. The chin should be clipped and cleaned prior to applying these topical medications. Examples of topical medications that have been used include salicylic acid pads (i.e., Stridex® pads), benzoyl peroxide 5% gel, 0.01 to 0.025% tretinoin cream or lotion, 0.75% metronidazole gel, clindamycin ointment, and mupiricin ointment.

Therapeutic Notes • Hot packing of the chin prior to treatment often makes the treatment more effective. A warm, moist cloth can be held on the chin for 30 seconds to open the pores and allow the medication to penetrate better.

Prognosis The prognosis is good for feline acne. Intermittent lifelong symptomatic treatment is often necessary. Feline acne is primarily a cosmetic concern. The exception is when a secondary infection is present. Bacterial skin infections often require systemic therapy to achieve control. Figure 2-1 Early acne is characterized by the presence of comedones. Image courtesy Dr. Gary D. Norsworthy.

The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.

Suggested Readings Jazic E, Coyner KS, Loeffler DG, et al. 2006. An evaluation of the clinical, cytological, infectious and histopathological features of feline acne. Vet Derm. 17(2):134–140.

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CHAPTER 3

Acromegaly Sharon Fooshee Grace

Overview Acromegaly is a well-recognized but rare disorder of cats caused by a functional growth hormone (GH) secreting tumor of the anterior pituitary. The disease is characterized by overgrowth of bone, viscera, and soft tissue and insulin-resistant diabetes mellitus. Most acromegalic cats are middle-aged to older males; a breed predisposition has not been recognized. Severe insulin-resistant diabetes mellitus is the most common and important clinical manifestation. GH exerts significant diabetogenic activity through its ability to create peripheral insulin resistance. Some acromegalic cats require 30 to 130 units of insulin per day to control concurrent diabetes. Historical and clinical findings include polyphagia, polyuria, polydipsia, weight gain despite poorly controlled diabetes, enlargement of the head, widened interdental spaces, inferior prognathism, large paws, rapid growth of toenails, thickened skin, degenerative arthritis, thickening of pharyngeal tissues, and organomegaly (especially cardiac, hepatic, and renal). Cats presented late in the course of disease may show signs of heart disease or failure (i.e., systolic murmur, pulmonary edema, pleural effusion) and chronic renal failure.

Diagnosis Primary Diagnostics • Change in Physical Appearance: Owners often fail to recognize gradual changes in their cat’s appearance. When possible, it is helpful to compare the appearance of the cat to a photograph taken several years before onset of signs to evaluate for changes consistent with acromegaly. • Minimum database (complete blood count, chemistry profile, and urinalysis): Hyperglycemia and glucosuria are consistent findings. Other common findings include hyperphosphatemia, hyperproteinemia, hypercholesterolemia, and mild increases in liver enzymes. Proteinuria can precede development of azotemia, which usually occurs late in the course of disease. • Insulin-Like Growth Factor-I (Somatomedin C) Levels: This is a commercially available test that provides an indirect assessment of GH levels. It is currently available through the endocrine laboratory at Michigan State University (phone 1-517-353-1683). The laboratory reports a sensitivity of 84% and specificity of 92%. The normal range is 12 to 92; a value greater than 200 is strongly suggestive of acromegaly. • Growth Hormone Assay: Measurement of serum GH can provide a definitive diagnosis. This test is offered at the University of Minnesota Veterinary Diagnostic Lab. See www.vdl.umn.edu. • Computed Tomography (CT) or Magnetic Resonance Imaging (MRI): At present, advanced imaging techniques are the most reliable means for detecting a pituitary mass. Pituitary imaging is also helpful in defining the size and progression of the tumor. See Figure 3-1. The presence of a mass is not diagnostic of a GH-secreting tumor because other types of pituitary tumors occur in cats (e.g., adrenocorticotropic hormone [ACTH]-secreting pituitary tumor). However,

Figure 3-1 A large pituitary mass can be seen at the tip of the arrow. This computerized tomography scan is typical for a cat with acromegaly. Image courtesy of Linda Abraham BSc, BVetMed, MRCVS, PhD, FACVSc and Steven Holloway, BVSc, DACVIM, PhD, The University of Melbourne, Australia. the likelihood that a pituitary tumor is secreting GH rises significantly if clinical signs of acromegaly are present, and if hyperadrenocorticism is ruled out via lack of clinical signs and results of adrenal testing. See Chapter 101.

Secondary Diagnostics • Radiographs: Survey radiographs of the chest, abdomen, and bones may reveal cardiomegaly, pulmonary edema, pleural effusion, hepatomegaly, splenomegaly, renomegaly, degenerative arthropathy, and a periarticular periosteal reaction. • Echocardiography: This may reveal hypertrophic changes in the septum and left ventricular free wall. • Adrenal Function Testing: Adrenal function should be evaluated to eliminate hyperadrenocorticism as a cause of insulin-resistant diabetes mellitus. Available tests include ACTH stimulation, dexamethasone suppression, endogenous plasma ACTH concentrations, and urinary cortisol-to-creatinine ratio. See Chapter 101 for details. • Thyroid Testing: Hyperthyroidism is common in elderly cats and may be a cause of insulin resistance in cats with naturally occurring diabetes mellitus. All geriatric cats should be evaluated with a total T4 value. However, the presence of unregulated diabetes often results in lowered total T4 values.

Diagnostic Notes th

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• GH assays that have been designed for humans will not accurately assess feline GH levels.

Acromegaly

• Hypertension is a common attendant problem in humans with acromegaly but has not been evaluated in affected cats.

Treatment Primary Therapeutics • Radiation Therapy: Radiation therapy offers the best chance for control of the disease. Results have varied from minimal to dramatic shrinkage of the tumor. Unfortunately, it is common for the tumor to regrow and signs to recur after cessation of therapy (6–18 months). • Medical Therapy: Drugs that lower circulating GH levels (e.g., dopamine agonists or somatostatin analogues) have been tried with mixed results; most cats fail to demonstrate a positive response. Therapy is not generally recommended unless other management techniques (i.e., high dose insulin, managing other secondary conditions, or radiation therapy) have been attempted and are not successful.

Secondary Therapeutics • Insulin: Increasing doses of insulin will be required to manage insulin-resistant diabetes mellitus.

Therapeutic Notes • Monitoring for secondary conditions (e.g., renal disease or cardiac disease) and provision of appropriate therapy will be necessary in most cases of feline acromegaly.

• Cryosurgical ablation of the pituitary gland has been reported in two cats; one had a positive outcome and the other was euthanized several months later.

Prognosis Many cats will do well for 1 to 2 years without specific treatment for acromegaly if the diabetes is managed reasonably well. One study of 14 acromegalic cats reported a mean survival time of 22 months and a median survival time of 21 months. Most cats will eventually die or are euthanized from secondary conditions (i.e., congestive heart failure, renal disease, and so on).

Suggested Readings Berg RIM, Nelson RW, Feldman EC, et al. 2007. Serum insulin-like growth factor-I concentration in cats with diabetes mellitus and acromegaly. J Vet Intern Med. 21(5);892–898. Dunning MD, Lowrie, CS, Bexfield NH, et al. 2009. Exogenous insulin treatment after hypofractionated radiotherapy in cats with diabetes mellitus. J Vet Intern Med. 23(2):243–249. Hurty CA, Flatland B. 2005. Feline acromegaly: A review of the syndrome. J Vet Intern Med. 41(5):292–297. Mayer M, Greco DS, LaRue SM. 2006. Outcomes of pituitary tumor irradiation in cats. J Vet Intern Med. 20(5):1151–1154. Niessen SJM, Petrie G, Gaudiano F, et al. 2007. Feline acromegaly: An underdiagnosed endocrinopathy. J Vet Intern Med. 21(5):899–905. Peterson ME, Taylor RS, Greco DS, et al. 1990. Acromegaly in 14 cats. J Vet Intern Med. 4(4):192–201.

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CHAPTER 4

Actinomycosis Sharon Fooshee Grace

Overview Feline actinomycosis is a suppurative to pyogranulomatous disease caused by infection with the filamentous, gram-positive, non-acid-fast bacterium Actinomyces spp. It is an anaerobic or facultative anaerobic organism found as a saprophytic inhabitant of mucous membranes, most notably the oral cavity. Endogenous species are not normally considered highly pathogenic. Typically, disease will not develop until the organism is inoculated into a wound in association with other bacteria, usually other commensal organisms from the oral cavity. Though it is occasionally seen in cats, few cases have been detailed in the literature. However, several different species of the organism have been recovered from cats. Establishment of infection in cats is thought to most commonly occur through bite wounds, although other modes are possible. It spreads locally by dissection through local tissue planes; hematogenous dissemination is thought rare. This disease has a variety of presentations that are clinically indistinguishable from other infectious diseases, particularly nocardiosis. Affected cats most often have cutaneous/subcutaneous and thoracic disease (i.e., empyema or pyothorax). Cutaneous/subcutaneous lesions may appear acutely or peracutely and are often around the head or neck. One case had local extension of a subcutaneous abscess into the spinal canal. Wounds are often non-healing and may be abscessed or fistulous with a serosanguinous to purulent exudate that is yellow to reddishbrown in color. See Figure 4-1. Abscesses may have a foul odor that is suggestive of an anaerobic infection. Drainage sometimes contains grossly visible clusters of bacterial macrocolonies called “sulfur granules.” Occasionally, cutaneous lesions are nodular in appearance and devoid of drainage. The lung and pleural space may become involved by

aspiration or inhalation of infected material, direct extension from more superficial disease, or perhaps through a bite wound to the chest. Respiratory infection may involve the lung itself or only the pleural space, and clinical signs are consistent with pulmonary or pleural disease. Important differential diagnoses for actinomycosis include but are not limited to nocardiosis (Chapter 152), mycobacteriosis (Chapter 144), leprosy (Chapter 127), plague (Chapter 169), sporotrichosis (Chapter 202), dermatophyte kerion (Chapter 48), dermatophilosis (Chapter 48), and panniculitis (Chapter 162). No cases of human actinomycosis have been reported from direct contact with an infected cat, although it may feasibly be transmitted through the bite wound of an animal.

Diagnosis Primary Diagnostics • Cytology and Gram Staining: Specimens for cytology may be collected by aspiration of abscesses, nodules, or body cavity fluid; impression smears may be made from the discharge of draining tracts. The organisms, easily visualized microscopically, are filamentous and occasionally branched; neutrophils are present, but macrophages may or may not be present. (See Chapter 282.) A polymicrobial infection is usually noted. In contrast, exudate from lesions of nocardiosis does not usually contain a mixed bacterial population. Fibrous masses without drainage may yield little diagnostic material. On Gram stain, the organisms are gram-positive. • Culture: Because actinomycosis (variably anaerobic or facultative anaerobic) is clinically indistinguishable from nocardiosis, which is an aerobe, (Chapter 152), both aerobic and anaerobic cultures of should be submitted. Most diagnostic laboratories can provide supplies for anaerobic submission of a sample. Culture for actinomycosis is often unrewarding because anaerobes are difficult to grow in culture, although some species are facultative anaerobes and may grow aerobically. Other organisms are likely to grow in addition to Actinomyces because it is usually a mixed bacterial infection. Presence of these other organisms may complicate isolation of Actinomyces. • Biopsy/Histopathology: Histologic study of tissue reveals a suppurative to pyogranulomatous reaction. There may be a core of neutrophils encapsulated by granulation tissue containing macrophages, plasma cells, and lymphocytes. Organisms may not be evident with routine hematoxylin/eosin stain and special stains may be needed. • Acid-fast Staining: A small amount of exudate can be smeared onto a microscope slide and submitted for acid-fast staining with ZiehlNiessen stain. Actinomyces is a non-acid-fast organism.

Secondary Diagnostics

Figure 4-1 Multiple draining fistulas are seen on the ventral abdomen of this cat with actinomycosis. Image courtesy Dr. Gary D. Norsworthy.

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• Complete Blood Count, Chemistry Profile, and Urinalysis: There are no laboratory abnormalities specific for actinomycosis. However, this information is helpful in evaluating overall health of the cat. • Retroviral Testing: All cats with nonhealing wounds or pyothorax should be tested for feline leukemia virus and feline immunodeficiency virus. • Diagnostic Imaging: Radiographs are indicated if pleural or peritoneal involvement is suspected. Abdominal ultrasound may be needed to investigate possible abdominal abscesses.

Actinomycosis

Diagnostic Notes • It is important to distinguish actinomycosis from nocardiosis because different antibiotics are required to treat the two diseases.

Treatment Primary Therapeutics • Antibiotics: Antibiotics must be administered for weeks to months beyond clinical resolution of disease to prevent relapse. Preferred protocols include amoxicillin (20–40 mg/kg q6h IM, SC, or PO) or clindamycin (5 mg/kg q12h PO, SC). Oral medication may be given if the patient is not anorexic or vomiting; it should be given on an empty stomach. Other drugs reported to have efficacy include doxycycline, tetracycline, erythromycin, and first-generation cephalosporins. Antibiotics are not a substitute for drainage of free fluid and abscesses. • Surgery: When possible, focal lesions should be surgically debrided and adequate drainage established. • Thoracic or Abdominal Drainage: Pyothorax should be addressed with a thoracic drainage system and saline lavage twice daily. This therapy should be continued until the thoracic fluid is clear and no organisms are found on cytologic examination of the fluid. This normally requires 4 to 10 days. Some have advocated thoracic lavage

with fluids containing sodium penicillin (not potassium penicillin). Surgical exploration of the abdomen will likely be required for abdominal infections.

Therapeutic Notes • Penicillin was considered the drug of choice, but poor absorption makes it less effective than once thought. • Drug penetration into granulation tissue can be problematic. • In some cases, the course of therapy has extended beyond a year.

Prognosis Prognosis is variably reported from guarded to good in cats with actinomycosis.

Suggested Readings Edwards DF. 2006. Actinomycosis and nocardiosis. In C Greene, ed., Infectious Diseases of the Dog and Cat, 3rd ed., pp. 451–456. Philadelphia: Saunders Elsevier. Thomovsky E, Kerl ME. 2008. Actinomycosis and nocardiosis. Compend Contin Educ. 10(3):4–10.

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CHAPTER 5

Adenocarcinoma and Carcinoma Mark Robson

Overview Carcinomas are malignant tumors of epithelial origin. If the tumor forms glands and ducts and has therefore arisen from glandular tissue it is termed an adenocarcinoma (AC). Therefore, these malignancies can arise from any epithelial or glandular tissue at any location in the body. The cytological features of these tumors are outlined in Chapters 281 and 288. With a few exceptions, there is a relative paucity of peer-reviewed literature specifically concerning carcinomas and ACs of cats when compared to the canine and human body of knowledge. Hence, a great deal of our approach to these tumors in cats is extrapolated from similar lesions in dogs and to a lesser extent people. Commonly recognized carcinomas include squamous cell carcinoma (SCC; see Chapter 203) and transitional cell carcinoma (TCC). AC is well recognized in the nasal cavity, lung, gastrointestinal tract, pancreas, liver, and mammary gland (see Chapter 132). Clinical signs of carcinomas and ACs are highly variable and related to their location. The nasal cavity of cats can give rise to SCC, AC, and undifferentiated carcinomas. In one study 60% of 320 cats with nasal tumors had carcinomas of various types, and males were more commonly affected than females. Nasal SCC or AC may cause sneezing, nasal discharge, and abnormal respiratory noises. Primary lung tumors are rare in cats but 70 to 85% of them are ACs, and the terminology can vary depending on whether site of origin (difficult to confirm in many cases) or cellular morphology is used to classify them. They may be described as an AC, an undifferentiated carcinoma, an SCC, or a bronchoalveolar carcinoma. Other similar terms may also be used. These tumors can be advanced before any clinical signs are seen. Cats do not cough as readily as dogs and humans so this sign can be variable. Weight loss, reduced appetite, and lethargy are more likely but are, of course, non-specific. Wheezing, cyanosis, fever, and hemoptysis are occasionally seen, along with lameness if musculoskeletal metastasis has occurred. Lung tumors in cats are often discovered incidentally after radiographs have been taken for other reasons. Metastasis to digits is discussed in Chapters 55 and 163. Epithelial tumors of the pancreas are termed carcinomas if they arise from the ductal epithelium and AC if they arise from acinar cells. Metastasis and local spread is common, with the liver often being the first tissue affected. Any gastrointestinal or pancreatic carcinoma or AC may result in anorexia, weight loss, vomiting, diarrhea, lethargy, and dyschezia, but none of these signs are specific; and the disease can be advanced before any signs are seen. Sometimes these tumors will be discovered in the abdomen serendipitously when ultrasound is performed for other reasons. Primary tumors of the liver are rare in cats, but cholangiocellular carcinoma and hepatocellular carcinoma have been well described, with a mean age at diagnosis of 11 years. Clinical signs include detection of an abdominal mass, polyuria/polydipsia, anorexia, and vomiting. Icterus may not be a common finding. Intestinal ACs are well recognized in cats but are less common than lymphoma. In contrast to the dog, most of these tumors occur in the ileum and jejunum rather than the colon. Mean age at time of diagnosis

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is 11 years, and most have metastasized at the time of surgery. Despite this, survival times can be prolonged, and in one study 11 of 32 cats that survived more than 2 weeks postoperatively showed a mean survival time of 15 months. Prostatic neoplasia is rare in the cat and, as in the dog, may be classed as AC or TCC depending on the precise appearance of the cells. Epithelial tumors of the reproductive tract of female cats are extremely rare. Renal carcinomas and ACs are rare in the cat. In contrast to dogs, lymphoma is the most common renal tumor in the feline. In the few reports that exist in cats the mean age at diagnosis was 9.3 years, the tumors metastasized widely, and clinical signs were variable and nonspecific. A case report documenting the resolution of paraneoplastic polycythemia after surgical resection of a renal AC in two cats has been published, though one cat died 8 months later from metastatic lesions. The biological behavior of a carcinoma or AC is highly variable with regard to metastasis, but they all show local invasion. Nasal carcinomas and ACs usually metastasize quite late if at all, whereas pancreatic, hepatic, and intestinal tumors often metastasize, and in many cases this will have already occurred at the time of diagnosis. Pancreatic tumors often metastasize to the liver, and clinical signs may be more obvious from liver involvement than from the pancreas. Any abdominal carcinoma or AC can spread locally across abdominal structures and the peritoneum, leading to the phenomenon of carcinomatosis (see Chapter 29). The actual tissue of origin may be difficult to define in these cases. The differential diagnosis of any particular carcinoma or AC will depend on the location. For instance, in the nasal cavity an AC could present in a similar way to lymphoma, deep fungal diseases, or a foreign body. In the gastrointestinal tract an AC needs to be distinguished from lymphoma, foreign body, or a leiomyosarcoma.

Diagnosis Primary Diagnostics • Cytology and Histology: These are the cornerstones of diagnosis. Lesions that are visible or palpable will be more amenable to sampling, but ultrasound-guided aspiration/biopsy, laparoscopy, or exploratory laparotomy may be required for abdominal lesions. See Chapter 281. • Imaging: Radiography will often be the first step in diagnosing pulmonary neoplasia, but ultrasonography will likely be the primary modality in the abdomen. Computerized tomography (CT) may be useful in some cases. Assessment of metastasis to local nodes, distant nodes, lung, and liver must be performed if surgery is considered, using ultrasound, radiography, advanced imaging, and guided aspiration. • Pancreatic Tumors: These can be difficult to distinguish from the lesions of pancreatitis. The ultrasound appearance, blood changes (including pancreatic lipase immunoreactivity [PLI]) and cytology of these two diseases can be similar. Often it requires biopsy by ultrasound guidance, laparoscopy, or laparotomy to reach a firm diagnosis. In one study comparing cats with pancreatic neoplasia with cats with nodular hyperplasia the existence of a single mass that exceeded 2 cm (3/4 inch) in any dimension was predictive of neoplasia. • Pulmonary Tumors: Diagnosis of pulmonary tumors may require bronchoscopy with bronchoalveolar lavage, lung aspiration, or

Adenocarcinoma and Carcinoma

lobectomy (complete or partial) via thoracoscopy or thoracotomy. Significant risk is involved with all pulmonary diagnostic procedures in the cat, and these should be discussed with the owner. • Prostatic Neoplasia: This rare tumor may be classed as carcinoma or AC, and lesions can be so undifferentiated that it is impossible for the pathologist to be sure. Cells from the urinary tract are notoriously difficult for cytologists to define accurately, with dysplasia and neoplasia having a large overlap in appearance. Histopathology will almost always be needed for a definitive diagnosis.

dipitously at laparotomy exist. At my practice partial remission of a biopsy-confirmed pancreatic AC was achieved using carboplatin and piroxicam. Survival time thus far has been 10 months. • Radiation Therapy: This may be appropriate, especially for lesions in accessible regions such as the nasal cavity, and consultation with a radiation oncologist is encouraged. • Nasal AC: A single case report exists of the treatment of a nasal AC with long-term oral piroxicam and then chemoembolization with carboplatin. This cat lived 744 days after first presentation.

Diagnostic Notes

Therapeutic Notes

• When considering ultrasound-guided aspiration or biopsy of abdominal structures, thought must be given to the undesirable possibility of “seeding” the abdominal cavity or needle track with neoplastic cells.

• Because surgery for cancer is a field filled with possible pitfalls, consultation with or referral to a specialist surgeon should be considered. • There is little peer-reviewed information concerning medical treatment of carcinoma and AC in the cat other than TCC and mammary carcinoma. Anecdotally, many internists will try a combination of carboplatin and a nonsteroidal anti-inflammatory drug (NSAID) such as piroxicam or meloxicam. The use of NSAIDs in this setting is extrapolated from their original use in TCC of dogs.

Treatment Primary Therapeutics • Surgical Feasibility Decision: The clinician must first consider whether surgery is appropriate and possible for the individual patient. The presence of metastasis may make surgery a poor option, but in some cases resection of a tumor can result in dramatic improvement in clinical signs even if metastasis is known to have occurred. An example is AC of the intestine in which functional obstruction can be relieved and the patient may have many months of good quality life even if metastasis to nodes is detected. • Pancreatic Tumors: These are generally regarded as resistant to treatment, even in humans. Isolated reports of prolonged survival time after surgical resection of a lesion that was discovered seren-

Prognosis The outlook for cats with carcinoma and AC is guarded overall but highly variable and dependent on the location and tissue of origin of the tumor. Lesions that are amenable to surgical resection carry a much better prognosis.

Suggested Readings Kosovsky JE, Matthiesen DT, Patnaik AK. 1988. Small intestinal adenocarcinoma in cats: 32 cases. J Am Vet Med Assoc. 192:233–235.

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CHAPTER 6

Amyloidosis Andrew Sparkes

Overview Amyloidosis is a diverse group of diseases characterized by deposition of inert, insoluble extracellular protein fibrils (amyloid) that have a distinctive three-dimensional conformation. Although more than 25 chemical types of amyloid have been identified in man and animals, they all share the morphology of being composed of non-branching fibrils, approximately 7- to 10-nm thick and of variable length. Histologically, amyloid deposits in tissues are amorphous and demonstrate apple-green birefringence when stained with Congo red. Amyloid fibrils have the potential to form when there is an accumulation of an amyloidogenic protein (increased synthesis or decreased degradation). Some normal proteins may have the ability to form amyloid fibrils if present in high enough concentrations; other proteins may become amyloidogenic as a result of genetic mutation (leading to production of an abnormal, amyloidogenic protein) or as a result of posttranslational events that affect the protein. Over time, accumulation of amyloid in tissues can lead to interference with their structure and function and thus lead to development of disease. A variety of amyloid-related diseases have been identified and described in cats. Importantly, these include: • Diabetes Mellitus: Many, although not all, diabetic cats have an accumulation of amyloid in their pancreas, which is derived from the hormone amylin that is co-secreted with insulin from β cells. Amylin is an amyloidogenic protein in a few species including man and cats, and pancreatic amyloidosis is an important part of the pathogenesis of humans with type-2 diabetes and also in many cats with diabetes. • Alzheimer-like Pathology in the Brains of Aging Cats: Studies have demonstrated amyloid plaques and fibrils in the brains of aging cats, which bear close resemblance to the changes seen in humans with Alzheimer ’s disease and related conditions. The clinical significance of these changes in cats is yet to be determined but may, for example, be related to cognitive dysfunction. • Prion Diseases: These are a form of amyloidosis, and although no longer recognized in cats, the emergence of bovine spongiform encephalopathy led to its spread to cats in the form of feline spongiform encephalopathy. • Immunoglobulin Light-Chain Associated Amyloidosis: As in other species, cats with plasmacytomas may produce excessive quantities of immunoglobulin light chain fragments, and these may be amyloidogenic. Generally the amyloid appears to be deposited locally and predominantly within the neoplastic tissue. • Reactive Amyloidosis (AA-amyloid): This is the most commonly described form of amyloid in veterinary medicine and is well recognized in cats. The amyloid is derived from serum amyloid-A (SAA), an acutephase protein produced in the liver as part of the inflammatory process. In this disease, amyloid deposits have been found in the liver, spleen, adrenals, small intestine, stomach, endocrine and exocrine pancreas, thyroids, parathyroids, heart, tongue, and kidneys. Despite the generalized nature of the deposits, the heaviest deposits usually occur in the liver (leading to spontaneous hepatic rupture)

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or the kidneys (leading to chronic renal disease as the deposits are primarily in the medullary interstitial space). Reactive amyloidosis may occur sporadically secondary to inflammatory or neoplastic diseases in any breed of cat, but predispositions have been described in Abyssinian cats and in Oriental Shorthair cats. Familial amyloidosis in Abyssinian cats has been well characterized in the United States, where AA-amyloid accumulates in a wide variety of tissues but clinical signs relate to accumulation in the renal medullary interstitium that leads to chronic renal disease. Affected cats have typically developed renal disease at around 1 to 5 (average 3) years of age, but some older cats that die of other causes have also been found to have subclinical renal amyloidosis. It has been suggested that this might be inherited as an autosomal dominant trait with incomplete penetration. A number of publications have now appeared identifying systemic amyloidosis in Siamese and Oriental cats. In contrast to Abyssinians, in many of these cats the liver is most severely affected, although widespread amyloid deposits are typical; this may include renal amyloidosis and thus concomitant chronic renal disease may also be present. Heavy amyloid accumulation in the liver leads to dramatic friability of the liver with spontaneous or easily induced rupture, evidenced by recurrent or catastrophic bleeding episodes into the abdomen. Current research suggests that affected Siamese and Oriental Shorthair cats have genetic mutations resulting in amino acid substitutions in the serum AA protein that renders it more amyloidogenic, but similar to the situation in Abyssinians, for the disease to develop there probably also needs an inflammatory process(es) to increase the production of SAA in most cases. Further studies are necessary to clarify the heritability of the disease in these breeds.

Diagnosis Primary Diagnostics • Histopathology: Examination of biopsies stained with Congo red is usually sufficient for a diagnosis to be made, but additional investigations, including the use of immunostains, are necessary for characterising the nature of the amyloid. Due to the friable nature of the liver, if biopsy is being contemplated and amyloidosis is suspected, it is preferable to perform surgical biopsies with laparotomy rather than ‘blind’ or ultrasound-guided needle biopsies in which the risk of significant haemorrhage is high.

Secondary Diagnostics • Clinical Signs: These may be diverse in cats with systemic amyloidosis. There may be progressive chronic renal disease (that may develop at a relatively young age), although the rate of progression is variable. When hepatic amyloidosis predominates there may be mild to profound elevations in liver enzymes, and cats often present with recurrent bouts of lethargy associated with acute onset anemia (due to abdominal hemorrhage) or acute death or life-threatening anemia due to a catastrophic hemorrhagic event. Clotting times are prolonged in some affected cats.

Amyloidosis

Figure 6-1 Lateral radiograph of a cat with severe hepatic amyloidosis. Irregular hepatomegaly is evident.

Figure 6-2 Hepatic ultrasound of the same cat showing that the normally homogenous echogenic pattern has been replaced by a mixed echogenic pattern.

• Radiographs: Abdominal radiographs may show an irregular enlargement of the liver. See Figure 6-1. • Ultrasound: The hepatic parenchyma may display a diffuse increase in echogenicity on ultrasound, and there may be a speckled or “sparkling” appearance. See Figure 6-2. Following acute episodes of hemorrhage, ascites (hemoperitoneum) may also be detectable by ultrasound.

ments should be considered. See Chapters 190 and 191. When liver hemorrhage occurs, blood transfusion should be considered. These cats should have a lifestyle that will minimize the risk of even mild abdominal trauma.

Diagnostic Notes • Although biopsy material is preferable for confirmation, in some cases a diagnosis of amyloidosis may be possible from fineneedle aspirates from affected tissues.

Treatment Primary Therapeutics • Amyloidosis is not a curable disease. • Efforts should be made to identify and treat any other concomitant diseases that may be predisposing to amyloid deposition (e.g., infectious/inflammatory diseases) or may be the result of amyloidosis.

Secondary Therapeutics • Medical Treatment: Treatments that have been attempted include vitamin K therapy (e.g., 10 mg/cat q7d PO), especially if there is evidence of prolonged clotting times, and prednisolone at antiinflammatory doses (1–2 mg/kg q24–48h PO). However, it is unclear whether either of these approaches produces genuine clinical benefit. Colchicine (0.03 mg/kg q24–48h PO) has been suggested because it may reduce SAA production in other species and thus reduce the accumulation of amyloid, but its efficacy (if any) in cats is unknown. • Supportive Therapy: This is important in cats with amyloidosis. When chronic renal disease develops, the usual supportive treat-

Therapeutic Notes • Prevention of systemic amyloidosis may be possible through selective breeding programs. Because many cats with systemic amyloidosis develop disease at a relatively young age, breeding from older healthy cats may be beneficial. Further work is needed to identify underlying genetic abnormalities (and thus diagnostic tests) in affected breeds/lines of cats.

Prognosis The prognosis for cats with clinical systemic amyloidosis is grave. Currently there is no known effective treatment, and the disease is progressive, usually leading to death from renal disease or liver rupture.

Suggested Readings Beatty JA, Barrs VR, Martin PA, et al. 2002. Spontaneous hepatic rupture in six cats with systemic amyloidosis. J Small Anim Pract. 43(8): 355–363. Godfrey DR, Day MJ. 1998. Generalised amyloidosis in two Siamese cats: spontaneous liver haemorrhage and chronic renal failure. J Small Anim Pract. 39(9):442–447. Gunn-Moore DA, McVee J, Bradshaw JM, et al. 2006. Ageing changes in cat brains demonstrated by beta-amyloid and AT8-immunoreactive phosphorylated tau deposits. J Fel Med Surg. 8(4):234–242. Rand J. 1999. Current understanding of feline diabetes: part 1, pathogenesis. J Fel Med Surg. 1(3):143–153.

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CHAPTER 7

Anal Sac Disease Gary D. Norsworthy

Overview The anal sacs are located lateral to the anus in the 4- to 5-o’clock and 7- to 8-o’clock positions. They are positioned between the internal and external anal sphincters and contain sebaceous and apocrine tubular anal glands, which secrete a malodorous substance that is used for scent marking, individual recognition, and defense purposes. This substance is temporarily stored in the paired anal sacs (paranal sinuses), which empty voluntarily when the cat feels threatened or involuntarily with bowel movements. If the sacs are not emptied periodically, the anal gland secretion desiccates and thickens. See Figure 7-1. At this stage, the anal sacs are said to be impacted; the cat exhibits pain when defecating and may experience tenesmus. The cat responds by licking or biting at the tailhead region. If infection occurs within the sacs, pain will increase. Abscess formation may follow resulting in expulsion of purulent material through a draining tract over one or both anal sacs. See Figure 7-2. Thus, the three stages of anal sac disease are impaction, infection, and abscessation. An unrelated anal sac condition is incompetence of the anal sac sphincters. When affected, cats spontaneously release normal anal sac material involuntarily. Although uncommon and of no health threat to the cat, this condition is not well tolerated by owners of indoor cats.

Diagnosis

Figure 7-2 The left anal sac of the cat in Figure 7-1 was abscessed. It was surgically opened with an incision over the abscess. Blood tinged purulent material drained freely.

release of anal sac material is characteristic of anal sac sphincter incompetence.

Primary Diagnostics • Clinical Signs: The signs of tenesmus, licking at the perineal region, and a draining tract are characteristic of anal sac disease. Spontaneous

Diagnostic Notes • Anal sac disease of dogs usually produces scooting. Scooting is not a common finding in cats with anal sac disease. • Some cats with anal sacculitis may lick the perineal area and the caudal thighs, producing a symmetrical pattern of alopecia.

Treatment Primary Therapeutics • Manual Expression: This procedure should permit removal of thickened secretions. Anesthesia or sedation is required in many cats because of the cat’s tight anal sphincter and small anal size. The first phalanx of one’s index finger or thumb is inserted into the anus. The anal sac is squeezed between it and the other mentioned digit. See Figure 7-1. • Irrigation: An antiseptic solution, such as dilute chlorhexidine, is used to flush remaining dried debris from the anal sacs. Sedation of the cat generally is required. • Antibiotic Instillation: Local treatment with antibiotics is indicated. Drugs expected to be effective against Escherichia coli, Streptococcus fecalis, and Clostridium spp. should be considered. • Systemic Antibiotics: Systemic antibiotics with the characteristics above speed recovery and should be given for 7 to 14 days. Figure 7-1 Desiccated, thick anal sac material was expressed from the right anal sac of the cat in Figure 7-2. This is a predisposing factor to anal sac abscessation.

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Secondary Therapeutics • Surgical Drainage: Anal sac abscesses that have not drained spontaneously should be opened surgically to establish drainage through the skin.

Anal Sac Disease

• Anal Sacculectomy: This procedure should be considered in recurrent cases but should not be performed until infection is resolved. It is the treatment of choice for incompetent anal sphincter disease. Fecal incontinence is a possible sequel, but it occurs infrequently if careful dissection is performed. If it occurs, it usually resolves spontaneously in 7 to 21 days.

Suggested Readings Zoran DL. 2005. Rectoanal Disease. In SJ Ettinger, EC Feldman, eds., Textbook of Veterinary Internal Medicine, 6th ed., pp. 1408–1420. St. Louis: Elsevier Saunders.

Prognosis The prognosis is good; however, aggressive therapy as outlined should occur.

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CHAPTER 8

Anaplasmosis Sharon Fooshee Grace

Overview Although molecular technology has greatly expanded our understanding of bacterial organisms in recent years, it has also created confusion as large numbers of bacteria have been reclassified and renamed. In 2001, the families Rickettsiaceae and Anaplasmataceae, members of the order Rickettsiales, underwent major reorganization. The genera Ehrlichia and Wolbachia were moved from the family Rickettsiaceae to the family Anaplasmataceae. The genus Rickettsia remained in the family Rickettsiaceae. Additionally, species within the genus Ehrlichia were significantly reorganized: E. phagocytophila, E. equi, and E. platys now reside in the genus Anaplasma; E. risticii and E. sennetsu have been moved to the genus Neorickettsia. Feline ehrlichiosis continues to be an area of active research, but little is known about this disease in cats. The family Anaplasmataceae contains gram-negative obligate intracellular organisms that parasitize leukocytes, erythrocytes, platelets, and endothelial cells. Ehrlichia phagocytophila, the granulocytic Ehrlichia, has been renamed Anaplasma phagocytophilum. This is a tick-borne organism found in many parts of the world, including the United States. Cats are not infected with tick-transmitted diseases as often as dogs, a finding which has been attributed to the fastidious grooming behavior of cats. Ticks are likely removed by cats before the 24- to 48-hour time frame required for transmission of most tick-transmitted diseases. A. phagocytophilum is transmitted transtadially by nymph and adult forms of Ixodes scapularis (the deer tick or black-legged tick) or Ixodes pacificus (the western black-legged tick). The deer tick is common in the eastern, southeastern, and midwestern United States, and depending upon geographic location, it feeds primarily on mammals, birds, or lizards. The western black-legged tick is found in the western United States. Larval forms feed on the white-footed mouse and other small rodents whereas nymphs and adults have a diverse range of hosts, including white-tailed deer, dogs, cats, and humans. The disease, formerly called ehrlichiosis, is now called feline granulocytotropic anaplasmosis or simply anaplasmosis. At present, little is known about the pathogenesis of the disease, although it is likely similar to infection in other species. In the limited number of cases described in the literature, clinical findings have included acute onset fever, lethargy, weight loss, vomiting, lameness (polyarthritis), and ocular discharge. Most cats have vague, nonspecific signs of illness. This organism has public health significance because humans are known to be susceptible to the organism. However, there is no evidence that human infection has resulted from contact with a cat.

Diagnosis Primary Diagnostics • History: The few cats reported with disease have had access to the outdoors. • Complete Blood Count, Biochemical Profile, and Urinalysis: Thrombocytopenia, the presence of morulae in neutrophils, mild hyperglycemia, and hyperglobulinemia have been reported in

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infected cats. The organism has been found to rarely infect eosinophils.

Secondary Diagnostics • Serology: Published studies have used immunofluorescent assays and enzyme-linked immunosorbent assay (ELISA) methodology to detect antibodies against the organism. • Polymerase Chain Reaction (PCR) Test: PCR testing is available at several commercial veterinary laboratories. Consult the diagnostic lab prior to sample submission for additional details on sample collection and shipping.

Diagnostic Notes • Clinical illness may develop prior to seroconversion. Therefore, a single negative antibody test does not exclude infection.

Treatment Primary Therapeutics • Antibiotics: Reported cases have appeared to improve when treated with doxycycline (5–10 mg/kg q24h PO) for 28 to 30 days.

Therapeutic Notes • Inadequate duration of therapy or selection of antibiotics without efficacy against A. phagocytophilum may result in incomplete response to treatment or relapse. • Antibodies may persist beyond the end of treatment, in some cases for months.

Prevention The disease can be prevented if tick-control measures are implemented. Cats going outdoors should be treated with topical acaricidal products approved for cats.

Prognosis Little is known about the disease in cats, but based on cases reported to date, prognosis is generally good if the cat is treated with doxycycline.

Suggested Readings Billeter SA, Spencer JA, Griffin B, et al. 2007. Prevalence of Anaplasma phagocytophilum in domestic felines in the United States. Vet Parasitol. 147(1–2):194–198. Lappin MR, Bjoersdorff, Breitschwerdt EB. 2006. Feline granulocytic ehrlichiosis. In C Greene, ed., Infectious Diseases of the Dog and Cat, 3rd ed., pp. 227–229. Philadelphia: Saunders Elsevier. Lappin MR, Breitschwerdt EB, Jensen WA, et al. 2004. Molecular and serologic evidence of Anaplasma phagocytophilum infection in cats in North America. J Am Vet Med Assoc. 225(6):893–896. Magnarelli LA, Bushmich SL, Ijdo JW, et al. 2005. Seroprevalence of antibodies against Borrelia burgdorferi and Anaplasma phagocytophilum in cats. Am J Vet Res. 66(11):1895–1899. Stuen S. 2007. Anaplasma phagocytophilum—the most widespread tickborne infection in animals in Europe. Vet Res Comm. 31(1):79–84.

CHAPTER 9

Anemia Sharon Fooshee Grace

Overview Anemia is a reduction below normal of the number of circulating red blood cells (RBCs) and hemoglobin. It is important to note that the cat’s RBC count is normally lower than that of dogs, and they tend to have a less vigorous marrow response to anemia. There are numerous causes of anemia in the cat. Historical findings depend on the chronicity of the anemia with acute, rapidly progressing anemias causing more severe signs than chronic, slowly progressing anemias. Cats may demonstrate mild or severe decreases in activity or tolerance for exercise and mild or severe increases in respiratory effort; pica is often present. Physical examination may reveal pale mucous membranes, increased ventilatory effort (especially with stress), a soft systolic heart murmur, tachycardia, and weakness. In examining the feline patient with anemia, particular attention should be given to the size of the peripheral lymph nodes and the spleen because common neoplastic, infectious, and immune causes of anemia often lead to enlargement of these organs. The initial step in the evaluation of any anemia involves defining the anemia as regenerative or nonregenerative. Circulating reticulocytes (immature RBCs) should be counted whenever the hematocrit is less than 20% to assess bone marrow responsiveness. The cat is unique in that two types of reticulocytes may be present. Aggregate reticulocytes are more

reflective of a recent regenerative response and contain numerous darkstaining clumps of ribosomes, whereas punctate reticulocytes contain small clumps or specks of ribosomal material. The presence of aggregate reticulocytes is the most reliable indicator of a regenerative response. Regenerative anemias are associated with three main categories of causes: blood loss, hemolysis, or sequestration. Nonregenerative anemias are caused by decreased production of erythrocytes; the underlying cause may be a disease of the bone marrow or may be secondary to an extramedullary disorder.

Diagnosis Differential Diagnoses There are many known diseases that cause anemia in cats. They are classified and listed in Table 9-1.

Primary Diagnostics • Complete Blood Count (CBC): A CBC should be performed if anemia is suspected. Diagnosis of anemia requires identification of erythrocyte numbers or a hematocrit lower than normal for the individual

TABLE 9-1: Known Causes of Anemia in Cats Regenerative

Hemolysis Erythrocyte parasites: Mycoplasma hemofelis and Candidatus Mycoplasma hemominutum (formerly known as Hemobartonella felis) Cytauxzoon felis, and Babesia spp. Immune-mediated destruction (i.e., drug-induced, idiopathic, paraneoplastic, or toxicity) Microangiopathic hemolysis (DIC) Oxidative injury (i.e., zinc, methylene blue, acetaminophen, benzocaine, phenazopyridine, or onions) Neonatal isoerythrolysis Blood Loss Trauma or surgical loss Coagulopathy External loss (i.e., urinary tract, trauma, or epistaxis) Internal or poorly visualized loss (i.e., gastrointestinal, peritoneal, or pleural) Sequestration Splenic disease with splenomegaly

Non-Regenerative

Intramedullary Hematopoietic neoplasia with or without feline leukemia virus or feline immunodeficiency virus infection Lymphoproliferative neoplasia Myelodysplasia Myeloproliferative neoplasia Red blood cell aplasia Extramedullary Chronic inflammatory disease (e.g., fungal disease, Feline Infectious Peritonitis, and so on) Chronic renal disease Neoplasia Poor nutrition or starvation

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SECTION 1: Diseases and Conditions Corrected reticulocyte count = ( reticulocyte % ) × ( patient′s HCT normal HCT* ) *Normal hematocrit = 37.5%

MacroC

• Feline Retroviral Screen: The cat should be evaluated with an antigen test for feline leukemia virus (FeLV) and an antibody test for feline immunodeficiency virus (FIV).

Secondary Diagnostics

MetaR

Figure 9-1 Signs of a regenerative anemia include the presence of nucleated red blood cells and reticulocytes. A metarubricyte (MetaR) and several macrocytes (MacroC) are shown. Macrocytes are reticulocytes stained with a modified Wright’s stain that demonstrate increased cell diameter but do not show the reticulum. The organisms on the red blood cells are Mycoplasma haemofelis.

A

P

• Serum Chemistry Profile: A serum chemistry profile is indicated to detect underlying diseases, especially in cases of nonregenerative anemia. Particular attention should be given to serum color (look for hemolysis or icterus), blood urea nitrogen (BUN), creatinine, alanine aminotransferase (ALT), alkaline phosphatase (ALP), total bilirubin, and total protein. • Bone Marrow Examination: With unexplained nonregenerative anemia, bone marrow aspiration and cytology are indicated. Several sites are available for aspiration: the humeral head, femoral shaft, or wing of the ilium is commonly used sites. See Chapter 296. The bone marrow slides should be submitted to a veterinary clinical pathologist, along with a tube of EDTA-anticoagulated blood drawn at the time of marrow aspiration. In some cases, a core biopsy of the marrow may be indicated. • Coombs’ Test: A Coombs’ test may be performed when an immunemediated cause of anemia is suspected. It should be remembered that a positive test is not diagnostic of immune-mediated hemolysis; a variety of disorders may produce a positive Coombs’ test. An EDTA-anticoagulated tube of blood should be submitted to a veterinary diagnostic laboratory. See Chapter 119. • Radiography: Thoracic and abdominal radiographs may be a useful component of the minimum data base in cats with unexplained anemia. • Coagulation Tests: If a coagulopathy is suspected, clotting tests and a manual platelet count are indicated.

Diagnostic Notes

Figure 9-2 When stained with new methylene blue stain, reticulocytes demonstrate the reticulum as either younger aggregate reticulocytes (A) or more mature punctuate reticulocytes (P). Aggregate reticulocytes are counted to generate the reticulocyte count.

laboratory. The blood smear should be evaluated for the presence of young RBC types (see Figure 9-1), RBC parasites, Heinz bodies and other morphologic changes, and cytopenias. Because of the small size of feline erythrocytes, spherocytosis (indicative of immune-mediated destruction) is not detectable on feline blood smears. • Reticulocyte Count: Equal parts of ethylenediaminetetra-acetic acid (EDTA) anticoagulated blood and new methylene blue stain are gently mixed, and the solution allowed to incubate at room temperature for 10 to 15 minutes. A smear is made, and then 500 to 1,000 red cells are examined. The percentage that is aggregate reticulocytes is recorded (see Figure 9-2). After 5 or 6 days and with sufficient anemia to stimulate erythrocyte production, the percentage of aggregate reticulocytes should be 1 to 5%. The feline regenerative response is more subtle than that of the dog with a comparable anemia. Additionally, some peculiarities of the feline erythron occasionally make it difficult to interpret the significance of a response; a veterinary clinical pathologist should be consulted, as needed. The reticulocyte count should be corrected for the hematocrit (HCT):

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• Mucous membrane color is a poor indicator of anemia in cats because normal feline mucous membranes are relatively pale, especially when compared with those of dogs, and excitement or stress may raise blood pressure and increase the color in the mucous membranes. • Circulating nucleated RBCs do not indicate a regenerative response unless accompanied by an increase in reticulocytes. Causes of circulating nucleated red bloods in the absence of a regenerative anemia include neoplasia, hypoxic or toxic bone marrow injury, lead toxicity, and splenic disease. • Regenerative anemias may take 5 to 6 days to respond with an appropriate peripheral reticulocytosis. This timeframe should be taken into consideration when the initial hemogram and reticulocyte count are consistent with nonregenerative anemia, but blood loss, hemolysis, or sequestration is likely. • Mycoplasma haemofelis and Candidatus Mycoplasma haemominutum (previously known as Hemobartonella felis) organisms may detach from red blood cells after incubating in EDTA anticoagulant. A fresh blood smear should accompany the anticoagulated blood when hemotrophic Mycoplasma spp. are suspected. • Whole blood or bone marrow may be submitted for PCR detection of Mycoplasma haemofelis and Candidatus Mycoplasma haemominutum circulating DNA. The receiving laboratory should be contacted for sample requirements. • New methylene blue stain, as described for the reticulocyte count, will allow Heinz bodies to be identified easily.

Anemia

• Increased numbers of Heinz bodies have been associated with hyperthyroidism, lymphoma, and diabetes mellitus.

Treatment Primary Therapeutics • Transfusion with Blood or Hemoglobin Solutions: Administration of whole blood or hemoglobin solutions (e.g., Oxyglobin®) may be useful in cats with severe anemia (see Chapter 295); however, Hct alone is a poor indicator of the need to transfuse because cats with chronic severe anemia (packed cell volume as low as 10%) may often be relatively stable. Acute hemolysis or hemorrhage would warrant transfusion if the Hct falls below 20%. Transfusion in cats with chronic anemia should be assessed on a case-by-case basis, though transfusion is usually needed when the Hct is less than 12%. Oxyglobin (maximum dose 5–15 ml/kg), a hemoglobin-based oxygen carrier solution derived from bovine hemoglobin, is available but is expensive. It has the potential to cause volume overload in cats so slow infusion rates of 0.5 to 5 ml/kg per hour are recommended.

Secondary Therapeutics • Erythropoietin: Feline recombinant erythropoietin is not commercially available for veterinary use at this time. Human recombinant erythropoietin may be used in cases of nonregenerative anemia owing to renal failure. See Chapter 190. For other causes of anemia, this treatment is not indicated because serum erythropoietin levels are already elevated.

• Initial blood samples for diagnostic testing should be collected pre-transfusion. • A standard reference should be consulted for details of managing the donor cat, performing blood typing and cross-matches, and specific information on transfusion protocols. See Chapter 295. • For cats with anemia of chronic disease, specific treatment of the anemia is rarely indicated. The practitioner should focus on identification and treatment of the underlying cause. If this treatment is successful, the anemia should resolve.

Prognosis Prognosis is dependent upon identification and successful management of the underlying cause of anemia. Generally, the prognosis is better for acute and regenerative than for chronic and nonregenerative anemias.

Suggested Readings Cotter SM. 2003. A diagnostic approach to anemic patients. Vet Med. 98(5):420–430. Haldane S, Roberts J, Marks S, et al. 2004. Transfusion medicine. Compend Contin Educ Pract Vet. 26(7):502–518. Loar AS. 1994. Anemia: Diagnosis and treatment. In JR August, ed., Consultations in Feline Internal Medicine, 2nd ed., pp. 469–487. Philadelphia: WB Saunders. Webb CB, Twedt DC, Fettman MJ, Mason G. 2003. S-adenosylmethionine (SAMe) in a feline acetaminophen model of oxidative injury. J Fel Med Surg. 5(2):69–75.

Therapeutic Notes • Emphasis should be placed on stabilizing the patient while aggressively pursuing the underlying disesase process.

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CHAPTER 10

Anorexia Mitchell A. Crystal

Overview Anorexia is the loss of appetite for food. Anorexia can result from numerous pathologic and nonpathologic conditions, including metabolic, gastrointestinal, oropharyngeal, cardiopulmonary, or neurologic disorders, inflammatory/infectious diseases, reactions to drugs/toxins, neoplasia, fever, pain, environmental stress, and lack of diet palatability. Because so many conditions may lead to anorexia, other accompanying clinical signs are variable. Some cats will demonstrate anorexia or anorexia/lethargy/weight loss as the only presenting complaint of a disease process. Unlike many other animals, cats are obligate carnivores with special nutritional requirements. This is due to the cat’s persistent use and loss of some nutrients and inadequate synthesis of others (see Table 10-1). As a result, persistent or prolonged anorexia can lead to serious metabolic derangements, complicating a pre-existing condition. An additional concern in prolonged anorexia is the cat’s potential to develop hepatic lipidosis. See Chapter 93. Therefore, anorexia in the cat warrants prompt diagnostic investigation and therapeutic intervention.

Diagnosis

• History: Question the owner about the cat’s environment (i.e., indoor versus outdoor, any recent moves, any new or departed pets or members of the household), travel history (i.e., to areas endemic for infectious diseases), recent drug therapy (i.e., prescription, nonprescription, otic, ophthalmic, topical), exposure to toxins, foreign bodies or other animals, signs of other disease processes (e.g., polyuria/polydipsia, vomiting, diarrhea), or change in diet. Review the cat’s vaccination history. • Physical Examination: Examine closely for wounds and abscesses, internal or external masses, organ size (enlargement or reduction), lymphadenopathy, abnormal cardiopulmonary auscultation, and pain. A complete oral examination is warranted to look for gingival

TABLE 10-1: Special Nutrient Requirements of the Cat Nutrient

Clinical Signs of Deficiency

Arginine

Ptyalism, hyperesthesia, vomiting, tremors, and ataxia; signs can develop within hours to days. Retinal degeneration, dilated cardiomyopathy, reproductive problems, and decreased growth in kittens; signs develop over weeks to months Dermatitis, dry hair coat, anemia, reproductive problems, and decreased growth in kittens; signs develop over weeks to months Retinal degeneration, weakness, dry/unkempt hair coat, and decreased growth in kittens; signs develop over weeks to months

Arachidonic Acid

Vitamin A

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Secondary Diagnostics • Thoracic Radiography or Ultrasound: Abnormalities may suggest inflammatory/infectious, neoplastic, or cardiopulmonary disease. • Abdominal Radiography or Ultrasound: Abdominal imaging may reveal abnormalities in organ size and architecture, gastrointestinal obstruction, or neoplasia.

Diagnostic Notes

Primary Diagnostics

Taurine

or dental disease and to look under the tongue for a linear foreign body. A complete ophthalmologic examination (anterior chamber and retina) will sometimes disclose evidence of inflammatory/ infectious diseases, or lymphoid neoplasia. See Chapter 299. • Database (Complete Blood Count, Chemistry Profile, and Urinalysis): Abnormalities may suggest metabolic disorders, inflammatory/ infectious diseases, or neoplasia. • Retroviral Tests: Positive results are not confirmatory but strongly support illnesses related to feline leukemia virus (FeLV) or feline immunodeficiency virus (FIV) as the source of anorexia.

• Dental disease is a rare cause of anorexia except for painful resorptive lesions. A complete evaluation of any cat with anorexia is indicated prior to anesthesia and dental prophylaxis, despite the presence of dental tartar. A complete evaluation will rule out the more common causes of anorexia and will determine if anesthesia is safe. • If a foreign body is suspected and a complete oral (including sublingual) examination cannot be completed in the awake cat, sedation is recommended.

Treatment Primary Therapeutics • Treat Underlying Disease: This is essential in restoring appetite. • Fluid Support: Fluids may be administered orally or parenterally if needed to correct or maintain hydration. See Chapter 302. • Nutritional Support: Indications for nutritional support include weight loss of greater than 10% of body weight (greater than 5% in kittens), anorexia persisting more than 3 to 5 days (longer than 1–2 days in kittens), hypoalbuminemia, lymphopenia, anemia, increased nutrient losses (i.e., vomiting, diarrhea, burns, large wounds, intestinal malassimilation, protein-losing nephropathies, peritonitis, pleuritis), diseases associated with high metabolic demand (e.g., neoplasia), and inability to eat because of a disease or therapy (e.g., oropharyngeal disease, chemotherapy). Each cat must be individually evaluated when deciding whether one or several of the aforementioned criteria should be present before initiating nutritional support. Nutrients may be provided via enteral tube (i.e., gastrostomy, esophagostomy, jejunostomy, or nasoesophageal tube placement or intermittent orogastric intubation), forced hand feeding or parenterally (total or partial parenteral nutrition). See Chapters 253, 255, 256, and 308. • Therapy for Nausea: This should be attempted if there are signs or suspicion that nausea may be present (e.g., dolacetron, metoclopramide, maropitant, and so on; see Chapter 229).

Anorexia

Secondary Therapeutics • Appetite Stimulants: Appetite stimulants should only be used to help promote voluntary eating in cases in which a diagnosis has been achieved, specific therapy has been instituted, and immediate nutritional support is not feasible. Prior to using chemical agents, an attempt to stimulate eating should be made by offering a variety of foods of different flavors, odors, and textures, by warming foods, by placing foods in a wide shallow bowl to prevent the sides of the bowl from contacting the cat’s whiskers, and by stroking and petting the cat at the time of feeding (or providing a quiet environment for the stressed cat such as a covered cage or a cardboard box). Chemical appetite stimulants reported effective in the cat include mirtazapine (3.75 mg/cat q48–72h PO), vitamin B12 (2000 mcg/cat SC), cyproheptadine (1–2 mg/cat 5–20 minutes prior to feeding up to q12h PO), diazepam (0.1–0.2 mg/kg immediately prior to feeding up to q12h IV), and oxazepam (1.25–2.5 mg/cat 5–20 minutes prior to feeding up to q12h PO).

as a 5% solution contains 0.17 kcal per milliliter which, when delivered at maintenance for 24 hours for a 5-kg cat, provides only 50 kcal or about one-fifth of the daily caloric need. Providing a fraction of the caloric need via a carbohydrate source can contribute to muscle wasting by promoting protein over fat catabolism. • Glucocorticoids (prednisone or prednisolone 1–2 mg/kg up to q12h PO or dexamethasone 0.1–0.2 mg/kg up to q12h PO) may be helpful in stimulating appetite in some cats; however, undesirable catabolic and immunosuppressive side effects may occur. • If no significant response is seen after chemical appetite stimulants have been used for 24 hours, chemical appetite stimulants should be discontinued and nutritional support started. • Mirtazapine dosing should be decreased by 50% in cats with hepatic disease.

Prognosis The prognosis varies depending on the underlying disorder causing the anorexia.

Therapeutic Notes • It is best to provide nutrition via the enteral route. This maintains gastrointestinal mucosal health, is less expensive, and provides a more natural means of nutrient absorption and utilization. If the gastrointestinal tract is unable to absorb and digest food, total or partial parenteral nutrition can be used. • Forced hand feeding is a less optimal means of enteral nutrition than tube feeding because it significantly increases patient stress and generally cannot deliver the volumes necessary to meet the patient’s nutritional requirements. • Intravenous fluids with 2.5 or 5% dextrose do not supply significant calories when delivered at rates at or moderately above maintenance; thus, they are only indicated in patients with hypoglycemia or in patients that require hypotonic fluids (e.g., heart disease). Dextrose

Suggested Readings Case LP, Carey DP, Hirakawa DA, Daristotle D. 2000. Canine and Feline Nutrition. A Resource for Companion Animal Professionals, 2nd ed. St. Louis: Mosby. Marks SL. 1998. Demystifying the anorectic cat. In Proceedings of the Sixteenth Annual Veterinary Medical Forum, pp. 62–64. Sanderson S, Bartges JW. Management of anorexia. 2000. In JD Bonagura, ed., Kirk’s Current Veterinary Therapy XIII. Small Animal Practice, pp. 69–74. Philadelphia: WB Saunders Company. Streeter EM. 2007. Anorexia. In LP Tilley, FWK Smith, Jr., eds., Blackwell’s 5-Minute Veterinary Consult: Canine and Feline, 3rd ed., pp. 86–87. Ames, IA: Blackwell Publishing Professional.

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CHAPTER 11

Aortic Stenosis Larry P. Tilley

Overview Congenital narrowing of the left ventricular outflow tract, aortic valves, or supravalvular aorta has been reported in the feline. Although there are several acquired abnormalities that cause left ventricular outflow obstruction, most notably hypertrophic cardiomyopathy, congenital aortic stenosis in the cat is rare. Of the different types of aortic stenosis noted in the cat, supravalvular stenosis appears to be most commonly encountered lesion. Aortic stenosis may be seen concurrently with other congenital defects such as mitral valve dysplasia. Left ventricular concentric hypertrophy occurs when significant outflow obstruction is present. The elevated left ventricular pressures may eventually result in left-sided congestive heart failure in severely affected cats. Physical examination reveals a left basilar systolic ejectiontype murmur and potentially late-rising femoral pulses, which are difficult to note at high heart rates.

Diagnosis Primary Diagnostics • Echocardiography: Left ventricular concentric hypertrophy, left atrial enlargement, high-velocity turbulent systolic flow in the left ventricular outflow tract as demonstrated by spectral or color-flow Doppler echocardiography, systolic anterior movement of the anterior mitral valve leaflet, mitral regurgitation, aortic regurgitation, and premature closure of the aortic valves may be present. A pressure gradient can be estimated from the flow velocity (pressure gradient = 4 × flow velocity squared) with variable accuracy.

Secondary Diagnostics • Electrocardiography: Increased R-wave amplitude and wide QRS complexes, suggestive of left ventricular enlargement; wide P-waves, suggestive of left atrial enlargement; and atrial and ventricular tachyarrhythmias may be present. • Thoracic Radiography: Left atrial and ventricular enlargement, dilation of the ascending aorta, and signs consistent with left-sided congestive heart failure, such as pulmonary edema, may be present. Heart enlargement is usually not seen because myocardial hypertrophy from pressure overload usually does not increase the size of the cardiac silhouette (concentric hypertrophy). • Advanced Imaging: Cardiac catheterization and selective angiocardiography may be used for definitive diagnosis but often is unnecessary. See Figure 11-1.

Diagnostic Notes • This congenital abnormality is rare in the cat.

Figure 11-1 Angiography can be used to diagnose aortic stenosis. A catheter (open arrows) is passed through the carotid artery into the left ventricle. Contrast material is injected and lateral thoracic radiographs are made. The supravalvular stenotic area (closed arrow) is seen in the outflow of contrast from the left ventricle into the aortic outflow tract.

Treatment Primary Therapeutics • Medical management of left-sided congestive heart failure consists of the use of diuretics, vasodilators (such as angiotensin-converting enzyme [ACE] inhibitors) and moderate dietary salt restriction. • Surgical intervention or balloon valvuloplasty of the stenotic lesion is not recommended in cats.

Secondary Therapeutics • Atenolol: Giving 6.25 mg q12–24h PO may be effective in reducing ventricular and supraventricular arrhythmias, slowing the heart rate, and limiting myocardial oxygen requirements. • Diltiazem: Giving 1.75–2.4 mg/kg q8h PO may have benefits in this disease if atenolol not effective.

Therapeutic Notes • Medical management of this abnormality often is unrewarding, especially if significant aortic regurgitation is present. • Prophylactic antibiotic therapy is indicated at times of potential bacteremia (i.e., dental procedures) because these patients (even those with mild stenosis) are predisposed to valvular endocarditis.

Prognosis th

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The prognosis of aortic stenosis is directly related to the severity of the outflow obstruction. Patients with significant pressure gradients across

Aortic Stenosis

their outflow tract (i.e., 75–100 mmHg) have a guarded-to-poor prognosis. As with other causes of ventricular concentric hypertrophy, there is an increased risk of sudden cardiac death. Considering the genetic potential, breeding of affected cats should be discouraged.

Oyama MA, Sleeper MM, Strickland K. 2008. Congenital Heart Disease. In LP Tilley, ed., Manual of Canine and Feline Cardiology, 4th ed., pp. 223–227. St. Louis: Elsevier.

Suggested Readings Brown DJ. 2007. Aortic Stenosis. In LP Tilley, FWK Smith, Jr., eds., Blackwell’s 5 Minute Veterinary Consult, 4th ed., pp. 96–97. Ames: Blackwell Publishing.

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CHAPTER 12

Arrhythmias Larry P. Tilley and Francis W. K. Smith, Jr.

Overview The essentials of electrocardiography include the assessment of heart rate, heart rhythm, and the P-QRS-T wave forms. The electrocardiogram (ECG) is needed to accurately diagnose cardiac arrhythmias because it is extremely sensitive for this purpose. The ECG should be a standard part of the systemic disease workup, as well as part of the database in cats with suspected heart disease. An arrhythmia can be defined as (a) an abnormality in the rate, regularity, or site of origin of the cardiac impulse, or (b) a disturbance in conduction of the impulse such that the normal sequence of activation of atria and ventricles is altered. It is important to establish the causes of arrhythmias because such information affects prognosis and therapy. The possible sources of arrhythmias in dogs and cats can be divided into three basic categories: (a) autonomic nervous system; (b) cardiac sources; and (c) extracardiac sources. A classification of cardiac arrhythmias is listed in Table 12-1. See Figure 12-1.

Normal sinus rhythm

Sinus tachycardia

Sinus bradycardia

TABLE 12-1: Classification of Cardiac Arrhythmias Sinus Rhythm

Normal sinus rhythm Sinus tachycardia Sinus bradycardia Sinus arrhythmia Wandering pacemaker

Abnormalities of Impulse Formation

Supraventricular Sinus arrest Atrial premature complexes (APC) Atrial tachycardia Atrial flutter Atrial fibrillation Atrioventricular (AV) junction AV junctional escape rhythm (secondary arrhythmia) Ventricular Ventricular premature complexes (VPCs) Ventricular tachycardia Ventricular flutter, fibrillation Ventricular asystole Ventricular escape rhythm (secondary arrhythmia)

Abnormalities of Impulse Conduction

Sinoatrial (SA) block Atrial standstill (i.e., hyperkalemia or sinoventricular conduction) AV block: first degree, second degree, or third degree (complete heart block)

Abnormalities of Both Impulse Formation and Impulse Conduction

Pre-excitation (Wolff-Parkinson-White) syndrome and reciprocal rhythm (re-entry) Parasystole

Sinus arrhythmia

Figure 12-1

Examples of different rhythms from the sinoatrial node.

Diagnosis Differential Diagnoses There are several physiologic and pathologic conditions that must be considered. They are listed in Table 12-2.

Primary Diagnostics • Thoracic Auscultation: A markedly irregular cardiac rhythm on auscultation with an arterial pulse deficit may implicate arrhythmias such as ventricular premature complexes and atrial fibrillation, but it will require an ECG to differentiate among them. • Electrocardiography: A systematic method for an accurate ECG analysis of a rhythm strip (usually lead II) should always include the following steps: (a) general inspection of the rhythm strip; (b) identification of P-waves; (c) recognition of QRS complexes; (d) relationship between P-waves and QRS complexes; and (e) summary of findings and final classification of the arrhythmia.

Secondary Diagnostics th

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• Vagal Stimulation: This includes the mechanical application of pressure to receptors that cause a reflex increase in vagal tone (either by

Arrhythmias

TABLE 12-2: Differential Diagnoses of Feline Cardiac Arrhythmias Autonomic Nervous System

Excitement, exercise, pain, or fever (sympathetic influence) Respiratory influences on vagal tone (not as pronounced in cats as in dogs) Organic brain disease causing sympathetic or vagal stimulation

Cardiac Sources

Hereditary (rare) Acquired damage to the conduction system, hypertrophic cardiomyopathy, or neoplasia Diseases of the atria and ventricles; arrhythmias occurring in neoplasia, hypertrophic cardiomyopathy, and myocarditis (many causes)

Extracardiac Sources

Hypoxia Disturbances of acid-base balance Electrolyte imbalance Drugs Endocrine disease: hyperthyroidism, diabetes mellitus

ocular pressure or carotid sinus massage). The effects of increasing vagal tone are mainly supraventricular, causing a slowing of the heart rate and a decrease in conduction through the atrioventricular (AV) junction. • Long-Term Ambulatory Recordings: A Holter™ Monitor records the ECG for extended periods of time. The long-term ECG recording technique is the most sensitive noninvasive test to demonstrate transient arrhythmias. • Echocardiography: Arrhythmias can often be picked up as an incidental finding during an ultrasound study, or in some cases, can affect the hemodynamics.

used in the specific treatment of arrhythmias in the cat. Diltiazem (1.75–2.4 mg/kg PO q8h) and atenolol (6.25 mg/cat q12–24h PO) are currently the drugs of choice in cats because of their broad antiarrhythmic effects.

Secondary Therapeutics • Treat the Underlying Disease: Specific treatment for many of the arrhythmias present in cats often is not required. In the majority of cases, arrhythmias disappear when the underlying disease is brought under control. For example, the correction of hyperkalemia resulting from urethral obstruction by relieving the obstruction and restoring normal acid-base status and fluid volume may eliminate the associated arrhythmias. See Chapters 106 and 220. • Digoxin: Because of the recent use of angiotensin-converting enzyme (ACE) inhibitors in the cat and the side effects of digoxin, digoxin is used infrequently. Digoxin (0.008–0.01 mg/kg [approximately one-quarter of a 0.125 mg tablet] q48–72h PO) is used mainly to control the ventricular rate in atrial arrhythmias and for its inotropic effect in the improvement of cardiac performance in dilated cardiomyopathy.

Therapeutic Notes • Other antiarrhythmic drugs, including quinidine, procainamide, and lidocaine, have been shown to be dangerous in the cat. These drugs have not been used extensively in the cat because of their high risk of reactions and because ventricular arrhythmias are not common in the cat. Lidocaine could be used as an emergency ventricular antiarrhythmic drug in the cat, but very low doses should be used and only if the arrhythmia has not resolved by the treatment of the underlying cause.

Prognosis Diagnostic Notes • A pronounced sinus arrhythmia, normally auscultated in dogs, is rare in cats. Therefore, an irregular cardiac rhythm auscultated in the cat is generally an abnormal finding. • It should be emphasized that severe, life-threatening arrhythmias, such as ventricular tachycardia or atrial tachycardia, may easily be missed on auscultation as the cardiac rhythm is often regular on auscultation. An ECG is the only way to accurately make this diagnosis.

Treatment

The prognosis is variable depending upon the exact cause of the arrhythmia. In the majority of cases, arrhythmias disappear when the underlying disease is brought under control.

Suggested Readings Tilley LP. 1992. Essentials of Canine and Feline Electrocardiography. Interpretation and Treatment, 3rd ed. Ames, IA: Blackwell Publishing. Tilley LP, Smith FWK, Jr., Oyama MA, Sleeper MM. 2008. Manual of Canine and Feline Cardiology, 4th ed. St. Louis: Elsevier.

Primary Therapeutics • Antiarrhythmic Drugs: Beta-blockers (i.e., atenolol, propranolol) and calcium channel blockers (i.e., diltiazem) are different drug groups

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CHAPTER 13

Ascites Larry P. Tilley

Overview Ascites is the accumulation of fluid within the peritoneal cavity. Ascites is indicative of an underlying disease process (exception: overzealous fluid administration) and may be clinically significant if it restricts diaphragmatic excursions, impeding respiration.

•

• •

Diagnosis Differential Diagnoses The most common causes of ascites in the cat are listed in Table 13-1.

Primary Diagnostics • Mucous Membrane Color and Capillary Refill Time (CRT): Pallor and delayed CRT may be present in cases of congestive heart failure or hemorrhage. • Thoracic Auscultation: In most cases of cardiomyopathy, a murmur or a gallop rhythm is present. Heart sounds are muffled when pericardial effusion is present. • Abdominal Palpation: This technique helps to confirm the presence of ascites and grades severity. Organomegaly is suggestive of con-

TABLE 13-1: Differential Diagnosis List for Ascites in Cats Abdominal Neoplasia (This is the most common cause of ascites in adult cats.)

Carcinomatosis; carcinomas and adenocarcinomas in abdominal organs.

Peritonitis

Feline infectious peritonitis (This is the most common cause of ascites in cats less than 1 year of age.) Chylous peritonitis Bacterial peritonitis

Congestive Heart Failure

Dilated cardiomyopathy Hypertrophic cardiomyopathy Congenital cardiac anomaly (i.e., tricuspid dysplasia or cor triatriatum dexter) Pericardial effusion

Hypoalbuminemia

Chronic hepatic disease Urinary loss (glomerulonephritis) Protein-losing enteropathy Malnutrition (parasitic or dietary)

Hemorrhage

Anticoagulant (i.e., warfarin and so on) toxicity Trauma Surgery

•

gestive heart failure or neoplasia. It is important to rule out pregnancy, bladder distension, and obesity. Peritoneal Fluid Analysis: Determine whether fluid is a transudate, exudate, hemorrhage, or chyle. Transudates are suggestive of congestive heart failure or hypoalbuminemia. Modified transudates are suggestive of feline infectious peritonitis and other infectious diseases or neoplasia. Complete Blood Count (CBC): This is to evaluate for anemia. Chemistry Profile: These tests may reveal hypoalbuminemia, elevation of liver enzymes, or low blood urea nitrogen (BUN), which are suggestive of hepatic insufficiency. Radiography: This is usually unrewarding when ascites is present other than to confirm the presence of ascites. See Figure 292-1.

Secondary Diagnostics • Bile Acids: Elevation of prepandial and postprandial bile acids is supportive of chronic liver disease. • Abdominal Ultrasonography: Ultrasound is indicated if abdominal disease is suspected. It is more diagnostic of ascites than radiography. See 292-4. • Echocardiography: An echocardiogram is indicated if cardiac disease is suspected. • Coronavirus Test: This is one of several tests indicated when feline infectious peritonitis (FIP) is suspected. See Chapter 76. FIP is uncommon in cats over 2 years of age and an unlikely disease in older cats with ascites. • Urinalysis: This test is used to detect proteinuria.

Diagnostic Notes • The first condition to be ruled out when ascites is present in cats less than 2 years of age is FIP; neoplasia should be highly suspected in older cats. • Analysis of peritoneal fluid should always be performed when ascites is present. • Conditions that may mimic ascites include hepatomegaly, splenomegaly, obesity, large neoplasms, pyometra, hydrometra, pregnancy, and advanced obstipation.

Treatment Primary Therapeutics • Primary Disease: The goal of diagnostics is to confirm ascites and diagnose the underlying disease. Successful treatment of the underlying disease is paramount to a successful outcome. • Abdominocentesis: This is essential when effusion is interfering with respiration. Approximately 50 to 75% of the ascites may be removed with minimal risk if a moderately sized (18-–22-gauge) catheter is used.

Secondary Therapeutics th

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• Furosemide: This drug is indicated only if ascites is secondary to congestive heart failure. A dose of 0.25 to 0.50 mg/kg q24h IV, IM,

Ascites

SC, PO is usually effective, although the dose can be increased. Using furosemide in noncardiogenic ascites will do little to remove the ascites and will dehydrate the patient.

Therapeutic Notes

Suggested Readings Thornhill JA. 2007. Ascites. In LP Tilley, FWK Smith, Jr., eds., Blackwell’s 5 Minute Veterinary Consult, 4th ed., pp. 108–109. Ames, IA: Blackwell Publishing.

• Periodic abdominocentesis is better tolerated than long-term aggressive diuretic use.

Prognosis The prognosis is variable depending upon the exact cause of the ascites. Most cats with respiratory distress can be stabilized with abdominocentesis.

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CHAPTER 14

Aspergillosis Sharon Fooshee Grace

Overview Aspergillosis is a relatively uncommon fungal disease of cats. A large number of cats with disseminated disease have been described in the literature; however, until recent years, there have been few published reports of localized infection involving the nasal, sinus, or orbital cavities. It is unclear why localized infections are being reported with increased frequency. Aspergillosis is caused by a saprophytic fungus, which is ubiquitous in the environment. The most important species in small animal medicine are Aspergillus fumigatus and Aspergillus terreus, with the former being most common. Infection is established through inhalation of airborne conidia, spores that are released from the free-living asexual form of the organism. Aspergillus is considered an opportunistic invader, which, once inside the host, adheres to and penetrates respiratory epithelium. Both host factors (i.e., immune competence, concurrent disease) and fungal characteristics (i.e., virulence of the invading species and size of inoculum) determine whether the infection will become established. The role of immunosuppression in facilitating infection remains unclear, although it does appear more common in cats with disseminated disease. One retrospective study reported that aspergillosis was more common in young adult cats and another found a higher prevalence in middleaged to older cats. The observed duration of illness reported by owners is typically a few weeks to a few months. No sex or breed predisposition has been noted, but brachycephalic breeds (Persians) have been suggested to have a marginally higher incidence of sino-nasal infection compared to other breeds. One report speculated that this could be due to disrupted nasal airflow and abnormal mucociliary clearance in Persians. Though not a consistent finding in all cases, a number of cats have been reported to have various diseases and infections concurrent with aspergillosis, including diabetes mellitus, feline infectious peritonitis (FIP), feline leukemia virus (FeLV), and panleukopenia. One review of 40 cases found an association with administration of glucocorticoids, long-term antibiotics, or both. Two distinct forms of aspergillosis have been described in cats: localized sino-nasal/orbital disease and disseminated disease. Localized disease is much less common than disseminated disease and involves the nasal cavity and frontal sinus. Local extension into the orbit may cause exophthalmos, although orbital disease has been described in one cat with no evidence of sino-nasal or disseminated disease. Sinonasal infection is associated with extensive and irreversible turbinate destruction. Clinical signs of nasal and sinus involvement include inspiratory dyspnea and stertor, sneezing, chronic mucopurulent nasal discharge, epistaxis, facial swelling, and mandibular lymphadenopathy. A mass lesion may be visualized within the nasal cavity. Localized infection has also been described in the urinary bladder of a cat with cystitis. Cats with disseminated disease have nonspecific signs of lethargy, fever, anorexia, and depression; vomiting and diarrhea have been reported in a few cats. Necropsy of cats with disseminated disease has demonstrated fungal hyphae in the lungs, heart, bladder, kidney, liver, and brain.

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Diagnosis Primary Diagnostics • Diagnostic Imaging: Radiographs of the nasal cavity and paranasal sinuses demonstrate increased soft-tissue density (sometimes with areas of mineralization) and bone destruction. See Figure 14-1. Computerized tomography (CT) is superior to conventional radiography in determining extent of disease and degree of bone destruction (including turbinates) because it can provide cross-sectional images. See Figure 14-2. Thoracic radiographs should be taken to evaluate the patient for pulmonary involvement. • Rhinoscopy: Rhinoscopy can be used to obtain tissue for histopathology, cytology, and culture. White-to-yellow masses, copious white-to-gray discharge, mucosal erythema, and turbinate destruction have been observed in cats with nasal infection. • Histopathology: Biopsy specimens may be placed in 10% formalin for submission. The cellular infiltrate contains lymphocytes, plasma cells, and neutrophils. Microscopic study demonstrates large mats of branching septate fungal hyphae consistent with Aspergillus. Superficial biopsies may be inconclusive.

Secondary Diagnostics • Complete Blood Count, Biochemical Profile, Urinalysis, and Retroviral Testing: Aspergillosis does not produce any pathognomonic changes in routine bloodwork, but the information gained is

Figure 14-1 The bony destruction caused by aspergillosis in the nasal cavity can be seen on this radiograph (arrow).

Aspergillosis

may be of potential use, although pharmacokinetic data is unavailable; it has been used at 10 mg/kg q24h PO. It is unknown how long therapy should continue, but a minimum of 6 months has been suggested. • Topical Therapy: Noninvasive infusion of clotrimazole through the nasal cavity over a period of 1 hour is the treatment of choice for nasal aspergillosis in dogs; results have been promising. Contact time of 1 hour seems to be critical in allowing the drug adequate time to damage the fungal cell membrane. The technique has had limited use in the cat but shows promise. The reader is referred to Suggested Readings section (Tomsa, Glaus, Zimmer, and Greene and Furrow and Groman) for more information. Potential complications include fatal aspiration of clotrimazole, laryngeal edema, leakage of medication across a disrupted cribriform plate, neurologic deficits, and death. Topical enilconazole therapy has been used in dogs, but it requires placement of indwelling catheters and repeated administration of the drug over 1 to 2 weeks.

Figure 14-2 This computerized tomography image shows aspergillosis in the frontal sinuses (small arrow) and the nasal cavity (large arrows). Images courtesy of Dr. Carolyn O’Brien, The Cat Clinic, Melbourne, AU.

helpful in assessing overall health of the cat and the potential for concurrent disease. Feline immunodeficiency virus (FIV) and FeLV testing should be performed in all debilitated cats. See Chapters 75 and 77. • Fungal Culture: Culture material should be taken directly from fungal colonies within the respiratory passage. Because fungal culture may yield false-positive or false-negative results, it is considered unreliable as the sole basis of diagnosis and should be used in conjunction with other tests. Urine culture is reported to have a high yield in cases of disseminated disease. • Serology: Several serologic tests are available for detection of Aspergillus-specific antibodies. It should not be used as the sole basis for ruling in or ruling out a diagnosis. It is unclear how prevalent these antibodies might be in the general population of uninfected, healthy cats. • Polymerase Chain Reaction (PCR) Testing: PCR tests have been developed, but their value in documenting disease in cats is still under investigation.

Diagnostic Notes • Aspergillus and Penicillium appear grossly and histologically similar. Culture is required to distinguish the two organisms.

Treatment Primary Therapeutics • Systemic Therapy: Effective therapy for aspergillosis has been elusive. Itraconazole has been used (10 mg/kg q24h PO) but has not been effective in all cases. In many cats, it appears to offer improvement but not resolution of disease. Posaconazole (5 mg/kg q24h PO, 40 mg/ml suspension) resulted in cure of one cat; disease had not recurred 20 months after therapy ended. Fluconazole has been used successfully to treat Aspergillus in the urinary bladder (7.5 mg/kg q12h PO). Voriconazole is another antifungal, which

Secondary Therapeutics • Nutritional Support: A feeding tube should be placed while the cat is under anesthesia if nutritional support is not needed. See Chapter 253 for placement of an esophagostomy tube.

Therapeutic Notes • Erosion of the cribriform plate is a contraindication for infusion of topical medications under pressure. • Rhinotomy and turbinectomy were used in the past, but these procedures are no longer considered of benefit in treating aspergillosis and may be detrimental to the patient. They cause additional pain and distress and do not appear to improve the success rate.

Prognosis Aspergillosis generally carries a poor prognosis, regardless of whether the disease is disseminated or localized.

Suggested Readings Adamama-Moraitou KK, Paitaki CG, Rallis TS, et al. 2001. Aspergillus species cystitis in a cat. J Fel Med Surg. 3(1):3–34. Day MJ. 2006. Feline disseminated aspergillosis. In C Greene, ed., Infectious Diseases of the Dog and Cat, 3rd ed., pp. 626–627. Philadelphia: Saunders Elsevier. Furrow E, Groman RP. 2009. Intranasal infusion of clotrimazole for the treatment of nasal aspergillosis in two cats. J Amer Vet Med Assoc. 235(10):1188–1193. Hamilton HL, Whitley RD, McLaughlin SA. 2000. Exophthalmos secondary to aspergillosis in a cat. J Amer Anim Hosp. 36(4):343–347. Mathews KG, Sharp NJH. 2006. Feline nasal aspergillosis-penicilliosis. In C Greene, ed., Infectious Diseases of the Dog and Cat, 3rd ed., p. 620. Philadelphia: Saunders Elsevier. McLellan GJ, Aquino SM, Mason DR, et al. 2006. Use of posaconazole in the management of invasive orbital aspergillosis in a cat. J Amer Anim Hosp. 42(4):302–307. Tomsa K, Glaus TM, Zimmer C, et al. 2003. Fungal rhinitis and sinusitis in three cats. J Am Vet Med Assoc. 222(10):1380–1384. Whitney BL, Broussard J, Stefanacci JD. 2005. Four cats with fungal rhinitis. J Fel Med Surg. 7(1):53–58.

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CHAPTER 15

Aspirin Toxicosis Sharon Fooshee Grace

Overview The cat has a slow rate of drug metabolism compared to other species because of a relative deficiency of some hepatic glucuronyl transferases, enzymes that are important for drug conjugation and excretion. This group of enzymes participates in the most common phase II reaction of drug metabolism—glucuronidation. Glucuronidation adds a water soluble glucuronide molecule to either the parent drug or a phase I metabolite, enhancing renal elimination. Delayed drug conjugation renders the cat sensitive to a variety of drugs and compounds, including phenols and phenolic derivatives, amines, and aromatic acids. As a phenol, aspirin falls into the category of drugs that have delayed elimination in the cat. Aspirin may be safely given at a dose of 10 to 20 mg/kg with a dosing interval of 48 to 72 hours. The increased dosing interval is required because the half-life of aspirin is approximately 40 hours in the cat as compared to 7.5 hours in the dog. Failure to adhere to recommended dosages and dosing intervals may lead to salicylate toxicity in the cat. Also, because the drug is highly-protein bound, cats with hypoalbuminemia may be more at risk for toxicity with aspirin administration. With aspirin toxicosis, nonspecific signs such as anorexia, depression, vomiting, tachypnea, and hyperthermia may initially occur. It is difficult to make a specific diagnosis of aspirin toxicosis if a history of aspirin ingestion is unrecognized. The likelihood of respiratory distress, acid-base disturbances, seizures, generalized bleeding tendencies, and gastrointestinal hemorrhage (with potential perforation) is increased with repeated dosing of the drug. Drug-induced hepatitis may lead to icterus. Muscle weakness, ataxia, seizures, coma, and death may follow within days.

Diagnosis Primary Diagnostics • History: Because the clinical signs are non-specific, it is important to question the owner about the administration of aspirin. The presence of a condition requiring analgesic or antithrombotic medication may prompt the clinician to suspect aspirin toxicosis in the patient. • Complete Blood Count (CBC): Anemia due to bone marrow suppression and the presence of Heinz bodies are occasionally noted on the CBC, especially with chronic exposure. Thrombocytopenia and leukocytosis with a left shift are also reported. • Acid-Base Evaluation: An initial respiratory alkalosis with subsequent high anion gap metabolic acidosis may be noted.

Secondary Diagnostics • Serum Salicylate Levels: Commercial laboratories may be equipped to measure salicylate levels in the blood, but toxic concentrations are not well defined for dogs and cats. • Ethylene glycol toxicity is an important differential diagnosis.

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Treatment Primary Therapeutics • Removal: If early intervention is possible, emesis may be induced or gastric contents removed by lavage. Activated charcoal should be given orally at 2 g/kg followed by an appropriate cathartic or as directed on the product label. Some activated charcoal products contain a cathartic. • Gastrointestinal Ulceration: This should be treated with appropriate protectants (sucralfate [0.25 g (one-fourth of 1-g tablet) q8–12h PO] or H2-receptor antagonists).

Secondary Therapeutics • Supportive Care: This should include fluid and electrolyte therapy as needed and attention to the patient’s body temperature. • Acid-Base Management: The patient should be monitored and treated for ongoing acid-base disturbances. Sodium bicarbonate therapy (based on blood gas results or, if these are unavailable, 0.5– 1.0 mEq/kg total dose delivered over 30 minutes to several hours depending on severity of lab changes/signs) may combat metabolic acidosis and hasten elimination of the drug.

Therapeutic Notes • No specific antidote is available for aspirin toxicity. • Therapy with sodium bicarbonate can exacerbate or lead to hypokalemia. • Aspirin should always be used with caution in young or old cats and in those suffering from renal or liver dysfunction, asthma, coagulation disorders, gastrointestinal ulceration, or hypoalbuminemia. It may delay parturition so should not be used in late gestation. Aspirin should be discontinued 1 week prior to elective surgery because of the impact on bleeding time.

Prognosis The prognosis should be favorable with early intervention and the cessation of aspirin administration. Chronic administration of aspirin to cats may lead to bone marrow suppression, which is life-threatening.

Suggested Readings Groff RM, Miller JM, Stair EL, et al. 1993. Toxicoses and Toxins. In GD Norsworthy, ed., Feline Practice, pp. 551–569. Philadelphia: JB Lippincott. Kore AM. 1997. Over-the-counter analgesic drug toxicosis in small animals. Vet Med. 92(2):158–165. Rumbeiha WK, Oehme FW, Reid FM. 1994. Toxicoses. In RG Sherding, ed., The Cat: Diseases and Clinical Management, pp. 215–249. Philadelphia: WB Saunders.

CHAPTER 16

Atopic Dermatitis Christine A. Rees

Overview Atopic dermatitis, or atopy, is an exaggerated response to one or more environmental allergens. These allergens are thought to be inhaled or absorbed percutaneously into the skin. This allergy is an immediate or immunoglobulin E-mediated disease that is thought to be inherited. Although the genetics of atopy in cats have not been determined, the familial predisposition suggests a genetic component to feline atopy. Feline atopy is currently thought to be the second most common allergy in cats. The exact pathogenesis has not been determined, but an inappropriate T helper-2 response, ultimately leading to allergic inflammation in the skin, is the most widely accepted theory. More recently, Langerhans cells have been found to be important in feline atopy. These are antigen presenting cells found in the skin. Therefore, percutaneous absorption of allergens may be more important than previously thought.

some cats will have nonseasonal atopy or respiratory signs associated with their allergies. • Progression: Many patients’ symptoms will become perennial as the duration progresses. • Intradermal Allergy Testing: Most veterinary dermatologists agree that the intradermal allergy testing is the method of choice. • Diagnose Secondary Infections: Secondary infections may be present and must be identified and treated to get a true picture of the underlying baseline allergic symptoms. Tape cytology to evaluate for presence of secondary bacterial or Malassezia spp. is indicated. Dermatophytosis must be ruled out by direct hair examination and dermatophyte test media (DTM®) culture.

Secondary Diagnostics • Serology: In vitro serologic testing is controversial at this time.

Diagnosis Primary Diagnostics • Dermatologic History: History is extremely important. Diagnosis begins by exclusion of other pruritic diseases such as other hypersensitivities, parasitic infections, dermatophytosis, neoplastic conditions, and immune-mediated conditions. • Clinical Appearance: The clinical signs for feline atopy are variable. Recurrent otitis externa, pruritus, miliary dermatitis, eosinophilic plaque, and other forms of eosinophilic granuloma complex, excessive grooming, and seasonal waxing and waning dermatitis are typical clinical findings. See Figure 16-1. Although not as common,

Treatment Primary Therapeutics • Immunotherapy: The only specific therapy available at this time is allergen-specific immunotherapy based on intradermal allergy testing or serologic in vitro testing. This is the therapy of choice by dermatologists for moderately-to-severely affected patients due to low therapeutic risk and the ability to potentially interrupt the sensitization and elicitation phases of the atopic state, thus offering the potential of more complete allergy control. • Technique: An allergy test is performed, either by intradermal or in vitro means. Specific allergens are selected to which the patient appears to be to allergic. An allergen-based serum is formulated and injected subcutaneously according to various protocols. If the patient responds, injections must be continued for life. • Disadvantage: The primary drawback is the delayed therapeutic response (1–3 months, range of 1–12 months). Symptomatic management may be needed during the first 3 months of the immunotherapy. Potential risks include worsening of symptoms, which can be controlled by modification of injection protocol, and immediate adverse reaction to the injection, manifested as diarrhea, vomiting, weakness, or collapse. Severe reactions are rare when the immunotherapy is administered properly.

Secondary Therapeutics

Figure 16-1 Atopic dermatitis can have many presentations. This cat exhibits patchy alopecia due to licking and scratching. Image courtesy Dr. Gary D. Norsworthy.

The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.

• Treat Secondary Causes of Pruritus: Secondary infections of the skin or ears need to be treated. In addition, exposure to external parasites, such as fleas, can cause an increase in pruritus. Therefore, cats should be on flea control products during immunotherapy. • Control Pruritus Pharmacologically • Corticosteroids: Corticosteroids are typically effective in reducing atopic pruritus, but long-term side effects are a concern. Prednisolone given at anti-inflammatory doses (2.2–4.4 mg/kg q12h PO for 1 week then taper) is the drug of choice because some cats have difficulty metabolizing prednisone to prednisolone. Triamcinolone (0.15%; Genesis Spray®) has been used as an extra-label adjunct in some cats. This medication appears to have relatively

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TABLE 16-1: Antihistamines for Cats Drug

Dose

1. Chlorpheniramine 2. Clemastine 3. Amitriptyline

1. 0.4–0.6 mg/kg q12h PO 2. 0.05–0.1 mg/kg q12h PO 3. 5–10 mg/cat/day q24h or divided q12h PO; initial trial of 3 weeks; Note: This is a tricyclic antidepressant that has antihistaminic properties in some cats. 4. 0.5–1.0 mg/kg q8–12h PO 5. 1–2 mg/kg q8–12h PO 6. 2.2 mg/kg q8–12h PO 7. 5 mg q24h PO

4. 5. 6. 7.

Cyproheptadine Hydroxyzine Diphenhydramine Cetrizine

minimal systemic absorption and may be of benefit in some patients. However, it is not completely without potential steroid side effects. Furthermore, the spray contains alcohol, which some cats find objectionable. • Modified Cyclosporine (Atopica®): Modified cyclosporine is not labeled for use in cats, but it may be useful for symptomatic management of some cats with atopy. Drug-to-drug interactions are of significant clinical importance; many drugs can potentially raise or lower cyclosporine blood levels. Interactions should be doublechecked for each patient before prescribing. This drug appears to ultimately inhibit T-cell function and can interrupt the symptoms of atopic dermatitis. There is currently no labeled indication for cats, but it is used for cats by dermatologists at 4 to 7 mg/kg q24h PO initially, then tapered to the least frequent effective dose. There is usually a lag phase before pruritus reduction is noted (2–3 weeks). Cyclosporine suppresses the immune system and may predispose patients to opportunistic infection and neoplasia. Therefore, its use is strictly contraindicated in patients with a history of malignant neoplasms or in patients infected with a retrovirus, and it should not be used without careful thought. In addition, a case of fatal toxoplasmosis has been reported in a cat administered cyclosporine. The serostatus for Toxoplasma should be checked in cats that are on cyclosporine and develop respiratory signs. Gastrointestinal upset is the primary clinical side effect noted and, in my

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experience, approximately 25 to 30% of patients will experience some form of transient upset (i.e., decreased appetite, vomiting, loose stools, or diarrhea) during the first 1 to 2 weeks of therapy. Little is known about the validity of cyclosporine blood levels in the cats. • Prevent Secondary Pruritus: Antihistamines combined with omega3 fatty acids supplemented at high doses (5–10 mg/kg based on eicosapentaenoic acid [EPA®] content) may benefit patients with less intense itching. These medications are better suited to prevent allergic itching than actually stopping it. It is typically better to start at the upper end of the antihistamine dosage and frequency to see if the cat responds because it can be difficult to convince an owner to repeat an antihistamine that has been tried previously with little success. See Table 16-1.

Prognosis Most cats with atopy can be reasonably controlled with corticosteroids. The long-term prognosis depends upon one’s ability to either restrict the patient’s contact with the allergen or one’s ability to desensitize the patient.

Suggested Readings Barrs VR, Martin P, Beatty JA. 2006. Antemortem diagnosis and treatment of toxoplasmosis in two cats on cyclosporine therapy. Aust Veter J. 84(1):30–35. Roosje PJ, van Kooten PJ, Thepen T, et al. 1998. Increased numbers of CD4+ and CD 8+ T cells in lesional skin of cats with allergic dermatitis. Vet Pathol. 25(4):268–273. Moriello KA. 2001. Feline Atopy in Three Littermates. Vet Dermat. 12(3):177–181. Last RD, Suzuki Y, Manning T, et al. 2005. Veterinary Drug Handbook, 5th ed. Ames, IA: Blackwell. Reedy LM, Miller WH, Willemse T. 1997. Atopy. In LM Reedy, ed., Allergic skin diseases of dogs and cats. 2nd ed., pp. 116–149. Philadelphia: WB Saunders. Last RD, Suzuki Y, Manning T, et al. 2004. A case of fatal systemic toxoplasmosis in a cat being treated with cyclosporin A for feline atopy. Vet Dermat. 15(3):194–198.

CHAPTER 17

Bartonellosis Mark Robson and Mitchell A. Crystal

Overview Bartonella spp. (previously named Rochalimaea spp.) are fastidious, arthropod-transmitted, hemotropic, intraerythrocytic, facultative, gramnegative bacteria. These coccobacilli or rod bacteria are 1 to 2 µm in length, appear slightly curved in shape, and stain positive with silver stain. Although Bartonella organisms are most well known as the causative agent of the human ailment cat-scratch disease (CSD), they are also associated in people with bacillary angiomatosis (proliferations of blood vessels), visceral bacillary peliosis (extravasation of blood), septicemia, granulomatous hepatitis or splenitis, meningitis, encephalitis, endocarditis, retinitis and optic nerve swelling, osteolysis, and granulomatous pneumonia. Immunocompetent individuals tend to contain infection to local or regional lymph nodes resulting in pyogranulomatous lymphadenitis; immunocompromised individuals often develop bacteremia and disseminated disease. Although over 20 species of Bartonella have been recognized, only four species have been identified in cats: B. henselae, B. clarridgeiae, B. koehlerae, and B. bovis (formerly B. weissii); currently, only B. henselae and B. clarridgeiae have clinical or zoonotic significance. There are two main genotypes of B. henselae. The Marseille genotype is the most common in the western United States, Australia, and western Europe, whereas in the eastern United States the Houston-1 genotype is equally prevalent. Arthropod vectors, especially the cat flea Ctenocephalides felis, play a major role in the cat to cat transmission of Bartonella spp. Transmission may occur via contact with flea excrement rather than by bites. Direct transmission from cat to cat in a flea-free environment and vertical transmission from queen to kitten have not been detected. Transmission of Bartonella spp. from cat to human occurs primarily via contact with cats (i.e., scratches, bites). A small number of human Bartonella cases (5%) lack feline exposure, suggesting that insect transmission may play a role in human transmission as well. Cat saliva/ bites seem to be a less common means of Bartonella transmission compared to scratches. Prevalence of Bartonella antibodies in cats is variable from region to region. Overall prevalence in North America is 28%. Climates that support the flea life cycle have higher prevalence rates than do those where fleas are less common (i.e., Southeast 60%, Hawaii 53%, Pacific Coast 40%, Midwest 7%, and Rocky Mountain region 4%). Japan has a prevalence of 6 to 22%. Kittens and possibly feral cats have a higher prevalence than do adult cats. Feline leukemia virus (FeLV) status does not appear to influence the prevalence of Bartonella. The role of Bartonella as a disease-causing organism in cats is uncertain. Experimental infections in cats have resulted in inoculation swelling, lymphadenopathy, febrile episodes lasting from 2 days to a few weeks, reproductive disorders (i.e., infertility and stillbirths), and splenic hyperplasia. Inflammatory lesions have been documented in the liver, spleen, myocardium, and kidney of chronic experimentally infected cats. It has been suggested that naturally infected cats (based on serology) have a higher incidence of stomatitis/gingivitis and some urologic diseases. Intracellular Bartonella-like organisms have been demonstrated in some cats with idiopathic peripheral lymphadenopathy. Recent studies have failed to demonstate a correlation between Bartonella infection and disease in cats with anemia, uveitis, and neu-

The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.

rological disease. A Japanese study has shown that coinfection with feline immunodeficiency virus (FIV) and Bartonella was more likely to result in gingivitis or lymphadenopathy than either agent alone. There has been a report of a single cat in which B. henselae deoxyriboneucleic acid (DNA) was found in an aortic valve damaged by endocarditis; however, a causal relationship was not proven. In a recent study by Lappin and colleagues it was found that afebrile control cats were significantly more likely to be antibody positive than febrile cats with clinical illness. There was found to be no significant difference in frequency of detection of Bartonella DNA in blood between afebrile and febrile cats. The authors concluded that “in cats Bartonella species antibody tests cannot predict whether fever is due to Bartonella species infection and should not be used to determine the Bartonella species infection status.” Bartonella vinsonii subsp berkhoffii has been identified as a cause of endocarditis, myocarditis, granulomatous lymphadenitis, and granulomatous rhinitis in dogs. It should be emphasized that although large numbers of cats have been exposed to Bartonella and might be positive on serology, polymerase chain reaction (PCR), or even culture, there is almost no evidence that clinical disease will ensue. A sick cat that is positive for Bartonella is far more likely to be suffering from another illness, and many clinicians doubt the wisdom of testing for Bartonella at all. Clinical signs of CSD in humans include lymphadenopathy, fever, malaise, myalgia, anorexia, weight loss, and headache. Bartonella is considered of zoonotic importance to humans, regardless of immune status. Any person demonstrating clinical signs consistent with CSD or other Bartonella-induced diseases should be referred to a physician for confirmation. If Bartonella is confirmed, discontinuation of exposure to and contact with the affected animal should be recommended.

Diagnosis Primary Diagnostics • PCR: Amplification of Bartonella DNA from whole blood, fresh tissues, and frozen tissues via PCR is sensitive and specific. See Table 17-1 for testing laboratories. • Culture and Sensitivity of Blood or Tissues: Blood or tissue cultures are performed using blood agar media in a 5% carbon dioxide and high humidity environment at 35°C and may require up to 56 days to grow visible colonies.

Secondary Diagnostics • Western blot, indirect immunofluorescent antibody (IFA) or enzymelinked immunosorbent assay (ELISA) for antibodies to Bartonella: These may be helpful in screening cats prior to adoption by immunocompromised individuals. Serologic testing provides helpful epidemiologic information but is of limited clinical utility for identifying actively infected cats. Serologic testing is used to confirm cat scratch disease in people. • Other Disease Tests: Because an illness in a cat is highly unlikely to be due to Bartonella infection, testing for diseases with a higher likelihood of being the causative agent is indicated. These would include feline leukemia virus (FeLV), FIV, Toxoplasma, Histoplasma, and so on.

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TABLE 17-1: Laboratories Performing Polymerase Chain Reaction Testing for Bartonella Antech Diagnostics

Colorado State University

IDEXX Reference Laboratories

University of California, Davis

Galaxy Diagnostics

VCA ANTECH, 12401 West Olympic Blvd., Los Angeles, CA 90064; Phone: 1-800745-4725; www.antechdiagnostics.com Veterinary Diagnostic Laboratory, 300 West Drake, Fort Collins, CO 80523. Phone: 1-970-297-1281 Fax: 1-970-297-0320, www.dlab.colostate.edu 2825 KOVR Drive, West Sacramento, CA 95605 Phone: 1-916-267-2454 Fax: 1-916-267-2413 www.idexx.com/ animalhealth/laboratory/realpcr/tests/ vectorbornedisease.jsp Lucy Whittier, Molecular and Diagnostic Core Facility, Department of Medicine and Epidemiology, School of Veterinary Medicine, 2108 Tupper Hall, University of California, Davis, CA 95616. Phone: 1-530-752-7991 Fax: 1-530-754-6862 www.vetmed.ucdavis.edu/vme/ taqmanservice/diag_home Animal Health Division, 2 Davis Drive, Durham, NC 27709; Phone: 1-919-3541056; Fax: 1-919-287-2476; www. galaxydx.com

• Bartonella culture in humans and dogs is typically unsuccessful; PCR has proven more successful in these species.

Treatment Primary Therapeutics • Antibiotics: Antibiotic therapy in cats may reduce bacteremia but is unlikely to eliminate infection. Therapy is not indicated unless significant illness is present, which is unlikely. There is no definitive proof that any drug is effective, but antibiotics that have been reported to be helpful in the cat include azithromycin (10 mg/kg q24h PO for 7 days then q48h for 5 weeks) doxycycline (10 mg/kg q12h PO), rifampin (10 mg/kg q24h PO), and enrofloxacin (5 mg/kg q24h PO; note the possibility of retinal damage especially at higher doses) for 2 to 4 weeks. Follow-up screening 3 weeks post-treatment may be indicated. For humans, azithromycin, rifampin, ciprofloxacin, and trimethoprim-sulfamethoxazole are recommended. Immunocompetent patients are treated for 2 weeks, immunocompromised patients are treated for a minimum of 6 weeks. • External Parasite Control: This will help prevent bartonellosis.

Therapeutic Notes • The treatment of choice in humans remains controversial as a result of limited clinical studies.

Prognosis Diagnostic Notes • The potential infectivity of a cat cannot be definitively predicted by serology because cats may be serologically positive and culture negative, although higher titers are frequently associated with bacteremia. A negative antibody IFA titer has a high predictive value and may be of use when assessing the risk of infection from a cat to an immunocompromised owner. • Culture is often accurate in cats but bacteremia may be intermittent and repeated cultures may be necessary. A negative result is not, therefore, definitive. Using special collection tubes and at least 1.5 mL of blood will aid in recovery of bacteria. It is advisable to check with the laboratory for submission requirements.

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Cats with Bartonella usually have inapparent infections and thus have an excellent prognosis. They will rarely develop any serious illness as a result of the infection. CSD in humans is usually self-limiting or responds well to antibiotic therapy, although relapses requiring prolonged treatment may occur in immunocompromised individuals.

Suggested Readings L Guptill-Yoran. Bartonellosis. 2006. In C Greene, ed., Infectious Diseases of the Dog and Cat, 3rd ed., pp. 510–524. St Louis: Saunders-Elsevier. Lappin MR, Breitschwerdt E, Brewer M, Hawley J, Hegarty B, Radecki S. 2009. Prevalence of Bartonella species antibodies in the blood of cats with and without fever. J Fel Med Surg. 11:141–148.

CHAPTER 18

Basal Cell Tumors Bradley R. Schmidt and Mitchell A. Crystal

Overview Basal cell tumors are common, making up 11 to 30% of feline skin tumors. Basal cell tumors occur in older adult cats (mean age 10–11 years) and may be benign (i.e., benign basal cell tumor, basal cell epithelioma, basaloid tumor, basaloma) or malignant (basal cell carcinoma). As most basal cell tumors are benign (>90%) and carcinomas are generally of low-grade malignancy with a low metastatic potential, the preferred nomenclature is “basal cell tumor” for both benign and malignant tumors. Basal cell carcinomas are more common in the cat than in the dog. Tumors arise from epidermal basal cells and usually affect the head, neck, limbs, and thorax. See Figure 18-1A. Basal cell carcinomas more commonly arise from the nasal planum and eyelids. See Figure 18-1B. They appear as well circumscribed, solitary, 0.5- to 10.0-cm (0.25- to 4-inch) raised, ulcerated, hairless, lesions, which are occasionally melanotic or cystic. Occasionally multiple tumors may be found in the same patient. Tumors are typically fixed to the overlying skin and are freely movable. Tumors are often slow growing and may be present for months prior to diagnosis. All breeds are affected, although Siamese (carcinoma) and Himalayan and Persian (benign basal cell tumor) breeds may be predisposed to basal cell tumor development. There is no known etiology, although a strong correlation exists in humans between ultraviolet light exposure and tumor formation. Clinical signs are limited to the presence of the mass. Differential diagnoses include squamous cell carcinoma, melanoma, mast cell tumor, cutaneous hemangioma or hemangiosarcoma, hair follicle tumors, and sebaceous gland tumors.

(A)

Diagnosis Primary Diagnostics • Surgical Removal or Biopsy/Histopathology: This is the most accurate means of diagnosis.

Secondary Diagnostics • Fine-Needle Aspiration/Cytology: This may reveal the diagnosis prior to surgery. • Fine-Needle Aspiration/Cytology of the regional lymph nodes: may be indicated in cases of basal cell carcinoma; however, metastasis is rare. • Thoracic Radiographs: Metastasis is extremely rare; however, thoracic radiographs may be indicated in cases of basal cell carcinoma and to evaluate for other cardiopulmonary disorders. • Minimum Data Base: The complete blood count, serum chemistry profile, urinalysis, retrovirus tests are generally unremarkable; however, they are recommended to evaluate the overall health of the patient.

(B) Figure 18-1 Although benign, some basal cell tumors can be large (A) or in difficult surgical locations (B). Photos courtesy Dr. Gary D. Norsworthy.

Treatment Primary Therapeutics • Surgical Excision: Complete removal of the tumors is curative in most cases of both benign and malignant tumors.

Diagnostic Notes

Secondary Therapeutics

• Basal cell tumors usually behave in a benign manner even if assessed as a carcinoma by histopathology or cytology.

• Laser Ablation, Cryotherapy, Electrosurgery: These methods have been successful in treating small lesions. • Radiation Therapy: This may be indicated for incompletely resected malignant basal cell tumors. • Chemotherapy: Efficacy of chemotherapy has not been determined but may be considered in the rare metastatic event.

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Prognosis The prognosis for cure is excellent with complete surgical excision in nearly all cases, regardless if the tumor is classified as malignant or benign. In the rare event of metastasis, the prognosis would be guarded to poor. The effectiveness of chemotherapy in treating metastatic lesions is unknown.

Suggested Readings Elmslie RE. 2004. Basal cell tumor. In LP Tilley, FWK Smith, Jr., eds., Blackwell’s 5-Minute Veterinary Consult, 3rd ed., p. 147. Baltimore: Williams & Wilkins.

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Moore AS, Ogilvie GK. 2001. Skin Tumors. In Moore AS, Ogilvie GK, eds., Feline Oncology, pp. 398–428. Trenton: Veterinary Learning Systems. Scott DW, Miller WH, Griffin CE. 2001. Miller & Kirk’s Small Animal Dermatology, 6th ed., pp. 1260–1263. Philadelphia: WB Saunders. Vail DM, Withrow SJ. 2007. Tumors of the skin and subcutaneous tissues. In SJ Withrow, DM Vail, eds., Small Animal Clinical Oncology, 4th ed., pp. 375–401. Philadelphia: Elsevier Saunders.

CHAPTER 19

Biliary Cysts Michele Fradin-Fermé

Overview Biliary cysts are cystic lesions delineated by thin walls and filled with serous or mucoid fluid; they can be observed either at the surface of the liver or within the hepatic parenchyma. They arise from primitive bile ducts (intra- or extrabiliary ducts) but develop into retention cysts lacking a connection with the biliary tree. They grow by expansion and bulge at the surface of the liver although they may remain intrahepatic. Their number, color, degree of lobulation, and size are variable. Cyst walls are composed of connective tissue lined by flattened or cuboidal biliary epithelium. Biliary cysts can be acquired or congenital. Acquired cysts are usually solitary and contain bile or blood. They are initiated by an inflammatory process such as trauma, chronic cholangiohepatitis, or neoplasia. Congenital cysts are usually multiple and may be associated with cysts in other organs (i.e., pancreas, kidneys, and so on). Congenital cysts are often seen in Persian cats and Himalayans, but they are not always related to polycystic kidney disease (PKD). Their content is usually clear and acellular. As they develop, they can create compression on the adjacent parenchyma leading to secondary inflammation and fibrosis. Most biliary cysts are asymptomatic; they are incidental findings on ultrasound or necropsy. In some cases they may become large and can produce increasing pressure on abdominal organs leading to reduced appetite and vomiting. See Figure 19-1. Acquired cysts accompanying cholangiohepatitis may produce symptoms that are rather related to the affected parenchyma rather than the cysts. Congenital cysts tend to be multiple; therefore, extensive fibrosis can occur leading to portal hypertension and hepatic dysfunction with encephalopathy and ascites.

Diagnosis Primary Diagnostics • Ultrasound: It is used to identify, enumerate, and confirm their connection with the liver. Cysts have usually thin, well-defined walls with anechoic contents causing distal acoustic enhancement. See Figure 19-2. Cysts with thicker, irregular walls and internal echoes are more likely to be clinically significant. Percutaneous aspiration with ultrasound guidance of a cyst for cytology and bacterial culture may be indicated. Serial ultrasound examinations also may be helpful in following cyst progression over time; generally, benign lesions do not change over time. The common bile duct may be compressed but typically remains patent even though it may become tortuous. • Radiographs: Biliary cysts are radiolucent, but, in cases of large cysts, displacement of abdominal organs by a fluid-density mass can be observed.

Secondary Diagnostics • Complete Blood Count and Chemistry Profile: These tests are usually unremarkable unless the cysts are linked to chronic cholangiohepatitis or they are numerous and associated with extensive fibrosis. • Analysis of the Contents of the Cyst: Congenital cysts usually have a clear, acellular content. Acquired cysts often contain blood or bile. • Computerized Tomography (CT): This imaging modality may be helpful in confirming the connection of the cyst to the liver. It also permits an assessment of cyst numbers and size prior to surgery. • Histopathology: Histologic examination is useful because it allows identification of the lesion and permits the differentiation between a cyst and a malignant tumor. However, there are some difficulties for the pathologist. When inflammation is associated with the cyst,

Figure 19-1 A large, solitary biliary cyst is seen attached to the periphery of one lobe of liver. At this size, biliary cysts may cause pressure on nearby viscera. This cyst was surgically excised. Image courtesy Dr. Gary D. Norsworthy.

The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.

Figure 19-2 A large biliary cyst is seen in the parenchyma of the liver. Image courtesy Dr. Gary D. Norsworthy.

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a determination should be made of primary inflammation as an etiology, as in chronic cholangiohepatitis, versus secondary inflammation due to adjacent organ impingement by the cyst. A large biliary cyst compressing hepatic parenchyma will create inflammation of the surrounding parenchyma. The pathologist must also differentiate between a biliary cyst and a cystadenoma, benign tumor. However, even with histopathology, distinction between the two may not be assured. The main difference is the amount of supporting stroma around the lesion. Biliary cysts have scant stroma; moderate stroma occurs around a cystadenoma. The fibrovascular stroma surrounding the epithelium of a cystadenoma may contain frequent islands of entrapped hepatocytes and occasional muscle fibers and inflammatory cells. This benign tumor arises primarily in cats over 10 years of age. It is a slow-growing tumor that requires surgical excision, if possible. In humans it can undergo malignant transformation; however, this has not been documented in cats. The histologic examination will also permit differentiation of a biliary cyst from an abscess, a parasitic cyst, cystadenocarcinoma, and hemangiosarcoma. • Liver Biopsy: Biopsy of the liver should also be performed at the time of surgery to rule in or out cholangiohepatitis or lymphoma. If the former is suspected, intestinal biopsy is also recommended to look for concurrent inflammatory bowel disease.

performed during a laparotomy to avoid bile spillage into the abdomen and to permit abdominal lavage if this occurs. Ultrasoundassisted drainage followed by alcoholization can also be used with success.

Secondary Therapeutics • Cystectomy: If a cyst is drained but the fluid reforms quickly, laparotomy and cyst removal should be considered. If the cyst cannot be completely removed, partial excision accompanied by marsupialization and possible omentalization may be considered. • Lobectomy: In case of numerous biliary cysts located on the same liver lobe, partial lobectomy may be indicated. • Biliary Diversion Surgery: If biliary cysts impinge bile flow of the extrahepatic ducts, biliary diversion surgery should be considered.

Prognosis The prognosis is generally good for congenital biliary cysts as most of them are asymptomatic. For acquired cysts, the prognosis is guarded as cysts are often associated with cholangiohepatitis or neoplasia.

Suggested Readings Treatment Primary Therapeutics • No Treatment: This is appropriate for biliary cysts if they are asymptomatic. • Drainage: In the case of a large cyst compressing other organs and inducing vomiting, ultrasound-guided aspiration to empty the cyst is indicated. However, if the cyst content is bile, aspiration should be

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Maxie MG. 2007. The Liver and Biliary System. In MG Maxie, ed., Jubb, Kennedy, Palmer ’s Pathology of Domestic Animals, 5th ed., pp. 301–302. Philadelphia: Saunders Elsevier. Zatelli A, D’Ipollito P, Bonfanti U, et al. 2007. Ultrasound-assisted drainage and alcoholization of hepatic and renal cysts: 22 cases. J Am Anim Hosp Assoc. 43(2):112–116. Laurence HJ, Erb HN, Harvey HJ. Nonlymphomatous Hepatobiliary Masses in Cats: 41 Cases (1972–1991). Vet Surg. 23:365–368.

CHAPTER 20

Bite Wounds: Canine Gary D. Norsworthy

Overview Cats are frequently the victims of bite wounds from dogs. Most cats are attacked by stray or free-roaming dogs, and often by more than one dog. Occasionally, a cat will stray into a fenced yard that contains a dog, and an attack will occur. Although dogs and cats frequently coexist in amiable relationships, if a cat suddenly runs from a dog, hunting instincts may override the previously friendly relationship, resulting in a seemingly inappropriate attack. When a cat bites a dog, a relatively small hole is made in the skin. However, dogs frequently hold their prey and shake their heads, resulting in much more severe damage to underlying tissues, including bones and thoracic or abdominal walls. The canine jaw is capable of applying 150 to 450 psi of crushing force. Wounds that penetrate thoracic or abdominal organs occur frequently. In addition to the physical trauma that occurs, canine oral bacteria and environmental contamination frequently occur. Dirt and plant material may contaminate the superficial and deep aspects of the wound. Wound healing has four stages: (a) The inflammatory phase lasts about 5 days. In addition to hemorrhaging and clotting, inflammatory mediators, including histamine, serotonin, proteolytic enzymes, kinins, and prostaglandins, contribute to inflammation; (b) during the debridement phase, an exudate composed of white blood cells, dead tissue, and wound fluid forms. Neutrophils infiltrate, releasing enzymes that facilitate the breakdown of extracellular debris and necrotic material. Monocytes enter tissue and transform to macrophages for removal of necrotic tissue, bacteria, and foreign material. Lymphocytes stimulate or inhibit protein synthesis and migration of other cells; (c) the repair stage begins 3 to 5 days after the injury. Fibroblasts migrate along fibrin strands to synthesize and deposit collagen, elastin, and proteoglycans that mature into fibrous tissue. Capillaries invade wounds to increase oxygen tension and augment fibroplasia. Granulation tissue begins to form at the wound edges about 3 to 5 days post-injury. Healthy granulation tissue is highly resistant to bacterial colonization. Granulation tissue proliferates and matures as wound contraction begins; (d) The maturation phase results in scar tissue formation and final healing. Cats that are bitten by dogs often have widespread tissue necrosis that will prevent primary wound healing. Therefore, these wounds must close by second intention healing that involves the healing phases described above.

Diagnosis Primary Diagnostics • History: The owner will often witness the attack and describe the head-shaking of the dog and the wounds sustained by the cat. In some cases, the cat is able to return home on its own despite the injuries; in other cases, the cat is found at or near the attack scene. • Physical Examination: The cat is often non-ambulatory and in pain; it is often non-responsive. The cat’s hair is often wet with canine saliva and the cat’s blood. Open wounds may be observed although they usually appear less serious than the deeper wounds. The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.

Treatment Primary Therapeutics • Stabilization: The cat must be stabilized. These measures will vary depending on the degree of injury. Some cats need intravenous fluids for shock. If a penetrating chest wound or tracheal injury has occurred, oxygen therapy may be needed. • Emergency Surgery: Immediate surgery is needed if penetrating chest or tracheal wounds have occurred. If abdominal dehiscence has occurred, surgery is needed immediately to replace, repair, or remove damaged abdominal organs. Surgery may be needed to control hemorrhage. See below regarding closing contaminated wounds. • Analgesics: An analgesic, such as buprenorphine, at 0.005 to 0.01 mg/ kg IV, q4 to 8 h IM or SC should be started at presentation. • Antibiotics: Injectable broad-spectrum antibiotics (cefovecin) or antibiotic combinations (fluoroquinolone plus ampicillin or amoxicillin) should be started at presentation and given until the time of discharge from the hospital. • Circulation Assessment: Wounds to an extremity may compromise or destroy circulation, making amputation necessary. Blood pressure determination at the level of the foot can be helpful in assessing circulatory viability. • Wound Cleaning: If thoracic or abdominal injuries do not necessitate emergency surgery, wound cleaning should be done after the cat is stabilized. This may occur on the day of hospital admission or the next day. Sedation or generally anesthesia is usually required. Hair should be removed from the wound and should be clipped from the cat’s skin near the wound. Copious, vigorous flushing with sterile saline or tap water is used to remove environmental debris, canine saliva, and contamination. Flushing with dilute (0.05%) chlorhexadine solution is advised due to its broad spectrum of activity and residual activity; 1 or 0.1% povidone-iodine is acceptable. Deep and contaminated wounds should either be not sutured or should be closed with loosely applied sutures just to approximate skin apposition. Drain tubes should be considered if the skin is closed.

Secondary Therapeutics • Tissue Viability Assessment: Skin circulation may deteriorate for about 5 days. If skin closure is performed prior to 5 days, the owner should be told that skin sloughing and future surgery are likely. Nonviable skin becomes black, bluish-black, or white during those 5 days, at which time it will slough. • Open Wound Phase: About 3 to 5 days post-injury, granulation tissue begins to form. Depending on the size of the wound, it may take several more days to weeks for all nonviable tissue to slough. Final closure should not occur prior to that. See Figures 20-1A, 20-1B, and 20-1C. • Final Wound Closure: Clinical judgment is used to determine when the open wound phase appears completed. The wound should be filled with pink granulation tissue with no or minimal nonviable skin or deeper tissue. Surgical closure is performed even though drain tubes may still be needed to prevent seroma formation when the wounds are deep or extensive. Any nonviable tissue is excised prior to closure. See Figure 20-1D.

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(A)

(B)

(C)

(D)

(E) Figure 20-1 A 7-year-old, female, spayed, domestic short-hair cat was pulled from a tree by two dogs as she tried to escape. Extensive bite wounds occurred on the ventral abdomen. A, At 7 days post-trauma sloughing and granulation are underway. B, At 9 days, most of the necrotic tissue had sloughed. C, At 16 days a clean bed of granulation tissue is present. The cat is ready for primary closure (D), which was performed the next day. By 3 months post-trauma healing was complete, hair had regrown, and the cat was clinically normal (E).

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Bite Wounds: Canine

• Skin Grafting: Extensive wounds may require closure using various reconstructive techniques such as V-to-Y plasty, Z plasty, and pedicle flaps. • Buprenorphine (at 0.01 to 0.02 mg/kg q8 to 12h PO) or meloxicam (0.05–0.1 mg/kg q24 to 48h PO) should be dispensed to be given by the owner for 3 to 7 days. • Antibiotics: Broad-specturm antibiotics should be given at home until it is obvious that primary healing without wound drainage is occurring.

Therapeutic Notes • Many cats will not eat until most of the necrotic tissue sloughs. Anorexia may last for 2 or more weeks. Placement of an esophagostomy or gastrostomy tube may be needed to prevent non-healing and the onset of hepatic lipidosis. See Chapters 253 and 255.

days, the prognosis is good. See Figure 20-1E. Owners should be prepared for a healing period of several weeks that may include two or more surgeries.

Selected Readings Fossum TW. 1997. Surgery of the Integumentary System. In TW Fossum, ed., Small Animal Surgery, pp. 91–152. St. Louis: Mosby. Griffin GM, Hold DE. 2001. Dog-Bite Wounds: Bacteriology and Treatment Outcome in 37 cases. J Am Anim Hosp Assoc. 37:453–460. Waldron DR, Zimmerman-Pope N. 2003. Superficial Skin Wounds. In D Slatter, ed., Textbook of Small Animal Surgery, 3rd ed., pp. 259–273. Philadelphia: Saunders Elsevier. Trout NJ. 2003. Principles of Plastic and Reconstructive Surgery. In D. Slatter, ed., Textbook of Small Animal Surgery, 3rd ed., pp. 274–292. Philadelphia: Saunders Elsevier.

Prognosis Dog bites to cats can be a fatal event depending on the extent of the injuries. If the cat is successfully stabilized and survives the first few

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CHAPTER 21

Bite Wounds: Felines Gary D. Norsworthy

Overview The territoriality of the cat is largely responsible for its fighting behavior, whether it is the aggressor or the territory defender. The typical feline bite wound is due to a tooth that penetrates the skin and underlying tissue, leaving a lesion of minimal diameter but substantial depth. Within a few hours, the skin puncture closes, entrapping bacteria from the cat’s mouth and debris, which were carried into the wound. Aerobic and anaerobic bacterial infections are common. The three stages are preabscess (swelling and pain), abscessation (focal pocket of pus), and postabscess (abscess drains spontaneously through the skin). Abscessation occurs about 3 to 5 days after the bite. If not surgically opened, it will usually rupture and drain spontaneously by 5 to 7 days. See Figure 21-1. Some cats develop chronic draining tracts due to resistant bacteria, Mycoplasma, Mycobacterium, or fungal infections, the presence of foreign bodies or bone sequestra within the wound, or immunosuppressive states associated with the feline immunodeficiency virus (FIV) or the feline leukemia virus (FeLV).

Diagnosis Cellulitis is a variant of this process. See Figure 21-2. If a bite wound occurs in a location that does not have loose skin, such as a distal extremity, infection will dissect through fascial and muscle planes, resulting in diffuse swelling instead of an abscess. Lethargy, inappetence, fever, and lameness are the early signs.

Diagnosis There are specific body regions that are more likely to be bitten based on the cat being the aggressor or the defendant. See Figure 21-3. Areas of swelling anywhere on the body of a cat showing the appropriate

Figure 21-2 This cat’s right foreleg was bitten by another cat. Because there is minimal loose skin in this location, cellulitis developed.

clinical signs should arouse suspicion of a bite wound abscess. Draining tracts, especially if the material has a putrid odor, indicates an advanced stage of the process and usually the presence of anaerobic bacteria.

Diagnosis Primary Diagnostics • History: Outdoor cats or cats in multicat households with a history of fighting are at highest risk. • Clinical Signs: The presence of a painful swollen area or a draining tract, accompanied by fever, should arouse one’s suspicion for a bite wound abscess.

Secondary Diagnostics

Figure 21-1 Two bite wounds occurred on this cat’s head about 5 days prior. The abscesses had ruptured and were draining at the time of presentation.

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• Culture and Sensitivity: This is generally not necessary as most infections are due to Pasturella multocida; however, chronic draining wounds should be cultured for aerobes, anaerobes, fungi, and Mycobacterium. In addition to Pasturella, commonly isolated organisms include Fusobacterium, Bacteroides, Eubacterium, Peptococcus, Peptostreptococcus, Corynebacterium, Actinomyces, and Micrococcus. • Complete Blood Count: Marked neutrophilic leukocytosis with a left shift is typical. • Retroviral Tests: Cats with recurrent or nonresponsive abscesses should be tested for FeLV and FIV. Although the FeLV antigen test will usually be positive within a few days after the bite occurs, the FIV antibody test may take up to 8 weeks to turn positive. Testing at 8 weeks post-presentation is recommended because it is unlikely to miss incubating infections. However, testing at the time of initial presentation has been recommended due to poor owner compliance for testing at 8 weeks. If both tests are negative retesting at 8 weeks should still be recommended.

Bite Wounds: Felines

Figure 21-3 Certain body regions are more likely to sustain fight wounds. These are largely influenced by whether the cat is the aggressor or the defendant. Adapted drawing courtesy of Journal Feline Medicine and Surgery and Dr. Richard Malik.

Diagnostic Notes • Because of the high incidence of this disease, a bite wound infection should be suspected first when draining tracts are present, especially if fever and outdoor exposure are present.

Treatment Primary Therapeutics • Antibiotics: The high incidence of Pasturella multocida makes penicillins and cephalosporins the drug families of choice. If begun within the first 24 hours after the bite, they may abort abscess formation and be curative. Antibiotic therapy is the treatment of choice for cellulitis. • Surgical Drainage: Surgically opening an abscess enhances rapid resolution. A drainage hole should be made in the ventral aspect of the abscess to facilitate drainage of purulent material. Flushing or swabbing the abscess with an antibacterial solution is appropriate. Placement of a drain tube is optional; if it is used, it should be placed so it exits the skin in the ventral aspect of the abscess. Suturing should not occur for 3 to 4 days; however, an abscess will generally granulate and close within 2 to 5 days without suturing. Surgical drainage is not appropriate for cellulitis.

Secondary Therapeutics • Surgical Exploration and Excision: Abscesses that do not heal promptly should be surgically explored to identify and remove foreign material. Chronic fistulous tracts should be excised, if surgically feasible. • Alternative Antibiotics: Bite wound infections that are not responsive to penicillins may be due to unusual organisms, including Mycobacterium or bacterial L-forms. Culture of the lesion and antibi-

otic sensitivity testing are recommended. Doxycycline or enrofloxacin may be effective for abscesses resistant to other antibiotics. These should be tried if culture is not feasible or while culture and sensitivity results are pending. • Cefovecin: The third-generation cephalosporin cefovecin (Convenia®, Pfizer) has proven efficacy for abscesses and cellulitis and avoids the use of oral antibiotics; dosage is 8 mg/kg q14d SC. One injection lasts about 2 weeks which is typically long enough for infection resolution. Client acceptance is good for cats that are resistant to oral administration of medications.

Therapeutic Notes • Castration should be recommended because the nature of the tom cat is to enlarge his territory by fighting. Fighting often leads to abscesses and FeLV or FIV infections. • If further fighting activity is likely, vaccination with FeLV and FIV vaccines is recommended.

Prognosis The prognosis for fight wound infections is excellent with proper diagnosis and antibiotic therapy. Cats with nonhealing wounds should have the wound exudate cultured and should also be tested for FeLV and FIV. These viral organisms make the cat susceptible to repeated and resistant infections.

Suggested Readings Dowers KL, Lappin MR. 2006. The pyrexic cat. In R. Jacquie, ed., ProblemBased Feline Medicine, pp. 364–392. Philadelphia: Elsevier Saunders. Greene CE. Feline abscesses. 2006. In CE Greene, ed., Infectious diseases of the dog and cat, 2nd ed. pp. 328–330. Philadelphia: WB Saunders.

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CHAPTER 22

Blastomycosis Sharon Fooshee Grace

Secondary Diagnostics

Overview Blastomyces dermatitidis, the etiologic agent of feline blastomycosis, is a dimorphic, saprophytic fungus. The disease is uncommon in the cat. Most reports indicate no breed, age, or sex predisposition in cats, although one study found a preponderance of cases in young adult males. To date, an association between blastomycosis and feline retroviral infections has not been made. The organism is worldwide in distribution. In North America, it is endemic in the Mississippi, Ohio, and Missouri River valleys, near the Great Lakes, and in Ontario, Manitoba, and Southern Saskatchewan. Attempts to isolate the organism from soil have met with only limited success. Increased risk has been demonstrated for dogs living near water with soil that is moist, acidic, and enriched with organic matter. The disease has been identified in cats confined to the indoors. Inhalation of infective conidia is the primary means for establishment of infection. Once in the lung, the conidium transforms to a thick-walled yeast, with dissemination by hematogenous and lymphatic routes. Reproduction in the host animal occurs asexually by budding from the parent organism. Disseminated disease is common in the feline cases reported, and the course of illness has ranged from weeks to months. Vague signs such as anorexia, fever, weight loss, and depression are expected. Pulmonary involvement appears to provide the most organ-specific findings (i.e., coughing, dyspnea, tachypnea, and increased lung sounds). Also reported are inflammatory ocular lesions (i.e., anterior uveitis and chorioretinitis), central nervous system (CNS) signs (i.e., ataxia and circling), lymphadenopathy, draining tracts/nodules, and osteomyelitis. The yeast (tissue) phase is not considered contagious to humans or other pets though caution should be exercised with open draining tracts. Public health risk is derived from a shared environmental exposure.

• Complete Blood Count (CBC), Biochemical Profile, Urinalysis, and Retroviral Tests: Nonregenerative anemia has been reported. Other changes reflective of specific organ involvement may be seen. • Radiography: The most common radiographic finding is a diffuse miliary or nodular interstitial lung pattern. Pleural and peritoneal effusions and perihilar lymphadenopathy have been reported. See Figure 291-39. • Urine Antigen Assay: MiraVista Labs (Indianapolis, IN, www. miravistalabs.com) has developed a urinary antigen test for Blastomyces in humans that also appears quite sensitive for diagnosis of canine blastomycosis. Because few cases of the disease have been reported in cats, use of the test has been limited, but it shows promise. • Serologic and Intradermal Skin Testing: These tests are not reliable indicators of infection in the cat.

Diagnostic Notes • The broad-based bud attachment that is present during reproduction is helpful in distinguishing Blastomyces from Cryptococcus neoformans. • Respiratory signs are not a reliable indicator of degree of pulmonary involvement. Therefore, thoracic radiographs should be taken prior to initiation of therapy. If lung disease is severe, worsening of respiratory signs should be anticipated following initiation of treatment. Supportive care may be needed. • Blastomyces may not stain reliably with routine histopathologic stains. If blastomycosis is suspected, the pathologist should be advised so that other stains (periodic acid-Schiff reaction [PAS], Gomori’s methenamine silver, or Gridley’s) may be used. • Travel history and prior geographic residence should always be obtained for any sick cat. Cats housed exclusively indoors are still at risk for infection.

Treatment

Diagnosis Primary Diagnostics • Clinical Signs: Respiratory signs, ocular disease (especially posterior chamber), draining tracts and nodules, and evidence of systemic disease in cats residing or traveling in the endemic area should raise one’s index of suspicion for blastomycosis. • Cytology: Identification of the organism is essential for definitive diagnosis. The organism is easily recognized in samples collected from exudative lesions and infected organs via impression smears or fine-needle aspirates. With Wrights-type stains, the organism appears as a moderate to large (5–20 µm) basophilic yeast with a characteristic thick, refractile double-contoured wall. Budding organisms are attached to the parent organism by a broad base. The associated inflammatory response is usually pyogranulomatous in nature. See Figure 289-5.

Primary Therapeutics • Itraconazole: At present, this is the antifungal drug of choice, although fluconazole is being increasingly utilized. Itraconazole is dosed at 5 mg/kg q12h PO and given with a meal to promote absorption of the drug. The capsule may be opened and the contents divided into gelatin capsules or mixed into canned food. The oral solution has better bioavailability than the capsules. Treatment duration should be a minimum of 60 days. If clinical signs are still present, continue for 2 months beyond resolution of signs. • Fluconazole: This newer azole has superior penetration of the ocular and CNS tissues compared to itraconazole. It is gaining in popularity since its release in generic form. One recent report showed recovery of several cats with 3 to 5 months of treatment at 5 mg/kg q12h PO. • Placement of a feeding tube, when needed, permits the owner to administer proper nutritional support at home.

Secondary Therapeutics th

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• Fluconazole and Amphotericin B are alternative treatments if the cat does not respond to itraconazole. A subcutaneous protocol has

Blastomycosis

become available for administration of amphotericin B; this protocol appears to reduce associated nephrotoxicity. See Chapter 43 for the protocol. • Affected cats should be periodically monitored after therapy is discontinued for possible relapse.

Therapeutic Notes • Although itraconazole is usually well tolerated, serum chemistries should be periodically checked during itraconazole therapy to assess for hepatotoxicity. For cats with clinical evidence of hepatotoxicity (i.e., anorexia, jaundice), the drug should be discontinued, at least temporarily. Asymptomatic cats with increased liver enzymes do not necessarily need cessation of therapy but should be closely monitored.

those severely debilitated by pulmonary disease must be given a guarded prognosis.

Suggested Readings Bromel C, Sykes JE. 2005. Epidemiology, diagnosis, and treatment of blastomycosis in dogs and cats. J Small Anim Pract. 20(4):233–239. Gilor C, Graves TK, Barger AM, et al. 2006. Clinical aspects of natural infection with Blastomyces dermatitidis in cats: 8 cases (1991–2005). J Am Vet Med Assoc. 229(1):96–99. Legendre A. 2006. Blastomycosis. In CE Greene, ed., Infectious Diseases of the Dog and Cat, 3rd ed., pp. 569–576. Philadelphia: Saunders Elsevier.

Prognosis In general, the prognosis for infected cats has improved with the introduction of itraconazole and fluconazole. Cats with CNS involvement or

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CHAPTER 23

Blindness Karen R. Brantman and Harriet J. Davidson

Overview Loss of vision may be caused by various diseases involving the eyes or the brain. It is important to determine the cause of the blindness to treat any serious or painful conditions. In some cases, vision may be restored, whereas in others the cat and owner must learn to adapt. Owners may bring their cats in for examination of acute blindness or gradual vision loss. Cats that have slowly lost vision frequently learn to compensate so well that the owner may be unaware of any change. As a result, the veterinarian may be the first person to detect vision loss during a routine examination. Visually impaired or blind cats still make wonderful house pets; however, some minor adaptations to the environment may be helpful.

Diagnosis Primary Diagnostics • History: A complete medical history is vital. It should include current diseases, all medications the cat has taken recently, and the patient’s overall status at home. Because owners frequently use several veterinarians, it is necessary that information be taken with each visit. Direct questions regarding vision should focus on changes in the patient’s behavior, navigation of surroundings, and the general appearance of the eyes. What the owner first noticed about the cat’s vision, the duration of the problem, any changes over time, and changes to the cat’s environment, such as a new home, new furniture, or recent rearrangement of furniture should be noted. Initially, ask questions in an open manner to prevent leading the owner to a particular answer. Direct questions should come at the end to confirm or deny particular findings. • Vision Assessment, Observation: Measuring vision is a challenge in the cat, and at its best, is a subjective test. The best method of assessing vision takes behavioral observations, physical manipulation of the cat, as well as ophthalmic examination results into account. Proceed first with simply observing how the cat holds itself, how its eyes appear without manipulation, and how it maneuvers within the examination room. Placing the cat in a new environment may help. Blind animals are more reluctant to walk, will bump into objects, and will not be able to jump onto elevated objects. They will sometimes walk with an accentuated gait of the forelegs, as if they are using their legs to test for objects. Keep in mind that if the cat does not move, it does not necessarily mean the cat is blind. Attempt to test the ability of the cat to see and track objects by tossing an object, such as a cotton ball. Again, be aware that the cat may choose to simply ignore the object and not move its eyes or head even though vision is intact. Likewise, maze testing is another challenge if the cat does not wish to walk. • Vision Assessment, Hands On: To test a cat’s visual placing, hold the cat with its chest supported and approach a flat surface. Animals with normal vision and normal proprioception will hold their paws out in anticipation of standing. A blind animal may not hold its paws out until they touch the surface. Next, assess the cat’s menace The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.

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and palpebral responses. The menace response is a learned response and does not become fully developed until about 10 to 16 weeks of age. It is important to note, however, that cats are able to override the menace response; they may not blink or respond even when they see an object coming toward them. In addition, take caution when menacing not to move air currents at the corneal surface. Air current sensation tests the corneal-palpebral reflex and not necessarily vision. If a negative menace is detected, touch the face near the eyelids to be certain that the cat is able to blink (palpebral reflex). If there is no palpebral reflex, the facial nerve is affected. When the facial nerve is not functional, any positive menace response will be subtle, such as retraction of the globe or pulling the face away. • Ophthalmic Examination: Due to the variable types of ocular diseases that can cause vision loss, a thorough ophthalmic examination should be completed including pupillary light and dazzle reflexes, measurement of intraocular pressures, and pupillary dilation for a complete lenticular and fundic examination. Stimulating a dazzle reflex involves shining a bright light into the eye and watching for a blink, narrowing of the palpebral fissure, or turning away of the head. Pupillary light and dazzle reflexes are subcortical responses and do not alone determine vision. A cat may have a cortical brain lesion and be blind, yet still maintain a positive pupillary light reflex (PLR) and dazzle response. In this instance, it is also likely that there will be other neurologic lesions. Thus, all cranial nerves should be assessed following PLR, dazzle, and menace.

Secondary Diagnostics • Electroretinogram: Measurement of the electrical activity of the retina may be used to determine retinal function. This is a specialized test performed by an ophthalmologist. The test can be done in the awake animal to determine mass retinal effect; specialized testing for subtle changes frequently requires general anesthesia. • Visual-Evoked Potentials: This is another form of electrodiagnostics and tests the integrity of the optic nerve, optic tracts, and the occipital cortex. • Brain Imaging: Magnetic resonance imaging (MRI) is the best method for evaluation of the soft tissues of the eyes, optic nerves, optic tracts, and the brain. This evaluation should be considered when no specific form of ocular disease can be identified.

Treatment Primary Therapeutics • Specific Treatments: The exact form of treatment is based on the particular disease. Uveitis, glaucoma, cataracts, and retinal disease can result in blindness and, in many instances, are treatable. See Chapters 31, 85, 223.

Secondary Therapeutics • Adaptation: If vision cannot be returned, it is important that the owner realize the cat may need some adjustments to its care and environment.

Blindness

• Environment: When a blind cat is placed into a new environment, it may experience a temporary change in behavior. Not knowing its surroundings may result in aggression or extreme timidity and hiding. A blind cat needs to be given time to adjust to its surroundings. To prevent problems, a cat’s food and water bowls, as well as litter pan, should be kept in the same location and on the ground floor of the home. Most blind cats become accustomed to their surroundings; they easily adapt and memorize where objects can be found. Cats that have learned their environment rarely bump into objects unless they have recently been moved. Due to their extraordinary senses, cats can learn to jump and climb, although this ability varies from cat to cat. • Playtime: The use of objects with a sound or scent may enhance the blind cat’s quality of life by allowing it to play, but playing is not necessary. Some cats are able to compensate for their lack of vision and may resume normal activity, including jumping on furniture and chasing objects. Blind cats have been observed “gazing” out windows. It is always hard to tell what is really in the mind of a cat.

• Outdoors: A blind cat should never be left outdoors unrestricted. Although its other senses remain alert and potentially greater than normal, allowing it to sense aspects of its environment. It can easily be lead astray by a scent or a sound and not have the ability to find its way home. • Enucleation: Cats that have suffered ocular trauma with possible lens capsule rupture and those with intraocular tumors or intractable glaucoma are candidates for enucleation. Sarcomas are usually malignant with local invasion along the optic nerve See Chapter 122.

Suggested Readings Martin CL. 2001. Evaluation of patients with decreased vision or blindness. Clin Tech Small Animal Pract. 16(1):62–70.

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CHAPTER 24

Bordetella Infection Teija Kaarina Viita-aho

Overview Bordetella bronchiseptica is an aerobic, gram-negative bacterium that causes respiratory tract infections in many mammals. In dogs it causes infectious tracheobronchitis, also known as kennel cough. B. bronchiseptica is considered to be a primary pathogen of cats, but it also may act as a secondary pathogen or co-pathogen with other respiratory tract pathogens such as the feline herpesvirus (FHV-1), feline calicivirus (FCV), and Chlamydophila felis. Exposure to the organism is common, and infection is widespread in the cat population. The prevalence of B. bronchiseptica is 3 to 14% in cats with respiratory tract disease, and 1 to 10% in clinically healthy cats. It has been isolated in 21% of cats with history of respiratory tract disease. Seroprevalence is reported to be much higher, up to 60% in diseased cats and up to 40% in clinically healthy cats. Seroprevalence is highest in high population density conditions such as rescue shelters and multicat households. Overcrowding, stress, and poor hygiene predispose to infection. The bacterium is shed in oral and nasal secretions. The primary route of infection is via the oronasal cavity. Transmission occurs primarily with direct contact because the organism does not survive long periods of time outside the host. However, in a heavily contaminated environment the organism can survive long enough outside the host to allow it to be transmitted indirectly with infected oral or nasal secretions. The bacterium is easily killed by many common disinfectants and by extremes of pH and temperature. The incubation time is 2 to 5 days. The most common clinical signs are sneezing, ocular and nasal discharge, and coughing. However, coughing is not as usual in cats than in dogs with kennel cough. Nevertheless, infection should be considered in any coughing cat. See Chapter 42. Other clinical signs include increased lung sounds, fever, and lymphadenopathy. Usually the clinical signs resolve after about 10 days. Poor hygiene and overcrowding may contribute to a heavy burden of infection and increase the severity of clinical signs. Severe signs such as pneumonia, dyspnea, and cyanosis may occasionally occur. Pneumonia, which may be generalized or localized, is usually seen in kittens younger than 10 weeks old, but older cats may be affected as well. Many of the clinical signs of B. bronchiseptica infection in cats mimic those observed with other respiratory pathogens (with the exception of coughing). Therefore, the disease cannot be determined solely by a visual or physical examination. Cats living in direct proximity with dogs have shown to have elevated prevalence of B. bronchiseptica. Therefore, it is believed that the infection can be transmitted between dogs and cats. Additionally, cats with B. bronchiseptica infection may act as reservoirs to the dog population, especially in an animal shelter setting. Because B. bronchiseptica is also a human pathogen, there is a potential for B. bronchiseptica to transmit between cats and their owners. Immunocompromised people are suggested to be in the highest risk of zoonotic infection. Some cats may become carriers of B. bronchiseptica after recovering from the acute disease and continue to shed the organism for several weeks after infection. The infection may also be clinically asymptomatic.

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Long-term asymptomatic carriage has been reported, and carrier cats only shed the bacterium during periods of stress.

Diagnosis Primary Diagnostics • Polymerase Chain Reaction (PCR) Testing: Some laboratories offer a PCR test for diagnosis of B. bronchiseptica. PCR is rapid, and it has high sensitivity and specificity. Samples are collected from the oropharynx or nasal cavity using sterile cotton swabs. • Bacterial Isolation: Samples for isolation can be obtained from the oropharynx with a sterile cotton swab or through transtracheal wash or bronchoalveolar lavage. If there is a nasal discharge, a nasal swab can also be obtained. The swab is placed immediately in charcoal transport medium. The sample is cultured on selective charcoal-cephalexin agar.

Diagnostic Notes • Serology is of limited diagnostic value due to the high seroprevalence in the cat population. • Isolation of B. bronchiseptica from oropharyngeal swabs should be interpreted with caution because many cats are asymptomatic carriers. However, the identification of B. bronchiseptica from bronchoalveolar lavage samples of cats with lower respiratory tract signs is diagnostic. • Chronic carrier cats often shed relatively few organisms and may require repeated oropharyngeal culturing. Furthermore, isolation does not confirm that the bacterium is the only causative agent of the respiratory disease.

Treatment Primary Therapeutics • Doxycycline: This is the drug of choice. It is dosed at 5 mg/kg q12h PO or 10 mg/kg q24h PO for 4 weeks. Doxycycline has been reported to cause esophageal strictures and esophagitis. To minimize the risk, doxycycline suspension is preferred over tablets. Alternatively, water should be syringed into the cat’s mouth or the tablet lubricated with butter or similar. Doxycycline, as other tetracyclines, may cause discoloration of teeth if used in pregnant queens or young kittens. Nevertheless, doxycycline is safer than other tetracyclines. I have used doxycycline in kittens of 4 to 5 months of age without dental problems.

Secondary Therapeutics • Fluoroquinolones: This group of drugs is also effective. Enrofloxacin is dosed at 5 mg/kg q24h PO. Overdosing should be avoided because enrofloxacin may cause blindness if higher doses are used. In contrast to dogs, cats treated with enrofloxacin are not predisposed to developing chondrotoxic side effects. Marbofloxacin has not shown to have adverse ophthalmic effects. It is dosed at 2.75 to 5.55 mg/kg q24h PO.

Bordetella Infection

• Clavulanic Acid-Potentiated Amoxicillin: Give at 20 mg/kg q12h PO for 4 weeks. It can be safely used in young kittens and pregnant queens. However, B. bronchiseptica is not as susceptible to it as to doxycycline and another course of treatment with doxycycline may be needed later to ensure that the organism is eliminated from the body. • Cats with severe signs may require supportive treatment such as intravenous fluid administration to correct the dehydration and restore electrolyte and acid-base balance.

Therapeutic Notes • Asymptomatic or mild disease does not usually require antimicrobial therapy. Treatment is indicated for cats with more severe or persistent signs. However, it has been suggested that antibacterial therapy should be used even in mild cases because B. bronchiseptica may colonize the lower respiratory tract and lead to more severe disease.

Prevention • An avirulent live intranasal vaccine for B. bronchiseptica is available in some European countries and in the United States. Because the infection is usually mild, it is not considered a core vaccine. Vaccination should be considered for cats living in or moving into high-density populations with a history of bordetellosis, such as shelters with endemic B. bronchiseptica. The intranasal vaccination is easy to perform and is well tolerated. After vaccination, cats may exhibit mild transient sneezing or clear ocular discharge. • Vaccination does not prevent the infection but significantly reduces clinical signs. The protection starts within 72 hours after the administration of vaccine. Such rapidly induced protection is particularly valuable if an outbreak of disease occurs. The immunity lasts for at

least a year and annual vaccination should provide continuous protection. • Cats receiving live vaccines will shed the bacteria for 4 to 5 days. Therefore, vaccination must be avoided if the owner is immunocompromised because B. bronchiseptica may transmit to humans. Alternatively, if vaccination is indicated, isolation of the cat for 1 week following vaccination should prevent any transmission to susceptible individuals. Additionally, immunocompromised cats should not be vaccinated.

Prognosis The prognosis is good in mild cases, but it can be poor in severe pneumonia occurs, which is more likely in young kittens.

Suggested Readings Binns SH, Dawson S, Speakman AJ, et al. 1999. Prevalence and risk factors for feline Bordetella bronchiseptica infection. Vet Record. 144:575–580. Egberink H, Addie D, Belák S, et al. 2009. Bordetella bronchiseptica infection in cats ABCD guidelines on prevention and management. J Fel Med Surg. 11:610–614. Helps CR, Lait P, Damhuis A, et al. 2005. Factors associated with upper respiratory tract disease caused by feline herpesvirus, feline calicivirus, Chlamydophila felis, and Bordetella bronchiseptica in cats: experience from 218 European catteries. Vet Record. 156:669–673. Speakman AJ, Dawson S, Binns SH, et al. 1999. Bordetella bronchiseptica infection in the cat. J Small Anim Pract. 40:252–256. Williams J, Laris R, Gray AW, et al. 2002. Studies of the efficacy of a novel intranasal vaccine against feline bordetellosis. Vet Record. 150:439–442.

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CHAPTER 25

Brachial Plexus Neuropathy Gary D. Norsworthy

Overview Brachial plexus neuropathy is a disease that affects the motor, and to some degree, sensory nerves that make up the brachial plexus. Etiology is unknown; an immune-mediated response directed at epitopes specific to nerves derived from the brachial plexus is postulated to play a role. The typical clinical presentation is paresis or paralysis of only the thoracic limbs with depressed spinal reflexes. Conscious proprioception (CP) is lacking in the thoracic limbs; however, it is normal in the pelvic limbs. See Figure 25-1. Muscle atrophy of the thoracic limbs may occur if the duration is sufficient. Although the affected nerves and muscles appear to be solely those of the thoracic limbs, other peripheral nerves are likely to be involved but less or not noticeable clinically. Spontaneous remission in 7 to 14 days was noted in the two cats and three dogs reported and in the one case treated by the author. Relapse occurred in one of the reported cats 13 months later, but spontaneous recovery occurred again.

Diagnosis Primary Diagnostics • Clinical Signs: Affected cats exhibit paresis or paralysis of the thoracic limbs. In limited cases studied, this is the only clinically observed clinical sign.

• Electromyographic Testing: Nerve conduction studies are abnormal in the affected peripheral nerves. This form of testing permits identification of affected nerves that are not associated with clinically apparent signs.

Diagnostic Notes • A tentative diagnosis can be made based on clinical signs. Other nontraumatic diseases causing paresis of the thoracic limbs but not the pelvic limbs are unreported.

Treatment Primary Therapeutics • Spontaneous remission has occurred in the observed cases. Within 7 days improvement is apparent. The cat may be normal within 14 days.

Secondary Therapeutics • Analgesics are indicated if pain is present.

Therapeutic Notes • Other forms of therapy have not been reported.

Prognosis The prognosis appears to be good with the possibility of relapse and subsequent recovery.

Suggested Readings Freeman PM, Harcourt-Brown TR, Jeffery ND, et al. 2009. Electrophysiologic evidence of polyneuropathy in a cat with signs of bilateral brachial plexus neuropathy. J Am Vet Med Assoc. 234(2):240–244.

Figure 25-1 Brachial neuropathy is characterized by neurological deficits, including loss of conscious proprioception (CP) in the front legs with normal CP in the rear legs.

The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.

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CHAPTER 26

Brachycephalic Syndrome Mac Maxwell and Gary D. Norsworthy

Overview The brachycephalic syndrome in dogs is a recognized constellation of conditions directly related to shortening of the nasal and oral cavities. One or more of the components may be found in brachycephalic dogs, with the English bulldog being the most consistently and severely affected. The canine components are stenotic nares, elongated soft palate, and hypoplastic trachea. Secondary changes that may occur are laryngeal edema, laryngeal collapse, tonsillar eversion, tracheal collapse, and laryngeal saccule eversion. Respiratory compromise is the overall net result. The clinical signs can vary from stridorous breathing or exercise intolerance to cyanosis and collapse. The brachycephalic syndrome in cats is not just a respiratory syndrome; it includes some of these respiratory components (i.e., stenotic nares, elongated soft palate), but it also affects the tongue, eyes, and teeth. Tonsillar, laryngeal, and tracheal induced respiratory compromise is rare in cats. Persians and Himalayan cats are the most consistently affected. Longevity of Persians is significantly less than eight other breeds studied in Sweden. It is likely that the conditions described in this chapter contribute to that.

Brachycephalic Corneal Disease Overview The feline cornea encompasses about 30% of the eyeball. Brachycephalism results in rostral protrusion of the eyeball resulting in more corneal contact with environmental factors than with other cats. Recurrent or chronic keratitis, corneal ulcers, corneal scarring, and corneal sequestra result. These are discussed in detail in Chapters 41 and 124.

Diagnosis

Prognosis The prognosis for treating brachycephalic corneal disease is good although the need for repeated treatment is likely because the facial conformation that underlies this disease cannot be changed. The recurrent nature often results in permanent scarring to significant portions of the cornea.

Idiopathic Facial Dermatitis of Persians Overview This is a facial dermatitis found in Persian and Himalayan cats that is also known as the Persian Dirty-face Syndrome. Because of its strong breed predilection, it is presumed that brachycephalism or other breedrelated genetic factors are involved. However, the nasolacrimal duct system of brachycephalic cats is usually inoperative so epiphora can keep the face moist. The characteristic finding is an accumulation of black waxy debris that mats in the hair principally around the eyes but also around the mouth and on the chin. See Figure 26-1. Otitis externa is also common. Initially it is not pruritic, but pruritus may develop if an inflammatory component develops. Exudative and erythematous facial folds and mucoid ocular discharge may occur. Erythema of the preauricular skin or ceruminous otitis externa with black, waxy debris in the ear canals may also be present. Secondary bacterial and Malassezia dermatitis may occur, but even if they are treated successfully the syndrome persists.

Diagnosis Primary Diagnostics • Clinical Appearance: The occurrence of the lesions described previously in a Persian or Himalayan cat is diagnostic. It is more difficult to detect in Himalayans due to the dark hair color in the affected areas.

Primary Diagnostics • Ophthalmic Examination: The corneal portion of the ophthalmic examination described in Chapter 299 should be employed. Fluorescein staining is essential for identifying active corneal ulcers. A corneal sequestrum is a focal, black, hard cicatrix usually located near the center of the cornea. See Figure 124-2.

Diagnostic Notes • The chronic or recurrent nature of the keratitis, corneal scarring, and corneal ulceration are what makes these events characteristic of brachycephalism.

Treatment Primary Therapeutics • See Chapters 41 and 124. The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.

Figure 26-1 A buildup of dark, waxy material ventral to the eyes is typical of the idiopathic facial dermatitis of Persian cats.

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(B)

(A)

(C)

Secondary Diagnostics • Cultures and Cytology: Fungal and bacterial cultures and cytology preps may identify secondary infections that need to be treated.

Treatment Primary Therapeutics • Successful treatment for the primary disease has not been found; it is, at this time, incurable.

Secondary Therapeutics • Seborrhea: Antisecorrheic products to reduce the waxy buildup may be of some benefit. Chlorhexidine (3%) wiping pads (Douxo, chlorhexadine 3% PS Pads; Sogeval, Coppell, TX) are helpful for some cats, but the owner should not get chlorhexidine in the eyes. • Antifungal Drugs: An azole antifungal drug (itraconazole, fluconazole) is indicated for Malassezia. • Others: One report documents promising results using oral cyclosporine. Steroids, doxycycline, hyposensitization, and food trials have been inconsistently effective in some cats.

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Figure 26-2 A, The nares are so stenotic in this cat that they nearly closed during inspiration. B, The nares are open so airway impairment is not a problem at 2 months post-operatively. A CO2 laser was used to sculpt the nares. Notice that this cat also has diverging strabismus. C, Stenotic nares can also be corrected using this surgical technique. A vertically oriented wedge-shaped incision is made (arrow) so tissue can be removed. When the wedge is closed with sutures, the naris is pulled open.

Stenotic Nares Overview Stenotic nares are the most common respiratory component of the feline brachycephalic syndrome. It results in nares that are minimally open during expiration and almost closed during inspiration. See Figure 262A. If exercise occurs the cat may be forced to breathe through its mouth.

Diagnosis Primary Diagnostics • Physical Examination: This disease is diagnosed by observing the narrow nasal openings. When the respiratory rate or the depth of respiration increases, the nares may be even more stenotic.

Treatment Primary Therapeutics • Surgery: The treatment for this condition is surgical reconstruction of the nares. A CO2 laser can be used to sculpt the nares. See Figure

Brachycephalic Syndrome

26-2B. Alternatively, a wedge of tissue can be removed lateral to each naris as will be described.

Surgical Procedure • See Figure 26-2C. Grasp the naris with forceps, and make a vertically oriented wedge-shaped incision using a No. 11 blade. The medial incision should be made first followed by the lateral aspect. • Appose the cut edges of the nostril using 3-0 or 4-0 polydiaxanone. • Repeat on the opposite nostril taking care to excise a similarly shaped wedge.

Malocclusion Overview Malocclusion is defined as faulty contact between the upper and lower teeth when the jaw is closed. When brachycephalism occurs, the teeth often become rotated dorsally and displaced due to crowding. Any of the teeth may be affected, but the canines are affected most commonly.

Figure 26-3 Malocclusion, usually involving the canine teeth, is common in brachycephalic cats.

Prognosis Diagnosis Primary Diagnostics • Oral Examination: An examination of the oral cavity will easily reveal the presence of malocclusion. See Figures 26-2A and 26-3.

The prognosis is good because it is unlikely that ocular perception is hindered significantly.

Elongated Tongue Overview

Treatment • No Treatment: In most cases, the mouth remains functional so treatment is not needed. In these cases, the condition is strictly cosmetic. • Orthodontics: In some cases the misdirected teeth may be returned to their normal position with orthodontics. Consult a veterinary dental textbook for technique or consider a referral to a veterinary dentist. • Extractions: Teeth that interfere with chewing or closing of the mouth or that cause the owner personal concern are candidates for extraction. See Chapter 243.

Prognosis Generally the prognosis is excellent because most affected cats have no trouble with prehension of food. The prognosis is also excellent if extraction or orthodontia is employed.

Diverging Strabismus Overview Strabismus is a disorder of vision due to a deviation from normal orientation of one or both eyes so that both cannot be directed at the same object at the same time. It occurs as a converging abnormality (cross eyes) or a diverging abnormality (walleyed).

Diagnosis Primary Diagnosis • Physical Examination: On physical examination the lines of sight of the two eyes diverge. See Figure 26-2A and 26-2B.

Treatment Primary Therapeutics • None: There is no treatment for this disorder.

Occasionally the tongue will not experience the same degree of shortening as the mandible and maxilla. This results in protrusion of the tongue from the mouth. This is common in brachycephalic cats, but it is usually not severe enough to justify treatment. When it is severe, the tongue is so long that it protrudes 1 cm (3/8 inch) or more, and it cannot be withdrawn into the mouth. This results in drying of the tip of the tongue. See Figure 26-4A. Infection or ulceration of the tongue may result.

Diagnosis Primary Diagnostics • Physical Examination: Observation of the tongue with the mouth closed is diagnostic. If there are signs of chronic desiccation near the tip, treatment should be recommended.

Treatment Primary Therapeutics • Surgery: Surgical excision of the rostral 1- to 2-cm (3/8- to 3/4-inch) of the tongue (partial glossectomy) is curative. Surgical Procedure • With the cat under general anesthesia, mark the portion of the tongue that extends rostral to the incisor teeth. • Place a noncrushing clamp (e.g., Doyen) across the rostral aspect of the tongue just proximal to the area to be resected. See Figure 26-4B. • Excise the rostral aspect of the tongue using a No. 10 scalpel blade. See Figure 26-4B. • Control hemorrhage as needed with electrocautery, digital pressure, or ligation. • Appose the epithelial edges with 4-0 or 3-0 polydiaxanone in a simple interrupted pattern. • Healing generally takes about 10-14 days. See Figure 26-4C.

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SECTION 1: Diseases and Conditions

(A)

(A)

(B) (B) Figure 26-5 A, This lateral radiograph shows the caudal aspect of the soft palate (arrow) overlying the epiglottis. B, Note the length of a normal soft palate (arrow) in another brachycephalic cat.

Elongated Soft Palate Overview

(C) Figure 26-4 (A) More than 1 cm (3/8 inch) of this elongated tongue protrudes from the mouth. The tip shows signs of constant drying. (B) A Doyen-type clamp is used to control hemorrhage during amputation of the tip of the tongue. (C) One month following surgery the tongue is healed and retracts normally into the mouth.

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Elongated soft palate in a brachycephalic dog can be severe enough to create significant respiratory impairment. The brachycephalic cat may also have a soft palate that is elongated enough to cause snoring sounds, especially when it is asleep, or that causes respiratory impairment similar to affected dogs. The decision to treat should be based on the severity of the clinical signs.

Diagnosis Primary Diagnostics • History and Clinical Examination: If the owner reports snoring the cat should be examined to determine if the soft palate is the cause. • Examination Under Anesthesia: The use of a laryngoscope will permit visualization of whether or not the caudal aspect of the soft palate contacts the epiglottis during inspiration.

Brachycephalic Syndrome

• Radiography: A lateral view of the cervical region using high quality radiographic equipment and technique will permit visualization of how far caudal the soft palate extends. See Figure 26-5.

Treatment Primary Therapeutics • None: If the clinical signs are mild (snoring) and the owner is tolerant of the snoring sounds, no treatment is needed. • Surgery: If the soft palate is so long that it interferes with unobstructed passage of air into the larynx or if the owner is intolerant of the snoring, surgery is indicated. A CO2 laser can be used to simultaneously cut and cauterize the caudal (elongated) portion of the soft palate. Alternatively, conventional surgery can be used; however, surgical access is limited. Surgical Technique: Soft Palate Resection • Place the patient in sternal recumbency and elevate the head. The endotracheal tube should be secured to the lower jaw to allow visualization of the soft palate. • Identify the landmarks for resection: the rostral tip of the epiglottis and the caudal aspect of the tonsillar crypts. • Place stay sutures on the lateral aspects of the soft palate just rostral to the anticipated site of resection. • Transect the soft palate using Metzenbaum scissors at the point where it touches the tip of the epiglottis. • Appose the dorsal and ventral aspects of the mucosa with 3-0 or 4-0 polydiaxanone in a simple continuous pattern. Alternatively, the palate may be partially transected and sutured to minimize hemorrhage.

Prognosis For mild cases causing snoring, the prognosis is excellent as long as the owner can tolerate the snoring and respiratory impairment does not occur. For severe cases the prognosis is excellent with surgical resection of the soft palate.

Suggested Readings Bond R, Curtis CF, Ferguson EA, et al. 2000. An idiopathic facial dermatitis of Persian cats. Vet Dermatol. 11:35–41. Egenvall A, Nodtvedt A, Haggstrom J, et al. 2009. Mortality of lifeinsured Swedish cats during 1999–2006: Age, breed, sex, and diagnosis. J Vet Intern Med. 23:1175–1183. Fontaine J, Heimann M. 2004. Idiopathic facial dermatitis of the Persian cat: three cases controlled with cyclosporine. Vet Dermatol. 15:64. Griffon DJ. 2000. Upper airway obstruction in cats: Pathogenesis and clinical signs. Compendium. 22(9):822–829. Griffon DJ. 2000. Upper airway obstruction in cats: Diagnosis and treatment. Compendium. 22(9):897–906. Malik R, Sparkes A, Bessant C. 2009. Brachycephalia—a bastardisation of what makes cats special (editorial). J Fel Med Surg. 11:889–890. Ordeix L, Galeotti, F, Scarampella F, et al. 2007. Malassezia spp overgrowth in allergic cats. Vet Dermatol. 18(5):316–323. Schlueter C, Budras KD, Ludewig E, et al. 2009. Brachycephalic Feline Noses: CT and anatomical study of the relationship between head conformation and the nasolacrimal drainage system. J Fel Med Surg. 11:891–900.

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CHAPTER 27

Bronchial Disease, Chronic Philip Padrid

Overview Chronic bronchial disease in cats occurs most commonly in two forms: chronic bronchitis and asthma. Chronic bronchitis is defined as an inflammatory disorder of the lower airways that causes a daily cough, for which other causes of cough (i.e., heartworm disease, pneumonia, lungworms, neoplasia, and so on) have been excluded. Asthma is more loosely defined as a disorder of the lower airways that causes airflow limitation that may resolve spontaneously or in response to medical treatment. Airflow limitation is generally the result of some combination of airway inflammation and airway smooth muscle contraction. The symptoms of asthma can be dramatic, including acute wheeze and respiratory distress. Sometimes however, the only symptom of asthma-induced airflow limitation is a daily cough, and in human patients, this is referred to as “cough-variant” asthma. Clinical signs are variable. Bronchitic cats have a daily cough and may be absolutely symptom free in between episodes of cough. Alternatively, cats with bronchitis may be tachypneic at rest. Asthmatic cats may cough, wheeze, and struggle to breathe on a daily basis. In mild cases, symptoms may be limited to occasional and brief coughing. Some cats with asthma may be asymptomatic between occasional episodes of acute airway obstruction. Severely affected cats may have a persistent daily cough and experience many episodes of life-threatening acute bronchoconstriction. The pathogenesis of asthmatic airway inflammation and hyperreactivity is clearly multifactorial. Numerous investigations suggest that the interaction between T lymphocytes and eosinophils within airways may play an important role in the generation of airway inflammation and airway hyperreactivity in human asthma. Most of the recent research in asthma pathogenesis includes the notion that effector lymphocytes may be broadly defined in terms of the pattern of cytokine secretion that they demonstrate, with the Th2-lymphocyte subtype generating the cytokines that drive asthmatic inflammation. Importantly, a Th2-driven cytokine profile has been demonstrated in antigen-induced asthma models in the feline species. There are no other disorders besides asthma that cause acute reversible, nonprogressive wheezing and tachypnea. Other causes of cough and tachypnea in the feline species include:

chitis from asthma in the feline patient. Nevertheless, the diagnosis, prognosis, and treatment options for both diseases overlap with great frequency.

Diagnosis Primary Diagnostics • History: The cat’s history should include of one or more of these clinical signs: cough (most consistent), acute wheeze, tachypnea, or respiratory distress including labored, open mouth breathing. These signs are usually relieved quickly with some combination of oxygen, bronchodilators, and corticosteroids. • Radiographs: Radiographic evidence of bronchial wall thickening, usually described as “doughnuts” and “tramlines.” See Figure 291-23. Air trapping may be assumed if the lungs are hyperinflanted. This is seen most prominently on the lateral view and can be appreciated by recognizing the position of the diaphragmatic crus at approximately the level of L1-L2. See Figure 27-1. Radiographs may also demonstrate atelectasis, most commonly of the right middle lung lobe. It is usually easier to see this pattern on a dorsal-ventral or ventral-dorsal exposure because the right middle lung lobe silhouettes with the cardiac silhouette on the lateral view. Atelectasis most commonly occurs in the right middle lung lobe because of mucus accumulation within the bronchus, and this airway is most commonly involved because it is the only airway that has a dorsal-ventral orientation within the bronchial tree and, therefore, subject to the effects of gravity (see Figure 27-2). In more extreme cases, you may appreciate fluffy illdefined heavy interstitial infiltrates in multiple lung lobes. The cause of these changes in cats with lower airway disease may be multiple small areas of atelectasis in multiple lung lobes resulting from multiple diffuse small mucus plugs. This presents a diagnostic challenge because this radiographic change is consistent with a number of disorders including neoplasia and diffuse interstitial pneumonitis.

• • • • • •

Chronic noninfectious bronchitis. Parasitic tracheobronchitis including Aelurostrongylus. Viral or bacterial tracheobronchitis. Infectious pneumonia (i.e., bacterial, viral, or parasitic). Interstitial lung disease (usually idiopathic). Cardiac disease (i.e., hypertrophic and congestive cardiomyopathy); few cats have a cardiac-generated cough, in contrast to dogs. • Primary or metastatic lung neoplasia; tracheobronchial neoplasia is uncommon. • Heartworm infestation. Definitive diagnosis of asthma is usually based on specific pulmonary function studies that require patient cooperation. Because both disorders, bronchitis and asthma, can cause a daily cough as the only clinical sign, there are many times when it is not possible to distinguish bronThe Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.

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Figure 27-1 Air trapping may be assumed if the lungs are hyperinflated. This is seen most prominently on the lateral view and can be appreciated by recognizing the position of the diaphragmatic crus at approximately the level of L1–L2.

Bronchial Disease, Chronic

bacteria does not by itself confirm airway infection. If a positive culture truly reflects infection, bacteria may be found intracellularly, or the bacteria should have grown on a primary culture plate without the need for enrichment broth; the bacteriology report will state this.

Treatment Primary Therapeutics Emergency Treatment

Figure 27-2 Lateral radiograph of a cat with asthma demonstrating right middle lung lobe collapse. The increased density of the atelectatic lung lobe is not readily apparent because the lung (arrow) silhouettes over the heart shadow.

Chest radiographs can also rule out other common causes of cough and tachypnea. See Figure 291-22. • Response to Therapy: Cats with asthma may stop coughing or wheezing within 10 minutes after administration of a bronchodilator (terbutaline [0.01 mg/kg IM, SC] or albuterol [2 puffs followed by 7–10 breaths from a spacer and mask]). The great majority of cats with bronchitis or asthma respond to high dose corticosteroid therapy within 5 to 7 days, and a patient with a diagnosis of bronchitis or asthma that responds poorly should be reevaluated and the diagnosis revisited.

Secondary Diagnostics • Heartworm Testing: An antibody test should be performed in regionally selected cases. If the antibody test is positive follow it with an antigen test and echocardiography. • Echocardiography: This to rule out cardiomyopathy or to demonstrate adult heartworms in endemic areas. Note that many cats with cardiomyopathy do not cough as a primary clinical sign. See Chapters 88 and 110. • Bronchoalveolar Lavage (BAL) with Cytology and Culture: Common cytologic findings include large numbers of eosinophils found in the recovered tracheobronchial secretions in asthmatic airways and nonseptic neutrophils in bronchitic airways of some cats. BAL eosinophilia is consistent with but not a good marker for asthma because of the large number of eosinophils found the recovered fluid from cats with normal pulmonary function and quiescent airways. The primary indication for bronchoscopy is when there is not an otherwise predictable cessation or minimization of clinical signs after 7 to 10 days of aggressive corticosteroid treatment.

Diagnostic Notes • Bronchoscopy is rarely required to make an accurate diagnosis of asthma in feline patients. Bronchoscopy in healthy cats is not a trivial undertaking. In cats with cough and respiratory compromise, bronchoscopy may be a life-threatening procedure and should only be performed by persons adequately and formally trained in the technique. • Cats with asthma do not generally have airway infection with bacteria. In fact, one well designed study showed that cats with signs of bronchial disease had fewer positive airway cultures than a cohort population of healthy cats. Thus, BAL fluid that harbors

• Oxygen: An oxygen cage with 100% ambient oxygen will deliver less than 40% inspired oxygen to patients; this is nevertheless effective, safe, and is the least stressful method of delivering oxygen to these unstable patients. • Parenteral Corticosteroids: Dexamethasone sodium phosphate is effective with a wide dose range; I recommend 0.2 to 0.5 mg/kg IV. The best understood effect of corticosteroid treatment in asthmatic patients is to inhibit cytokine and inflammatory protein expression the level of mRNA transcription. This process takes hours and days. Clearly then, we do not fully understand why intravenous corticosteroids work quickly, but they do. • Inhaled Bronchodilators: Albuterol sulfate (Ventolin™, Proventil™) is the drug of choice. Two puffs into a spacer are followed by 7 to 10 breaths through a mask connected to the spacer. In emergency cases, albuterol can be used q30m for up to 6 hours without serious side effects; it will last for 2 to 4 hours • Systemic Bronchodilator: If an inhaled bronchodilator is not available or possible, give terbutaline (0.01 mg/kg IM). Terbutaline is a selective beta2-receptor agonist that produces relaxation of bronchial smooth muscle. It is available as a 1-mg/ml suspension. For a 5-kg (11-lb) cat, dilute terbutaline with sterile saline in a 1:9 ratio to produce terbutaline 0.1 mg/ml. Administer 0.5 ml of this concentration (0.05 mg) to achieve a dose of approximately 0.01 mg/kg.

For the Stable Asthmatic • Oral Corticosteroids: Newly diagnosed patients should receive prednisolone 1.0 mg/kg q12h PO for 5 days. If there are positive therapeutic effects begin to wean to lowest effective dose that controls >75% of the clinical signs. • Inhaled Corticosteroids: Fluticasone (Flovent™) is dosed as a 110 µg inhaler. Give two puffs into the spacer followed by 7 to 10 breaths. This is an excellent replacement for oral corticosteroids once the oral medications have been used and found to be effective. Because inhaled fluticasone may take 10 days to reach peak effectiveness begin inhaled steroid therapy while the patient is receiving oral corticosteroids and wean off the oral steroid over a 10- to 14-day period. See Figure 27-3. • Oral Bronchodilator: Terbutaline can be given at 0.1 to 0.2 mg/kg per 8 hours PO q8 to 12h. • Injectable, Long-Acting Corticosteroids: Parenteral administration of long acting corticosteroids is limited to patients for whom no other method of drug administration is feasible. In this setting, injection of a Depo-Medrol™ (10–20 mg IM total dose) once every 2 to 8 weeks may be effective. This therapy is likely to result in significant/serious side effects including weight gain, diabetes mellitus, and reduced immunity, and represents the treatment of last resort.

Therapeutic Notes • Albuterol only comes in a single strength (90 µg per acuation). Albuterol usually results in relaxation of airway smooth muscles within 1 to 5 minutes, so the effect is almost immediate. This drug

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SECTION 1: Diseases and Conditions

be relatively unaffected by their disease most weeks of every month and most months of every year. • It is critically important to understand that human (and perhaps feline) asthmatic and bronchitic airways show evidence of chronic ongoing inflammation whether the patient is symptomatic or not. Therefore, treatment strategies are most successful if they are directed toward decreasing the underlying inflammatory component of the disease in addition to addressing the acute clinical signs of cough, wheeze, and increased respiratory effort. • Patients with symptoms that occur less than once weekly (without medication) are generally not considered to have chronic active inflammatory airways. These patients may be safely treated with bronchodilators when needed.

Secondary Therapeutics Figure 27-3 with asthma.

•

•

•

•

60

Proper position of spacer device to deliver inhaled medications to cat

should be used in cats with bronchoconstriction. Symptoms that may indicate bronchoconstriction include wheezing, noisy lower airway breathing, prolonged expiratory phase of ventilation, and coughing. Albuterol can be used once or twice daily prior to administering fluticasone or as needed for acute coughing and wheezing. Flovent comes in three strengths: 44 µg, 110 µg, and 220 µg per actuation. Dosing with the 44 µg q12h does not consistently result in acceptable clinical responses. For cats with mild/moderate disease 110 µg q12h frequently results in clinical responses equivalent to that achieved by administration of 5 mg of prednisone q12h PO. Cats with more serious disease may require 220 µg inhaled q12h. Administration of fluticasone more than twice daily has not resulted in clinical benefit in my experience. Administration of inhaled medications requires special technique. Fluticasone and albuterol are administered using a small, aerosolholding chamber (spacer; AeroKat™, Trudell Medical, Ontario CA) attached to a metered dose inhaler (MDI) on one end and a face mask on the other. The spacer is approximately the size of the inner cardboard roll used with toilet paper. The MDI supplies precise doses of the aerosol drug, and the holding chamber contains the aerosol so it can be inhaled when the patients inspires. The mask is designed to cover the nose of the cat. The choice of spacer is relevant as cats have a tidal volume of between 5 and 10 mL of inspired air per pound of body weight. Currently, only the AeroKat brand spacers have been designed specifically based on the tidal volume characteristics of the cat. Using these spacer devices, cats will inhale the majority of drug propelled into the spacer by breathing 7 to 10 times through the spacer-mask combination after actuation of the MDI. It is important to teach the owner to observe the pet actually breathing because cats may initially hold their breaths when introduced to this form of treatment. The procedure is not time consuming, but it can be helpful to acclimate the cat to the mask. When administering inhalation therapy, the MDI is first shaken to open an internal valve within the canister, and then it is attached to the spacer. The mask attached to the other end of the spacer is placed snuggly on the animal’s nose or muzzle, and the MDI is pressed to release the medication into the spacer. Patients with asthma may have clinical signs once a month, once a week, or multiple times every day. The frequency of signs may be stable for months and then suddenly worsen without obvious cause. This does not necessarily reflect a nonreversible worsening of disease. In contrast, asthmatic patients may have signs that wax and wane for many years without a predictable pattern. Therefore, drug doses and frequency of administration must be tailored to the individual patient. The goal of course is to make the patient symptom free. Realistically, the goal is for patients to cough less than daily and to

• Antibiotics: A fluoroquinolone, such as enrofloxacin (3–5 mg q24h PO for 10 days) should be given for documented bacterial infection or if a previously stable asthmatic patient suddenly becomes unstable. Because 25% of cats with signs of lower airway disease have Mycoplasma spp., enrofloxacin, doxycycline, and azithromycin are good antibiotic choices. • Cyproheptadine: This drug comes in both tablet and liquid form and is dosed at 2 to 4 mg q12h PO. The primary indication for this drug is a trial in the symptomatic asthmatic cat already receiving maximal doses of bronchodilators and corticosteroids. It has antiserotonin properties. Serotonin is a primary mediator released from activated mast cells into feline airways and causes acute smooth muscle contraction (bronchoconstriction) in cats but not in humans. A beneficial therapeutic response may not be seen for 4 to 7 days, but depression, the primary side effect of this drug, may be observed 24 hours after administration. Depression is not lifethreatening but may cause the owner to discontinue cyproheptadine therapy. • Anti-leukotrienes: Zafirlukast, montelukast, and zileuton have been recommended; however, there is no evidence that drugs that affect leukotriene synthesis or receptor ligation play a significant role in the treatment of feline or canine respiratory disease. Having said that, there is at least one undocumented claim of efficacy using zafirlukast (1–2 mg/kg q12h PO) or montelukast (0.5–1.0 mg/kg q24h PO) for treatment of feline asthma. • Methylxanthines: Theophylline and aminophylline (5–6 mg/kg q12h PO; sustained release: 25 mg/kg q24h PO) are purported to relax smooth muscle, particularly bronchial smooth muscle, as well as stimulate the central nervous system and act as a weak cardiac and diaphragmatic stimulant and diuretic. However, I do not use this class of drugs to treat feline patients with asthma; both inhaled albuterol and oral and injectable terbutaline are more effective bronchodilators in cats.

Prognosis Chronic bronchitis and asthma cause a constellation of symptoms in the feline patient, including cough, wheeze, and variable amounts of disability at rest. Other nonairway disorders can cause similar signs in these patients, and there are only a small number of diagnostic tests available to distinguish one disorder from another. Therefore, the clinician in general practice must rely on careful history taking, physical examination skills, and accurate interpretation of thoracic radiographs to insure that a proper diagnosis is made. Asthma may resolve spontaneously or become a lifelong disorder with a variable clinical presentation. In general, cats with asthma can be well controlled with aggressive treatment. The use of inhaled medications to treat asthma and bronchitis is considered the standard of care in humans and is now widely recommended for cats with chronic bronchial disease. This approach avoids

Bronchial Disease, Chronic

many of the side effects previously seen in patients treated with systemic medications.

Suggested Readings Boothe DM. 2006. Drugs affecting the respiratory system. In LG King, ed., Textbook of Respiratory Disease in Dogs and Cats, pp. 236–245. St. Louis: Elsevier. Chandler1 JC, Lappin MR. 2002. Mycoplasma respiratory infections in small animals: 17 cases (1988–1999). J Am Anim Hosp Assoc. 38(2):111–119. Johnson LR, Drazenovich, TL. 2007. Flexible bronchoscopy and bronchoalveolar lavage in 68 cats (2001–2006). J Vet Intern Med. 21(2): 219–225.

Kirchvink N, Leemans J, Delvauz F, et al. 2006. Inhaled fluticasone reduces bronchial responsiveness and airway inflammation in cats with mild chronic bronchitis. J Fel Med Surg. 8(1):45–54. Norris CR, Decile KC, Berghaus LJ, et al. 2003. Concentrations of cysteinyl leukotrienes in urine and bronchoalveolar lavage fluid of cats with experimentally induced asthma. Am J Vet Res. 64(11):1449–1453. Padrid PA. 2000. Feline Asthma. Diagnosis and Treatment. Vet Clin North Am Small Anim Pract. 30(6):1279–1293. Reinero CR, Byerly JR, Berghaus RD, et al. 2005. Effects of drug treatment on inflammation and hyperreactivity of airways and on immune variables in cats with experimentally induced asthma. Am J Vet Res. 66(7):1121–1127.

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CHAPTER 28

Calicivirus Infection Gary D. Norsworthy

Overview The causes of feline upper respiratory infections (URIs) include bacteria, fungi, and viruses. This chapter will concentrate on those diseases caused by the various strains of the feline calicivirus (FCV), a small, noneveloped single-stranded RNA virus of which there is wide antigenic variability. However, currently all strains are classified as a single serotype. The FCV and the feline herpesvirus-1 (FHV-1) account for about 80% of all feline URIs. These viruses are contagious and often endemic to multicat households and facilities. Both are likely to produce a carrier state in which stress-induced intermittent viral shedding (FHV-1) or continuous viral shedding (FCV) occurs. Maternal antibodies wane at about 5 to 7 weeks of age, so kittens in these environments are usually exposed before vaccine-induced immunity occurs. The clinical signs are based on the fact that the FCV replicates in epithelial cells of the upper respiratory tract, conjunctiva, tongue, and in pneumocytes in the pulmonary alveoli. The most consistent clinical sign of an FCV infection is sneezing; other common signs include fever, nasal discharge, oral ulceration, and hypersalivation. See Figure 28-1. Anorexia occurs due to fever, oral ulceration, or nasal congestion and can lead to dehydration and death. Less frequently, various strains of FCV cause polyarthritis, ulceration of the nasal planum, or interstitial pneumonia. The FCV can be isolated from the mouths of the vast majority of cats with lymphoplasmacytic stomatitis-gingivitis. If it is etiologically involved it is due to an immune response to the virus and not the virus itself. Transmission primarily occurs by direct contact between cats involving oral and nasal secretions. Indirect transmission via infectious discharges and fomites is also possible. Infection occurs via the nasal,

oral, or conjunctival routes. Sneezed macrodroplets are unlikely to be infectious beyond 2 meters (6 feet) from a sneezing cat, but they may persist in the environment for up to one month. The incubation period is typically 3 to 4 days; a transient viremia occurs at that time. The FCV is not transmissible to humans. Recently, a highly virulent strain of FCV, called the virulent systemic feline calicivirus (VS-FCV), has been reported to cause severe disease with a mortality rate of more than 40% of affected cats. It causes high fever, facial and paw edema, ulceration and hair loss on the face, feet, and ears, icterus, and hemorrhage from the nose and in the feces, in addition to the more typical respiratory signs. See Figure 28-2. It affects adult cats more than kittens; affected cats may die within 24 hours of the onset of clinical signs. When introduced into a naïve household,

(A)

Figure 28-1 The signature sign of an feline calicivirus infection is lingual ulceration. The ulcers typically affect the anterior or lateral margins of the tongue as seen in this cat.

The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.

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(B) Figure 28-2 A, The virulent systemic feline calicivirus (VS-FCV) causes a vasculitis resulting in swelling, edema, local alopecia, and ulcerative dermatitis as seen in this 10-week-old kitten. B, Other manifestations of the VS-FCV include icterus and lingual ulceration as seen in this 6-year-old cat that died of the disease.

Calicivirus Infection

hospital, or shelter, disease can spread rampantly directly between cats or via fomites and cause death in a large number of the affected cats. Newer vaccines include this strain.

Diagnosis Primary Diagnostics • History and Clinical Signs: Although there are several causes of sneezing in cats, sneezing that persists over 48 hours is highly suggestive of URI. Some or many of the other aforementioned clinical signs are usually present.

Secondary Diagnostics • Viral isolation: Many veterinary reference laboratories can isolate and identify the FCV in cell culture from oropharyngeal or conjunctival swabs. However, because of the asymptomatic carrier state, interpretation of a virus isolation result in terms of active infection versus carrier must not be misinterpreted. The presence of virus and clinical signs are poorly correlated. False-negative results are a problem. • Polymerase Chain Reaction (PCR) Testing: PCR testing can be used to identify the FCV. The same interpretation limitations as virus isolation apply. False-negative results are a problem.

Diagnostic Notes • The clinical signs of all viral URIs are similar. When secondary bacterial infections occur, these diseases are indistinguishable based on clinical signs except for the severe signs caused by the VS-FCV.

Diagnostic Notes • Virus neutralizing antibody titers are not reliable for diagnosing active respiratory viral infections due to natural infection and vaccination.

Treatment Primary Therapeutics • Antibiotics: An FCV infection can become complicated by bacteria. Although most strains of FCV produce a self-limiting disease of a few days duration, the bacterial infections can become lifethreatening if not treated. The drugs of choice for mild-to-moderate disease are amoxicillin (12.5 mg/kg q12h PO) or amoxicillinclavulanic acid (15 mg/kg q12h PO). If severe disease occurs, either azithromycin (10 mg/kg q24h PO for 10 days) or clavulanic acid/ amoxicillin plus a fluoroquinolone is preferred for outpatients; if the cat resists oral medications, cefovecin injectable (8 mg/kg q24h SC) can be used. Amoxicillin (12.5 mg/kg q12h SC) or ampicillin (10–20 mg/kg q12h SC) plus enrofloxacin (2 mg/kg q12h SC) is preferred for hospitalized cats. • Hydration: Nasal and ocular secretions thicken when dehydration occurs. To prevent this added discomfort, cats should receive rehydrating and maintenance doses of balanced electrolyte fluids IV or SC. • Nutritional Support: Anorexia is common and is the most serious common complication of URIs. Nutritional support using orogastric or nasoesophageal tubes should begin as early as possible. Contraindications include dyspnea and severe depression. Nasal secretions should be softened with water and removed before an orogastric tube is passed as cats with nasal blockage tend to panic when an orogastric tube is passed. Severe nasal congestion and irritation contraindicates the use of nasoesophageal tubes. See Chapters 253 and 308.

Secondary Therapeutics • Ophthalmic Antibiotics: These are indicated when conjunctivitis exists. Do not to use products containing corticosteroids if a corneal ulcer is present. • Nasal Decongestants: Oxymetazoline hydrochloride (Afrin Pediatric Nasal Drops®) is advocated by some. One drop is placed in one nostril once daily. However, most cats object to nasal drops; aftercongestion (also called “rebound congestion”) may develop, and efficacy has not been clearly demonstrated.

Therapeutic Notes • Antiviral drugs currently available are only effective against DNA viruses and retroviruses. There is not a proven antiviral drug that is effective against the FCV and that is safe. Ribavirin inhibits RNA viruses in vitro, but it is toxic to cats. • Cats should be treated in a hospital with isolation facilities when anorexia occurs or to prevent exposure of others cats in the household. If cats are treated at home, they should be isolated from other cats, if possible. • Cats infected with the VS-FCV should be treated aggressively with intravenous fluids, parenteral antibiotics, and nutritional support and strictly isolated from other cats. • Treatment of chronic gingivitis/stomatitis is discussed in Chapter 84.

Prevention • A vaccine containing FHV-1 and FCV should be considered a core vaccine to be given to all cats. However, neither antigen produces sterilizing immunity; they are only able to mute the severity of clinical signs rather than prevent infection, disease, and virus shedding. Their duration of immunity must be defined in terms of the expected outcome of vaccination. Most FCV-containing vaccines in the United States contain only one strain of FCV that was chosen over 30 years ago. Due to frequent mutation, there are many vaccine-resistant strains present in the feline population. • Newer vaccines contain a common FCV strain and the VS-FCV strain. Dual strain vaccines offer broader cross-protection to more strains of FCV. • Kittens should be vaccinated about every 3 to 4 weeks beginning at about 8 weeks of age. The last vaccine should not be administered before 16 weeks of age. Kittens in breeding colonies and catteries with endemic FCV should be vaccinated initially at 4 weeks of age then every 2 weeks until 12 weeks of age then at 16 weeks of age. • Intranasal vaccination has not been shown to shorten clinical infection or to terminate the carrier state. However, immunity develops more quickly with intranasal vaccines than with injectable vaccines, so they have merit in situations in which exposure is likely. Intranasal vaccines may also prevent the carrier state. Some cats receiving intranasal vaccine develop chronic sneezing. • Disinfection of premises is important in multicat situations. Effective disinfecting agents include sodium hypochlorite (5% bleach diluted 1:32), potassium peroxymonosulfate, chlorine dioxide, and commercial products approved for FCV inactivation. Note that bleach is only effective for 24 hours after dilution. • In a cattery situation queens should be boostered prior to mating. Vaccination during pregnancy is discouraged. • Vaccination of feline immunodeficiency virus (FIV) infected, feline leukemia virus (FeLV) infected, and chronically ill cats should continue as long as these cats are not febrile or showing signs of immunosuppression. However, immunity may be delayed and less than that produced in a normal cat so more frequent vaccinations should be considered. Inactivated vaccines are preferred over modified-live vaccines.

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Prognosis The prognosis is good except for cats infected with the VS-FCV if anorexia and dehydration do not occur or if they are treated aggressively. Cats that fail to respond to appropriate therapy within 4 to 6 days should be tested for the FeLV and the FIV, two viruses that can be immunosuppressive and prevent response to therapy. Cats infected with the VS-FCV have a much more guarded prognosis due to the aggressive nature of the virus.

Suggested Readings Gaskell RM, Dawson S. 2006. Other Feline Viral Diseases. In SJ Ettinger, EC Feldman, eds., Textbook of Veterinary Internal Medicine, 5th ed., pp. 667–671. St. Louis: Elsevier Saunders.

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Pedersen NC, Elliot JB, Glasgow A, et al. 2000. An isolated epizootic of hemorrhagic-like fever in cats caused by a novel and highly virulent strain of feline calicivirus. Vet Microbiol. 73:281–300. Radford D, Addie D, Belak S, et al. 2009. Feline calicivirus infection: ABCD guidelines on prevention and management. J Fel Med Surg. 11:556–564. Sykes JE. 2001. Feline upper respiratory tract pathogens. Herpesvirus-1 and calicivirus. Compend Contin Educ. 23:166–167.

CHAPTER 29

Carcinomatosis Bradley R. Schmidt

Overview Carcinomatosis (effusions containing malignant epithelial cells) is generally associated with the presence of a carcinoma of any organ in the thoracic or abdominal cavity and can be cytologically difficult to distinguish from a mesothelioma. As with mesothelioma, malignant epithelial effusions may develop secondary to exudation from the primary tumor, inflammation associated with the primary tumor, and diffuse lymphatic metastasis/obstruction. Malignant effusions are generally present within the body cavity where the primary tumor is identified but may also develop in other body cavities secondary to lymphatic metastasis. Solid metastasis to other organs may also be seen. See Figure 29-1A and Figure 29-1B. Reported cancers associated with carcinomatosis in the cat include, but are not limited to, carcinoma of the lung, pancreas, intestinal tract, and liver as well as aortic body tumors. See Chapter 5 for patient signalment associated with the various tumors. Clinical signs associated with pleural and pericardial effusion are related to respiratory compromise and cardiac tamponade and may include dyspnea, coughing, and progressive effusions resulting from right-sided heart failure. Nonspecific signs of malignant effusion arising in any body cavity include lethargy, anorexia, and intermittent vomiting. In addition to these clinical signs, clinical signs related to the primary and metastatic tumors may also be seen. Differential diagnoses for carcinomatosis includes lymphoma, malignant effusion secondary to a sarcoma, and benign effusions secondary to cardiac disease, protein-losing enteropathy and nephropathy, liver disease, heartworm disease, feline infectious peritonitis (FIP), and other infectious processes.

(A)

Diagnosis Primary Diagnostics • Fluid Analysis and Cytology: Fluid analysis and cytology may aid in the diagnosis of malignant effusion. Confirming and differentiating carcinomatosis or mesothelioma cytologically may be difficult as reactive mesothelial cells associated with benign effusions may also display marked atypia. Furthermore, mesothelioma and malignant epithelial cells may cytologically appear similar, further complicating the diagnosis. • Fine-Needle Aspiration and Cytology: Fine-needle aspiration of masses or enlarged organs may help determine the origin of the malignant pleural effusion. • Tissue Biopsy and Histopathology: Tissue biopsy of masses or enlarged organs via a surgical or laparoscopic approach may determine the origin of the malignant pleural effusion if fine-needle aspirations are negative.

Secondary Diagnostics • Immunohistochemistry: Immunohistochemical staining may aid in the diagnosis of carcinomatosis because these tumors generally stain positive for cytokeratin whereas most sarcomas do not.

The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.

(B) Figure 29-1 Carcinomatosis often produces solid metastasis the mesentery (A) and to other organs (B). Photo courtesy of Dr. Gary D. Norsworthy.

• Fibronectin: Elevations in fluid fibronectin is reported to be a sensitive but nonspecific test for malignant effusions in dogs and cats. Normal levels in effusion would help to rule out mesothelioma. • Thoracic Imaging: Thoracic radiographs or computerized tomography (CT) scan of the thorax should be performed to evaluate for the presence of pleural thickening or masses as well as pulmonary or mediastinal masses. Thoracocentesis prior to performing thoracic radiographs or CT scan may aid in the interpretation. • Ultrasound: Abdominal ultrasound should be performed in all cases of abdominal effusions, as well as in cases with malignant pleural effusion, to evaluate for tumors that may have metastasized to the thoracic cavity. Although radiographs or CT scans are the diagnostics of choice for the thoracic cavity, thoracic ultrasound may be performed when pleural fluid is present. Carcinomatosis

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SECTION 1: Diseases and Conditions

•

•

•

•

generally appears as a diffuse, hyperechoic thickening or as a nodular thickening of the pleural or peritoneal lining. Lymph Node Fine-Needle Aspiration and Cytology: A fine-needle biopsy should be performed if lymphadenopathy is present. Benign mesothelial cells have been reported within lymph nodes in dogs with nonmalignant pericardial effusions; therefore, interpret results with caution. Echocardiogram, Electrocardiogram (ECG), and Thyroid Tests: A cardiac evaluation and thyroid evaluation should be performed in all cats where hyperthyroidism or cardiac disease is suspected to be the cause of effusion, especially in cases of pericardial effusion. Minimum Data Base: A complete blood count, serum biochemistry profile, urinalysis, feline leukemia virus (FeLV) and feline immunodeficiency virus (FIV) serology, and heartworm antigen and antibody testing should be performed to evaluate the overall health of the patient and for nonneoplastic causes for effusion development. Fluid Culture and Sensitivity: This should be performed if primary or concurrent sepsis is suspected cytologically.

Diagnostic Notes • Carcinomatosis should be considered over mesothelioma when a mass lesion is identified in thoracic or abdominal organs and when histopathology or cytology distinguishes it as a primary tumor. • Effusion pH: One study suggested that fluid pH may be helpful in differentiating benign from malignant pericardial effusions; however, a subsequent study suggested that the pH values overlapped too much to be of any clinical use.

Treatment

these drugs appears to be minimal, the use of intracavitary chemotherapy alone may not be indicated when larger mass lesions are present.

Secondary Therapeutics • Intravenous Chemotherapy: Intravenous chemotherapy is indicated when larger nodules or masses are present or when nodal or organ metastasis is present. Responses to intravenous chemotherapy in most cases appear to be limited and short in duration. Common chemotherapy agents include doxorubicin (1 mg/kg or 25 mg/m2 q3w IV), mitoxantrone (6.0–6.5 mg/m2 q3w IV) and carboplatin (225–240 mg/m2 q3–4w IV). Careful monitoring of the white blood cell counts is recommended. Carboplatin is excreted by the kidneys; therefore, use with caution in cats with renal compromise. • Pericardectomy for Pericardial Effusion: In the rare event of malignant pericardial effusion, pericardectomy may be performed to alleviate signs related to cardiac tamponade. Adjunctive intravenous chemotherapy as above may also be considered. • Surgery: Surgery to remove a primary tumor (e.g., primary lung tumor or small intestinal tract tumor) may be palliative; however, survival times are generally short when malignant effusions or metastasis is present. • COX-1/COX-2 Inhibitors or COX-2 Inhibitors: These agents have been reported in the treatment of squamous cell carcinoma and other tumors in the cat. Although use of these drugs either as a single agent or in combination with carboplatin has been reported, no studies exist on the benefits of the use of these agents in the treatment of carcinomatosis. • Prednisone/Prednisolone: Corticosteroids may be used to palliate clinical signs.

Primary Therapeutics • Centesis: Thoracocentesis, pericardiocentesis, or abdominocentesis should be performed to alleviate potentially life-threatening clinical signs and discomfort associated with fluid accumulation. A 21- or 23-gauge butterfly catheter or 20- or 22-gauge over-the-needle catheter attached to an extension set and three-way stopcock may be used. Sedation may be indicated in some cats but must be used with caution if respiratory or cardiac compromise is present. • Intracavitary Chemotherapy: Intracavitary chemotherapy (pleural or peritoneal cavities only) delivers a higher concentration of chemotherapy to the tumor while minimizing systemic effects and may relieve lymphatic obstruction resulting in the resolution or slowing of fluid accumulation. Commonly used drugs include carboplatin (225–240 mg/m2) or mitoxantrone (6.0–6.5 mg/m2). Carboplatin is further diluted with 5% dextrose in water or sterile water and mitoxantrone with 0.9% sodium chloride to a total volume of 15 to 30 mL, depending upon the residual fluid volume present in the body cavity post-centesis, to aid in the diffusion of the drug into the body cavity. The chemotherapy drug is infused into the body cavity with a 21- or 23-gauge butterfly catheter or 20- or 22-gauge over-the-needle catheter attached to an extension set and three-way stopcock. In cases of pleural effusion, the dose may be divided and administered into the right and left pleural cavity. After infusion is complete, the patient is gently rolled to aid in the diffusion of the chemotherapy. Mild sedation may be indicated. Systemic absorption of these drugs is reported to be minimal; therefore, neutropenia and other adverse effects are generally not seen. However, monitoring the while blood cell count is recommended. Furthermore, carboplatin is excreted by the kidneys, and caution should be used in administering to cats with renal compromise. Because penetration of carboplatin and, most likely, mitoxantrone is only 2 to 3 mm or less and the systemic absorption of

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Therapeutic Notes • Radiation therapy has not been critically evaluated in the treatment of malignant effusions in the cat. • Intracavitary chemotherapy may be considered in cases where larger nodules or masses are not present. When larger tumor burdens are present, surgery or intravenous chemotherapy should be incorporated in the treatment. Some advocate dividing the chemotherapy and administering 50% intravenously and 50% intracavitary when treating malignant effusions with concurrent larger tumor burdens. • Pleurodesis: Pleurodesis with agents such as doxycycline or talc has generally been unsuccessful.

Prognosis The prognosis for most cats with carcinomatosis is generally poor due to the metastatic nature of most tumors and the inability of intracavitary or intravenous chemotherapy to result in durable remissions. Removal of effusion or the use of prednisone may be palliative for 1 to 5 months.

Suggested Readings Fine DM, Tobias AH, Jacob KA. 2003. Use of pericardial fluid pH to distinguish between idiopathic and neoplastic effusions. J Vet Intern Med. 17:525–529. Hirschberger J, Pusch S. 1996. Fibronectin concentrations in pleural and abdominal effusions in dogs and cats. J Vet Intern Med. 10:321–325. Monteiro CB, O’Brien RT. 2004. A retrospective study on the sonographic findings of abdominal carcinomatosis in 14 cats. Vet Radiol Ultrasound. 6:559–564.

CHAPTER 30

Cardiopulmonary Arrest Larry P. Tilley

Overview

Diagnosis

Cardiopulmonary arrest (CPA) is an immediately life-threatening condition that requires prompt recognition and appropriate intervention to restore circulatory function. In CPA, cessation of effective cardiac contractions and ventilation quickly lead to widespread hypoxia, with cerebral death occurring within 4 to 5 minutes. CPA is usually a grave development, with survival rates of 2 to 5% reported even with optimal therapy. Considering this, the clinician should place a major emphasis on the recognition of impending CPA. Reversal of abnormalities placing the cat at risk of CPA is generally much more successful than cardiopulmonary resuscitation itself. Signs of CPA include loss of consciousness, dilated pupils, agonal or absent respiration, absent heart sounds and arterial pulsations, cyanosis, and often opisthotonos. These signs may be abrupt and dramatic in a previously healthy cat or may occur rather subtly in a moribund case.

• Mucous Membrane Color and Capillary Refill Time (CRT): Look for pallor or cyanosis. CRT may be delayed. • Thoracic Auscultation: Look for absence of respiratory or heart sounds. In some cases, extreme bradycardia may be detected. • Electrocardiography: Look for asystole (absence of complexes), slow ventricular escape rhythm, and idioventricular rhythm.

Secondary Diagnostics • Blood Gas Analysis: Look for severe hypoxemia, hypercapnia, and acidosis.

Diagnostic Notes

Diagnosis Differential Diagnoses Virtually any pathophysiologic state can deteriorate to the point at which CPA occurs. The most common clinical disorders predisposing cats to CPA are listed in Table 30-1.

TABLE 30-1: Differential Diagnoses for Cardiopulmonary Arrest Cardiopulmonary Disease

Primary Diagnostics

Congestive heart failure (secondary to cardiomyopathy or other primary cardiac disease) Obstructive airway disease Heartworm disease Trauma (i.e., myocardial contusions and traumatic myocarditis) Pleural effusion Neoplasia Hemorrhage Trauma, surgery

Systemic Abnormalities

Severe acid-base disturbances Severe electrolyte disturbances (e.g., hyperkalemia secondary to urethral obstruction) Overwhelming sepsis or endotoxemia

Other

Drugs, particularly anesthetic agents Surges in parasympathetic tone (as may occur with tracheal intubation and manipulation of ocular, laryngeal, or pharyngeal areas)

The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.

• Intensive monitoring (i.e., vital signs, mucous membrane color, electrocardiograph) of cats with conditions predisposing them to CPA and during anesthesia is essential.

Prevention • Correct Hypoxemia: For anesthetized cats, discontinue anesthetic, increase oxygen flow, and confirm proper endotracheal tube placement. For cats with pulmonary edema, administer diuretics and supplemental oxygen. • Thoracocentesis: This should be performed if significant pleural effusion is present. • Intravascular Abnormalities: Correct fluid deficits and electrolyte or acid-base disturbances. • Correct Cardiac Arrhythmias: See Chapter 12.

Treatment Primary Therapeutics (see Figure 30-1) for Cardiopulmonary Resuscitation, follow ABCD • A = Airway: Clear the airway of any obstructive material. Endotracheal intubation should be performed, and tracheostomy should be considered if complete obstruction exists. • B = Breathing: Provide respiratory support if spontaneous respiration is absent or insufficient. Provide 100% oxygen with an Ambu® bag, through the reservoir bag of an anesthesia machine, or via a mechanical ventilator. Institute artificial ventilation; administer two short breaths of about 2 seconds duration each and reassess. If no spontaneous respiration occurs, continue ventilations at a rate suitable for this cat (normal respiratory rate 10–24 breaths per minute). Peak airway pressures should not exceed 20 cm H2O. • C = Circulation: External cardiac massage provides at best about 30% of normal cardiac output; internal cardiac massage is two to three times more effective in improving cerebral and coronary perfusion. Perform chest compressions rapidly, at a rate of between 80 and 100 compressions per minute; the chest should be displaced about 30%. With the patient in right lateral recumbency, perform compressions

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Cardiopulmonary Arrest Begin Basic Life Support Airway

Assess for airway obstruction. assess for breathing Perform intubation

Breathing

Ventilate with 100% oxygen. avoid hyperventilation Provide 10–24 breaths/minute

Circulation

Assess for heart beat and pulses If absent, begin chest compressions Provide 100–120 compressions/minute Minimize interruptions

Begin Advanced Life Support Place ECG and Determine Arrest Rhythm Obtain Access for Drug Therapy

VF/Pulseless VT Defibrillate

Drug Therapy

Asystole/Bradycardia/PEA

2–10 joules/kg (external) 0.2–1 joule/kg (internal) Provide up to 3 consecutive shocks before resuming CPR for 1–2 min.

Drug Therapy

Epinephrine (0.01–0.1 mg/kg IV) or Vasopressin (0.8 units/kg IV)

Atropine (0.04 mg/kg IV) Use lower dose if palpable pulse or suspected vagal arrest Epinephrine (0.01–0.1 mg/kg IV) May be repeated @ 3–5 min. intervals or Vasopressin (0.8 units/kg IV) Given one time only

Lidocaine (2 mg/kg IV) or Amiodarone (5 mg/kg IV) Repeat Defibrillation (escalating dose)

Anesthesia-Related Arrest Turn off vaporizer, flush circuit Administer specific drug reversal agent Low-dose epinephrine (0.01 mg/kg) where indicated

During CPR Consider Interposed Abdominal Compression Consider Open-Chest CPR Especially with prolonged arrests or in large patients. Transdiaphragmatic approach during laparotomy Consider Sodium Bicarbonate (1–2 mEq/kg IV) Indicated in patients with significant pre-existing metabolic acidosis, hyperkalemia, or with prolonged (>10 min.) CPA Consider Calcium Gluconate (50–100 mg/kg IV)

Indicated in patients with hyperkalemia or ionized hypoca/cemia

Consider Magnesium Sulfate (30 mg/kg IV)

Indicated in patients with hypomagnesemia

Monitor Ongoing Resuscitating

Use end-tidal CO2 monitoring available

Search for Underlying Causes of Arrest Figure 30-1

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Run ‘stat’ bloodwork (PCV/TS/BG/Blood Gas/Electrolytes)

Algorithm for performing cardiopulmonary resuscitation in veterinary patients.

Cardiopulmonary Arrest

directly over the heart (intercostal spaces 3–5); this can be performed using one hand. Different compression and ventilation regimes have been reported. The goals are to (a) provide appropriate compressions (80–100 per minute) and (b) provide appropriate ventilations (10–24 per minute) without stopping compressions for ventilations and without trying to synchronize ventilations with compressions. • D = Drugs: Administer atropine (0.02–0.05 mg/kg IV or 0.2– 0.5 mg/kg intratracheally [IT]) if asystole or severe bradycardia is present. Give epinephrine (0.01–0.1 mg/kg IV [1 mL per 5 kg or 11 lbs of the 1:1000 concentration] IV, or 2 ml per 5 kg [11 lb] IT). This may be repeated every 3 to 5 minutes. Give bicarbonate (1–2 mEq/kg IV) if acidosis or severe hyperkalemia present or if arrest duration has exceeded 10 minutes. Another agent to consider is vasopressin (0.8 mg/kg IV [or 0.8 units/kg IV]; can repeat at 5 minute intervals.)

• Defibrillation is rarely achieved with drugs. A defibrillator should be available for CPR, especially in critical care and emergency clinics. • A flowchart of ABCD steps should be placed in surgery and the intensive care area. Organization of efforts is essential. Prepare technicians with mock arrest situations. All technicians should be familiar with basic cardiopulmonary resuscitation (CPR). Establish a mobile “crash cart” of supplies and drugs needed for CPR.

Prognosis The prognosis is best when CPA is unexpected (e.g., during elective anesthesia), not associated with significant underlying disease, and promptly detected. Otherwise, the prognosis is poor.

Therapeutic Notes • Intracardiac administration of emergency drugs is not recommended. If a central venous catheter is not available, administer drugs (i.e., atropine, epinephrine, or lidocaine) intratracheally. Dilute the drugs with 5 to 10 mL of sterile saline and administer them through a catheter placed within the endotracheal (ET) tube. The tip of the catheter should be at the level of the carina. The IT dose of emergency drugs is twice the IV dose.

Suggested Readings Mark SL. 2007. Cardiopulmonary Arrest. In CE Greene, FWK Smith, Jr., eds., Blackwell’s 5 Minute Veterinary Consult. 4th ed., pp. 218–219. Ames, IA: Blackwell Publishing. Cole SG, Drobatz KJ. 2008. Cardiopulmonary resuscitation. In LP Tilley, ed., Manual of Canine and Feline Cardiology. 4th ed., pp. 333–341. St. Louis: Elsevier Saunders.

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CHAPTER 31

Cataracts Shelby L. Reinstein and Harriet J. Davidson

Overview The lens is an avascular, transparent tissue that functions to refract light onto the retina. When the lens is diseased, a loss of transparency often manifests as an opacity, or cataract, within the lens. Nuclear sclerosis is a normal aging change and should be differentiated from cataracts. Nuclear sclerosis results from an increased density of the central portion of the lens as it ages; it is visible as a bluish opacity in the center of the lens. Nuclear sclerosis does not affect vision unless advanced; however, cataracts can progress and cause blindness. Additionally, cataracts often induce a secondary uveitis (see Chapter 223), which can lead to glaucoma (see Chapter 85). There are many methods used to classify cataracts. It is helpful to determine the age of onset, stage of progression, location, and cause of a cataract.

Diagnosis Primary Diagnostics • Examination: Examining the lens is achieved following full dilation of the pupil, in a darkened room. The examination can be performed using a transilluminator with or without magnification, or a direct ophthalmoscope. The transilluminator may be held approximately 12 inches from the cat’s face. The normal tapetal reflex is seen, which creates back lighting, or retroillumination, of the lens. This helps to identify opacities within the lens, seen as dark spots in the tapetal reflex. If the entire lens is opaque (cataractous), no reflex is seen. Close examination of the lens with magnification will allow determination of the location and size or stage of the cataract. A slit beam of light can be used to examine a cataract and help determine size and location. When the slit beam is shone into the eye, three beams of light are visualized; called the pyrkinje reflexes. The first beam of light is seen as a convex reflex off the cornea, a second convex beam is seen reflecting off of the anterior lens surface, and lastly a concave beam is seen reflecting off of the posterior lens surface of the lens. By moving the slit beam of light across the lens, the reflected lights will also move, allowing identification of the location and size of the cataract. • Classification: Many methods exist to classify a cataract. Often, it is fitting to use multiple schemes to accurately describe the cataract. • Age of Onset: Cataracts may be described as congenital, juvenile, or senile. Differential diagnoses will differ based upon the age of onset, and it may suggest an etiology. • Stage of Progression: The size of a cataract is described based upon the percentage of the total lens it occupies. An incipient cataract involves 180 mEq/L [180 mmol/L]) is often associated with neurologic damage that can be residual or can result in coma or death.

Suggested Readings Gaschen FP, Jones BR. 2005. Feline Myopathies. In SJ Ettinger, EC Feldman, eds., Textbook of Veterinary Internal Medicine, 6th ed., pp. 906–912. St. Louis: Elsevier Saunders. Joseph RJ, Carrillo JM, Lennon VA. 1988. Myasthenia gravis in the cat. J Vet Intern Med. 2(2):75–79. Podell M. 2000. Neurologic Manifestations of Systemic Disease. In SJ Ettinger, EC Feldman, eds., Textbook of Veterinary Internal Medicine, 5th ed., pp. 548–552. Philadelphia: WB Saunders. Shelton D. 2007. Myasthenia gravis. In LP Tilley, FWK Smith, Jr., eds., Blackwell’s 5-Minute Veterinary Consult. Canine and Feline, 4th ed., pp. 908–909. Ames, IA: Blackwell Publishing.

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CHAPTER 34

Chemotherapy for Lymphoma Mitchell A. Crystal and Bradley R. Schmidt

Overview In the cat, lymphoma is broadly categorized into two histopathological categories based on behavior and response to chemotherapy: the more common large cell (lymphoblastic) lymphoma that arises from any anatomic location and is usually associated with rapid disease progression, and the less common small cell (lymphocytic) to intermediate cell lymphoma that has been described in the small intestinal tract as well as in other organs and may be associated with a more indolent course of progression. Although lymphoma is considered a chemosensitive malignancy, drug resistance has likely developed by a variety of genetic and cellular pathways by the time the neoplasm becomes clinically detectable. Combination chemotherapy attempts to overcome chemotherapy resistance and maximize tumor cell kill by using drugs with different mechanisms of action and minimize side effects by avoiding the use of drugs with overlapping toxicities. Chemotherapy drugs are administered by injection or orally on an outpatient basis or orally at home. Minimally, a complete blood cell count (CBC) assessment and a complete physical examination should be performed prior to and 1 week after each therapy until a pattern is established that indicates each agent is safe and well tolerated. If a serious side effect occurs, subsequent dose reduction, delay in therapy, or change in chemotherapy drugs used may be indicated.

TABLE 34-1: Cyclophosphamide, Vincristine, Prednisone (COP) Week 0 Week 1 Week 2 Week 3 Week 6

Reported first remission rate Reported median first remission duration Median survival time

Vincristine 0.75 mg/m2 IV and cyclophosphamide 300 mg/m2 PO Vincristine 0.75 mg/m2 IV Vincristine 0.75 mg/m2 IV Vincristine 0.75 mg/m2 IV and cyclophosphamide 300 mg/m2 PO Vincristine 0.75 mg/m2 IV and cyclophosphamide 300 mg/m2 PO Prednisone: 2 mg/kg per day PO given continuously for 1 year beginning week 0 Treatment is continued with vincristine and cyclophosphamide at 3-week intervals for 1 year 79 to 100% 84 to 180 days Not reported

Combination Protocols with Author’s Notes • Combination chemotherapy protocols are considered the mainstay in therapy of feline lymphoma and are generally associated with higher remission rates and longer remission times when compared to single agent protocols. Four combination chemotherapy protocols that have been successfully used in the treatment of feline lymphoma are listed in Tables 34-1, 34-2, 34-3, and 34-4. The overall first remission rates, durations, and survival times (when available) are listed. Variations of the aforementioned protocols are also described with similar response rates and survival times. • We commonly use one the following protocols to treat cats with large cell (lymphoblastic) and some forms of intermediate cell lymphoma of various anatomic locations: • cyclophosphamide, Oncovin® (vincristine), prednisone (COP) • L-asparaginase, Oncovin® (vincristine), cyclophosphamide, chlorambucil, Adriamycin® (doxorubicin), prednisone (CHOP) • cyclophosphamide, Oncovin® (vincristine), prednisone, Adriamycin® (doxorubicin) (COPA). • Whereas responses may vary, remission rates associated with these protocols are generally high, however survival times are typically less than 1 year. • The chlorambucil/prednisone protocol is generally reserved for the treatment of cats with small to intermediate cell lymphoma of the small intestinal tract, small cell lymphoma of other anatomic locations, and chronic lymphocytic leukemia. These cats may enjoy prolonged survival times with this less aggressive protocol (11 months or more).

The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.

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• L-asparaginase may be used in the first week of therapy in many of the combination protocols described; however, when used concurrently with vincristine, myelosuppression may occur anecdotally. Some advocate the use of L-asparaginase only in critical cases or as part of a rescue protocol. Efficacy of L-asparaginase in the cat is coming under question, as a recent study reported only a 30% response rate in feline lymphoma. • Vincristine and cyclophosphamide doses reported in the combination protocols may result in toxicities that are not acceptable to the cat owner. Dose reduction may be indicated initially and may be increased in subsequent administrations if the patient is tolerating therapy well. See Commonly Used Drugs in the Therapy of Lymphoma listed in this chapter.

Single-Agent Protocols • Doxorubicin: In contrast to dogs, doxorubicin has demonstrated poor efficacy when used as a single-agent therapy for feline lymphoma (26% complete response, median first remission duration 92 days, median survival time 84 days). It has been demonstrated, however, that the addition of doxorubicin to a combination chemotherapy protocol such as COP may significantly prolong remission times. Doxorubicin is generally administered at 1 mg/kg or at 25 mg/m2 diluted with saline, IV every 21 days. A recent study comparing these two dosages reported that the latter dose was associated with a lower posttreatment neutrophil count but not associated with more clinical toxicities. It was not determined if there was a difference in tumor response between the two dosages. In cats, renal toxicity is more of a concern than cardiomyopathy. Monitor blood urea nitrogen (BUN) and creatinine prior to each administration for evidence of evolving renal disease.

Chemotherapy for Lymphoma

TABLE 34-2: Modified Wisconsin—L-asparaginase, Vincristine, Cyclophosphamide, Chlorambucil, Doxorubicin, Prednisone (Modified CHOP) Week 0 Week Week Week Week Week Week Week Week Week Week Week Week Week Week Week

1 2 3 5 6 7 8 10 12 14 16 18 20 22 24

First remission rate Median first remission duration Median survival time

2

Vincristine 0.5–0.7 mg/m IV and L-asparaginase 400 u/kg SC Cyclophosphamide 200 mg/m2 PO or IV Vincristine 0.5–0.7 mg/m2 IV Doxorubicin 25 mg/m2 IV Vincristine 0.5–0.7 mg/m2 IV Cyclophosphamide 200 mg/m2 PO Vincristine 0.5–0.7 mg/m2 IV Doxorubicin 25 mg/m2 IV Vincristine 0.5–0.7 mg/m2 IV Cyclophosphamide 200 mg/m2 PO or IV Vincristine 0.5–0.7 mg/m2 IV Doxorubicin 25 mg/m2 IV Vincristine 0.5–0.7 mg/m2 IV Cyclophosphamide 200 mg/m2 PO or IV Vincristine 0.5–0.7 mg/m2 IV Doxorubicin 25 mg/m2 IV Prednisone: 2 mg/kg per day PO weeks 0 and 1, then 1 mg/kg/day PO weeks 2 and 3, then discontinue unless clinically indicated. If sterile hemorrhagic cystitis occurs, substitute chlorambucil at 1.4 mg/kg PO. For renal or central nervous system lymphoma, substitute cytosine arabinoside (Cytosar®, 600 mg/m2 SC) every 8 weeks beginning at week 6. 68% 273 days

225 days

TABLE 34-3: Cyclophosphamide, Vincristine, Prednisone, Doxorubicin (COP Induction + Doxorubicin Maintenance; COPA) Week 0 Week Week Week Week Week Week Week Week Week Week

1 2 3 6 9 12 15 18 21 24

First remission rate Median first remission duration Median survival time

Vincristine 0.75 mg/m2 IV and Cyclophosphamide 300 mg/m2 PO Vincristine 0.75 mg/m2 IV Vincristine 0.75 mg/m2 IV Doxorubicin 25 mg/m2 IV Doxorubicin 25 mg/m2 IV Doxorubicin 25 mg/m2 IV Doxorubicin 25 mg/m2 IV Doxorubicin 25 mg/m2 IV Doxorubicin 25 mg/m2 IV Doxorubicin 25 mg/m2 IV Doxorubicin 25 mg/m2 IV Prednisone: 2 mg/kg per day PO beginning week 0 and ending at onset of week 3. Treatment ends week 24. 47% 281 days

TABLE 34-4: Chlorambucil + Prednisone for Lymphocytic Alimentary Lymphoma (Chlorambucil, Prednisone) Day 0 Day 1 Day 2 Day 3 Prednisone Chlorambucil Protocol end point not reported First remission rate Median first remission duration Median survival time

Chlorambucil 15 mg/m2 PO Chlorambucil 15 mg/m2 PO Chlorambucil 15 mg/m2 PO Chlorambucil 15 mg/m2 PO 10 mg/cat per day PO beginning day 0 4-day pulse treatment is repeated every 3 weeks

69% 615 days 510 days

• Idarubicin: Idarubicin is an oral anthracycline agent that has been shown to have efficacy in feline lymphoma (2 mg q24h PO for 3 consecutive days, repeated every 21 days). Furthermore, the addition of idarubicin as a single agent in 18 cats that achieved remission with COP induction resulted in median remission times of 183 days. • CCNU (CeeNU®, Lomustine®): This oral alkylating agent is being investigated for use in feline lymphoma. It is renally and hepatically metabolized and crosses the blood-brain barrier. Limited information is available regarding the use of CCNU in cats. Dogs with resistant lymphoma demonstrate a 20% response rate to CCNU. CCNU can be considered as a rescue agent for cats with resistant lymphoma. It is dosed at 50 to 60 mg/m2 (typically 10 mg/average to large-sized cat) q4 to 6w PO. Acute dose limiting toxicity is neutropenia, which can occur 7 to 28 days after treatment; gastrointestinal toxicity can also occur. Cumulative dose limiting toxicity is thrombocytopenia, which can occur 14 to 21 days after treatment. Further chronic effects of CCNU have not yet been evaluated in the cat; delayed liver damage has been documented in the dog (9 of 228 dogs receiving chronic therapy). Monitoring of the CBC (prior to and 7 to 10 days following each treatment) and chemistry profile (prior to every other treatment) is indicated if CCNU is used. • Miscellaneous Notes: Single agent use of cyclophosphamide, chlorambucil, vincristine, vinblastine, L-asparaginase, and prednisone have all anecdotally resulted in prolonged survival times; however, their use is generally reserved to combination protocols.

Commonly Used Drugs in the Therapy of Lymphoma Chlorambucil • Supplied as 2 mg tablets. • Drug type: Alkylating agent. • Dosage: 0.1 mg/kg q24h PO or 6 to 8 mg/m2 q24h PO. Because the tablets should never be split, this usually translates to 2 mg q24h PO to q3d PO days depending upon the weight of the cat. Also, it may be dosed as indicated in combination chemotherapy protocols. It is generally used as a substitute for cyclophosphamide if hemorrhagic cystitis occurs or in the treatment of small cell lymphoma or chronic lymphocytic leukemia. • Toxicities: It is generally well tolerated; however, gastrointestinal side effects and myelosuppression may occur.

Not reported

Cyclophosphamide • Supplied as 25- and 50-mg tablets; 100-, 200-, and 500-mg and 1- and 2-g vials.

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• Drug type: Alkylating agent. • Dosage: 50 mg/m2 orally in the morning q48h PO or 200 to 300 mg/m2 q21d PO. Do not split the tablet; adjust the actual dose based on tablet size. For example, if a dose is calculated at 12 mg q48h with the cumulative 2-week dose being 84 mg divided over 7 doses, administer 25 mg tablets in 3 doses equally spaced in that 2-week interval. The intravenous dose is 200 to 300 mg/m2 mixed with any volume of 0.9% saline, administered over 20 to 30 minutes. Cyclophosphamide is eliminated by the kidneys; reduce the dose if renal disease is present. • Toxicities: Anorexia, vomiting, or diarrhea is seen more commonly with intravenous administration. Neutropenia may occur uncommonly to occasionally with the nadir being 7 to 14 days after therapy; it usually returns quickly to normal. The low count does not cause signs of illness unless infection or sepsis occurs. Decrease the dose by 20% if severe neutropenia (12 µg/L), cobalamin supplementation alone or together with a dietary trial is a rational first approach for cats with cobalamin deficiency. Depending on the size of the cat 100 to 250 µg/cat of cobalamin (most commonly cyanocobalamin) are injected subcutaneously q7d for 6 weeks, followed by 100 to 250 µg/

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cat q14d SC for 6 weeks, and another injection of the same dose four weeks later. Serum cobalamin concentration should be rechecked 4 weeks after the last dose of cobalamin to evaluate the patient’s need for further cobalamin supplementation.

Prognosis

Therapeutic Notes

The overall prognosis for cats with cobalamin deficiency is dependent on the underlying cause. However, once cobalamin deficiency has been diagnosed and appropriately addressed therapeutically, cobalamin deficiency does not continue to contribute to the overall morbidity and mortality of the patient.

• If the cat does not respond to cobalamin supplementation alone, it is crucial to carefully evaluate the patient for the underlying cause for the cobalamin deficiency. This involves evaluation of the cat for chronic small intestinal disease and may include fecal examination for intestinal parasites and treatment with a broadspectrum anthelmintic agent, feeding trials, abdominal ultrasound, endoscopic or surgical biopsy with histopathological evaluation, and other diagnostic tests that may be deemed necessary in a specific case. Then, the underlying cause of the cobalamin deficiency can be addressed therapeutically in addition to cobalamin supplementation. • It has also been speculated that cobalamin may have a direct pharmacologic effect on appetite. Many cats with cobalamin deficiency have a poor appetite and start eating well after cobalamin supplementation has been instituted. In some of these patients the poor appetite recurs as soon as cobalamin supplementation is discontinued even though serum cobalamin concentration may be well within the reference range. In these patients cobalamin supplementation should resume and may need to be continued long term.

Ruaux CG, Steiner JM, Williams DA. 2001. Metabolism of amino acids in cats with severe cobalamin deficiency. Am J Vet Res. 62:1852–1858. Ruaux CG, Steiner JM, Williams DA. 2005. Early biochemical and clinical responses to cobalamin supplementation in cats with signs of gastrointestinal disease and severe hypocobalaminemia. J Vet Int Med. 19:155–160. Ruaux CG, Steiner JM, Williams DA. 2009. Relationships between low serum cobalamin concentrations and methlymalonic acidemia in cats. J Vet Int Med. 23:472–475. Simpson KW, Fyfe J, Cornetta A, et al. 2001. Subnormal concentrations of serum cobalamin (Vitamin B12) in cats with gastrointestinal disease. J Vet Int Med. 15:26–32. Thompson KA, Parnell NK, Hohenhaus AE, et al. 2009. Feline exocrine pancreatic insufficiency: 16 cases (1992–2007). J Fel Med Surg. 11(12): 935–940.

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Suggested Readings

CHAPTER 38

Coccidioidomycosis Sharon Fooshee Grace

Overview Of all the deep (systemic) mycotic agents, Coccidioides has the most limited geographic distribution. Cats and dogs are infrequently infected outside the endemic areas of the dry, southwestern United States, Mexico, and Central and South America. This ecologic niche, the Lower Sonoran life zone, is well suited to support growth of the organism. C. immitis is found in the San Joaquin Valley, whereas C. posadasii is found in other areas. Endemic areas are characterized by sandy alkaline soil, low annual rainfall, and high summer temperatures. During periods of high temperature and scant rainfall, the organism survives below the soil surface. When a period of heavy rainfall follows such a dry spell, the organism replicates in the upper soil surface and sporulates, and the infective arthrospores are dispersed through the environment by wind or any activity that creates dust. Increased numbers of human cases have occurred in endemic areas following dust storms and earthquakes. Cats appear relatively immune to the disease as compared to dogs, though cats are often more debilitated than dogs at the time of initial presentation. Although only a limited number of cases have been described in cats, the primary route of infection appears to be inhalation of airborne arthrospores, as occurs in other species. Infection of cats by direct inoculation of the organism has been rarely reported. Dissemination occurs through hematogenous and lymphatic routes. A competent cellmediated immune response must be present to contain infection. Infection with the feline leukemia virus (FeLV) and feline immunodeficiency virus (FIV) does not appear to predispose cats to coccidioidomycosis. Traditionally, it has been considered that humans are not at risk for the disease from contact with infected cats but that they may become infected because of shared environmental exposure. A recent report described an unusual case of direct transmission of the disease from a cat to a human via a bite wound. This case represents an uncommon scenario for disease transmission. The incubation period from inhalation of the organism until respiratory signs appear is presumed to be a few weeks, as it is in dogs. Nonspecific signs of fever, anorexia, and weight loss are common. Dermatologic abnormalities, such as draining tracts and abscesses, with regional lymphadenopathy are the most common findings in infected cats. Though the lungs are often subclinically involved, overt lower respiratory signs (i.e., coughing or dyspnea) are not frequently observed. Ocular inflammation and lameness due to bone involvement have been reported. Pericardial infection was seen at necropsy in 26% of infected cats in one study, although there were no antemortem signs of heart disease. Hyperesthesia, seizures, behavior changes, and ataxia are reported but nervous system involvement appears uncommon.

Diagnosis Primary Diagnostics • Clinical Signs: Clinical signs are non-specific; however, cats from the endemic area with signs of systemic disease should be suspected of being infected.

• Cytology: This disease typically has low numbers of organisms in lesions, making cytological diagnosis a challenge. Negative findings do not rule out the disease, but visualization of organisms will confirm it. Samples may be obtained by aspiration of cutaneous nodules, lung parenchyma, or lymph nodes; performing impression smears from draining tracts; or by making slides from bronchioalveolar lavage specimens, though airway washing is considered a lowyield procedure. See Chapter 289. The associated inflammatory response is usually pyogranulomatous. Routine in-office stains will sometimes fail to stain the organism. The organism is basophilic and has a thick cell wall which shrinks during fixation, giving it a folded appearance. • Histopathology: Histological identification of organisms confirms infection. Routine hematoxylin and eosin stains may detect the organism, but special stains will sometimes be needed. GrocottGomori methenamine silver and periodic acid-Schiff (PAS) stains are often useful. The pathologist should be alerted when coccidioidomycosis is a differential diagnosis.

Secondary Diagnostics • Minimum Data Base: The minimum data base will not provide a diagnosis but is useful as a general health screen for the patient. Nonregenerative anemia and hyperproteinemia have been reported in a number of cases. • Radiography: Hilar lymphadenopathy, interstitial lung disease, and pleural disease may be present. See Figure 291-39. Hilar lymphadenopathy appears to be a useful indicator of canine disease in endemic areas, but this relationship has not been established for cats. Bone lesions are infrequent but are a mixture of osteoproductive and osteolytic lesions. • Serologic Testing: Though experience with serologic testing in cats is limited, there is increasing evidence that serology is more valuable than previously thought. Precipitin antibodies and complement-fixing antibodies were present in most infected cats tested in one study, and both persisted for a long period of time. Although further evaluation is needed to assess the usefulness of serologic testing, at present, seropositivity does seem to correlate well with the disease in cats. However, serology is a questionable tool for detecting progression of disease and response to therapy.

Diagnostic Notes • The organism is not always present in large numbers so cytological identification sometimes requires an extended microscopic search. • A thorough travel history should be obtained for any sick cat. • Culture should not be attempted in clinic. Infectious arthroconidia are easily aerosolized, placing personnel at risk. In endemic areas, a veterinary diagnostic lab should be contacted before culturing material from any draining lesion.

Treatment Primary Therapeutics

th

The Feline Patient, 4 Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.

• Azole drugs: Itraconazole and fluconazole have both been used to treat the disease. Itraconazole is safely dosed at 5 mg/kg q12h PO

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and should be given with a meal; an acid environment in the stomach enhances absorption of the drug. The capsule may be opened and the contents divided into gelatin capsules or mixed into canned food. An oral solution is available and has greater bioavailability than the capsule. Itraconazole becomes concentrated in the skin and may be especially useful for cutaneous involvement. Fluconazole has the added benefit of superior penetration into the CNS and eye and is now available in relatively inexpensive generic form. Several dosing protocols are published with a recent review article suggesting 25 to 50 mg/cat q12-24h PO. Unlike itraconazole, fluconazole does not need to be administered with food for enhanced absorption.

• Recovery confers lifelong immunity in people, but it is unknown whether recovered animals have the same ability. • Although itraconazole is usually well tolerated, serum chemistries should be periodically checked during therapy to assess for hepatotoxicity. For cats with clinical evidence of hepatotoxicity (i.e., anorexia, jaundice), the drug should be discontinued, at least temporarily. Asymptomatic cats with increased liver enzymes do not necessarily need cessation of therapy but should be closely monitored.

Prognosis The long-term prognosis for cats with coccidioidomycosis is guarded.

Secondary Therapeutics • The imidazole drugs are considered fungistatic, not fungicidal. Treatment duration should be long term (i.e., 2 months past resolution of clinical signs). • Amphotericin B is an alternative treatment if the cat does not respond to itraconazole or fluconazole. A subcutaneous protocol has become available for administration of amphotericin B; this protocol appears to significantly reduce the nephrotoxic potential of the drug. See Chapter 43 for the protocol. • At diagnosis, many cats are debilitated due to prolonged anorexia. Placement of a feeding tube permits the owner to administer proper nutritional support.

Therapeutic Notes • Relapse is fairly common following cessation of therapy, even with long-term therapy.

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Suggested Readings Gaidici A, Saubolle MA. 2009. Transmission of coccidioidomycosis to a human via a cat bite. J Clin Microbiol. 47(2):505–506. Graupmann-Kuzma A, Valentine B, Shubitz LF, et al. 2008. Coccidioidomycosis in dogs and cats: A Review. J Am Anim Hosp Assoc. 44(5):226–235. Greene RT, Troy GC. 1995. Coccidioidomycosis in 48 cats: A retrospective study (1984–1993). J Vet Intern Med. 9(2):86–91. Shubitz LF. 2007. Comparative aspects of coccidioidomycosis in animals and humans. Ann NY Acac Sci. 111(10):395–403.

CHAPTER 39

Coccidiosis Mark Robson and Mitchell A. Crystal

Overview Coccidia are obligate intracellular parasites usually found in the small intestine. There are several genera of coccidia that infect cats, most commonly Isospora (see Table 39-1; for information regarding Toxoplasma gondii, refer to Chapter 214; for information regarding Cryptosporidium spp., refer to Chapter 44). Coccidia are acquired via ingestion of monozoic cysts in intermediate host tissue or sporulated oocysts from infected feces. There is generally no extra-intestinal involvement in the cat, and transplacental and transmammary infection does not occur. Cats are the definitive host for Isospora felis and Isospora rivolta, and infection with these species rarely causes disease. Kittens younger than 1 month old, and cats that are stressed, immunosuppressed, or in crowded (e.g., catteries) or unsanitary conditions are at a higher risk of developing clinical signs. Physical examination may be normal or reveal evidence of diarrhea, hematochezia, weight loss, and dehydration. Death may occur in severely affected animals. Cats are also the definitive host for Hammondia hammondi, Besnoitia wallacei, B. darlingi, and B. oryctofelisi. Cats become infected from ingesting tissue cysts in the intermediate host, commonly rodents. Infection is generally limited to the gastrointestinal tract; however, Besnoitia may be found in extra-intestinal organs. These species are considered to be non-pathogenic. Cats are an intermediate host for Sarcocystis neurona of which the definitive host is the opossum. Infection is acquired by direct ingestion of sporocysts shed in opossum feces. S. neurona can cause a fatal encephalomyelitis in kittens, although limited studies have found serum antibodies in 5% of domestic and 13% of feral cats indicating that exposure is not uncommon. Many other Sarcocystis spp. have been identified in the intestinal tract of cats and, rarely, skeletal and cardiac muscle; however, these species appear to be non-pathogenic.

Diagnosis

Figure 39-1 Coccidiosis: The top image is an oocyst of Isospora felis. The bottom image is a sporulated oocyst. Both were found in a fecal flotation and measure approximately 40 µm longitudinally. For comparison, Toxicara cati (ascarid) eggs are about 75 µm in diameter.

Primary Diagnostics

• Histopathology and Immunohistochemistry: S. neurona schizonts and merozoites can be seen in the brain and spinal cord.

• Fecal Flotation: Oocysts are seen on microscopic examination (51% false-negatives without centrifugation, 6% false-negatives with centrifugation). See Figure 39-1.

Secondary Diagnostics

TABLE 39-1: Coccidia Found in the Cat Coccidia Organism

Intermediate Host

Besnoitia spp. Cryptosporidium spp. Hammondia hammondi Isospora felis, Isospora rivolta Sarcocystis spp. Toxoplasma gondii

Rodents, opossum, rabbits, and lizards None Goats and rodents Various mammals Cat and various mammals Various mammals

• Direct Saline Smear: Oocysts are sometimes seen on microscopic examination (95% false-negatives).

Diagnostic Notes • Oocysts found in a cat without diarrhea are most likely an incidental finding. • Oocysts in an immunocompetent cat with diarrhea may be an incidental finding or indicate other concurrent disease. • Oocysts may be shed intermittently, so multiple fecal samples are recommended in cats with diarrhea.

Treatment Primary Therapeutics

The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.

• Trimethoprim-sulfonamide: Dose at 15 to 30 mg/kg PO for cats less than 4 kg (8.8 pounds). Dose at 30 to 60 mg/kg PO for cats greater than 4 kg (8.8 pounds). Give q24h for 6 days.

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• Sulfadimethoxine: Administer 50 to 60 mg/kg PO, SC once, followed by 27.5mg/kg q24h PO for 14 to 21 days. • Ponazuril: Administer 50 mg/kg q24h PO for 1 to 5 days. Repeat in 10 days if needed. This drug is extra-label for use in cats but appears to be safe in kittens. Some authors believe it is more effective than the sulfonamides. (Add 10 mL [10g] paste to 20 mL water to make a 50-mg/mL solution.)

Secondary Therapeutics • Furazolidone: Administer 8 to 20 mg/kg q24h PO for 7 to 10 days. • Toltrazuril: Administer 15 mg/kg q24h PO for 3 to 6 days. • Nitrofurazone: Available as a 4.59% soluble powder that can be added to drinking water (up to 1g/2L) for 7 days. • Amprolium: Administer 60 to 100 mg/cat q24h PO for 7 to 12 days. • Supportive Care: Fluid, electrolyte and blood product therapy may be needed if dehydration, electrolyte derangements, or anemia from gastrointestinal hemorrhage are present. Nutritional requirements should be managed.

Therapeutic Notes • Infections are often self-limiting, and therapeutic decisions should be based on clinical signs. • Recurrent or persistent infections warrant investigation of underlying disease or re-evaluation of the environment.

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• Infections can be avoided by preventing predatory behavior, maintaining appropriate sanitation, avoiding stress/overcrowding, insect control, and cooking all meat fed to cats. • Runs, cages, and food utensils should be disinfected with 10% ammonia solution or boiling water. • Queens should preferably be treated for coccidiosis prior to parturition. • Sarcocystis-associated encephalomyelitis has only been diagnosed post-mortem; thus, treatment has never been attempted. Ponazuril has been effective in the treatment of S. encephalomyelitis in horses.

Prognosis The prognosis for coccidiosis is excellent for most infected cats. The prognosis for Sarcocystis-associated encephalomyelitis is grave.

Suggested Readings De Santis-Kerr AC, Raghavan M, Glickman NW, et al. 2006. Prevalence and risk factors for Giardia and coccidia species of pet cats in 20032004. J Fel Med Surg. 8(5):292–301. Dubey JP, Greene CE. 2006. Enteric coccidiosis. In CE Greene, ed., Infectious Diseases of the Dog and Cat, 3rd ed., pp. 775–784. St. Louis: Saunders-Elsevier. Dubey JP, Higgins RJ, Barr BC, et al. 1994. Sarcocystis-associated meningoencephalomyelitis in a cat. J Diagnos Investig. 6:118–120.

CHAPTER 40

Constipation and Obstipation Sharon Fooshee Grace and Mitchell A. Crystal

Overview Constipation is defined as infrequent or difficult evacuation of hard or dry feces. It may be acute or chronic and is characterized by excessive straining to defecate in conjunction with a reduced volume of passed feces. Obstipation represents a state of intractable constipation that results from prolonged fecal retention; it is considered more refractory to therapy than constipation. There are many causes of constipation and obstipation. See Table 40-1. Both constipation and obstipation may eventually lead to development of acquired megacolon, a condition of extreme colonic dilation with colonic muscle dysfunction. See Chapter 136. Note that owners may confuse constipation and dysuria based on positioning in the litter box. The differentials for dysuria should also be considered. See Chapter 61.

TABLE 40-1: Causes of Constipation and Obstipation Environmental

Pain induced

Extraluminal colonic obstruction

Diagnosis Primary Diagnostics • History: A detailed history should record information related to defecation habits (often out of the litter box), over-the-counter or prescription medications given, recent or past trauma, tendency to eat foreign objects, propensity to engage in fights, recent weight loss or evidence of systemic illness, and changes in appetite. • Physical Examination: Careful attention should be given to inspection of the perineal area and anal sacs, as well as an assessment of neurologic status of the lumbar and sacral spinal cord. Pain upon lifting the tail, an easily expressible bladder, and poor anal tone could point to lumbosacral neurologic disease. Dysautonomia would present with signs of diffuse autonomic dysfunction (i.e., decreased lacrimation, pupillary dilation, regurgitation or vomiting, megaesophagus, or nictitans prolapse). See Chapter 58. Megacolon can usually be detected during abdominal palpation as an enlarged, firm, feces-distended colon. • Abdominal, Pelvic, and Hind Limb Radiographs: These help to confirm constipation, to assess the severity of colonic distension, and may identify predisposing factors, such as pelvic or limb fractures, luxations, or arthritis, mass lesions, rectal foreign bodies, and spinal column abnormalities and injuries. See Figures 40-1 and 1361. Megacolon is defined as a colonic diameter equal to or greater than twice the length of the body of L7. See Figures 136-2 and 292-36. Lumbosacral radiographs (with or without an epidurogram), computerized tomography (CT), or magnetic resonance imaging (MRI) may be helpful to further define neurologic disease caused by spinal column or cord abnormalities. • Minimum Data Base (Complete Blood Count [CBC], Biochemical Profile, Urinalysis): The database can give an assessment of the overall health of the cat. The CBC may suggest inflammation or infection (e.g., anal sacculitis or abscess) and may support dehydration (elevated hematocrit). The biochemical profile may reveal abnormalities that cause impaired motility (e.g., hypokalemia, hypercalcemia, evidence of dehydration, and disorders that predispose to dehydration).

The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.

Intraluminal colonic obstruction

Neuromuscular Disease

Drugs or Medications

Metabolic and Endocrine

Lack of exercise No litter box, dirty litter box, or change of litter brand Unfamiliar environment Anorectal disease or stricture Pelvic or hind limb fractures, dislocations, arthritis, or other joint disease (i.e., torn Anterior Cruciate Ligament (ACL) and such) Perianal bite wound or abscess Rectal foreign body Neoplasia Pelvic fracture Pseudocoprostasis (i.e., extreme perineal matting of hair, usually including feces, so stool cannot pass) Atresia ani Hair, bone, plant material, or foreign body Neoplasia Perineal hernia Colonic smooth muscle disease; idiopathic megacolon Spinal cord disease: cauda equina, sacral spinal cord deformations (Manx breed), lumbosacral disease, dysautonomia, or sacral nerve disorders (i.e., tail pull injury and so on) Antacids Anticholinergics Antihistamines Barium sulfate Diuretics Narcotic analgesics Sucralfate Vincristine Dehydration Generalized muscle weakness Hypercalcemia Hypokalemia Hypothyroidism (rare) Obesity

Secondary Diagnostics • Advanced Imaging: In some cases advanced imaging (CT or MRI) of the spinal cord and vertebrae may be necessary. • Digital Rectal Examination: This can be carefully performed under general anesthesia to identify pelvic fractures, masses, perineal hernias, anal sac disease, and strictures. • Colonoscopy: Fiberoptic examination of the rectum and colon can identify polyps, masses, foreign bodies, and strictures. Colonic evacuation and preparation with oral cathartic solutions (polyethyleneglycol solutions [GoLYTELY, Colyte] at 30 mL/kg PO via orogastric or nasogastric tube 18 to 24 and 8 to 12 hours prior to colonoscopy) are needed for good visualization.

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Treatment Primary Therapeutics

(A)

• Fluid Therapy: Fluid therapy is essential to aid in softening the stool in dehydrated cats. Intravenous or subcutaneous administration is preferred to oral rehydration therapy. See Chapter 302. • Enemas: This is indicated as the initial step in the medical management of constipation/obstipation. This is best performed following fluid administration and with the cat under anesthesia. The enema should utilize 15 to 20 mL/kg of warm water without soap or other additives (to minimize mucosal irritation and damage). The volume delivered should be repeated several times to completely empty the colon. Manual evacuation via abdominal palpation and rectal digital manipulation should be performed in conjunction with enema administration for maximal colonic evacuation. A small amount of water-soluble lubrication will help in removing feces. In cats with mild constipation, dioctyl sodium sulfosuccinate enemas may be sufficient. • Prokinetics: Cisapride has proven beneficial in managing constipation in cats. It has been removed from the human market because of side effects but is still available through veterinary compounding pharmacies. For cats up to 10 pounds, the dose is 2.5 mg/cat q8h PO given 30 minutes before feeding. Cats heavier than 10 pounds may receive a dose up to 5 mg/cat q8h PO given 30 minutes before feeding. • Diet: Easily digestible, low-bulk diets are indicated. Supplementation with small amounts of fiber (e.g., psyllium [Vetasyl, Metamucil]) at 2.5–5 mL (1/2–1 teaspoons or 1.7–3.4 g) q12 to 24h PO with food or canned pumpkin at 2.5 to 5 mL (1–2 teaspoons) q12 to 24h PO with food may help soften the stool and stimulate defecation; however, diets high in fiber often create excessive fecal bulk and may complicate or worsen colonic distention. • Lactulose: This is an osmotic stool softener that may help in managing constipation when used in combination with cisapride. The dose is 0.5 to 1.0 ml/kg q8 to 12h PO.

Secondary Therapeutics • Subtotal Colectomy: This is an effective therapy for megacolon and should be recommended if obstipation has occurred more than two or three times despite medical and dietary management or if medical and dietary management are not possible See Chapters 136 and 249.

(B) Figure 40-1 A, This radiograph confirms constipation by the presence of segmented fecal balls in the colon. It also shows potential causes of pain when positioning to defecate. There is spondylosis at T12–T13, L1–L2, L2–L3, and L7–S1. B, A ventral-dorsal view of the pelvis and rear legs also reveals degenerative joint disease of both coxofemoral joints. Radiographic assessment of the knees should also occur because this is another source of pain to the defecating cat. Images courtesy of Dr. Gary D. Norsworthy.

Therapeutic Notes • Phosphate-containing enemas should not be used in cats. Severe hyperphosphatemia may lead to rapid development of severe hypocalcemia and seizures or death. • Enemas given too rapidly may cause nausea and vomiting. Cats receiving enemas for colon evacuation should be under anesthesia with a cuffed endotracheal tube in place.

Prognosis

• Total Thyroxin (TT4): Hypothyroidism is rare in the cat, but it has been associated with obstipation and megacolon.

Diagnostic Notes • Barium enemas are sometimes helpful in identifying mural/intraluminal masses, but colonoscopy is preferred over this technique because more information is typically achieved (i.e., direct visualization of the lesion, tissue biopsy collection for histopathology).

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Constipation has a better prognosis than obstipation and megacolon, though typically all can be successfully managed.

Suggested Readings Jergens AE. 2007. Constipation and obstipation. In LP Tilley, FWK Smith, Jr., eds., Blackwell’s 5-Minute Veterinary Consult. Canine and Feline, 4th ed., pp. 294–295. Ames, IA: Blackwell Publishing. Washabau RJ, Hasler AH. 1997. Constipation, obstipation, and megacolon. In JR August, ed., Consultations in Feline Internal Medicine, 3rd ed., pp. 104–112. Philadelphia: WB Saunders.

CHAPTER 41

Corneal Ulcer Gwen H. Sila and Harriet J. Davidson

Overview A corneal ulcer is defined as loss of epithelial tissue from the surface of the cornea due to instantaneous or progressive erosion and necrosis of the tissue. Any trauma to the corneal surface may result in ulceration. In a normal cat a simple superficial ulcer heals quickly. During the initial stage of healing epithelial cells spread and slide across the ulcer to rapidly cover the defect. The next stage is replication and maturation of these cells as the epithelial layers thicken to fill in the defect. Finally, the basement membrane is replaced completing the healing process. If the ulcer is deeper and the stroma is affected the ulcer will take longer to heal because the keratocytes of the stroma must replicate new collagen. Tears and epithelial cells are a significant barrier to infective organisms in a healthy eye. Whenever the corneal epithelium is disrupted the underlying stroma is at risk for infection by opportunistic bacteria. Stromal degradation may occur through enzymatic breakdown of the collagen fibers once the bacteria begin to colonize. The most common bacterial organisms resulting in infection are Staphylococcus spp., Streptococcus spp., Corynebacterium spp., and Pseudomonas spp. Corneal fungal infections are extremely uncommon in the cat. Sources of corneal trauma may be external to the cat or secondary to facial conformation or eyelid abnormalities. External injury may be as simple as a grass stem or weed whipped across the eye or severe injuries, such as a cat fight. Although the eyelid reflexes are normally quick, the cornea can be damaged. Entropion, distichia, trichiasis, and ectopic cilia are uncommon conditions in the cat, but they should be ruled out prior to treatment. Untreated chronic, irritating conditions will prevent a corneal ulcer from healing. Nasal folds and lagophthalmos (incomplete eyelid closure) with exposure keratitis are seen in certain brachycephalic breeds. These conditions more commonly result in conjunctivitis and keratitis rather than direct corneal ulceration. If the cat develops an ulcer from another cause, these concurrent conditions may slow healing and predispose to infection. Keratoconjunctivitis sicca may predispose the cornea to ulceration and prevent normal healing. These conditions need to be treated concurrently with the corneal ulcer. Feline herpesvirus-1 (FHV-1) is an extremely common ocular disease in cats. Cats are frequently exposed to the virus at birth. Although vaccination against herpesvirus is common, the vaccine does not produce sterilizing immunity. Therefore, infection and ocular disease may still occur in vaccinated cats. The virus has a propensity for the corneal epithelium but may replicate within the conjunctiva. The virus may become latent and establish itself within the trigeminal ganglia. After an initial corneal infection, nearly 80% of cats will have latent infections, with upward of 45% of those cats having reoccurrence of clinical disease. Cats can develop keratitis at anytime in their life cycle, but kittens and elderly cats are most likely to become symptomatic as they have a lower immune defense. Cats that are latently infected are prone to re-ulceration during the juvenile state at the onset of estrus and under stress. Stress of any type or systemic steroid administration can allow viral recrudescence resulting in development of clinical signs.

The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.

Diagnosis Primary Diagnostics • Clinical Appearance: Corneal ulceration usually causes blephrospasm, epiphora, and accompanying conjunctivitis. A transilluminator held close to the eye while looking across the corneal surface may help to establish the depth of the ulcer. The surrounding cornea should be evaluated for cellular infiltrate, marked edema, or collagenolysis (melting). Any of these findings suggests an infected cornea. Examine the entire eye including the lids, conjunctiva, and anterior chamber to ensure no other abnormalities or causative lesions are present. • Schirmer Tear Test: This is done prior to staining to insure normal tear production. • Fluorescein Stain: This is used to confirm the presence of an ulcer. The cornea should be evaluated after placement of the stain to access the size and depth of the ulcer. Ulcers with a dendritic pattern are considered pathognomonic for herpesvirus infection. See Figures 41-1 and 124-4. Herpesvirus should be suspected in any case of superficial ulcers or those that are recurrent in nature. • Laboratory Testing: Polymerase chain reaction (PCR), enzymelinked immunosorbent assay (ELISA), virus isolation, and so on may be helpful to confirm the diagnosis of FHV-1 infection; however, none of the current tests are sensitive or specific for predicting clinical disease. Due to the variability in testing, many veterinary ophthalmologists recommend treatment for cats suspected of having FHV-1 despite negative test results. See below.

Secondary Diagnostics • Bacterial Culture and Sensitivity: An aerobic swab should be collected for initially severe or complicated ulcers or ulcers that fail to respond to standard therapy. The sample should be collected from

Figure 41-1 Feline cornea: Note pale linear streaks on the corneal surface that are typical of feline herpesvirus lesions.

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the ulcer margin and not the conjunctiva. Care should be taken to touch only the cornea with the swab and not to rupture the eye if the ulcer is deep. • Cytology/Gram Stain: This may be used to help identify any bacteria present. • Topical Anesthetics: These can be an important aspect of the diagnostic process. However, they should not be used prior to a Schirmer Tear Test because they will alter the test results. The use of topical anesthetics can be a diagnostic tool that may provide direction on determining the etiology. Corneal pain from an external stimulus, such as a foreign body, will be greatly reduced when a topical anesthetic is applied. If the cat is significantly improved following topical anesthetic application, the eye and eyelids should be inspected for the source of corneal irritation. Corneal ulcer pain is a combination of direct simulation of the corneal nerve and the axonal reflex. Corneal nerve stimulation results in release of prostaglandins within the ciliary body. A topical anesthetic will not eliminate this intraocular inflammatory response so the eye may remain painful.

Diagnostic Notes • Prior to taking a sample for PCR testing for FHV-1 the diagnostic laboratory that will perform the test should be contacted for instructions on sample collection. A Dacron swab is usually used to sample the cornea or conjunctiva. Unvaccinated clinically normal cats may test positive for the virus and modified live FHV-1 vaccine strains can cause false-positives. Known infected cats may also test negative. • The majority of cats will have an ELISA or serum titer. A recent study found no correlation between FHV-1 disease status (i.e., acute, chronic, and asymptomatic) and magnitude of FHV-1 titer. • Sample collection is crucial to the success of virus isolation of FHV-1. The reference laboratory should be contacted prior to sample collection.

Treatment Primary Therapeutics • Ophthalmic Antibiotics: These are the most essential part of the treatment regime. If used to prevent infection, they should be administered every 6 to 8 hours. If they are being used to eliminate an infection, they should be used at a minimum of every 6 hours and may be needed as often as every 2 hours in the initial phase of treatment. Ophthalmic antibiotics include combination antibiotics (i.e., polymyxin, gramicidin, or bacitracin), tetracycline, erythromycin, gentamicin, tobramycin, ciprofloxacin, ofloxacin, and levofloxacin. Oral antibiotics do not take the place of topical medications. The use of oral antibiotics is generally only helpful if there is extensive corneal vascularization or corneal perforation. • Ophthalmic Atropine: This is used once or twice daily to control ciliary spasm due to the axonal reflex. It has the additional effect of preventing synechia (iris adhering to lens or cornea) in severe ulcers. The ointment causes less salivation than the solution because it does not travel down the tear duct and into the cat’s mouth as easily. However, in cases of imminent corneal perforation ointments should be avoided because they are toxic to the tissues within the eye. • Other Analgesics: Systemic non-steroidal anti-inflammatory medications will also aid in the reduction of pain and uveitis from the axonal reflex. Meloxicam (0.1 mg/kg q24h PO) is recommended on a short term basis (1.030 (or osmolality >1,000 mOsm/l) is regarded as an adequate renal response. If this is not achieved, DI is confirmed in the absence of any other identified cause. It is imperative that the patient is monitored closely during a water deprivation test as life-threatening dehydration may occur. • Vasopressin Response Test: The modified water deprivation test simply assesses whether vasopressin is produced or responded to in the face of challenge with dehydration.

Protocol: Vasopressin Response Test • Immediately following the water deprivation test, a vasopressin response test is performed. • Urine concentration is determined, and the bladder emptied of urine. • Aqueous vasopressin (DDAVP®, desmopressin) is given by intramuscular injection (about 0.5–1.0 µg/kg). • Urine concentration is assessed 1 to 2 hours post-injection. • Following the test, water is reintroduced gradually (in small amounts).

Interpretation • An appreciable increase in USG (>1.015) following administration of vasopressin is indicative of central DI. • Failure to concentrate suggests nephrogenic DI. • Due to the presence of partial disease or renal medullary washout, results of testing are not always straightforward to interpret. In some cases repeat DDAVP injections over 2 to 5 days may be required to achieve a good response.

Secondary Diagnostics • Gradual Water Deprivation Test: Some clinicians prefer a gradual water deprivation test in the first part of this trial with water intake being restricted from approximately 150 ml/kg down to 70 ml/kg over 2 to 3 days prior to the abrupt water deprivation. The theory of this is that severe PU/PD may cause medullary washout in the kidneys and the gradual water deprivation may reverse this, permitting appropriate responses to the abrupt water deprivation. The disadvantage is that if there is significant obligatory PU there may be significant dehydration prior to beginning the abrupt water deprivation study.

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• Therapeutic Trial: To avoid the potential hazards of a water deprivation test, or where equivocal results are obtained, a therapeutic trial may be given with vasopressin. Other diseases should again be eliminated first (limiting the diagnosis to DI or psychogenic PD) and DDAVP can then be administered for 3 to 5 days with response being carefully monitored by measuring water intake and USG. In theory this is a less satisfactory test than a water deprivation test, as nonspecific responses are possible, but in some situations this may be the most appropriate course of action, and a good response is generally good evidence of the presence of DI.

Treatment • Thiazide Diuretics: Hydrochlorothiazide or chlorothiazide can reduce the polyuria (and hence polydipsia) by as much as 30 to 50% in DI cases through reducing proximal tubular sodium and water resorption and thus reducing the volume of urine reaching the distal tubule. It is the only form of therapy suitable for nephrogenic cases. Doses of the thiazides have to be titrated to the individual, and monitoring is required to ensure hypokalemia does not develop. Initial doses of 1 to 2 mg/kg of hydrochlorothiazide q12h PO or 10 to 20 mg/kg of chlorothiazide q12h PO have been recommended. • DDAVP: DDAVP is a synthetic analogue of AVP with a longer halflife. It is available in human-licensed preparations and can be given by injection, by conjunctival drops, or orally in tablet formulation for the treatment of complete or partial central DI. DDAVP injection is usually given at a dose of 2 to 5 µg/cat q12 to 24h SC. The nasal spray (100 µg/ml) can be administered as conjunctival drops. One to four drops are given q12 to 24h. Conjunctival reaction can occur limiting

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the value of this route of administration. DDAVP is absorbed after oral administration but relatively poorly. Tablets are available and can be used successfully to treat cats at 25 to 50 µg/cat q8 to 12h PO as a suggested starting dose. This needs to be adjusted according to response, and some cats may need a higher dose. • Chlorpropamide: This drug has the ability to potentiate the effect of vasopressin in the renal tubules. It is only of value in the treatment of partial central DI, but success has been reported in at least one cat when given at 40 mg q24h PO. Care is necessary as this is a sulfonylurea and can cause hypoglycemia as well as hepatotoxicity.

Prognosis The prognosis in most cases is good as clinical signs can usually be controlled well enough to manage the condition effectively. The prognosis must be downgraded with some underlying conditions, such as pituitary neoplasia.

Suggested Readings Aroch I, Mazaki-Tovi M, Shemesh O, et al. 2005. Central diabetes insipidus in five cats: clinical presentation, diagnosis and oral desmopressin therapy. J Feline Med Surg. 7(6):333–339. Campbell FE, Bredhauer B. 2008. Trauma-induced central diabetes insipidus in a cat. Aust Vet J. 86(3):102–105. Campbell FE, Bredhauer B. 2005. Trauma-induced central diabetes insipidus in a cat. Aust Vet J. 83(12):732–735. Court MH, Watson AD. 1983. Idiopathic neurogenic diabetes insipidus in a cat. Aust Vet J. 60(8):245–247.

CHAPTER 50

Diabetes Mellitus: Chronic Complications Gary D. Norsworthy Overview Cats are relatively free of chronic complications of diabetes. Unlike dogs, they do not get diabetic cataracts and their sequela, lens-induced uveitis. They do not have peripheral vascular disease which causes necrosis and sloughing of extremities, as occurs in humans. However, three chronic complications are possible. (a) Diabetic neuropathy occurs in about 10% of diabetic cats. (b) Diabetic nephropathy occurs infrequently in diabetic cats. (c) Specific foot diseases have been reported infrequently.

Diabetic Neuropathy Overview Diabetic neuropathy is thought to be due to polyols (sorbitol and fructose) that collect excessively in Schwann cells. Several differences have been noted in the nerves of diabetic versus normal cats. In diabetic cats, the nerve water content, glucose (8-fold), and fructose (12-fold) are increased, and nerve myoinositol is decreased as compared to normal cats. The latter results in decreased nerve conduction velocity.

Diagnosis

Secondary Diagnostics • Electrodiagnostics: Electrophysiologic testing reveals motor and sensory nerve conduction changes typical of demyelination. Electromyographic testing is normal or reveals abnormalities consistent with denervation. • Histopathology: This reveals Schwann cell injury and axonal degeneration.

Treatment Primary Therapeutics • No specific therapy is known. • Good control of hyperglycemia over several weeks to months usually results in improvement or a return to a near normal state. However, not all cats respond due to permanent peripheral nerve damage.

Secondary Therapeutics • Anecdotally, the use of Vitamin B12 seems to hasten recovery. Injections of 250 µg are given q3 to 4d SC.

Primary Diagnostics • Clinical Signs: Hindlimb weakness often preventing jumping, a plantigrade posture, muscle atrophy of the hindlimb, and depressed limb reflexes and postural reaction tests. Affected cats usually walk with their hocks touching the floor. See Figure 50-1. Rarely, weakness progresses to the forelimbs.

Diagnostic Notes • The use of an oral sulfonylurea, such as glipizide or glyburide, frequently does not control hyperglycemia as well as it controls clinical signs. This will delay or prevent recovery from diabetic neuropathy.

Prognosis The prognosis for cats with diabetic neuropathy is variable. Some cats have a return to normal leg function. Others show no response even with good regulation of the diabetes.

Diabetic Nephropathy Overview

Figure 50-1 A plantigrade stance, in which the cat’s hocks touch the floor when it is walking or standing, is characteristic of diabetic neuropathy.

The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.

Diabetic nephropathy is thought to occur in diabetic cats; however, its detection is complicated by the fact that most diabetic cats are geriatric, and most geriatric cats have chronic renal deterioration. Diabetic nephropathy results in membranous glomerulonephropathy, glomerular and tubular basement membrane thickening, and an increase in mesangial matrix material, subendothelial deposits, glomerular fibrosis, and glomerulosclerosis. Some of these changes overlap with some of the changes of geriatric renal deterioration so it is difficult to attribute chronic renal failure directly to diabetes. In humans, diabetic nephropathy develops and becomes clinically significant over several decades. Diabetic cats rarely live more than 10 years after diagnosis, principally because they are typically geriatric at the time of diagnosis; therefore, the relatively shorter life span of diabetic cats may preclude sufficient time to develop, or at least recognize, diabetic nephropathy.

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Diagnosis Primary Diagnostics • Biochemical Profile and Urinalysis: Diabetic nephropathy results in azotemia then uremia. Laboratory changes are not different from those of chronic renal insufficiency and failure. Serum creatinine and blood urea nitrogen (BUN) are elevated above normal, and urine specific gravity is decreased below 1.020. Hyperphosphatemia and hypokalemia are common sequels.

Diagnostic Notes • It is not possible to distinguish diabetic nephropathy from geriatric chronic renal disease without renal biopsy, and even then there are many overlapping features that may make diagnosis unsure. Therefore, renal biopsy is not recommended.

Prognosis The prognosis for cats with diabetic nephropathy is good as long as azotemia remains controlled.

Diabetic Foot Disease Overview There are two foot diseases that occur in diabetic cats in increased frequency: overgrown toe nails and cutaneous xanthomatosis. Overgrown toe nails occur in older cats and in sick cats that do not sharpen their nails. Because diabetic cats are usually over 10 years of age and suffering the ill effects of this disease, they are predisposed to nail overgrowth. Nail trimming should be performed on an as-needed basis. Cutaneous xanthomatosis present as whitish, waxy nodules in the skin of the feet. Their association with diabetes is somewhat presumptive. They usually resolve when diabetes is controlled.

Treatment Suggested Readings Primary Therapeutics • Renal Treatment: Affected cats are treated no differently than cats in chronic renal insufficiency (Chapter 191) or chronic renal failure (Chapter 190), depending on the level of renal dysfunction. • Diabetic Regulation: Good regulation of the cat’s diabetes is very important.

Secondary Therapeutics • Hypertension Control: Systemic blood pressure should be checked. Uncontrolled hypertension can be additionally detrimental to the kidneys. See Chapter 107.

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Bagley RS, Rand J, King T, et al. 2006. The cat with generalized weakness. In J Rand, ed., Problem-Based Feline Medicine, pp. 941–975. Philadelphia: Elsevier Saunders. Nelson RW. 2005. Diabetes Mellitus. In SJ Ettinger, EC Feldman, eds., Textbook of Veterinary Internal Medicine, 6th ed., pp. 1563–1591. St. Louis: Elsevier Saunders.

CHAPTER 51

Diabetic Ketoacidosis Jacquie Rand

Overview Diabetic ketoacidosis (DKA) in its severe clinical form is a medical emergency requiring prompt treatment to correct dehydration, electrolyte disturbances, and acidosis. In its mild form, cats with DKA appear as “healthy” diabetics. DKA is the result of marked insulin deficiency, and if uncomplicated by precipitating conditions, ketonemia and ketoacidosis can occur approximately 12 and 16 days, respectively, after insulin concentrations are suppressed to fasting levels. Marked insulin suppression occurs on average four days after blood glucose concentrations reach 30 mmol/L (540 mg/dL). However, many cats with DKA appear to have other intercurrent precipitating conditions including infection, pancreatitis, or renal insufficiency. Severe lack of insulin secretion results in accelerated breakdown of fat that releases free fatty acids into the circulation. Free fatty acids are oxidized in the liver to ketones that are used by many tissues as an energy source instead of glucose. This occurs when intracellular glucose concentrations are insufficient for energy metabolism as a result of severe insulin deficiency. In the liver, when insulin is deficient, instead of conversion to triglycerides, free fatty acids are oxidized to acetoacetate, which is converted to behydroxybutyrate or acetone. Ketones are acids that cause central nervous system (CNS) depression and act in the chemoreceptor trigger zone to produce nausea, vomiting, and anorexia. They also accelerate osmotic water loss in the urine. Dehydration results from inadequate fluid intake in the face of accelerated water loss secondary to glycosuria and ketonuria. Dehydration and subsequent reduced tissue perfusion compounds the acidosis through lactic acid production. In the severe form, cats with DKA have marked dehydration, hypovolemia, metabolic acidosis, and shock. There is whole body loss of electrolytes including sodium, potassium, magnesium, and phosphate, and some of these plasma deficiencies are compounded by the intracellular redistribution of electrolytes occurring after insulin therapy. Cats with severe DKA often present recumbent and may have hyperviscosity, thromboembolism, severe metabolic acidosis, and renal failure which may result in death. Differential diagnoses are in three categories. (a) Diabetic cats with another intercurrrent condition. For example, cats with acute necrotizing pancreatitis, sepsis, and acute renal failure need to be differentiated from those with DKA uncomplicated with other life-threatening conditions. Cats with DKA which do not respond within 1 to 2 days to fluid, electrolyte and insulin therapy should be suspected of having underlying disease. Acute necrotizing pancreatitis was a frequent cause of death in one study. (b) Nonketotic hyperosmolar diabetes. These cats have extreme hyperglycemia (>600 mmo/L [10,900 mg/dl]), hyperosmolality (>350 mOsm/L), severe dehydration, and severe depression but are not ketotic or acidotic. (c) Any severe illness resulting in severe depression, recumbency, and dehydration especially if there has been preceeding polyuria, and polydipsia, for example, acute renal failure superimposed on pre-existing chronic renal failure. These cats are easily differentiated from cats with DKA on the basis of the absence of ketonuria, glucosuria, and marked hyperglycemia.

The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.

Diagnosis Primary Diagnostics • Clinical Signs: Clinical signs of polydipsia, polyuria, and weight loss for several weeks prior to presentation of an acutely ill cat. However, in some cats, owners do not report polyuria and polydipsia. Ketone odor may be evident on the breath. Cats with mild DKA may have the same preceeding history but appear bright and alert on presentation. • Biochemistry and Urinalysis: Marked hyperglycemia (usually >24 mmol/L [436 mg/dl] and often over 30 mmol/L [540 mg/dl]), glucosuria, and ketonuria. Some cats have ketonemia without significant acidosis and usually present as “healthy” diabetic cats. In cats with blood glucose around 30 mmol/L (540 mg/dL), urine ketones appear at sufficient levels to result in a positive dipstick reaction approximately 5 days after beta-hydroxybutyrate is detectable in the urine and 11 days after beta-hydroxybutyrate is above the reference range in plasma (0.5 mmol/L). This is because the predominant ketone in plasma and urine in cats is beta-hydroxybutyrate, but the urinary test sticks detect mainly acetoacetate. Dipsticks and portable meters for measuring beta-hydroxybutyrate are available and are more sensitive for detecting ketosis in cats. However cats presenting with clinical signs of DKA typically are ketonuric. • Lipemia: This is visible approximately 1 week before ketonuria is evident

Secondary Diagnostics • Other Blood Values: Initially measure packed cell volume, total protein, potassium, phosphorus, total carbon dioxide, blood urea nitrogen (BUN), creatinine, and calcium as a minimum data base for guiding treatment. Serum electrolyte concentrations, particularly potassium and phosphate, and bicarbonate must be measured on admission and at least two to three times a day in the first 1 to 2 days. Although concentrations of potassium and phosphate may be elevated or normal (or subnormal) on admission, they need to be monitored two to three times daily in the first 24 to 48 hours because plasma concentrations of these electrolytes can drop rapidly once fluid and insulin therapy is begun. • Ultrasonography: Depending on signs of other intercurrrent disease, radiography and ultrasonography or other diagnostics may be indicated, for example, to assist in identifying pancreatitis. • Urinalysis: Urine sediment should be examined for signs of infection.

Diagnostic Notes • Diagnosis is rarely a problem in the severe form of DKA. • Using a cut-point of 1.5 mmol/L for urinary ketones, the sensitivity and specificity of urine dipsticks for detecting DKA in cats were reported to be 82% and 95%, respectively; when used with a cut-point of 4 mmol/L in plasma, sensitivity/specificity were 100% and 88% for detecting DKA. • Addition of hydrogen peroxide to urine does not improve the sensitivity of urine dipsticks to detect urinary ketones.

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SECTION 1: Diseases and Conditions

Treatment Primary Therapeutics • Fluid Therapy: Fluids are essential treatment and are lifesaving. Most cats are moderately to severely dehydrated (7–12%) on initial presentation. • Fluid Type: Both 0.9% or 0.45% saline are used, although 0.9% is more common. Use of hypotonic solutions (0.45%) are advocated by some because of the hyperosmality of the plasma but are controversial. Lactated Ringer ’s solution or Normosol-R are also used as a first choice of fluid type by some. • Fluid Volume: Typically fluid deficits are corrected over 12 to 18 hours with flow rates of 60 to 150 mls/kg per 24 hours. For cats with severe signs of dehydration and poor perfusion, use doses appropriate for shock therapy; however if depression worsens, suspect cerebral edema and reduce fluid rate. Approximately one-third of sick diabetic cats in one study were hyperosmotic (>350 mOsm/kg). Although sodium is the major contributor to osmolality, and whole body hyponatremia helps to protect many DKA cats from marked hyperosmolality, the magnitude of the glucose increase is much greater than the decrease in sodium, as can be seen from the equation: Osmolality = 2 (Na + K mE/L) + 0.05 (glucose mg/dL) + 0.33 (BUN mg/dL). The normal range is from 290 to 310 mOsm/kg. • Monitoring: Diabetic cats have high continuing fluid losses until urinary glucose and ketone loss is substantially reduced; therefore, they have relatively high maintenance fluid requirements. The cat must be monitored carefully to assess adequacy of hydration and urine output; weighing the cat is an important guide for detecting over- and under-hydration during hospitalization. (Use percentage of dehydration on admission as a guide to calculating target body weight and account for 0.5 to 1% body weight loss per day associated with fasting.) • Nonketotic Hyperosmolar Diabetes: Cats with this condition should have cautious fluid replacement; replace 60 to 80% of the deficit over 24 hours and avoid decreasing serum osmolarity by more than 0.5 to 1.0 osmol/hr. • Electrolytes: Supplement fluids with potassium if it is normal or decreased. If elevated, monitor carefully and supplement as soon as in the normal range. If potassium concentrations are not available initially, supplement at 30 to 40 mmol/L; otherwise, supplement fluids using standard dosing protocols. See Chapter 114. Depending on the potassium concentration and rate at which it is falling, 40 to 80 mEq/L or more may be required. • Phosphorus: Tissue phosphorus is usually depleted and plasma levels may be normal, decreased, or increased on presentation. Hypophosphatemia results in Heinz body formation and hemolytic anemia, which may be life-threatening. Supplement phosphate as potassium phosphate, if phosphorus is normal or subnormal, and monitor serum for hemolysis. Because potassium is also depleted, one method is to divide potassium equally as potassium chloride and potassium phosphate. Alternatively correct phosphorus by adding it to calcium-free fluid and infusing at 0.01 to 0.03 mmol/L per kilogram per hour. Provide a matched blood transfusion if hemolysis is evident in the face of a decreasing packed cell volume. Excessive phosphorus supplementation can cause hypocalcemia and resultant signs. • Acidosis: Fluid expansion, provision of sodium chloride containing fluids, and insulin administration rapidly correct acidosis. Generally mild to moderately severe acidosis (HCO3 ≥ 7 mmol/L) resolves with fluid and insulin therapy, and bicarbonate administration is only recommended when HCO3 is less than 7 mmol/L. Although severe acidosis is associated with depression, decreased cardiac contractility, and peripheral vasodilatation, the disadvantages of bicarbonate therapy outweigh the advantages, including accelerated

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development of hypokalemia and hypophosphatemia. If bicarbonate is being administered, add to fluids at the rate of HCO3(mEq) = body weight (kg) × 0.4 × (12 − patient’s HCO3-) × 0.5. If the patient’s HCO3- or total CO2 concentration is unknown, use 10 for the patient’s HCO3- value in the equation. • Insulin: Insulin therapy is needed to switch off excessive ketone formation and provide insulin sensitive tissues with glucose for energy metabolism. Because insulin therapy will worsen hypokalemia and hypophosphatemia, sometimes precipitously, commence fluid and electrolyte replacement first because severe electrolyte disturbances can be fatal. Generally wait 1 to 2 hours before beginning insulin. If potassium concentration is within the normal range after 2 hours of fluid and electrolyte therapy, begin insulin. If potassium is still below 3.5 mmol/L, insulin therapy can be delayed another 1 to 2 hours, but it should commence no longer than 4 hours after initiation of fluids. The goal with insulin treatment is to stimulate glucose uptake into cells for energy metabolism, and gradually decrease blood glucose concentrations by approximately 4 mmol/L/hr (75 mg/dL per hour) until 12 to 14 mmol/L (216–250 mg/dL). Several protocols for insulin therapy are available. Most intensive-care hospitals use continuous intravenous protocols, whereas for many practitioners, intramuscular protocols may be easier to manage. Once glucose is 10 to 14 mmol/L (180–250 mg/dL) and the cat is rehydrated, swap to subcutaneous regular insulin every 6 to 8 hours or subcutaneous maintenance insulin, which is preferred (glargine, detemir or PZI; or where a legal requirement, porcine Lente insulin) or maintain on regular insulin IM (q4–6h) until eating. • Intravenous Protocol: Add 25 units of soluble (regular or crystalline insulin; do not use Lente or NPH) to a 500-ml bag of fluids. This produces a concentration of 50 mU/mL which is infused at 1 ml/kg per hour and adjusted up or down as indicated by hourly blood glucose measurements to achieve a decrease in blood glucose concentration of 2.8 to 4.2 mmol/L per hour (50–75 mg/dL per hour). Alternatively add 1.1 U/kg body weight to a 250-ml bag of saline and infuse at 10 ml/hr to provide approximately 0.05 U/ kg per 24 hours and adjust as indicated based on blood glucose concentration. Administer insulin using an infusion or syringe pump via a second infusion line attached by a Y piece to the maintenance fluid line, or alternatively, through two separate catheters, to provide both insulin and adequate fluids. Let first 50 mL run out of the line and discard because insulin binds to plastic. Infuse insulin until glucose concentration falls to 12 to 14 mmol/L (216–250 mg/dL), then halve the rate of flow or switch to regular insulin given intramuscularly every 4 to 6 hours. Alternatively, if hydration status is good, switch to regular insulin SC every 6 to 8 hours or standard maintenance insulin SC. Glucose should be added to the fluids to prevent blood glucose concentration decreasing further, while enabling insulin therapy to be maintained to reverse ketone production. Add 50% dextrose to the fluids to create a 5% dextrose solution (e.g., 100 mL of 50% dextrose in 1 liter of fluids). • Intramuscular: There are several protocols, including regular insulin every hour or 4 hours and glargine. The advantage of the 4-hour protocol is that it is less time consuming for the staff; however, glucose concentration can drop precipitously presumably due to depots of insulin that are absorbed from previously poorly perfused muscles. • Regular Insulin; Hourly Intramuscular Protocol: Give a loading dose of 0.2 U/kg followed by 0.1 U/kg hourly, and, once blood glucose is 12 to 14 mmol/L (216–250 mg/dL), change to subcutaneous insulin (either regular insulin every 6 to 8 hours or standard maintenance insulin every 12 hours). Add dextrose to the fluids to maintain blood glucose concentration in the 12 to 14 mmol/L (216–250 mg/dL) range for the first 24 hours. • Four-Hour Intramuscular Protocol: Regular insulin or glargine can be administered every 4 hours.

Diabetic Ketoacidosis

• Glargine Protocol: Glargine administered IV or IM has the same pharmacodynamic and pharmokinetic effect as regular insulin. A simple and effective protocol in cats is to initially give glargine 2 U/ cat subcutaneously and 1 U/cat intramuscularly regardless of body weight, and repeat the intramuscular dose 4 or more hours later if the blood glucose concentration is greater than 14 to 16 mmol/L (250–290 mg/dL); repeat the subcutaneous dose every 12 hours. More than half the cats are on subcutaneous insulin only by 24 hours after admission. Add glucose to the fluids once blood glucose is 12 to 14 mmol/L (216–250 mg/dL). This protocol is simple and less time-consuming and costly for the client. Most cats are eating within 1 to 2 days if there is no other intercurrent condition. Recent research demonstrated that subcutaneous glargine twice daily and a simplified regime of intramuscular regular insulin resulted in a significantly faster time to resolution of metabolic acidosis than a constant rate infusion (CRI) of regular insulin in cats with DKA. • Nonketotic Hyperosmolar Diabetes: Reverse hyperglycemia slowly (eg. 1.1 U/kg per 24 hours regular insulin) and delay insulin for 2 to 4 hours after initiation of fluid therapy. • Food: Encourage cats to eat using palatable food or force feed, preferably low carbohydrate food; however, ingestion of food is more important than the kind of food.

Therapeutic Notes • Fluids are the number one priority together with supplementation of potassium and phosphorus. Careful monitoring of electrolytes during treatment is essential. • Insulin should be given starting 1 to 2 hours (occasionally 3–4 hours if the cat is severely hypokalemic) after fluid and electrolyte therapy.

• Other intercurrent disease is often present and needs an appropriate diagnostic and management plan.

Prognosis The prognosis for recovery from DKA to discharge from tertiary referral hospitals is reported to range from 75 to 82%, and varies depending on coexisting disease. Underlying conditions, delay in seeking treatment and inability to provide intensive care may all affect survival. One study reported that cats with DKA are no less likely to achieve remission than cats without DKA. Another study reported that cats with DKA were more likely to achieve remission than to die of DKA.

Suggested Readings DiBartola S, Panciera DL. 2006. Fluid therapy in endocrine and metabolic disorders. In S DiBartola, ed., Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice, 3rd ed., pp. 478–489. Nelson R. 2005. Diabetes Mellitus. In SJ Ettinger, EC Feldman, eds., Textbook of Veterinary Internal Medicine, 6th ed., pp. 1563–1591. St. Louis, MO: Elsevier Saunders. Feldman EC, Nelson RW. 2004. Diabetic Ketoacidosis. In EC Feldman, RW Nelson, eds., Canine and Feline Endocrinology and Reproduction, 3rd ed., pp. 580–615. Philadelphia: Elsevier Saunders. Hume DZ, Drobatz KJ, Hess RS, et al. 2006. J Vet Intern Med. 20: 547–555. Koenig A, Drobatz KJ, Beale AB, et al. 2004. Hyperglycemic, hyperosmolar syndrome in feline diabetics: 17 cases (1995–2001). J Vet Emerg Med Crit Care. 14:30–40. www.uq.edu.au/ccah. Maintenance protocols for insulin administration are available.

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CHAPTER 52

Diabetes: Uncomplicated Jacquie Rand

Overview Diabetes mellitus is defined as persistent hyperglycemia, regardless of cause. In primary care practice, approximately 1 in 200 cats are diabetic, with domestic shorthair cats the most commonly affected. In the United States, Maine Coon, Domestic Longhair, Russian Blue, and Siamese are overrepresented, and Burmese cats are at increased risk in the United Kingdom and Australasia. Peak age of onset is 10 to 13 years of age, and males outnumber females by 2 : 1. Risk factors include obesity, physical inactivity, confinement indoors, and administration of glucocorticoids or progestins. Multiple etiologies cause diabetes in cats, and the relative frequency depends on whether the practice is primary care or a referral hospital. In primary care practice, 85 to 95% of diabetic cats appear to have type 2 diabetes mellitus, previously called adult-onset diabetes or noninsulin dependent diabetes. Type 2 diabetes is characterized by decreased insulin secretion, insulin resistance, and amyloid deposition in the pancreatic islets. Other specific types of diabetes account for approximately 5 to 15% of cases in primary care practice, whereas in referral practice they may account for the majority of cases. Other specific types of diabetes result from disease causing either decreased insulin secretion or impaired insulin action (insulin resistance). Acromegaly causes marked insulin resistance and appears to be the most common other specific type of diabetes in cats (approximately 25–30% in referral institutions in the United Kingdom and United States). See Chapter 3. Less common specific types of diabetes include hyperadrenocorticism, chronic end-stage pancreatitis, and pancreatic adenocarcinoma (reported to account for as many as 18% in tertiary referral practice in the United States). Regardless of the cause of diabetes, at diagnosis, endogenous insulin secretion is usually very low. This is likely the result of β cell failure from the underlying cause of the diabetes, combined with suppression of insulin secretion by glucose toxicity. Glucose toxicity is defined as suppression of insulin secretion by persistently high blood glucose greater than 24 hours duration. Insulin secretion is suppressed to minimal concentrations after 3 to 7 days of blood glucose concentrations of approximately 30 mmol/L (approximately 540 mg/dL); the severity of suppression is dose dependent. Good glycemic control is essential to reverse glucose toxicity. Suppression of insulin secretion by glucose toxicity is initially functional and reversible; however over weeks and months it causes irreversible damage to β cells and β cell loss. This largely explains why cats with poorly controlled diabetes for more than 6 months have significantly reduced probability of remission, even after good glycemic control is achieved.

Diagnosis Primary Diagnostics • Clinical Signs: Classical clinical signs are polyuria, polydipsia, and weight loss. These signs are combined, at least initially, by polyphagia; however, at diagnosis many cats have reduced appetite. Signs are

The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.

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usually present for weeks to months, but may be missed by some owners. Cats are often overweight initially, and then lose weight secondary to the disease. Muscle wasting and diffuse peripheral neuropathy are commonly reported, and result in weakness, difficulty jumping, and unsteadiness of gait. A plantigrade stance is less common, but likely indicative of more longstanding diabetes. See Chapter 50. Depression, anorexia and dehydration are present in about 50% of cats, whereas many others are otherwise healthy at initial presentation. • Laboratory Data: Persistent hyperglycemia is the hallmark of diabetes. Clinical signs are present once glucose concentrations exceed the renal threshold (14–16 mmol/L [250–290 mg/dL]). Acute stress, particularly if associated with struggling, can increase blood glucose by 10 mmol/L [180 mg/dL], but usually resolves within 3 to 4 hours. Transient illness-associated hyperglycemia may persist for several days. If blood glucose is 290 mg/dL), and more often glucose concentrations range from 7 to 12 mmol/L (126–216 mg/dL). Cats with blood glucose of ≥20 mmol/L (≥360 mg/dL) should be treated as diabetic until proven otherwise, even if the owner has not reported any signs. • Fructosamine concentration is not sufficiently sensitive for differentiating cats with stress hyperglycemia from diabetes. • Although 60 to 80% of diabetic cats are ketonemic based on betahydroxybutyrate measurements, ketonuria is present in a smaller percentage of cats. • Any diabetic cat with visible lipemia should be considered ketotic and treated with insulin because a diabetic ketoacidosis crisis can occur within days.

Diabetes: Uncomplicated

Treatment Primary Therapeutics • Cats with marked depression and dehydration, with or without ketoacidosis, should be initially treated as for cats with diabetic ketoacidosis until they are stable. See Chapter 51. • In newly diagnosed cats with type 2 diabetes and correctable causes of other specific types of diabetes, the primary goal of therapy should be diabetic remission or noninsulin dependence. The primary goal of therapy in cats with long-term diabetes (>12–24 months) and uncorrectable causes of other specific types of diabetes is control of clinical signs and avoidance of clinical hypoglycemia. • Remission is defined as euglycemia without the need for insulin or oral hypoglycemic agents. The most important positive predictive factors for remission are early institution of rigorous glycemic control (delaying diligent management of blood glucose concentration reduces the frequency of remission significantly), and prior use of glucocorticoid treatment. Negative predicative factors are the presence of neuropathy including weakness and inability to jump, and a high maximal insulin dose required to achieve glycemic control. • Insulin Therapy: The aim of insulin therapy is to obtain blood glucose concentrations that are 4 to 11 mmol/L (72–200 mg/dL) throughout the day. In newly diagnosed diabetic cats, remission rates of ≥85% can be obtained using a protocol designed for tight glycemic control using glargine or detemir, diligent monitoring and appropriate dose adjustment, and an ultra-low carbohydrate diet. Because of the short duration of lente action, there is usually no exogenous insulin action several hours before each insulin injection. Therefore, preinsulin blood glucose is typically ≥20 mmol/L (≥360 mg/dL), and the goal of achieving glucose concentrations between 4 and 11 mmol/L (72 and 200 mg/dL) is not usually achievable throughout the day, except for cats going into remission. Remission rates are typically only 25 to 30% for lente. Published remission rates for PZI are less than for determir and glargine. • There are three phases of insulin dose adjustments. Initially there is a phase of increasing dose every 5 to 7 days by (0.25) 0.5 to 1 U, depending if on a low (