Today's Veterinary Practice, January 2017

IN THIS ISSUE 26 FELINE GINGIVOSTOMATITIS 40 T REATMENT GUIDELINES FOR CHRONIC KIDNEY DISEASE 77 MANAGING CANINE DEMODICOSIS

Reviewing Dental Radiographs Findings That Indicate Healthy Teeth

JANUARY/FEBRUARY 2017 VOLUME 7, NUMBER 1

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JANUARY/FEBRUARY 2017

VOLUME 7, NUMBER 1

An official journal of the NAVC, Today’s Veterinary Practice is the trusted source for peer-reviewed clinical information in small animal veterinary medicine.

Our goal is to enhance knowledge and encourage

Editor in Chief

confidence, inspiring

Simon R. Platt

the highest quality of

BVM&S, MRCVS, DACVIM (Neurology) & DECVN University of Georgia College of Veterinary Medicine SRPlatt@NAVC.com

veterinary care. As an NAVC publication, our audience has access to world-class continuing professional

NAVC BOARD OF DIRECTORS PRESIDENT Melinda D. Merck, DVM IMMEDIATE PAST PRESIDENT

Christine Navarre, DVM, MS, DACVIM (LAIM) PRESIDENT-ELECT Gail Gibson, VMD

development developed for the global veterinary health

VICE PRESIDENT K . Leann Kuebelbeck, DVM, DACVS

care community.

TREASURER Laurel Kaddatz, DVM DIRECTORS Paige Allen, MS, RVT

An official journal of the

Better care through knowledge

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Harold Davis, Jr, BA, RVT, VTS (Emergency & Critical Care) (Anesthesia & Analgesia)

Chief Executive Officer, NAVC

Cheryl Good, DVM

Thomas M. Bohn, MBA, CAE

Sally Haddock, DVM

TBohn@NAVC.com

Bob Lester, DVM

12/14/16 5:30 PM

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12/14/16 5:34 PM

JANUARY/FEBRUARY 2017

VOLUME 7, NUMBER 1

EDITORIAL ADVISORY BOARD SENIOR VICE PRESIDENT OF SALES & PUBLISHING

P. Jane Armstrong

Laura C.S. Walker

LWalker@NAVC.com

DVM, MS, MBA, DACVIM (SAIM) University of Minnesota College of Veterinary Medicine

PUBLISHER

Nick Paolo, MS, MBA NPaolo@NAVC.com

EXECUTIVE EDITOR

Robin Henry

RHenry@NAVC.com

Mark Cofone

EDITORIAL DIRECTOR

VMD, DACVS Veterinary Specialty Center Wilmington, Delaware

Kelly Soldavin

KSoldavin@NAVC.com DIRECTOR OF SALES

Renee Luttrell

610.558.1819 • RLuttrell@NAVC.com DIRECTOR OF AUDIENCE DEVELOPMENT

Sheila Grosdidier

SReynolds@NAVC.com

RVT, PHR Veterinary Management Consultation Evergreen, Colorado

Sondra Reynolds

SENIOR ART DIRECTOR

Michelle Taylor

MTaylor@NAVC.com ART DIRECTOR

David Beagin

Garret Pachtinger

ASSISTANT EDITOR

VMD, DACVECC Veterinary Specialty & Emergency Center Levittown, Pennsylvania

DBeagin@NAVC.com

Julie Butler

STAFF WRITER

Megan Cox

STAFF EDITORS

Maureen McKinney; Suzanne B. Meyers; Jennifer DiSanto; Lisa Wirth, VMD

Michael Schaer DVM, DACVIM, DACVECC University of Florida College of Veterinary Medicine

GRAPHIC DESIGNER

Courtney Ballauer

WARRANTIES, LIMITATIONS. Except as expressly set forth herein, Eastern States Veterinary Association, Inc (NAVC) makes no warranties whatsoever, express, implied, or statutory. NAVC specifically disclaims any implied warranty of merchantability or fitness for a particular purpose. In no event will NAVC be liable to you or any third party for any indirect, punitive, special, incidental, or consequential damages (including loss of profits, use, data, or other economic advantage), however it arises, even if NAVC has previously been advised of the possibility of such damage. All rights reserved. No part of this publication may be reproduced in any form without written permission from the publisher. Entire contents ©2017 Eastern States Veterinary Association, Inc (NAVC).

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Change Name/Address or Cancel. Please use online form at tvpjournal.com or contact us by phone, fax, or email subscriptions@CDS1976.com.

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*Qualifying Subscribers: Veterinarians, members of the veterinary health care team, veterinary school faculty, veterinary students, and other professionals allied to the field.

Eastern States Veterinary Association, Inc (NAVC) reserves the right to determine eligibility for a free subscription.

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12/16/16 1:30 PM

FEATURES 26 RACE-APPROVED CE CREDIT ARTICLE

Chronic Feline Gingivostomatitis: Proven Therapeutic Approaches & New Treatment Options Barden Greenfield, DVM, DAVDC, FAVD Chronic gingivostomatitis (CGS) in the cat is a very painful disease, characterized by severe inflammation of the gingiva, buccal mucosa, and caudal oral mucosa. This article reviews clinical signs of CGS, current treatment modalities, and promising treatment options that may be available soon.

RACE-APPROVED CE CREDIT ARTICLE

40

Treatment Guidelines for Chronic Kidney Disease in Dogs & Cats: International Renal Interest Society Recommendations Gregory F. Grauer, DVM, MS, DACVIM The International Renal Interest Society (IRIS) was created to advance the scientific understanding of kidney disease in small animals and to help practitioners better diagnose, understand, and treat canine and feline renal disease. This article discusses the latest IRIS guidelines on treatment of chronic kidney disease.

IN THIS ISSUE 26 FELINE GINGIVOSTOMATITIS 40 TREATMENT GUIDELINES FOR CHRONIC KIDNEY DISEASE 77 MANAGING CANINE DEMODICOSIS

February is National Pet Dental Health Month

Reviewing Dental Radiographs Findings That Indicate Healthy Teeth

JANUARY/FEBRUARY 2017 VOLUME 7, NUMBER 1

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10 14 16

6 TVP-0102_Contents.indd 6

ON OUR COVER

Dental health is a key component of overall pet health, and dental problems can cause, or be caused by, other health problems. A pet’s teeth and gums should be examined and radiographed at least annually to assess for early signs of disease. The American Veterinary Medical Association (AVMA) reports that 80% of dogs and 70% of cats have some kind of oral disease by the age of 3. Read more at avma.org.

Cover photo courtesy of Shutterstock.com/rawpixel.com

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ADVERTISER INDEX NAVC PERSPECTIVES TODAY’S VETERINARY NEWS

TABLE OF CONTENTS

To read this issue online, visit tvpjournal.com

12/14/16 6:15 PM

AMOXICILLIN TRIHYDRATE AND CLAVULANATE POTASSIUM TABLETS DOGS: Indicated in the treatment of periodontal and skin and soft tissue infections such as wounds, abscesses, cellulitis, and superficial/juvenile and deep pyoderma due to susceptible strains of bacteria.

CATS: Indicated in the treatment of urinary tract infections (cystitis) and skin and soft tissue infections such as wounds, abscesses, and cellulitis/dermatitis due to susceptible strains of bacteria.

Backed by the newly combined Veterinary Technical Services and Sales Support Teams of both Dechra and Putney.

Available in 62.5 mg, 125 mg, 250 mg, and 375 mg tablets supplied in foil strip packs. Each carton holds 15 foil strip packs with 14 tablets per strip (210 tablets per carton).

PUTNEY IS NOW PART OF DECHRA VETERINARY PRODUCTS

Ask your Dechra or distributor representative for further information or visit www.dechra-us.com.

As with all drugs, side effects may occur. Amoxicillin Trihydrate and Clavulanate Potassium Tablets contain a semisynthetic penicillin (amoxicillin) and have the potential for producing allergic reactions. This product should not be used in animals with a history of an allergic reaction to any of the penicillins or cephalosporins. If an allergic reaction occurs, administer epinephrine and/or steroids. Refer to the prescribing information for complete details or visit www.dechra-us.com.

To order, please contact your Dechra or distributor representative or call (866) 683-0660.

24-hour Technical Support available (866) 933-2472.

Nonurgent Technical Support available via email support@dechra.com.

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Dechra Veterinary Products US and the Dechra D logo are registered trademarks of Dechra Pharmaceuticals PLC.

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COLUMNS 12 EDITOR’S NOTE

One Health—How Does It Help Veterinary Medicine?

Simon R. Platt, BVM&S, MRCVS, DACVIM (Neurology) & DECVN

55

RACE-APPROVED CE CREDIT ARTICLE

IMAGING ESSENTIALS

95

Interpretation of Dental Radiographs in Dogs & Cats

ASPCA PRACTICAL TOXICOLOGY

The Decontamination Dilemma: Bromethalin Ingestion Renee Tourdot, DVM

Santiago Peralta, DVM, DAVDC, and Nadine Fiani, BVSc, DAVDC

69

ACVN NUTRITION NOTES

103

Understanding Types of Fiber & Clinical Uses

CLINICAL INSIGHTS

A Cancer Diagnosis Is Not a Death Sentence Sue Ettinger, DVM, DACVIM (Oncology)

Deborah E. Linder, DVM, MS, DACVN

77

DERMATOLOGY DETAILS

109

Updates on the Management of Canine Demodicosis

NAVC KEYNOTE COMMENTARY

A Regulatory Road Map for Telehealth & Pet Health Care Mark Cushing, JD

Sandra N. Koch, DVM, MS, DACVD

87

AHS HEARTWORM HOTLINE

114

Heartworm Disease: The Science, the Practice, the Future

HOW I TREAT

Otitis Media/Interna An Interview with Dr. Lori Thompson

Clarke Atkins, DVM, DACVIM (SAIM & Cardiology)

22 PET HEALTH BY THE NUMBERS

Canine Periodontal Disease Featuring AVDC Periodontal Stages Copyright AVDC, used with permission.

Today’s Veterinary Practice does not, by publication of ads, express endorsement or verify the accuracy and effectiveness of the products and claims contained therein. The publisher, Eastern States Veterinary Association, Inc (NAVC), disclaims any liability for any damages resulting from the use of any product advertised herein and suggests that readers fully investigate the products and claims prior to purchasing. The opinions stated in this publication are those of the respective authors and do not necessarily represent the opinions of the NAVC nor its Editorial Advisory Board. NAVC does not guarantee nor make any other representation that the material contained in articles herein is valid, reliable, or accurate; nor does the NAVC assume any responsibility for injury or death arising from any use, or misuse, of same. There is no implication that the material published herein represents the best or only procedure for a particular condition. It is the responsibility of the reader to verify the accuracy and applicability of any information presented and to adapt as new data becomes publicly available.

Today’s Veterinary Practice (ISSN 2162-3872 print and ISSN 2162-3929 online) is published bi-monthly (Jan/Feb, Mar/Apr, May/June, Jul/Aug, Sept/ Oct, Nov/Dec; 6x per year) by North American Veterinary Conference, 37 Paul Lane, Glen Mills, PA 19342. Periodicals postage paid at Glen Mills, PA 19342 and additional mailing offices. POSTMASTER: Send all UAA to CFS (See DMM 507.1.5.2); NON-POSTAL AND MILITARY FACILITIES: send address corrections to CDS/Today’s Veterinary Practice, 440 Quadrangle Drive, Ste E, Bolingbrook, IL 60440.

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TABLE OF CONTENTS

To read this issue online, visit tvpjournal.com

12/16/16 1:36 PM

YOU’VE GOT HER BACK. VETMEDIN® HAS HER HEART.

No other canine CHF drug offers the same level of research and support as Boehringer Ingelheim Vetmedica, Inc. Industry-trusted VETMEDIN gives dogs with congestive heart failure (CHF) better days and longer lives.1 It’s backed by years of groundbreaking canine cardiology research.

And only VETMEDIN offers free tools that educate your clients to recognize the signs of CHF faster—which can lead to treatment sooner. Contact your Boehringer Ingelheim Vetmedica, Inc. representative today for a heart to heart about VETMEDIN. Reference: 1. Lombard CW, Jöns O, Bussadori CM; for the VetSCOPE Study. Clinical efficacy of pimobendan versus benazepril for the treatment of acquired atrioventricular valvular disease in dogs. J Am Anim Hosp Assoc. 2006;42(4):249–261.

IMPORTANT SAFETY INFORMATION: Use only in dogs with clinical evidence of heart failure. The safety of VETMEDIN has not been established in dogs with asymptomatic heart disease or in heart failure caused by etiologies other than atrioventricular valvular insufficiency or dilated cardiomyopathy. Please refer to the package insert for complete product information or visit www.vetmedin.com.

VETMEDIN is a registered trademark of Boehringer Ingelheim Vetmedica GmbH, licensed to Boehringer Ingelheim Vetmedica, Inc. © 2016 Boehringer Ingelheim Vetmedica, Inc. VET0515009

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Amoxicillin Trihydrate and Clavulanate Potassium Tablets ANADA 200-592, Approved by FDA CAUTION: Federal (USA) law restricts this drug to use by or on the order of a licensed veterinarian.

INDICATIONS: Amoxicillin Trihydrate and Clavulanate Potassium Tablets are indicated in the treatment of: Dogs: Skin and soft tissue infections such as wounds, abscesses, cellulitis, superficial/juvenile and deep pyoderma due to susceptible strains of the following organisms: β-lactamase-producing Staphylococcus aureus, non-β-lactamaseproducing Staphylococcus aureus, Staphylococcus spp., Streptococcus spp., and E. coli.

Periodontal infections due to susceptible strains of both aerobic and anaerobic bacteria. Amoxicillin Trihydrate and Clavulanate Potassium Tablets have been shown to be clinically effective for treating cases of canine periodontal disease.

Cats: Skin and soft tissue infections such as wounds, abscesses, and cellulitis/dermatitis due to susceptible strains of the following organisms: β-lactamase-producing Staphylococcus aureus, non-β-lactamase-producing Staphylococcus aureus, Staphylococcus spp., Streptococcus spp., E. coli, and Pasteurella spp.

Urinary tract infections (cystitis) due to susceptible strains of E. coli.

Therapy may be initiated with Amoxicillin Trihydrate and Clavulanate Potassium Tablets prior to obtaining results from bacteriological and susceptibility studies.

A culture should be obtained prior to treatment to determine susceptibility of the organisms to Amoxicillin Trihydrate and Clavulanate Potassium Tablets. Following determination of susceptibility results and clinical response to medication, therapy may be reevaluated.

CONTRAINDICATIONS: The use of this product is contraindicated in animals with a history of an allergic reaction to any of the penicillins or cephalosporins.

WARNINGS: Safety of use in pregnant or breeding animals has not been determined.

ADVERSE REACTIONS: Amoxicillin Trihydrate and Clavulanate Potassium Tablets contain a semisynthetic penicillin (amoxicillin) and have the potential for producing allergic reactions. If an allergic reaction occurs, administer epinephrine and/or steroids.

ADVERTISER INDEX

Recombitek 4 Lepto Vaccines . . . . . 23

Advanced Veterinary Ultrasound Veterinary Ultrasound . . . . . . . . . . . . . . . 13 advancedveterinaryultrasound.com

ACVIM ACVIM Conference . . . . . . . . . . . . . . . . . . 53 acvim.org

Antech Diagnostics Lab Diagnostics . . . . . . . . . . . . . . . . . . . . . 99

merial.com

Midmark VetPro Dental Solutions . . . . . . . . . . . . 63 midmarkanimalhealth.com

NAVC NAVC Conference 2017 . . . . . . . . . . . . . . 19 navc.com/conference

antechdiagnostics.com

NAVC Discovery 2017 . . . . . . . . . . . . . . . 20

Blue Buffalo Natural Veterinary Diet . . . . . . . . . . . . . 68

navc.com

NAVC Institute 2017 . . . . . . . . . . . . . . . . . 39

truebluevets.com

navc.com/institute

Boehringer Ingelheim Vetmedin . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9, 11

Veterinary Innovation Summit . . . . . . 64 navc.com

boehringer-ingelheim.com

NAVC Live . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 91

Care Credit Financing . . . . . . . . . . . . . . . . . . . . . . . . . . . . 102

navc.com/live

carecredit.com

New Product Gallery . . . . . . . . . . . . . . . . 101 navc.com/conference

Ceva Animal Health DOUXO . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3

NAVC Bookstore . . . . . . . . . . . . . . . . . . . . 108

ceva.us

bookstore.navc.com

Vectra 3D . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15 ceva.us

Dechra Amoxicillin Trihydrate and Clavulanate Potassium Tablets . . 7, 10 dechra-us.com

Nutramax Laboratories Products . . . . . . . . . . . . inside front cover nutramaxlabs.com

Patterson Veterinary Sirona Schick . . . . . . . . . . . . . . . . . . . . . . . . . 54 schickbysirona.com

Elanco Interceptor Plus . . . . . . . . . . . . . bellyband elanco.com

PNC Financial Services Financing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 25 pnc.com

Trifexis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 86, 84 elanco.com

Idexx Laboratories SDMA Test . . . . . . . . . . . . . . . . . . . . . . . . insert idexx.com/sdma

Protege Biomedical ClotIt VET . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18 clotitvet.com

SCIL Vet Diagnostics Blood Chemistry Analyzer . . . . . . . . . 67 scilvet.us

SDMA Test . . . . . . . . . . . . . . . . . . . . . . . . 112-113 idexx.com/sdma

Kane Biotech Inc STRIX NB . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 66 strixnb.com

Masterfoods USA Royal Canin . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17 royalcanin.com

Merck Bravecto . . . . . . . . . . . . . . . . . . . . . . . . . . 75, 76

TriLogic Pharma Clindoral . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 35 trilogicpharma.com

Vetoquinol Family of Products . . . . . . . . . . . . . . . . . . . . 5 vetoquinolusa.com

Virbac Sentinel Spectrum . . . . . . . . . . . . . . . 21, 20 virbacvet.com

bravectovets.com

Manufactured for: Putney, Inc., a wholly owned subsidiary of Dechra Pharmaceuticals, PLC. Portland, ME 04101 USA 1-866-683-0660 Made in Austria.

Rebound . . . . . . . . . . . . inside back cover virbacpets.com

The Merck Veterinary Manual . . . . . . . 85 merckvetmanual.com

Merial NexGard . . . . . . . . . . . . . . . . . . . . . . . . . . 93, 94 nexgardfordogs.com

Oravet . . . . . . . . . . . . . . . . . . . . . . . back cover

Virox Technologies Disinfectants . . . . . . . . . . . . . . . . . . . . . . . . . 37 virox.com

Zoetis Simparica . . . . . . . . . . . . . . . . . . . . . . . . . 49, 51

oravet.com

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simparica.com

AD INDEX

12/16/16 1:39 PM

090340591/0 NADA 141-273, Approved by FDA

Vetmedin® (pimobendan) Chewable Tablets

Cardiac drug for oral use in dogs only Caution: Federal law restricts this drug to use by or on the order of a licensed veterinarian.

Description: Vetmedin (pimobendan) is supplied as oblong half-scored chewable tablets containing 1.25, 2.5, 5 or 10 mg pimobendan per tablet. Pimobendan, a benzimidazole-pyridazinone derivative, is a non-sympathomimetic, non-glycoside inotropic drug with vasodilatative properties. Pimobendan exerts a stimulatory myocardial effect by a dual mechanism of action consisting of an increase in calcium sensitivity of cardiac myofilaments and inhibition of phosphodiesterase (Type III). Pimobendan exhibits vasodilating activity by inhibiting phosphodiesterase III activity. The chemical name of pimobendan is 4,5-dihydro-6-[2-(4-methoxyphenyl)-1H-benzimidazole5-yl]-5-methyl-3(2H)-pyridazinone. The structural formula of pimobendan is:

Indications: Vetmedin (pimobendan) is indicated for the management of the signs of mild, moderate, or severe (modified NYHA Class IIa, IIIb, or IVc) congestive heart failure in dogs due to atrioventricular valvular insufficiency (AVVI) or dilated cardiomyopathy (DCM).

Vetmedin is indicated for use with concurrent therapy for congestive heart failure (e.g., furosemide, etc.) as appropriate on a case-by-case basis. a

A dog with modified New York Heart Association (NYHA) Class II heart failure has fatigue, shortness of breath, coughing, etc. apparent when ordinary exercise is exceeded.

b

A dog with modified NYHA Class III heart failure is comfortable at rest, but exercise capacity is minimal.

c

A dog with modified NYHA Class IV heart failure has no capacity for exercise and disabling clinical signs are present even at rest.

Dosage and Administration: Vetmedin should be administered orally at a total daily dose of 0.23 mg/lb (0.5 mg/kg) body weight, using a suitable combination of whole or half tablets. The total daily dose should be divided into 2 portions that are not necessarily equal, and the portions should be administered approximately 12 hours apart (i.e., morning and evening). The tablets are scored and the calculated dosage should be provided to the nearest half tablet increment.

Contraindications: Vetmedin should not be given in cases of hypertrophic cardiomyopathy, aortic stenosis, or any other clinical condition where an augmentation of cardiac output is inappropriate for functional or anatomical reasons.

Warnings: Only for use in dogs with clinical evidence of heart failure. At 3 and 5 times the recommended dosage, administered over a 6-month period of time, pimobendan caused an exaggerated hemodynamic response in the normal dog heart, which was associated with cardiac pathology (See Animal Safety).

Human Warnings: Not for use in humans. Keep this and all medications out of reach of children. Consult a physician in case of accidental ingestion by humans.

Precautions: The safety of Vetmedin has not been established in dogs with asymptomatic heart disease or in heart failure caused by etiologies other than AVVI or DCM. The safe use of Vetmedin has not been evaluated in dogs younger than 6 months of age, dogs with congenital heart defects, dogs with diabetes mellitus or other serious metabolic diseases, dogs used for breeding, or pregnant or lactating bitches.

Adverse Reactions: Clinical findings/adverse reactions were recorded in a 56-day field study of dogs with congestive heart failure (CHF) due to AVVI (256 dogs) or DCM (99 dogs). Dogs were treated with either Vetmedin (175 dogs) or the active control enalapril maleate (180 dogs). Dogs in both treatment groups received additional background cardiac therapy (See Effectiveness for details and the difference in digoxin administration between treatment groups).

The Vetmedin group had the following prevalence (percent of dogs with at least one occurrence) of common adverse reactions/new clinical findings (not present in a dog prior to beginning study treatments): poor appetite (38%), lethargy (33%), diarrhea (30%), dyspnea (29%), azotemia (14%), weakness and ataxia (13%), pleural effusion (10%), syncope (9%), cough

TVP-0102_Contents.indd 11

of pimobendan and active metabolite and the maximum physiologic response (peak LV dP/dtmax). Blood levels of pimobendan and active metabolite began to drop before maximum contractility was seen. Repeated oral administration of pimobendan did not result in evidence of tachyphylaxis (decreased positive inotropic effect) or Adverse reactions/new clinical findings were seen in drug accumulation (increased positive inotropic effect). both treatment groups and were potentially related to CHF, the therapy of CHF, or both. The following adverse Laboratory studies indicate that the positive inotropic effect of pimobendan may be attenuated by the reactions/new clinical findings are listed according to concurrent use of a β-adrenergic blocker or a calcium body system and are not in order of prevalence: CHF channel blocker. death, sudden death, chordae tendineae rupture, left atrial tear, arrhythmias overall, tachycardia, syncope, Effectiveness: In a double-masked, multi-site, 56-day weak pulses, irregular pulses, increased pulmonary field study, 355 dogs with modified NYHA Class II, III, or edema, dyspnea, increased respiratory rate, coughing, IV CHF due to AVVI or DCM were randomly assigned gagging, pleural effusion, ascites, hepatic congestion, to either the active control (enalapril maleate) or the decreased appetite, vomiting, diarrhea, melena, weight Vetmedin (pimobendan) treatment group. Of the 355 loss, lethargy, depression, weakness, collapse, shaking, dogs, 52% were male and 48% were female; 72% were trembling, ataxia, seizures, restlessness, agitation, diagnosed with AVVI and 28% were diagnosed with pruritus, increased water consumption, increased DCM; 34% had Class II, 47% had Class III, and 19% urination, urinary accidents, azotemia, dehydration, had Class IV CHF. Dogs ranged in age and weight abnormal serum electrolyte, protein, and glucose from 1 to 17 years and 3.3 to 191 lb, respectively. The values, mild increases in serum hepatic enzyme levels, most common breeds were mixed breed, Doberman and mildly decreased platelet counts.

Pinscher, Cocker Spaniel, Miniature/Toy Poodle, See Table 1 for mortality due to CHF (including Maltese, Chihuahua, Miniature Schnauzer, Dachshund, euthanasia, natural death, and sudden death) and for and Cavalier King Charles Spaniel. The 180 dogs (130 the development of new arrhythmias (not present in a AVVI, 50 DCM) in the active control group received dog prior to beginning study treatments) by treatment enalapril maleate (0.5 mg/kg once or twice daily), and group and type of heart disease (AVVI or DCM) in the all but 2 received furosemide. Per protocol, all dogs 56-day field study. with DCM in the active control group received digoxin.

The 175 dogs (126 AVVI, 49 DCM) in the Vetmedin Table 1: CHF Death and New Arrhythmias group received pimobendan (0.5 mg/kg/day divided in the 56-Day Field Study into 2 portions that were not necessarily equal, and the Vetmedin® Active Control portions were administered approximately 12 hours Group Group apart), and all but 4 received furosemide. Digoxin was Dogs that 14.3% 14.4% optional for treating supraventricular tachyarrhythmia died n = 175 n = 180 in either treatment group, as was the addition of a due to CHF β-adrenergic blocker if digoxin was ineffective in 9 of 126 dogs 16 of 130 dogs controlling heart rate. After initial treatment at the clinic with AVVI with AVVI on Day 1, dog owners were to administer the assigned 16 of 49 dogs 10 of 50 dogs product and concurrent medications for up to 56±4 days. with DCM with DCM The determination of effectiveness (treatment success) Dogs that 39.4% 45.0% for each case was based on improvement in at developed n = 175 n = 180 least 2 of the 3 following primary variables: modified new 59 of 130 dogs NYHA classification, pulmonary edema score by a arrhythmiasa 45 of 126 dogs with AVVI with AVVI masked veterinary radiologist, and the investigator’s overall clinical effectiveness score (based on physical 24 of 49 dogs 22 of 50 dogs examination, radiography, electrocardiography, and with DCM with DCM clinical pathology). Attitude, pleural effusion, coughing, a New arrhythmias included supraventricular premature activity level, furosemide dosage change, cardiac beats and tachycardia, atrial fibrillation, atrioventricular size, body weight, survival, and owner observations were secondary evaluations contributing information block, sinus bradycardia, ventricular premature beats supportive to product effectiveness and safety. and tachycardia, and bundle branch block Based on protocol compliance and individual case Following the 56-day masked field study, 137 dogs integrity, 265 cases (134 Vetmedin, 131 active control) in the Vetmedin group were allowed to continue on were evaluated for treatment success on Day 29. See Vetmedin in an open-label extended-use study without Table 2 for effectiveness results. restrictions on concurrent therapy. The adverse reactions/new clinical findings in the extended-use Table 2: Effectiveness Results study were consistent with those reported in the 56-day for the 56-Day Field Study study, with the following exception: One dog in the Vetmedin® Active Control extended-use study developed acute cholestatic liver Group Group failure after 140 days on Vetmedin and furosemide.

Treatment 80.7% 76.3% In foreign post-approval drug experience reporting, the Success on n=134 n=131 following additional suspected adverse reactions were Day 29 88 of 101 dogs 77 of 100 dogs reported in dogs treated with a capsule formulation with AVVI with AVVI of pimobendan: hemorrhage, petechia, anemia, hyperactivity, excited behavior, erythema, rash, 20 of 33 dogs 23 of 31 dogs drooling, constipation, and diabetes mellitus. with DCM with DCM To report suspected adverse reactions, to obtain a Treatment 71.1% 67.2% Material Safety Data Sheet, or for technical assistance Success on n=113 n=110 call 1-866-638-2226.

Day 56 66 of 85 dogs 56 of 85 dogs Clinical Pharmacology: Pimobendan is oxidatively with AVVI with AVVI demethylated to a pharmacologically active metabolite 13 of 28 dogs 17 of 25 dogs which is then conjugated with sulfate or glucuronic with DCM with DCM acid and excreted mainly via feces. The mean extent of protein binding of pimobendan and the active No increase metabolite in dog plasma is >90%. Following a single in furosemide 78.3% 68.6% oral administration of 0.25 mg/kg Vetmedin tablets dose between n=130 n=126 the maximal mean (± 1 SD) plasma concentrations Day 1 and (Cmax) of pimobendan and the active metabolite were Day 29 3.09 (0.76) ng/ml and 3.66 (1.21) ng/ml, respectively.

Individual dog Cmax values for pimobendan and the At the end of the 56-day study, dogs in the Vetmedin active metabolite were observed 1 to 4 hours postgroup were enrolled in an unmasked field study to dose (mean: 2 and 3 hours, respectively). The total monitor safety under extended use, without restrictions body clearance of pimobendan was approximately on concurrent medications.

90 mL/min/kg, and the terminal elimination half-lives Vetmedin was used safely in dogs concurrently of pimobendan and the active metabolite were receiving furosemide, digoxin, enalapril, atenolol, approximately 0.5 hours and 2 hours, respectively. spironolactone, nitroglycerin, hydralazine, diltiazem, Plasma levels of pimobendan and active metabolite antiparasitic products (including heartworm were below quantifiable levels by 4 and 8 hours after prevention), antibiotics (metronidazole, cephalexin, oral administration, respectively. The steady-state amoxicillin-clavulanate, fluoroquinolones), topical volume of distribution of pimobendan is 2.6 L/kg ophthalmic and otic products, famotidine, theophylline, indicating that the drug is readily distributed into levothyroxine sodium, diphenhydramine, hydrocodone, tissues. Food decreased the bioavailability of an aqueous solution of pimobendan, but the effect of food metoclopramide, and butorphanol, and in dogs on on the absorption of pimobendan from Vetmedin tablets sodium-restricted diets. is unknown.

Palatability: In a laboratory study, the palatability of Vetmedin was evaluated in 20 adult female Beagle In normal dogs instrumented with left ventricular (LV) dogs offered doses twice daily for 14 days. Ninety pressure transducers, pimobendan increased LV dP/ percent (18 of 20 dogs) voluntarily consumed more dtmax (a measure of contractility of the heart) in a than 70% of the 28 tablets offered. Including two dogs dose dependent manner between 0.1 and 0.5 mg/ that consumed only 4 and 7% of the tablets offered, the kg orally. The effect was still present 8 hours after average voluntary consumption was 84.2%. dosing. There was a delay between peak blood levels

(7%), sudden death (6%), ascites (6%), and heart murmur (3%). Prevalence was similar in the active control group. The prevalence of renal failure was higher in the active control group (4%) compared to the Vetmedin group (1%).

Animal Safety: In a laboratory study, Vetmedin chewable tablets were administered to 6 healthy Beagles per treatment group at 0 (control), 1, 3, and 5 times the recommended dosage for 6 months. See Table 3 for cardiac pathology results. The cardiac pathology/histopathology noted in the 3X and 5X dose groups is typical of positive inotropic and vasodilator drug toxicity in normal dog hearts, and is associated with exaggerated hemodynamic responses to these drugs. None of the dogs developed signs of heart failure and there was no mortality.

Table 3: Incidence of Cardiac Pathology/ Histopathology in the Six-month Safety Study Severe left ventricular hypertrophy with multifocal subendocardial ischemic lesions

One 3X and two 5X dogsa

Moderate to marked myxomatous thickening of the mitral valves

Three 5X dogs

Myxomatous thickening of the chordae tendineae

One 3X and two 5X dogs

Endocardial thickening of the left ventricular outflow tract

One 1X, two 3X, and two 5X dogs

Left atrial endocardial thickening (jet lesions) in 2 of the dogs that developed murmurs of mitral valve insufficiency

One 3X and one 5X dog

Granulomatous inflammatory lesion in the right atrial myocardium

One 3X dog

Most of the gross and histopathologic findings occurred in these three dogs

a

Murmurs of mitral valve insufficiency were detected in one 3X (Day 65) and two 5X dogs (Days 135 and 163).

These murmurs (grades II-III of VI) were not associated with clinical signs.

Indirect blood pressure was unaffected by Vetmedin at the label dose (1X). Mean diastolic blood pressure was decreased in the 3X group (74 mmHg) compared to the control group (82 mmHg). Mean systolic blood pressure was decreased in the 5X group (117 mmHg) compared to the control group (124 mmHg). None of the dogs had clinical signs of hypotension.

On 24-hour Holter monitoring, mean heart rate was increased in the 5X group (101 beats/min) compared to the control group (94 beats/min). Not counting escape beats, the 3X and 5X groups had slightly higher numbers of isolated ventricular ectopic complexes (VEs). The maximum number of non-escape VEs recorded either at baseline or in a control group dog was 4 VEs/24 hours. At either Week 4 or Week 20, three 3X group dogs had maximums of 33, 13, and 10 VEs/24 hours, and two 5X group dogs had maximums of 22 and 9 VEs/24 hours. One 1X group dog with no VEs at baseline had 6 VEs/24 hours at Week 4 and again at Week 20. Second-degree atrioventricular heart block was recorded in one 3X group dog at Weeks 4 and 20, and in one dog from each of the 1X and 5X groups at Week 20. None of the dogs had clinical signs associated with these electrocardiogram changes.

Treatment was associated with small differences in mean platelet counts (decreased in the 3X and 1X groups), potassium (increased in the 5X group), glucose (decreased in the 1X and 3X groups), and maximum blood glucose in glucose curves (increased in the 5X group). All individual values for these variables were within the normal range. Three 1X and one 5X group dogs had mild elevations of alkaline phosphatase (less than two times normal). Loose stools and vomiting were infrequent and self-limiting.

Storage Information: Store at 20° to 25°C (68° to 77°F), excursions permitted between 15° and 30°C (between 59° and 86°F).

How Supplied: Vetmedin® (pimobendan) Chewable Tablets: Available as 1.25, 2.5, 5 and 10 mg oblong half-scored chewable tablets - 50 tablets per bottle.

NDC 0010-4480-01-1.25 mg - 50 tablets NDC 0010-4481-01-2.5 mg - 50 tablets NDC 0010-4482-01-5 mg - 50 tablets NDC 0010-4479-01-10 mg - 50 tablets Manufactured by: Boehringer Ingelheim Promeco S.A. de C.V. Mexico City, Mexico Manufactured for: Boehringer Ingelheim Vetmedica, Inc. St. Joseph, MO 64506 U.S.A. Vetmedin® is a registered trademark of Boehringer Ingelheim Vetmedica GmbH licensed to Boehringer Ingelheim Vetmedica, Inc. Copyright © 2013 Boehringer Ingelheim Vetmedica, Inc. or an affiliated company. All Rights Reserved.

448005-00 Revised 06/2013

12/14/16 6:17 PM

Simon R. Platt , BVM&S, MRCVS, DACVIM (Neurology) & DECVN University of Georgia EDITOR’S NOTE

EDITOR’S NOTE

One Health—How Does It Help Veterinary Medicine? “ Our essential connection with animals is ancient, and it runs deep. It extends from body to behavior, from psychology to society—forming the basis of our daily journey of survival. This calls for physicians and patients to think beyond the human bedside to barnyards, jungles, oceans, and skies.

Because the fate of our world’s health doesn’t depend solely on how we humans fare. Rather it will be determined by how all the patients on the planet live, grow, get sick, and heal.”

Barbara Natterson-Horowitz & Kathryn Bowers,

oobiquity: The Astonishing Connection Z Between Human and Animal Health

Much has been made of the recognition that animal health and human health have a multitude of parallels. Throughout many species, diseases have been documented and researched, and they share a plethora of similarities with the same diseases in humans. These similarities may be pathologic, genetic, or pathophysiological, creating windows of opportunity to investigate new diagnostic and therapeutic strategies that may potentially benefit animals, as well as humans, with a given disease.

Across the world, unions have formed between veterinary and human medicine teams under One Health directives and they are exploring the “naturally occurring” models of human disease that dogs and cats, for instance, now represent.

SHORTCOMINGS OF RODENT RESEARCH MODELS Oncologic diseases are just one group of health issues being investigated in dogs on a cytogenetic, diagnostic, and therapeutic basis. Many cancers

12 TVP-0102_Editors-Note.indd 12

in humans have retained their poor prognoses over several decades despite billions of dollars of investment into the use of murine models of these diseases. While these artificially created models, or “living Petri dishes,” have helped advance the understanding of cancers on histologic, molecular, and cytogenetic levels, they have consistently failed to identify “game changing” therapies in many of the most devastating cancers.

The main reason for this failure is that artificial rodent tumor-bearing models do not adequately reflect human tumor biology or tumor heterogeneity, and they may demonstrate different drug metabolism characteristics than tumors in humans.1 Rodent models often lack a competent immune system and their tumors often respond differently to cancer treatments than human tumors.2 Additionally, such small animals are inappropriate models to accurately evaluate novel treatments in conjunction with standard surgical resection.

DOGS ARE MORE THAN MAN’S BEST FRIEND Spontaneous “naturally occurring” cancer models offer an opportunity to apply a “comparative” perspective with translational applications to new drug discovery and development.3 We are all aware that dogs have a long history in biomedical research, based on their strong anatomical and physiological similarities to humans; the relatively high number of pet dogs that are diagnosed and treated with cancer each year have focused attention on this species.

Investigations of cancer in dogs have been pursued for over 40 years,4 but to date they represent an under-utilized model, one with an intact immune system that is more genetically outbred. The recent deciphering of the canine genome provides evidence of strong similarities with humans, particularly with respect to the gene families associated with cancer,

EDITOR’S NOTE

12/14/16 5:55 PM

EDITOR’S NOTE

which are significantly closer than the relationship between mice and humans.4-6

CLINICAL TRIALS PROVIDE TREATMENT OPTIONS Of significant advantage to the pursuit of One Health goals is that many dog owners are highly motivated and will often seek out new options for the management of cancer in their pets; many will have interest in receiving care that is provided as part of clinical trials when conventionally available treatments do not meet their goals.

Recent centralization of clinical trial information has been made available through the efforts of the American Veterinary Medical Association and can be viewed at ebusiness.avma.org/aahsd/study_search.aspx. This website provides a place where veterinarians and owners alike may search for clinical trials that are studying any number of canine health issues, including cancer.

Most of the trials are funded, which implies that there is a considerable financial incentive for the owner to pursue a treatment that may previously have been too expensive to consider.

FIRST, DO NO HARM: CONSIDERATIONS FOR CLINICAL TRIALS However, we must keep in mind several important issues that need to be front and center of any discussion surrounding use of a pet in a medical trial for the benefit of veterinary and human medicine.

First and foremost, we are dealing with a family member and, although it can be easily accepted that novel treatment strategies will be unproven in their success, it is difficult to justify use of an untested treatment if its safety cannot be guaranteed due to lack of sufficient preliminary data in this species. continued on page 24

JANUARY/FEBRUARY 2017

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â–

TVPJOURNAL.COM

13 12/14/16 5:56 PM

Melinda Merck, DVM Veterinary Forensics Consulting, LLC, Austin, Texas NAVC PERSPECTIVES

NAVC PERSPECTIVES

The Importance of Home As I sit here contemplating this column, I am struck by the amount of change we have seen in the past year. We have witnessed changes in many areas that affect our lives, including politically and socially—we may have been shocked, surprised, or expected the outcome.

Change can create hope or fear, confidence or insecurity, balance or uncertainty. This year’s NAVC Conference theme, Welcome Home, is both poignant and timely. That sense of “home” is an important element to navigating through life and its inevitable changes.

WHAT IS “HOME” TO YOU? Home can mean many things. It is where you recharge, refill your soul, and grow; where you feel connected and are loved. Home is where you feel safe.

For most of us, home is where the tail wags, where the favorite toy is dumped in your lap. It is doggie breath, tuna breath, and the smell of hay. Home is filled with neighs, snorts, barks, purrs, bleats, and moos. It is the clicking of nails across the floor or thundering hooves in the pasture. It is the lick, the nuzzle, and the feel of sleek fur under your fingers.

It is the eyes that knowingly connect with yours.

2017 Veterinary Community Events Veterinary Innovation Summit College Station, TX April 28–30 NAVC Institute

Orlando, FL

May 21–26

NAVC Discovery

Buffalo, NY

July 31–August 3

NAVC Live

Portland, OR

August 20–23

WHERE IS YOUR “HOME”?

Home can be more than one place. It can be wherever you are and whatever you create. It is the feeling of familiarity.

14 TVP-0102_NAVC-Perspectives.indd 14

We spend the majority of our time at work, our home away from home. This is where we grow personally and professionally. The veterinary medical profession is one of service and giving. It is important to build bits of “home” into our place of work—where we rejuvenate and regain a sense of balance and calm.

We need to create touchpoints at work that connect us with “home”: from textbooks we saved after graduation to decades of dusty journals to memorabilia from colleagues. “Home” is filled with the sights and sounds of lab machines, IV pumps, monitors, dental machines, clippers running, and rolling stall doors and cage doors latching.

COMING HOME Creating a place where you feel at home is important for individuals, clients, and patients. It is why the NAVC has new programs focused on the development of Fear Free practices and enhancing the health and wellbeing of the veterinary community. We are committed to building a physical and virtual home where you can learn, reach out, and grow.

NAVC has created a home for the veterinary community through the educational opportunities of Today’s Veterinary Practice and Today’s Veterinary Technician, the NAVC Conference and NAVC Institute, VetFolio, and NAVC Discovery and NAVC Live, coming this year. These resources provide continuous learning experiences and the power of connection to colleagues and experts on a world-wide level. A place where you can have a sense of home and make it your own.

We all look forward to coming home. So, welcome home.

—Melinda Merck, President, NAVC Board of Directors

NAVC PERSPECTIVES

12/14/16 5:57 PM

TVP-0102_NAVC-Perspectives.indd 15

12/16/16 1:29 PM

NAVC Conference News TODAY’S VETERINARY NEWS

TVP ACUTE ABDOMEN SYMPOSIUM Today’s Veterinary Practice (TVP) is presenting its second annual symposium on Sunday, February 5, at the NAVC Conference 2017. Diagnosis and Management of the Acute Abdomen has been organized by TVP Editor in Chief, Dr. Simon Platt, and NAVC Executive VP of Veterinary Education, Dr. Matt Winter. This topic will be explored through interactive lectures, case-based Q&A sessions, and roundtable discussion.

■L earn more about the NAVC Conference by turning to page 19 or visiting navc.com/conference.

NEW OPPORTUNITIES ANNOUNCED BY AFSCAN

FEBRUARY IS NATIONAL PET DENTAL HEALTH MONTH!

The African Small Companion Animal Network (AFSCAN) has finalized plans for the 2018 AFSCAN/NAVC and BSAVA International Scholar Programs (applications accepted in January 2017) and the 2017 AFSCAN Research and Studentship Awards (applications available at afscan.org/science). With the support of its sponsors, AFSCAN is funding up to 2 clinical research projects and up to 5 “studentships.” AFSCAN also announced 2 new initiatives for 2017:

Visit VetFolio (vetfolio.com), the partnership between the NAVC and AAHA, that provides online continuous education. Search “dental” and enjoy the extensive collection of RACE-approved CE materials, care guides, client handouts, and articles by dentistry experts.

• A pilot project in Kenya in which veterinarians will use a tablet-based app to collect demographic and health-related data from dogs visiting veterinary practices. The information will provide a valuable baseline perspective on canine health in Kenya.

• A “twinning program” sponsored by Zoetis that will offer African veterinarians the opportunity to partner with veterinary hospitals in the U.S. in long-term mentoring relationships.

■ For more information, visit afscan.net.

■C heck out TVP’s Practical Dentistry articles at tvpjournal.com.

ACVIM FOUNDATION AWARDS ONCOLOGY GRANT The American College of Veterinary Internal Medicine (ACVIM) Foundation has awarded funds to Annette Smith, DVM, DACVIM (Oncology & SAIM) and her colleagues at Auburn University College of Veterinary Medicine to perform research on canine breast cancer. This research will explore whether microRNA can be used to detect cancer cells and predict how well patients will respond to treatment.

■F or more information about the ACVIM Foundation, visit acvimfoundation.org.

NAVC LAUNCHES NEW ONLINE BOOKSTORE The NAVC has launched an online bookstore that features high-quality reference books categorized by Veterinary Medicine, Veterinary Technician/Nurse, and Veterinary Assistant. Each book listing includes a synopsis as well as the complete table of contents to help readers decide which book meets their specific needs. In addition, the bookstore will include NAVC Conference Proceedings, free subscriptions to Today’s Veterinary Practice and Today’s Veterinary Technician, and the NAVC’s inaugural book, Small Animal Radiography: Essential Positioning Guide.

■ For more information, visit bookstore.navc.com.

16 TVP-0102_News.indd 16

TODAY’S VETERINARY NEWS

12/16/16 1:33 PM

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Multifunction Canine Print TVP-0102_News.indd 17Ad 10.5x14.indd 1

11/29/16 5:59 12/14/16 1:34 PM

TODAY’S VETERINARY NEWS

TODAY’S VETERINARY NEWS

CANINE OSTEOARTHRITIS STUDY USING REMOTE MONITORING SEEKS PARTICIPANTS

The FASTEST way to stop bleeding and keep it stopped.

Recommended by veterinarians for use on biopsies, bleeding ulcers, dental procedures, and more.

■F or further details, visit vet.cornell.edu/ClinicalTrials/Trials/osteoarthritis.cfm.

HEALTH CARE PROFESSIONALS CALL FOR ONE HEALTH APPROACH TO PET AND HUMAN OBESITY A vision of a world where regular activity, a balanced diet, and healthy weight are part of every family’s life was presented at the recent Preventing Obesity in People and Their Pets: A One Health Approach. This conference was hosted by the One Health Committee of the World Small Animal Veterinary Association (WSAVA), in collaboration with the U.S. Centers for Disease Control and Prevention (CDC), and brought together speakers from human and veterinary medicine to discuss the problem of obesity in humans and companion animals. At the conclusion of the conference, speakers and delegates drafted a consensus statement on the One Health approach to obesity.

■W atch videos from the conference on the One Health Committee Facebook page: facebook.com/onehealthonemedicine/

shutterstock.com/Dora Zett

VET

i4C Innovations, Inc has announced its sponsorship of a study with Cornell University College of Veterinary Medicine to monitor pain and activity in canine patients with osteoarthritis using the remote Voyce Pro Wellness Monitoring Program. Through this monitoring, the clinicians are attempting to discern whether a difference exists in a dog’s pain response before and after the patient is given an oral pain medication. Enrollment for the study is open to dogs 2 years of age or older that weigh more than 30 pounds. They must be diagnosed with osteoarthritis and cannot currently be receiving NSAIDs, morphine-derived medications, or steroids.

VETERINARIANS EARN COMMUNITY SERVICE & NEXT GENERATION AWARDS Henry Schein, Inc has announced that Dr. Adriana Noacco is the recipient of the fourth annual Henry Schein Cares International Veterinary Community Service Award in recognition of her service to people and pets in Argentina. Dr. Julie Stafford has been named by WSAVA and Hill’s Pet Nutrition as the 2016 Next Generation Veterinary Award winner.

Today’s Veterinary Practice congratulates both recipients on these top honors.

www.ClotItVET.com

TODAY’S VETERINARY NEWS continued on page 94

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TODAY’S VETERINARY NEWS

12/16/16 1:34 PM

TREAT YOURSELF AND LEARN SOME NEW TRICKS

Orlando, Florida • February 4-8, 2017 (Exhibits 5-8) Orange County Convention Center • West Concourse

WELCOME

HOME

GET READY FOR A BIGGER, BETTER AND MORE EXHILARATING EXPERIENCE THAN EVER BEFORE.

EXPLORE the industry’s greatest and latest products and services with more than 650 exhibitors in ONE NAVC Conference Exhibit Hall.

ENJOY a wide selection of Small Animal, Large Animal, Exotics, Technician and Practice Management programs, as well as a Health & Wellbeing Center, IGNITE! 10-minute talks, FEAR FREE sessions and Hospital Design Workshop.

RECHARGE with entertainment and events featuring Grammy Award-winning artist Darius Rucker, “Dirty Jobs” host and “Deadliest Catch” narrator, Mike Rowe, and “Good Morning America” host, Robin Roberts! Also – NEW this year – Sunday’s “Big Game” event, a 5k Fun(d) Run/Walk and Fun(d) Golf Tournament to benefit the WSAVA Foundation.

REGISTER NOW AT NAVC.COM /TheNAVC

TVP-0102_News.indd 19

/The_NAVC

@THE_NAVC

#NAVC2017

12/14/16 6:00 PM

SAVE THE DATE FOR AN ALL NEW EDUCATIONAL EVENT

TODAY’S VETERINARY NEWS

Caution Federal (USA) law restricts this drug to use by or on the order of a licensed veterinarian.

Indications SENTINEL® SPECTRUM® (milbemycin oxime/lufenuron/praziquantel) is indicated for the prevention of heartworm disease caused by Dirofilaria immitis; for the prevention and control of flea populations (Ctenocephalides felis); and for the treatment and control of adult roundworm (Toxocara canis, Toxascaris leonina), adult hookworm (Ancylostoma caninum), adult whipworm (Trichuris vulpis), and adult tapeworm (Taenia pisiformis, Echinococcus multilocularis and Echinococcus granulosus) infections in dogs and puppies two pounds of body weight or greater and six weeks of age and older.

Dosage and Administration SENTINEL SPECTRUM should be administered orally, once every month, at the minimum dosage of 0.23 mg/lb (0.5 mg/kg) milbemycin oxime, 4.55 mg/lb (10 mg/kg) lufenuron, and 2.28 mg/lb (5 mg/kg) praziquantel. For heartworm prevention, give once monthly for at least 6 months after exposure to mosquitoes.

Dosage Schedule Praziquantel per Number of chewable chewables

Milbemycin Oxime per chewable

Lufenuron per chewable

2 to 8 lbs.

2.3 mg

46 mg

22.8 mg

One

8.1 to 25 lbs.

5.75 mg

115 mg

57 mg

One

25.1 to 50 lbs.

11.5 mg

230 mg

114 mg

One

50.1 to 100 lbs.

23.0 mg

460 mg

228 mg

One

Body Weight

Over 100 lbs.

Administer the appropriate combination of chewables

To ensure adequate absorption, always administer SENTINEL SPECTRUM to dogs immediately after or in conjunction with a normal meal.

SENTINEL SPECTRUM may be offered to the dog by hand or added to a small amount of dog food. The chewables should be administered in a manner that encourages the dog to chew, rather than to swallow without chewing. Chewables may be broken into pieces and fed to dogs that normally swallow treats whole. Care should be taken that the dog consumes the complete dose, and treated animals should be observed a few minutes after administration to ensure that no part of the dose is lost or rejected. If it is suspected that any of the dose has been lost, redosing is recommended.

Contraindications There are no known contraindications to the use of SENTINEL SPECTRUM. Warnings Not for use in humans. Keep this and all drugs out of the reach of children.

Precautions Treatment with fewer than 6 monthly doses after the last exposure to mosquitoes may not provide complete heartworm prevention.

Prior to administration of SENTINEL SPECTRUM, dogs should be tested for existing heartworm infections. At the discretion of the veterinarian, infected dogs should be treated to remove adult heartworms. SENTINEL SPECTRUM is not effective against adult D. immitis.

Mild, transient hypersensitivity reactions, such as labored breathing, vomiting, hypersalivation, and lethargy, have been noted in some dogs treated with milbemycin oxime carrying a high number of circulating microfilariae. These reactions are presumably caused by release of protein from dead or dying microfilariae.

Do not use in puppies less than six weeks of age.

Do not use in dogs or puppies less than two pounds of body weight.

Veterinarians from around the world are invited to take part in an immersive, hands-on educational event filled with cutting-edge veterinary medical techniques in a destination location. The event offers three distinct courses meant to challenge practitioners, improve practical skills and enhance the entire practice. Set in the summertime in upstate New York, attendees will be able to explore the Buffalo area and visit Niagara Falls when not in the classroom.

The safety of SENTINEL SPECTRUM has not been evaluated in dogs used for breeding or in lactating females. Studies have been performed with milbemycin oxime and lufenuron alone.

Adverse Reactions The following adverse reactions have been reported in dogs after administration of milbemycin oxime, lufenuron, or praziquantel: vomiting, depression/lethargy, pruritus, urticaria, diarrhea, anorexia, skin congestion, ataxia, convulsions, salivation, and weakness.

To report suspected adverse drug events, contact Virbac at 1-800-338-3659 or the FDA at 1-888-FDA-VETS. Information for Owner or Person Treating Animal Echinococcus multilocularis and Echinococcus granulosus are tapeworms found in wild canids and domestic dogs. E. multilocularis and E. granulosus can infect humans and cause serious disease (alveolar hydatid disease and hydatid disease, respectively).

Owners of dogs living in areas where E. multilocularis or E. granulosus are endemic should be instructed on how to minimize their risk of exposure to these parasites, as well as their dog’s risk of exposure. Although SENTINEL SPECTRUM was 100% effective in laboratory studies in dogs against E. multilocularis and E. granulosus, no studies have been conducted to show that the use of this product will decrease the incidence of alveolar hydatid disease or hydatid disease in humans. Because the prepatent period for E. multilocularis may be as short as 26 days, dogs treated at the labeled monthly intervals may become reinfected and shed eggs between treatments.

Manufactured for: Virbac AH, Inc. P.O. Box 162059, Ft. Worth, TX 76161

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For details and to register for the event, visit NAVC.com/Discovery.

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NADA #141-333, Approved by FDA © 2015 Virbac Corporation. All Rights Reserved.

SENTINEL and SPECTRUM are registered trademarks of Virbac Corporation.

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Dogs should be tested for heartworm prior to use. Mild hypersensitivity reactions have been noted in some dogs Dogs should be number tested for prior to use. Mild hypersensitivity have been noted inthe some carrying a high of heartworm circulating microfilariae.

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References: 1. Data on file, Vetstreet Data Analytics. Virbac Corporation. 2. SENTINEL® SPECTRUM® (milbemycin oxime/ lufenuron/praziquantel) of Information Summary].

NC: Animal Health;®2011. ® References: 1. Data on[Freedom file, Vetstreet Data Analytics.

VirbacGreensboro, Corporation.

2.Novartis SENTINEL SPECTRUM (milbemycin oxime/ lufenuron/praziquantel) [Freedom of Information Summary]. Greensboro, NC: Novartis Animal Health; 2011. * Prevents flea eggs and maggot-like larvae from developing; does not treat adult fleas. † A. caninum. * Prevents flea eggs and maggot-like larvae from developing; does not treat adult fleas. ® ‡ † SENTINEL A. caninum.Brand Products. ‡ SENTINEL® Brand Products.

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PET HEALTH

BY THE NUMBERS

PET HEALTH BY THE NUMBERS

Canine Periodontal Disease shutterstock.com/Roger Costa Morera

Today’s Veterinary Practice and Banfield Pet Hospitals (banfield.com) have partnered together to bring you Pet Health by the Numbers. This column provides clinically relevant statistics extracted from medical record data of nearly 2.5 million dogs and nearly 500,000 cats presented to more than 920 Banfield Pet Hospitals in 2015.

February is National Pet Dental Health Month and, in honor of this important initiative, this column features statistics on the prevalence of periodontal disease in dogs presented to Banfield Pet Hospital in 2015. Read this issue’s dental articles, Interpretation of Dental Radiographs in Dogs & Cats and Chronic Feline Gingivostomatitis: Proven Therapeutic Approaches & New Treatment Options, on pages 55 and 26, respectively.

Prevalence of Periodontal Disease (PD) per 10,000 Dogs, Grouped by Age & Breed Size (2015) AGE & BREED SIZE

POPULATION IN CATEGORY

PD STAGE 1

PD GRADE 2

PD GRADE 3

PD GRADE 4

2,459,684

617.8

444.1

250.3

134.1

Juvenile (< 1 year)

505,847

35.4

2

0.3

0.1

Young adult (1 to < 3 years)

612,940

448.7

96.1

15.7

3.8

1,222,565

848.7

597.6

275

119.4

Geriatric (≥ 10 years)

323,068

706.9

991.2

858.8

573.7

Small

1,151,790

720

620

410

240

Medium

407,200

700

500

260

120

Large

939,805

490

230

70

20

Giant

72,209

420

180

40

10

Overall

Mature adult (3 to < 10 years)

Note: Age group and breed size totals will not match overall totals. Age groups are derived from visit age in 2015; some pets may have been counted in multiple age categories (eg, a pet that visited as a juvenile and then as a young adult in 2015). Breed size totals will not match due to animals of unknown breed. continued on page 24

22

PET HEALTH BY THE NUMBERS

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PET HEALTH

BY THE NUMBERS

PET HEALTH BY THE NUMBERS continued from page 22

Stages of Periodontal Disease1 The degree of severity of periodontal disease (PD) relates to a single tooth; a patient may have teeth that have different stages of periodontal disease.

Copyright AVDC, used with permission.

Normal (PD0)

Clinically normal; gingival inflammation or periodontitis is not clinically evident

Stage 1 (PD1)

Gingivitis only without attachment loss; height and architecture of alveolar margin are normal

Stage 2 (PD2)

Early periodontitis; less than 25% of attachment loss (measured by probing the clinical attachment level or evaluating dental radiographs*) or, at most, there is a stage 1 furcation involvement in multirooted teeth

Stage 3 (PD3)

Moderate periodontitis; 25% to 50% of attachment loss (measured by probing of the clinical attachment level or evaluating dental radiographs*) or there is a stage 2 furcation involvement in multirooted teeth

Stage 4 (PD4)

Advanced periodontitis; more than 50% of attachment loss (measured by probing of the clinical attachment level or evaluating dental radiographs*) or there is a stage 3 furcation involvement in multirooted teeth

* Radiographic determination of the distance of the alveolar margin from the cementoenamel junction relative to the length of the root

Reference 1.

Wolf HF, Rateitschak EM, Rateitschak KH, et al. Color Atlas of Dental Medicine: Periodontology, 3rd ed. Stuttgart: Georg Thieme Verlag, 2005.

EDITOR’S NOTE continued from page 13 EDITOR’S NOTE

Second, success in many clinical trials evaluating cancer therapies in humans is based upon survival.

This is a flawed marker of outcome in veterinary medicine, as we all know that quality of life and owner input determine survival in pet dogs.

Therefore, other, perhaps less well-defined, markers need to be used, potentially detracting from the pure translational information that the trial can provide.

Third, veterinary medicine can rarely offer a significant number of clinical cases for enrollment in these trials, which means that the resulting data documenting success is not very robust. Yet there is value in these clinical trials that must not be underestimated; it’s just that our expectations must be set appropriately.

Turn to page 16, Today’s Veterinary News, to read about the WSAVA/CDC Preventing Obesity in People & Pets One Health Conference (wsavaobesity.com) and the canine osteoarthritis study at Cornell University (vet.cornell.edu/ ClinicalTrials/Trials/Osteoarthritis.cfm), which is seeking remote participants.

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Success in clinical trials can help the species as a whole, which is the bystander effect that interests us veterinarians the most, as it directly benefits our own patients.

—Simon Platt, Editor in Chief References 1.

Huszthy PC, Daphu I, Niclou SP, et al. In vivo models of primary brain tumors: Pitfalls and perspectives. Neuro Oncol 2012; 14:979993.

2. Candolfi M, Curtin JF, Nichols WS, et al. Intracranial glioblastoma models in preclinical neuro-oncology: Neuropathological characterization and tumor progression. J Neurooncol 2007; 85:133-148.

Learn More

24

If this approach is thoughtfully achieved, our pet dogs can represent a valuable stepping stone in the battle to find better therapeutics in humans. In the interim, such financially supported studies can help some dogs that would otherwise have had no feasible treatment options.

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3. Hansen K, Khanna C. Spontaneous and genetically engineered animal models; use in preclinical cancer drug development. Eur J Cancer 2004; 40:858-880.

4. Paoloni M, Khanna C. Translation of new cancer treatments from pet dogs to humans. Nat Rev Cancer 2008; 8:147-156.

5. Lindblad-Toh K, Wade CM, Mikkelsen TS, et al. Genome sequence, comparative analysis and haplotype structure of the domestic dog.

Nature 2005; 438:803-819.

6. O'Brien SJ, Murphy WJ. Genomics. A dog's breakfast? Science 2003; 301:1854-1855.

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CHRONIC FELINE GINGIVOSTOMATITIS

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CHRONIC FELINE GINGIVOSTOMATITIS:

Proven Therapeutic Approaches & New Treatment Options Barden Greenfield, DVM, DAVDC, FAVD Memphis Veterinary Specialists, Cordova, Tennessee Arkansas Veterinary Specialists, Little Rock, Arkansas

Chronic gingivostomatitis (CGS) in the cat is a very painful disease, characterized by severe inflammation of the gingiva, buccal mucosa, and caudal oral mucosa.1 CGS affects 0.7% to 10% of the general cat population.2 This article reviews clinical signs of CGS, current treatment modalities, and promising treatment options that may be available soon.

IDENTIFYING INFLAMMATION It is important to differentiate gingivitis from stomatitis: gingivitis is inflammation of the gingiva (Figure 1), while stomatitis is inflammation of the mucous lining of any of the structures in the mouth. In clinical use, the term stomatitis should be reserved to describe wide-spread oral inflammation (beyond gingivitis and periodontitis) that may also extend into submucosal tissues (Figure 2).3 The mucogingival (MG) line provides a landmark at which the clinician differentiates disease entities. Routine gingivitis does not extend beyond the gingiva, while stomatitis always extends beyond the MG line.

shutterstock.com/Byelikova Oksana

TVP-0102_FEATURE_Feline-Gingivostomatitis-Therapy.indd 27

FIGURE 1. Gingivitis; note that inflammation is relegated to the gingival margin only.

FIGURE 2. Chronic gingivostomatitis of the right maxilla.

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Diagnostic Findings Etiology of Chronic Gingivostomatitis

Oral examination findings include:

This disease process of CGS is a result of an inappropriate immune response to oral antigenic stimulation and, unfortunately, there may be one or more initiating causes that trigger this event.

• Inflammation of the oral mucosa (Figure 2)

Dental plaque bacteria, even in very small amounts, have been shown to stimulate the immune system. At one time, it was thought that, in addition to plaque bacteria, this clinical phenomenon might have contributing factors, such as an infectious agent (ie, feline calicivirus [FCV], feline leukemia virus [FeLV], feline herpesvirus, feline immunodeficiency virus [FIV], and Bartonella henselae).

Recent studies focused on the shedding of FCV as an active virus in clinical cases of CGS and found no association of viral shedding with FeLV, FIV, herpesvirus, and Bartonella. 5,6 While it is clinically important to know the immunologic status (ie, FeLV or FIV positive/negative) of the patient at the time of the examination, these disease processes may not necessarily be causative agents, but can contribute to the morbidity of the patient in the healing phase of treatment.

• When stomatitis extends into the alveolar and buccal mucosa, it is defined as alveolar or rostral stomatitis.

• When inflammation occurs in the caudal oropharynx lateral to the palatoglossal folds, it is identified as caudal mucositis or stomatitis.1,3,4

DIAGNOSIS Clinical Signs Clinical signs of CGS can be quite variable among cats (Table 1), but most experience moderate to severe oral pain and, in severe cases, cats may cry when their mouths are opened.

• Inflammation of the alveolar and buccal mucosa of premolars and molars (most often symmetrical) and caudal oropharynx (Figure 3).

Simultaneous tooth resorption (TR) and/or periodontitis (inflammation at the tooth surface and of surrounding alveolar bone) may occur.1,4 In some patients, hyperglobulinemia is present.2 However, neutrophilia is not a hematologic finding in cats with CGS.

PARTIAL OR FULL MOUTH EXTRACTIONS Successful treatment of CGS requires the minimization of oral bacteria.1 The most favorable clinical control for resolution of oral inflammation is via partial or full mouth complete tooth extractions (Figures 4–6).

In addition to complete tooth extraction, the marginal bone should receive alveoplasty (smoothing bone and alveolus to remove ridges and spicules). Only American Veterinary Dental College (AVDC) specialists or veterinarians with extensive experience in feline extraction should consider approaching these cases surgically.

Recently, an article was published with the objective of evaluating the long-term response of cats with

TABLE 1 Clinical Signs of Chronic Gingivostomatitis Weight loss and/or reluctance to eat Dropping food Vocalization while eating; then “running away” from food Hypersalivation Failure to groom Oral malodor

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FIGURE 3. Caudal mucositis associated with chronic gingivostomatitis.

CHRONIC FELINE GINGIVOSTOMATITIS

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stomatitis to tooth extraction. The data concluded that “extraction of teeth in areas of oral inflammation provided substantial improvement or complete resolution of stomatitis in more than two-thirds of affected cats.”7 Furthermore, full mouth extractions did not appear to provide additional benefits.7 If there is any inflammation of the mucosa of the canine teeth or incisors, those teeth must be removed. The effectiveness of dental extractions has been shown to be: 55% cure, 35% markedly improved, and 10% no improvement.8,9

Efficacy of Periodontal Therapy Periodic periodontal therapy that includes scaling, polishing, and probing results in minimal success due to the fact that dental plaque bacteria repopulate and initiate the inflammatory cascade soon after therapy. Home care is usually

FIGURE 4. Postoperative image of mandible after full mouth extractions in a 3-year-old cat.

FIGURE 5. Postoperative radiograph confirming complete tooth extraction in Figure 4 cat.

unrewarding as cats are resistant to daily or twice-daily tooth brushing and oral rinses.

Dental Radiography With extractions, emphasis is placed on the absolute need that all root structures must be removed, as any tooth root remnant will not allow for resolution or improvement of clinical signs (Figure 7). It is my opinion and that of other AVDC specialists that extractions should only be completed with the aid of dental radiography to confirm complete tooth root extraction.

Histopathology Histopathology of inflamed mucosa and gingiva reveal plasma cells with varying numbers of lymphocytes, neutrophils, and macrophages.

FIGURE 6. Clinical resolution of chronic gingivostomatitis in a 3-year-old cat.

FIGURE 7. Tooth root remnants in patient with refractory CGS. This cat did not respond favorably to therapy due to incomplete tooth extractions.

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Learn More Read A Review of Feline Oral Squamous Cell Carcinoma in the November/December 2016 issue of Today’s Veterinary Practice, available at tvpjournal.com.

Mast cells may be seen in higher numbers, but they can also be seen in cases of periodontitis and tooth resorption.4 Rarely is histopathology warranted, unless unilateral lesions are seen.

Histopathologic differentiation between CGS and neoplasia is needed for those particular cases.

Patient Preparation For those cats that eat hard food as their sole diet, a transition to canned food is needed prior to surgery.

This canned diet should continue for all cats at least 2 to 3 weeks postoperatively. An appetite stimulant (eg, mirtazapine, 3.75 mg/cat PO Q 72 H) may help cats adjust to the new texture and diet and can be continued through the posttreatment phase.

Pain Management Pain management is recommended, not only in the pre- and postoperative phases, but also the intraoperative phase (Table 2).

• Buprenorphine provides pre- and postoperative analgesia for these patients.

• Compounded gabapentin has shown benefit in severely painful cats.

• Intraoperative regional nerve blocks provide

analgesia for 6 to 8 H and decrease anesthetic depth and mean alveolar concentration of inhalants.10 The addition of an opioid to bupivacaine is sufficient to provide analgesia for approximately 48 to 72 H.11,12

• Usage of an approved nonsteroidal antiinflammatory (NSAID) in the postoperative phase of therapy compliments analgesic therapy.

REFRACTORY CGS TREATMENT The author defines refractory as no improvement 60 days post full mouth extraction. As mentioned earlier, approximately 10% of CGS surgical cases are refractory, and these pose a very difficult therapeutic challenge to the clinician.

Following are the most current treatment modalities available, with a peek at one of the most promising options for refractory CGS.

Corticosteroids Historically, corticosteroids (eg, prednisolone) have been used for refractory cases, with limited to moderate success. Immunosuppressive dosages are recommended if this class of drug is chosen (Table 3). Assessment of clinical improvement is needed every 30 days.13 There are undesirable clinical and physiological effects of chronic corticosteroid usage, such as polyuria and polydipsia, thinning of haircoat, behavioral changes, and diabetes mellitus. In a recent study evaluating efficacy of prednisolone, 13 of 16 cats did not respond favorably, with deleterious clinical signs.1

TABLE 2 Recommended Perioperative Analgesics for Partial or Full Mouth Extractions DRUG

DOSAGE/ADMINISTRATION

PERIOPERATIVE PERIOD

Buprenorphine

0.02 mg/kg sublingually Q 8–12 H

Preoperative Postoperative

Gabapentin

5−10 mg/kg Q 12–24 H

Preoperative Postoperative

Regional nerve block: Buprenorphine + bupivacaine

Buprenorphine (0.3 mg/mL): 0.05 mL Bupivacaine (0.5 mg/mL): 0.95 mL Inject 0.25 mL per regional nerve block

Intraoperative

Robenacoxib*

1−2 mg/kg PO Q 24 H

Postoperative

*If previous corticosteroid therapy has been used, an appropriate washout period must be considered before administering an approved NSAID.

30

CHRONIC FELINE GINGIVOSTOMATITIS

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TABLE 3 Medical Therapy Options for Refractory CGS DRUG

DOSAGE

Prednisolone

•3 −4 mg/kg PO Q 24 H for 3−4 weeks • Taper by approximately 25% per month

Microemulsified cyclosporine suspension

2.5 mg/kg PO Q 12 H

Modified cyclosporine

7.5−10 mg/kg PO Q 24 H

Feline recombinant interferon omega

• • • • •

I nject 2.5 MU in the inflamed right caudal mucosa Inject 2.5 MU in the inflamed left caudal mucosa Dilute the remaining 5 MU in 100 mL sterile saline and separate into 10 mL fractions Keep 1 syringe in the refrigerator and freeze the remaining syringes Administer 1 mL PO Q 24 H, alternating sides of the mouth daily, until all 100 ML has been administered

Cyclosporine Cyclosporine is a potent immunosuppressive agent that inhibits T cell activation by blocking the transcription of genes coded for specific pro-inflammatory cytokines interleukin-2 (IL-2) and IL-4. If this positive feedback loop of T cell activation by IL-2 is suppressed, the inflammatory process can be minimized.

The mechanism of action of cyclosporine is to minimize IL-2 expression, which subsequently minimizes T cell numbers.1

A recent study showed significant clinical improvement using cyclosporine (Figures 8 and 9, page 32).1

• A notable outcome of this study revealed more favorable clinical success with patients that have not received previous corticosteroids (69% versus 45%).1,4 • This double-blind study evaluated 16 cats administered a microemulsified cyclosporine suspension (Neoral, novartis.com).1 The cyclosporine product was compounded at 2.5 mg/kg per 1 mL in a cod liver oil base, with tuna flavoring, and it was administered at 1 mL PO Q 12 H.

What You Will Need Proper equipment (Table 4) and knowledge of mucogingival flap presentation are essential to attain maximum clinical success.

Equipment A variety of burs and diamonds are needed to facilitate extraction and alveoplasty. Instruments, such as a Minnesota retractor and DeBakey tissue forceps, can help prevent tissue maceration during the procedure. Fine luxators or periotomes help fatigue the periodontal ligament without damaging the surrounding alveolar bone. Magnification and illumination are essential for this procedure, or any oral surgery.

Knowledge While this article does not address the step-by-step procedure to perform quadrant extractions, it is prudent to review current literature or even take one or multiple laboratories to attain clinical competency.

TABLE 4 Equipment Necessary to Successfully Perform Tooth Extractions EQUIPMENT LIST

#15 or 15C scalpel blades Minnesota retractor for isolation of the tongue and surrounding soft tissue DeBakey tissue forceps Fine, sharp luxators and/or periotomes Variety of burs: #½, #1, and #2 round; #701L or #699 crosscut; medium grit football and conical diamonds Periosteal elevators specific for cats or small dogs Sharpened #2, #3, and #4 winged elevators 5-0 poliglecaprone-25 or chromic gut with a P3 needle

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More recently, a once-daily modified cyclosporine (Atopica, us.atopica.com) is now available for cats (Table 3). The dosage for that product is 7.5 to 10 mg/kg Q 24 H, as it needs to be given at higher dosages than microemulsified cyclosporine to achieve adequate blood levels.

Establishing trough whole blood cyclosporine levels (attained 12 H after the last dosage given) > 300 ng/mL demonstrated the most significant clinical improvement (72%).1 Trough whole blood cyclosporine levels should be tested monthly if there is no clinical improvement. The goal of > 300 ng/mL should be attained and, if values are lower, treatment dosage is increased accordingly.

Transient vomiting and diarrhea are the most common side effect of cyclosporine. Informed consent of the usage of cyclosporine is important as well as future costs associated with this medication. Outdoor cats or cats eating a raw diet should be tested for Toxoplasma gondii prior to cyclosporine therapy.1,4

packaged in a 10 million (MU) vial (Table 3); there are no adverse side effects to rFeIFN-Ď&#x2030;.14

CO2 Laser Therapy CO2 laser therapy has been described as an adjunct therapy for refractory stomatitis (Figures 10 to 12).15 The goal of therapy is to char the inflamed tissue, which results in scar tissue formation, and this scar tissue is considerably less likely to become inflamed over time. However, the veterinarian must be extremely proficient in the usage of this laser; hospitalization, placement of an esophagostomy tube, and corticosteroid therapy are frequently necessary. This therapy may be repeated in 4 to 6 weeks, if needed.15

Adipose-Derived Mesenchymal Stem Cell (ASC) Therapy Mesenchymal stem cells have been associated with regenerative ability, in part due to their ability

Feline Recombinant Interferon Omega Feline recombinant interferon omega (rFeIFN-Ď&#x2030;) is available in the United States only through the Food and Drug Administration (FDA) Compassionate Use Program and is imported on an individual basis. This drug is licensed to treat retroviral infections and studies have shown that interferon delivered transmucosally was as effective as prednisolone in decreasing clinical signs. It is

FIGURE 8. Refractory caudal mucositis after full mouth extractions. Courtesy Milinda Lommer, DVM, DAVDC

32

FIGURE 9. Resolution of caudal mucositis after cyclosporine therapy. Courtesy Milinda Lommer, DVM, DAVDC

CHRONIC FELINE GINGIVOSTOMATITIS

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to modulate both innate and adaptive immune responses. These cells are adherent, fibroblastlike, multipotent stem cells derived from a variety of tissues, including adipose tissue.2 The goals of a recent study were to evaluate the effectiveness of adipose-derived mesenchymal stem cell (ASC) therapy in cats with CSG and possibly establish correlation of this therapy in human counterparts with similar pathology.2

• The study hypothesized that ASC therapy would result in systemic immune modulation, inflammatory lesion reduction, and clinical sign improvement, either by complete cure or substantial reduction in inflammatory lesions; this hypothesis was confirmed by clinical, histopathologic, and immunologic testing.

• Each cat was hospitalized posttransfusion for 2 to 3 days to monitor for possible adverse reactions.

The researchers also established that cats with < 15% CD8 cytotoxic T cells (with low expression of those cells) were 100% responsive to ASC therapy, while cats with > 15% CD8 cytotoxic T cells responded poorly.2 This biomarker may assist clinicians in predicting clinical response to ASC therapy.

Once the ability to preselect favorable clinical cases is standardized and proper culture expansion and characterization are made commercially available, this favorable treatment for CGS provides an excellent opportunity for substantial or total clinical resolution of previously nonresponsive cats.

• The 7 of 9 cats that completed this study received 2 IV injections of 20 million autologous ASCs administered 1 month apart.2 • Of those 7 remaining cats, 5 responded to treatment by either complete clinical remission (3 cats) or substantial clinical improvement (2 cats).2

FIGURE 11. CO2 laser ablation for refractory caudal mucositis; the canine teeth were extracted at the same time. Courtesy John Lewis, DVM, DAVDC, FAVD, and the University of Pennsylvania

FIGURE 10. Severe refractory caudal mucositis despite previous extraction of premolars and molars. Courtesy John Lewis, DVM, DAVDC, FAVD, and the University of Pennsylvania

FIGURE 12. Healed caudal oropharynx after treatment with CO2 laser. Courtesy John Lewis, DVM, DAVDC, FAVD, and the University of Pennsylvania

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Learn More Learn more about adipose-derived mesenchymal stem cell therapy by reading Regenerative Medicine for Soft Tissue Injury & Osteoarthritis in the July/August 2016 issue of Today’s Veterinary Practice, available at tvpjournal.com.

IN SUMMARY CGS is a complex syndrome for which a true cause-and-effect has yet to be established. Until that time, partial or full mouth extractions are the gold standard of therapy. Complete tooth removal—with absolutely no tooth root remnants remaining—is essential for progression to clinical improvement. Utilization of dental radiography is not an option but rather an essential diagnostic and confirmational tool to ensure complete removal of the entire tooth.

Confident knowledge of surgical flaps and quadrant extractions is highly recommended prior to undertaking this oral surgery. The veterinarian should have the appropriate armamentarium available to perform quadrant extractions in the cat, but the best tool for the clinician is patience.

Use of systemic antibiotics in lieu of partial or full mouth extractions is ill-advised, and only contributes to possible antibiotic resistance in patients. At the immediate intra- and postoperative phases of treatment, antibiotics may aid in soft tissue healing; however, chronic, long-term use of antibiotics has not been documented to be effective.

Transitioning the patient to canned food (with an appetite stimulant, if needed) prior to surgery, minimizing chronic oral pain with opioid therapy (eg, buprenorphine) and gabapentin, and removing all tooth structures provide the practitioner the best chance of clinical success.

Addressing the immediate postoperative phase is critical. Utilizing buprenorphine in the regional nerve blocks provides prolonged analgesia.

Additionally, an opioid and ketamine loading dose followed by a constant rate infusion (CRI) or a fentanyl CRI immediately prior to and following anesthesia can augment the opioid administered in the regional block.

Finally, refractory CGS cases should be treated with corticosteroids, cyclosporine, feline recombinant interferon omega, or CO2 laser. With ASC therapy available in the future, clinicians will have another option for treating refractory cases of CGS. References

Glossary ASC adipose-derived mesenchymal stem cell AVDC American Veterinary Dental College CGS chronic gingivostomatitis CRI constant rate infusion FCV feline calicivirus FeLV feline leukemia virus FIV feline immunodeficiency virus MG mucogingival MU million unit NSAID nonsteroidal anti-inflammatory drug

1. Lommer MJ. Efficacy of cyclosporine for chronic, refractory stomatitis in cats: a randomized, placebo-controlled, double-blinded clinical study. J Vet Dent 2013; 30(1):8-17.

2. Arzi B, Mills-Ko E, Verstraete FJ, et al. Therapeutic efficacy of fresh, autologous mesenchymal stem cells for severe refractory gingivostomatitis in cats. Stem Cells Transl Med 2016; 5(1):75-86.

3. AVDC accepted nomenclature, available at avdc.org.

4. Lommer MJ. Oral inflammation in small animals. Vet Clin North Am Small Anim Pract 2013; 43(3):558-571.

5. Belgard S, Truyen U, Thibault JC, et al. Relevance of feline calicivirus, feline immunodeficiency virus, feline leukemia virus, feline herpesvirus and Bartonella henselae in cats with chronic gingivostomatitis. Berl Munch Tierarztl Wochenschr 2010; 123(9-10):369-376.

6. Dowers KL, Hawley JR, Brewer MM, et al. Association of Bartonella species, feline calicivirus, and feline herpesvirus 1 infection with gingivostomatitis in cats. J Feline Med Surg 2010; 12(4):314-321.

7. Jennings MW, Lewis JR, Soltero-Rivera MM, et al. Effect of tooth extraction on stomatitis in cats: 95 cases (2000-2013). JAVMA 2015; 246(6):654-660.

rFeIFN-ω feline recombinant interferon omega

8. Hennet P. Feline chronic gingivostomatitis: Extraction and what else?

Veterinary Dental Forum, 2010.

TR tooth resorption

9. Hennet P. Chronic gingiva-stomatitis in cats: Long-term follow-up of 30 cases treated by dental extractions. J Vet Dent 1997; 14(1):15-21.

continued on page 38

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CHRONIC FELINE GINGIVOSTOMATITIS

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ONE MORE STEP FOR PERIODONTAL HEALTH:

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This helps in diagnosing the severity of the periodontal condition/periodontitis.

Periodontitis is a progressive condition and one of the major goals of periodontal care is to decrease pocket depth. There are effective, evidence-based products such as Clindoral® (TriLogic Pharma) and Doxirobe® (Zoetis) to reduce pocket depths in early periodontitis, however, there is still some hesitancy in using these products amongst practitioners. While neither product takes the place of thorough teeth cleaning and pocket debridement or periodontal surgery, both have proven to be effective in decreasing pocket depth.

New Periodontal Research Objective: To assess the efficacy of periodontal care options in improving stage 2 (early) periodontal disease as evidenced by changes (improvement) in periodontal pocket depth in a blinded, randomized study.

Summary of Procedures Day 0: Gather patient information and perform physical and oral examination for inclusion assessment. Closed root planing and periodontal pocket depth measurement of the whole mouth under anesthesia. All teeth/pockets with a pocket depth measurement of 3 – 5 mm were noted.

If all study requirements were met the dog was randomly assigned to one of the study groups.

Group I: Closed root planing alone Group II: Closed root planing followed by the placement of Doxirobe® gel in qualifying pockets.

Group III: Closed root planing followed by the placement of Clindoral® periodontal filler in qualifying pockets.

Day 90: The enrolled dogs were reexamined and whole mouth charting was done under anesthesia. The study ended on day 90. The study was blinded by doctor A performing the day 0 charting and providing periodontal care and doctor B charting the pocket depths at day 90. The study enrolled enough dogs so that each group had 25 treated sites to evaluate.

Results Within group: Pocket depth at day 90 was significantly better than pocket depth at day 0 irrespective of the options, when compared within the group.

Between groups: Improvement in pocket depth seen at day 90 with the addition of Clindoral® to closed root planing was significantly better when compared to the improvement in pocket depth seen at day 90 with closed root planing alone or closed root planing with Doxirobe®.

Periodontal Disease Classification The stage of the periodontal disease was

determined based on the periodontal disease classification (Veterinary Dental Nomenclature adopted by the American Veterinary Dental College [AVDC]) and was based on two measurements, probing depth and percent attachment loss (PAL).

Probing depth was measured on day 0 (following closed root planing) and day 90, using a constant force electronic probe (Florida probe). PAL was determined from radiographs (X-rays).

Conclusions: It can be concluded from the study results that the addition of Clindoral® to closed root planing was significantly better in reducing pocket depth. The data from this study provides evidence that adopting just one more step in veterinary dental care is beneficial to periodontal health.

Efficacy of the periodontal care options was determined by improvement in periodontal pocket depth at day 90 compared to periodontal pocket depth at day 0.

Visit clindoral.com for complete study and product information. Clindoral is available from your distributor representative.

Want to learn more?

trilogicpharma.com 866-562-8042 Toll Free

1 1 1

Bellows J. Go one step beyond in veterinary dental care. DVM360 Magazine 2016;Jan 04.

Johnston TP, Mondal P, Pal D, et al. Canine periodontal disease control using a clindamycin hydrochloride gel. J Vet Dent 2011;28(4):224-229.

Zetner K, Rothmueller G. Treatment of periodontal pockets with doxycycline in beagles. Vet Ther 2002;3(4):441-452.

Doxirobe® is a trademark of Zoetis Services LLC.

TVP-0102_FEATURE_Feline-Gingivostomatitis-Therapy.indd 35

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Chronic Feline Gingivostomatitis: Proven Therapeutic Approaches & New Treatment Options OVERVIEW

This article, page 26, provides an overview of current and future therapeutic options for management of cats with chronic gingivostomatitis (CGS) and refractory CGS.

LEARNING OBJECTIVES

After reading this article, participants will be able to recognize the signs of chronic CGS in cats and compare treatment options for CGS and refractory CGS.

1. Which of the following is TRUE with regard to the use of cyclosporine therapy in refractory CGS? a. Minimum whole blood cyclosporine trough values of 100 ng/dL are recommended for favorable treatment outcome. b. Modified cyclosporine has better oral absorption than the microemulsified version of cyclosporine. c. Patients receiving prior corticosteroid therapy respond better to cyclosporine therapy than those that have not received prior corticosteroids. d. The mechanism of action of cyclosporine is to minimize IL-2 expression, which subsequently minimizes T cell numbers.

2. CGS in cats affects approximately how much of the general cat population? a. 20% to 25% b. 15% to 20% c. < 10% d . 30% 3. Which of the following is FALSE with regard to clinical and hematologic signs of CGS? a. The mucogingival line provides a landmark by which the clinician differentiates disease entities of gingivitis and stomatitis. b. When inflammation occurs in the caudal oropharynx lateral to the palatoglossal folds, it is identified as faucitis. c. Oral submucosal tissues are often involved in chronic gingivostomatitis cases. d. Hyperglobulinemia is a common finding in these cases.

This article is RACE-approved for 1 hour of continuing education credit.

To receive credit, take the approved test online at vetmedteam.com/ tvp.aspx (CE fee of $5/article).

4. Which of the following has been implicated in active shedding during clinical cases of CGS? a Feline leukemia virus b. Feline immunodeficiency virus c. Bartonella henselae d. Feline calicivirus 5. Which of the following is FALSE with regard to perioperative pain management in a CGS case? a. Buprenorphine may be added to regional nerve blocks to enhance analgesia for up to 3 days. b. Robenacoxib may be used with corticosteroids to provide a balanced analgesic response. c. Gabapentin has shown benefit in severely painful cats. d. None of the above.

6. Which of the following is FALSE with regard to treatment options for CGS? a. Antibiotics should not be used regularly to control the bacterial plaque formation in CGS patients. b. Partial mouth extractions parallel full mouth extractions with resolution of clinical signs, provided the canines and incisors are not involved. c. CO2 laser therapy is a viable treatment option to char caudal mucositis lesions prior to extraction of teeth. d. Pre- and postoperative dental radiography must accompany all extractions in CGS patients. continued on page 38

NOTE

Questions online may differ from those here; answers are available once CE test is taken at vetmedteam.com/tvp.aspx. Tests are valid for 2 years from date of approval.

36

CHRONIC FELINE GINGIVOSTOMATITIS

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7. Which is TRUE with regard to adipose-derived mesenchymal stem cell (ASC) therapy and a recent study using this methodology? a. Commercially available adipose-derived stem cells provide an excellent alternative to other conventional treatments for refractory CGS cases. b. Cats with > 15% CD8 cytotoxic T cells with low expression of those cells were 100% responsive to ASC therapy. c. ASC therapy provides an excellent outpatient method for treatment of refractory CGS. d. Mesenchymal stem cells have been associated with regenerative ability due in part to their ability to modulate both innate and adaptive immune responses.

8. Which of the following is FALSE with regard to CGS? a. Tooth resorptions may occur simultaneously with CGS. b. Food allergies can be a contributing component to CGS. c. Calculus formation contributes to the exacerbation of clinical signs of CGS. d. None of the above.

9. Which of the following is TRUE with regard to the use of corticosteroids for the treatment of refractory CGS cases? a. When using this class of drugs, it is recommended to use the immunosuppressive dosage. b. Corticosteroids enhance cyclosporine therapy, but at a low clinical dosage of 1 mg/kg PO Q 48 H. c. Corticosteroids are contraindicated when using CO2 laser therapy. d. Thirteen out of 16 cats in a recent study responded favorably in treatment of CGS. 10. What is the percentage of refractory CGS cases after full mouth extractions? a. 10% b. 20% c. 30% d . 40%

NOTE

Questions online may differ from those here; answers are available once CE test is taken at vetmedteam.com/tvp.aspx. Tests are valid for 2 years from date of approval.

continued from page 34 10. Beckman B. Regional nerve blocks for oral surgery in companion animals. Compend Cont Ed Pract Vet 2002; 24(6):439-444.

11. Modi M, Rastogi S, Kumar A. Buprenorphine with bupivacaine for intraoral nerve blocks to provide postoperative analgesia in outpatients after minor oral surgery. J Oral Maxillofac Surg 2009; 67(12):2571-2576.

12. Snyder C. Do locally administered opioids with local anesthesia increase anesthetic duration? Veterinary Dental Forum, 2015.

13. Davis EM. How I treat refractory feline chronic gingivostomatitis. Clin Brief 2015; Jan:19-22.

14. Hennet PR, Camy GA, McGahie DM, Albouy MV. Comparative efficacy of a recombinant feline interferon omega in refractory cases of calicivirus-positive cats with caudal stomatitis: A randomised, multicentre, controlled, double-blind study in 39 cats. J Feline Med Surg 2011; 13(8):577-587.

15. Lewis JR, Tsugawa AJ, Reiter AM. Use of CO2 laser as an adjunct treatment for caudal stomatitis in a cat. J Vet Dent 2007; 24(4):240-249.

38

Barden Greenfield

Barden Greenfield, DVM, DAVDC, FAVD, practices in Memphis (Memphis Veterinary Specialists) and Little Rock (Arkansas Veterinary Specialists). He is also the founder of the Mississippi Valley Veterinary Dental Educational Center (MVVDEC) in Memphis, providing dental CE to veterinarians and technicians in the central U.S. Dr. Greenfield is the president of the AVDC and has been serving on the AVDC board for the past 4 years. In addition to his clinical practice, Dr. Greenfield enjoys lecturing at the local, state, national, and international levels. He has authored multiple articles for the Journal of Veterinary Dentistry. Dr. Greenfield received his DVM from Mississippi State University.

He may be reached at drg@yourpetdentist. com.

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40

CHRONIC KIDNEY DISEASE IN DOGS & CATS

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TREATMENT GUIDELINES FOR CHRONIC KIDNEY DISEASE IN DOGS & CATS:

International Renal Interest Society Recommendations Gregory F. Grauer, DVM, MS, DACVIM Kansas State University

Chronic kidney disease (CKD) affects an estimated 1% to 3% of all cats and 0.5% to 1.5% of all dogs.1 Nephron damage associated with CKD is usually irreversible and can be progressive (Figure 1, page 42).

CKD is a major cause of morbidity and mortality, especially in older dogs and cats.

Because renal replacement therapy (dialysis and transplantation) is not widely available in veterinary medicine, management of CKD in dogs and cats focuses on:

• Early detection • Renoprotective treatments designed to slow the progressive loss of nephrons.

INTERNATIONAL RENAL INTEREST SOCIETY Many different terms have been used to describe renal disease and decreased renal function. Unfortunately, these terms can be confusing due to a lack of standard definition and application (eg, renal insufficiency and end-stage renal disease/failure).

shutterstock.com/DuxX

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The International Renal Interest Society (IRIS, iris-kidney.com) was created to advance the scientific understanding of kidney disease in small animals and, specifically, to help practitioners better diagnose, understand, and treat canine and feline renal disease.

IRIS has created an internationally recognized set of guidelines for the classification and treatment of kidney disease; these guidelines are available on the IRIS website and address:

• Staging of CKD • Treatment recommendations for CKD • Grading of AKI (acute kidney injury).

View the IRIS Guidelines Staging of CKD iris-kidney.com/guidelines/staging.html Treatment Recommendations for CKD iris-kidney.com/guidelines/ recommendations.html Grading of AKI iris-kidney.com/guidelines/grading.html

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STAGING CANINE & FELINE CKD The IRIS Staging of CKD guidelines were developed as a guide to classifying stable canine and feline CKD in order to both improve communications surrounding CKD and link appropriate diagnostic and therapeutic efforts to patients with varying degrees of CKD. Learn More Read Early Diagnosis of Chronic Kidney Disease in Dogs & Cats: Use of Serum Creatinine & Symmetric Dimethylarginine in the March/ April 2016 issue of Todayâ&#x20AC;&#x2122;s Veterinary Practice, available at tvpjournal.com.

These guidelines have been published in well-known textbooks, such as Current Veterinary Therapy and Textbook of Veterinary Internal Medicine, and have been adopted by the American and European Societies of Veterinary Nephrology and Urology (asvnu.org and esvnu.eu, respectively).2,3

Decreased number of nephrons

This staging system is not used to make a diagnosis of CKD but is employed following a diagnosis of CKD in order to facilitate appropriate treatment, monitoring, and further diagnostics.

Serum Creatinine Concentration The IRIS staging system is based primarily on serum creatinine concentrations (Table 1) and applies only to dogs and cats that are well hydrated and have stable CKDâ&#x20AC;&#x201D;stability is documented by < 20% variation in serum creatinine concentrations over at least a 2-week interval.

Note that the lower end of serum creatinine concentrations in Stage 2 lies within the reference interval for many laboratories. Serum creatinine concentration is a relatively insensitive marker of renal function and, therefore, dogs and cats with serum creatinine concentrations near the upper end of the laboratory reference interval may have reduced glomerular filtration rates.

Systematic hypertension

Pre-glomerular vasodilation Post-glomerular vasoconstriction Glomerular hyperfiltration

High dietary protein?

Glomerular cell proliferation Glomerulosclerosis

Proteinuria

Tubulointerstitial Damage Protein depletion and weight loss Nephrocalcinosis

FIGURE 1. Potential mechanisms of progressive loss of nephrons in chronic kidney disease.

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TABLE 1 Stages of CKD: Classified by Serum Creatinine Concentration STAGES OF CKD

SERUM CREATININE CONCENTRATION (MG/DL)

Stage 1 Non-azotemic Stage 2 Non-azotemic to mild renal azotemia Stage 3 Moderate renal azotemia Stage 4 Severe renal azotemia

CATS

DOGS

< 1.6

< 1.4

TABLE 2 Substages of CKD: Classified by Urine Protein/Creatinine Ratio (UPC) CLASSIFICATION OF UPC

Non-proteinuric Borderline proteinuric

1.6−2.8

1.4−2

2.9−5

2.1−5

>5

>5

Serum creatinine concentrations must always be interpreted in light of the patient’s muscle mass, urine specific gravity, and physical examination findings in order to rule out pre- and postrenal causes of azotemia.

The IRIS CKD staging system cannot be applied to patients with:

• Pre- or postrenal azotemia • Acute or decompensated (sometimes termed acute on chronic) kidney disease.

Proteinuric

UPC RATIO CATS

DOGS

< 0.2

< 0.2

0.2−0.4

1.4−2

> 0.4

> 0.5

Renal proteinuria can be glomerular and/ or tubular in origin (ie, excessive filtration, decreased tubular reabsorption, or both).

Renal proteinuria is persistent—with at least 2 positive tests separated by 10 to 14 days—and associated with inactive urine sediments.

Urine protein/creatinine ratios (UPCs) > 2 suggest glomerular-range proteinuria, which is rare in cats compared with dogs.

It is important to recognize that the UPC does not differentiate renal proteinuria from proteinuria associated with lower urinary tract inflammation; the clinician needs to make this determination by assessing the patient and urine sediment.

Systolic Blood Pressure The IRIS stages of CKD are primarily defined by serum creatinine concentration (Table 1) and then further classified by: • Presence or absence of proteinuria (Table 2) • Systemic hypertension (Table 3).

SDMA Concentrations Interpretation of serum symmetric dimethylarginine (SDMA) concentrations, along with serum creatinine concentrations, may increase the sensitivity for early diagnosis of CKD.4,5

Renal Proteinuria Proteinuria is an important risk factor for the development of azotemia in cats and the progression of azotemia and decreased survival in both dogs and cats.6-8 Presence or absence of proteinuria is used to substage CKD (Table 2) in the IRIS staging system.

IRIS blood pressure substaging is based, in part, on risk of target organ—eye, brain, heart, and kidney—damage (Table 3). In the absence of target organ damage, persistence of hypertension should be documented.

Systolic blood pressure is typically measured by the Doppler methodology in dogs and cats.

TABLE 3 Substages of CKD: Classified by Systemic Blood Pressure & Risk of Target Organ Damage SYSTOLIC BLOOD PRESSURE (MM HG)

RISK OF TARGET ORGAN DAMAGE

< 150

Minimal

Borderline hypertensive

150−159

Low

Hypertensive

160−179

Moderate

CLASSIFICATION OF BLOOD PRESSURE

Normotensive

Severe hypertension

180

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Although it is preferable to measure blood pressure on different days, it is acceptable to perform 2 measurements at least 2 hours apart. Most clinicians consider systolic hypertension to be > 160 mm Hg and initiate treatment at that point.

DIAGNOSTIC APPROACH AFTER STAGING

2. Characterization of the stability of renal disease and function.

Stability of renal function should be assessed by serial monitoring of abnormalities identified during initial characterization of the renal disease (Table 5).

If the same laboratory and methodology are used, increases in serum creatinine > 0.3 mg/ dL are suggestive of changes in renal function rather than assay variability. It is important to rule out dehydration as a cause of increasing serum creatinine concentrations.

In general, the diagnostic approach to a patient once CKD has been identified and staged focuses on 3 areas (Table 4).

1. Characterization of primary renal disease and/or complicating disease processes.

Further definition of the renal disease—beyond a standard minimum database—should include diagnostics to rule out potentially treatable conditions/complications; for example, urine culture for urinary tract infection and kidney imaging for renal lymphosarcoma.

3. Characterization of patient problems associated with decreased renal function.

Patient problems associated with decreased renal function (Table 4) may include anorexia, nausea, vomiting, weight loss, dehydration, acidosis, potassium depletion, and anemia.

TABLE 4 Diagnostic & Treatment Considerations Linked to IRIS CKD Stages OPTIMUM IRIS STAGES

Stage 1 Stage 2 Early Stage 3

Stage 2 Stage 3 Early Stage 4

Late Stage 3 Stage 4

DIAGNOSTIC & TREATMENT FOCUS

Assess primary disease and complicating disorders

Monitoring at least Q 6 months

Assess CKD stability or progression

Monitoring at least Q 3 months

Assess patient problems

Monitoring at least Q 1–2 months

CONSIDERATIONS POTENTIAL PROBLEMS

DIAGNOSTICS/TREATMENT

Renal infiltrative disease Renal lymphosarcoma

Radiographs, ultrasound ± FNA, chemotherapy

Obstructive uropathy Ureteral obstruction

Radiographs, ultrasound ± FNA, chemotherapy, SC ureteral bypass

Hypercalcemic nephropathy

Serum Ca and iCa assessment, NaCl fluid therapy, furosemide diuresis

Nephrocalcinosis

Renal diets, intestinal phosphorus binders

Hypertension

CCAs, ACE inhibitors, ARBs

Proteinuria

ACE inhibitors, CCAs, ARBs

Anorexia, nausea, vomiting

Appetite stimulants, antiemetics, H2 receptor blocker, proton pump blockers

Metabolic acidosis

Dietary alkalization

Potassium depletion

Potassium supplementation

Dehydration

Fluid therapy

Anemia

Recombinant erythropoietin

Calorie malnutrition

Appetite stimulants, dietary variety, feeding tube placement

Uremia

Enteric dialysis

ACE = angiotensin-converting enzyme; ARB = angiotensin receptor blocker; Ca = calcium; CCA = calcium channel antagonist; CKD = chronic kidney disease; FNA = fine-needle aspiration; iCa = ionized calcium; NaCl = sodium chloride

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Timing of Diagnostics In the early stages of CKD, characterization of primary renal disease and/or complicating disease processes, as well as determining disease stability, are most important—when appropriate treatment has the greatest potential to improve or stabilize renal function.

In the later stages of CKD, characterization of patient problems becomes more important—when clinical signs tend to be more severe. In these later stages, diagnostic and subsequent therapeutic efforts should be directed at patient problems.

THERAPEUTIC APPROACH TO CKD

tailored to each individual patient and that patient’s stage of disease (Tables 4 and 6). Serial monitoring of the patient—after treatment has been initiated—allows the clinician to modify treatment based on patient response (Table 5).

TABLE 5 Serial Monitoring of Patients with CKD FREQUENCY OF MONITORING

MONITORING SHOULD INCLUDE:

Stage 1 Stage 2 Early Stage 3

At least Q 6 months

•S erum biochemistry profile

Stage 2 Stage 3 Early Stage 4

At least Q 3 months

Late Stage 3 Stage 4

At least Q 1–2 months

• Urinalysis •Q uantitation of proteinuria •B lood pressure measurement

Therapy Tailored to CKD Stage Similar to the diagnostic approach, the therapeutic approach to CKD should be

•± urine culture and ultrasound examination

TABLE 6 Therapeutic Approach Based on IRIS Stage of CKD STAGE 1 CKD

STAGE 2 CKD

STAGE 3 CKD

STAGE 4 CKD

Pursue additional diagnostics (eg, urine C/S, urinary tract imaging)

3

3

3

3

Discontinue all potentially nephrotoxic drugs

3

3

3

3

Prerenal or postrenal disorders

3

3

3

3

Primary disease processes or complicating disorders

3

3

3

Hypertension and renal proteinuria

3

3

3

3

3

3

3

3

3

3

Calcitriol a

3

3

3

Reduce phosphorus intake (eg, renal diet, enteric phosphate binders)

3

3

3

Monitor for metabolic acidosis b

3

3

3

3

3

3

3

3

3

Q 1–3 months

Q 1–2 months

IDENTIFY AND CORRECT/TREAT:

CONSIDER RENOPROTECTIVE TREATMENTS: Renal diet ACE inhibitor, CCA, ARB

3

Symptomatic treatment to improve quality of life Monitor serum creatinine c

3

3

Address anorexia and calorie malnutritiond Assess CKD stability/progression

Q 6 months

Q 3–6 months

a. Avoid calcium containing enteric phosphate binders or monitor closely for hypercalcemia. b. Consider adding oral sodium bicarbonate or potassium bicarbonate to renal dietary therapy. c. In patients receiving vasoactive drugs for hypertension and/or proteinuria. d. Consider appetite stimulants, antiemetics, and gastric acid blockings drugs, but correction of metabolic deficits/excesses is more important.

ACE = angiotensin-converting enzyme; ARB = angiotensin receptor blockers; CCA = calcium channel antagonist; C/S = culture and sensitivity

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For example, disease specific treatments for ureteroliths and bacterial pyelonephritis, as well as treatments designed to slow the progression of renal disease (renoprotective treatments), are of most value in the earlier stages of CKD. In the later stages of CKD, treatment tends to be focused on quality of life and managing clinical signs associated with decreased renal function.

Learn More Read Nutritional Management of Chronic CKD in Dogs & Cats (March/April 2016), which details the efficacy of therapeutic diets, key nutrients in CKD, and role of body condition, available at tvpjournal.com.

This article is RACE-approved for CE credit.

Renoprotective Treatments Renoprotective treatments include:

• Dietary change designed to reduce serum phosphorus concentrations and decrease soft tissue mineralization9,10 • Potentially angiotensin-converting enzyme (ACE) inhibitors, calcium channel antagonists (CCA), and angiotensin receptor blockers (ARB) to normalize systemic and intraglomerular blood pressures and reduce proteinuria (Table 7)11-14 • Potentially, calcitriol supplementation.

CCAs are typically the first line of defense for moderate to severe hypertension in cats, while ACE inhibtors

are typically the first line of defense for hypertension in dogs as well as proteinuria in dogs and cats.

There is some evidence in dogs and cats that CCAs upregulate the renin–angiotensin–aldosterone system and, therefore, combined treatment with an ACE inhibitor is often recommended.15,16 Vasoactive drugs (ACE inhibitors, CCAs, and ARBs) should not be administered to dehydrated patients.

In patients in which hypertension and/or proteinuria are refractory to initial ACE inhibitor treatment, the standard dose can be doubled at least once, combined with a CCA, or the ACE inhibitor may be replaced with an ARB (eg, telmisartan).

For patients with Stage 2 CKD, calcitriol supplementation (0.5–1 ng/kg PO, separate from feeding) is a potentially renoprotective treatment in dogs17 but unproven in cats. Patients should be normocalcemic, with serum phosphorus concentrations within the target range (see Treatment Goals), prior to calcitriol supplementation.

Phosphorus Reduction Reduction of phosphorus intake is a major treatment goal for dogs and cats with Stage 2 and beyond CKD. The first line of defense against higher serum phosphorus concentrations is a gradual transition to a renal diet. A gradual transition over several weeks from a maintenance diet to a renal diet helps avoid any aversion to the renal diet.

TABLE 7 Dosages of Drugs for Management of CKD DRUG CLASSIFICATION

DRUG

DOSAGE

Benazepril

0.5–1 mg/kg PO Q 24 H

Enalapril

0.5–1 mg/kg PO Q 24 H

Angiotensin receptor blocker

Telmisartan

Cats: 1 mg/kg PO Q 24 H

Antidepressant a

Mirtazapine

1.5–2 mg/cat PO Q 24 H

Antiemetic

Maropitant

1 mg/kg PO or SC Q 24 H

Calcium channel antagonist

Amlodipine

Dogs: 0.0625–0.25 mg/kg PO Q 24 H Cats: 0.625–1.25 mg/cat PO Q 24 H

Proton pump inhibitor

Omeprazole

Dogs: 0.7 mg/kg PO Q 24 H Cats: 1 mg/kg PO Q 12 H

ACE inhibitor

a. Used for appetite stimulation in cats

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CONTINUING EDUCATION

Most renal diets are not only phosphorus restricted but:

• Contain reduced amounts of protein and salt • Are supplemented with omega-3 fatty acids • Are alkalinized to help offset the metabolic acidosis associated with CKD. Feline renal diets are also often supplemented with potassium.

Enteric phosphate binders are the second line of defense if serum phosphorus is > 4.6 mg/dL after dietary phosphorus restriction (see Treatment Goals). Many different enteric phosphate binders exist but all need to be well mixed with the diet or administered at the time of feeding.

To increase efficacy, the binder should be in the gut when phosphorus from the diet is also there.

The dose of the binder required to meet the target serum phosphorus goal will vary with the amount of phosphorus being fed and the stage of CKD. Use of calcium containing enteric phosphate binders in dogs and cats receiving calcitriol should be avoided or monitored closely for hypercalcemia (total and ionized calcium concentrations). CKD dogs with a product of serum calcium × phosphorus concentrations > 70 mg/dL have reduced survival times.18

Treatment Goals Goals for antihypertensive treatment and antiproteinuric treatment are a systolic blood pressure < 160 mm Hg and a UPC < 0.4 in cats and 0.5 in dogs. Alternatively, a reduction of > 50% of the baseline UPC is an acceptable response.

Target serum phosphorus concentrations are:

• Stage 2 CKD: > 2.7 but < 4.6 mg/dL • Stage 3 CKD: > 2.7 but < 5 mg/dL • Stage 4 CKD: > 2.7 but < 6 mg/dL Note that most laboratory reference intervals for serum phosphorus include concentrations much higher than 4.6 mg/dL.

IRIS TREATMENT RECOMMENDATIONS Stage 1 CKD Patients 1. Identify and correct any prerenal or postrenal disorders. Dehydration is the most common prerenal abnormality encountered, especially if urine-concentrating ability is compromised.

Any clinical or suspected subclinical dehydration should be corrected with isotonic, polyionic replacement fluid solutions, such as lactated Ringer’s solution either IV or SC. 2. Identify and treat any treatable primary disease processes (eg, renal lymphoma and hypercalcemia) or complicating disorders (eg, urinary tract infections and ureteroliths).

3. Pursue additional diagnostics recommended for Stage 1 CKD patients, including:

• Urine culture and sensitivity: Many urinary tract infections are subclinical in CKD patients • Urinary tract radiography: Ideal for localization of radiopaque uroliths (Figure 2) • Urinary tract ultrasound: Ideal for assessing kidney tissue architecture and renal pelvic dilation.

FIGURE 2. Lateral abdominal radiograph of a cat with uroliths.

4. Identify and treat hypertension and renal proteinuria. In Stage 1 CKD patients, a systolic blood pressure > 160 mm Hg is indicative of hypertension, while a UPC > 0.4 in cats and JANUARY/FEBRUARY 2017

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> 0.5 in dogs indicates renal proteinuria. Dietary sodium and protein reduction (eg, a renal diet) combined with ACE inhibitors, CCAs, and ARBs are used to reduce hypertension and proteinuria.

5. Discontinue all potentially nephrotoxic drugs.

6. Assess CKD stability or progression by monitoring patients at least twice a year. Dogs and cats with Stage 1 CKD (Table 8) are at risk for kidney disease progression; however, not all Stage 1 CKD patients progress to become azotemic. Those with borderline hypertension and proteinuria should be monitored closely.

Stage 2 CKD Patients 1. In both dogs and cats, pursue all treatments for Stage 1.

2. Identify and treat any primary renal disease or complicating condition, which is still an important goal in Stage 2 CKD. Dogs and cats with mid to late Stage 2 CKD often have progressive loss of renal function, although the rate of renal disease progression can be variable.

3. Reduce phosphorus intake with renal diets and enteric phosphate binders (if needed to meet goals).—This is a major treatment goal for dogs and cats with Stage 2 and beyond CKD.

4. Consider calcitriol supplementation—a potentially renoprotective treatment in dogs and cats. In dogs and cats receiving calcitriol, avoid use of calcium containing enteric phosphate binders or monitor patients closely for hypercalcemia.

5. Monitor patients for metabolic acidosis.

Stage 2 CKD patients should be monitored for metabolic acidosis by measuring serum bicarbonate or total CO2 concentrations.

If necessary, renal dietary therapy may be supplemented with oral sodium bicarbonate or potassium bicarbonate in order to maintain serum bicarbonate concentrations in the 18 to 24 mmol/L range.

6. Assess CKD stability or progression by monitoring patients Q 3 to 6 months.

Stage 3 CKD Patients 1. In both dogs and cats, pursue all treatments for Stage 1 and 2 CKD. 2. Continue renoprotective treatments (eg, renal diets, antihypertensive and antiproteinuric treatments) as Stage 3 CKD patients have progressive renal disease and it is important—as in State 2 CKD patients—to slow disease progression.

TABLE 8 Abnormalities Compatible with Stage 1 Non-azotemic CKD Kidney palpation or imaging abnormalities Decreased urine concentrating ability without an identifiable nonrenal cause Persistent proteinuria of renal origin Increases in serum creatinine concentration (> 0.3 mg/dL over time) in which prerenal influences, such as dehydration and increases in muscle mass, have been ruled out a Persistent increases in SDMA (> 14 mcg/dL) with a serum creatinine concentration < 1.4 mg/dL in dogs or < 1.6 mg/dL in cats Kidney biopsy results (Figure 3) b

FIGURE 3. Histopathology of CKD showing tubular mineralization (purple).

NOTES a. Increases in serum creatinine concentration can occur within the laboratory reference interval (eg, an increase in serum creatinine concentration from 0.6 to 1.2 mg/dL over several years in a dog or cat can be associated with > 50% nephron loss). b. Kidney biopsy is not routinely recommended in CKD.

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NOT ALL FLEA AND TICK CHEWS ARE CREATED EQUAL

Flea and tick protection that goes on and on and on...all month long

Introducing Simparica Monthly chewables for dogs that offer persistent protection from fleas and ticks.

Simparica acts fast—it starts killing fleas within 3 hours and ticks within 8 hours1 —and keeps going strong for 35 days2 without losing effectiveness at the end of the month.

IMPORTANT SAFETY INFORMATION: Simparica is for use only in dogs, 6 months of age and older.

Simparica may cause abnormal neurologic signs such as tremors, decreased conscious proprioception, ataxia, decreased or absent menace, and/or seizures. Simparica has not been evaluated in dogs that are pregnant, breeding or lactating. Simparica has been safely used in dogs treated with commonly prescribed vaccines, parasiticides and other medications. The most frequently reported adverse reactions were vomiting and diarrhea. See full Prescribing Information on the back of this page and at www.zoetisUS.com/SimparicaPI.

Fetch more information about Simparica from Zoetis Customer Service at 1-888-ZOETIS-1 or 1-888-963-8471.

References: 1. Six RH, Geurden T, Carter L, et al. Evaluation of the speed of kill of sarolaner (Simparica™) against induced infestations of three species of ticks (Amblyomma maculatum, Ixodes scapularis, Ixodes ricinus) on dogs. Vet Parasitol. 2016;222:37-42. 2. Six RH, Everett WR, Young DR, et al. Efficacy of a novel oral formulation of sarolaner (Simparica™) against five common tick species infesting dogs in the United States. Vet Parasitol. 2016;222:28-32.

All trademarks are the property of Zoetis Services LLC or a related company or a licensor unless otherwise noted. © 2016 Zoetis Services LLC. All rights reserved. October 2016. SMP-00048

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PEER REVIEWED

Gregory F. Grauer

Gregory F. Grauer, DVM, MS, DACVIM (SAIM), is a professor and Jarvis Chair of Medicine, Department of Clinical Sciences, at Kansas State University College of Veterinary Medicine. His clinical and research interests involve the small animal urinary system. He is on the board of directors of the IRIS and American Society of Veterinary Nephrology and Urology. Dr. Grauer received his postgraduate training in internal medicine at Colorado State University. He has been a faculty member at University of Wisconsin and Colorado State University Colleges of Veterinary Medicine.

3. Initiate symptomatic treatment to improve quality of life (Table 4) because many dogs and cats with Stage 3 CKD, especially late Stage 3 CKD, begin showing clinical signs.

4. Assess CKD stability or progression by monitoring patients Q 3 months; those with early Stage 3 CKD can be monitored Q 6 months, while those with late Stage 3 CKD should be monitored Q 1 to 2 months.

Stage 4 CKD Patients 1. In both dogs and cats, pursue all treatments for Stage 1, 2, and 3 CKD. 2. Continue renoprotective treatments (eg, renal diets, antihypertensive and antiproteinuric treatments) as these treatments are still important in early Stage 4 CKD patients but invariably the management focus shifts to making the patient as comfortable as possible given its renal failure.

3. Continue symptomatic treatment to improve quality of life (Table 4). Owners frequently— and rightfully—equate nausea, decreased appetite, vomiting, and weight loss with poor quality of life.

4. S top the catabolic spiral of calorie malnutrition— one of the primary management goals in Stage 4 CKD (Table 4). Appetite stimulants, antiemetics, and gastric acid blocking drugs become important in these patients (Table 7), but correction of metabolic deficits (eg, dehydration) and excesses (eg, hyperphosphatemia) is a higher priority.19,20

50

5. Monitor serum creatinine concentrations closely in Stage 4 CKD dogs and cats that are being treated with vasoactive drugs for hypertension and/or proteinuria.

6. Reevaluate patients Q 1 to 2 months.

IN SUMMARY Understanding the diagnostic and therapeutic priorities based on the stage of CKD facilitates appropriate management of dogs and cats with CKD. Identification and correction of any primary or complicating diseases are most important in Stage 1 and 2 patients. Renoprotective treatments are most important in Stage 2 and 3 patients.

Symptomatic patient therapy to improve quality of life is most important in Stage 4 patients.

References 1. Brown SA. Management of chronic kidney disease. In Elliott J, Grauer GF (eds): BSAVA Manual of Canine and Feline Nephrology and Urology, 2nd ed. Gloucester (UK): BSAVA, 2007, pp 223-230.

2. Bonagura JD, Twedt DC. Kirk’s Current Veterinary Therapy XV. St. Louis: Elsevier, 2014.

3. Ettinger SJ, Feldman EC. Textbook of Veterinary Internal Medicine Expert Consult, 7th ed. St. Louis: Elsevier, 2010.

4. Hall JA, Yerramilli M, Obare E, et al. Comparison of serum concentrations of symmetric dimethylarginine and creatinine as kidney function biomarkers in cats with chronic kidney disease. J Vet Intern Med 2014; 28(6):1676-1683.

5. Hall JA, Yerramilli M, Obare E, et al. Serum concentrations of symmetric dimethylarginine and creatinine in dogs with naturally occurring chronic kidney disease. J Vet Intern Med 2016; 30(3):794802.

6. Jepson RE, Brodbelt D, Vallance C, et al. Evaluation of predictors of the development of azotemia in cats. J Vet Intern Med 2009; 23(4):806-813.

7. Jacob F, Polzin DJ, Osborne CA, et al. Evaluation of the association between initial proteinuria and morbidity rate or death in dogs with naturally occurring chronic renal failure. JAVMA 2005; 206(3):393-400.

References continued on page 53

Glossary ACE angiotensin-converting enzyme ARB angiotensin receptor blocker CCA calcium channel antagonist CKD chronic kidney disease IRIS International Renal Interest Society SDMA serum symmetric dimethyl arginine UPC urine protein/creatitine ratio

CHRONIC KIDNEY DISEASE IN DOGS & CATS

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TM

(sarolaner) Chewables FOR ORAL USE IN DOGS ONLY CAUTION: Federal (USA) law restricts this drug to use by or on the order of a licensed veterinarian.

Description: SIMPARICA is a flavored, chewable tablet for administration to dogs over 6 months of age according to their weight. Each tablet is formulated to provide a minimum sarolaner dosage of 0.91 mg/lb (2 mg/kg) body weight.

Sarolaner is a member of the isoxazoline class of parasiticides and the chemical name is 1-(5’-((5S)-5-(3,5-Dichloro-4-fluorophenyl)-5-(trifluoromethyl)-4,5-dihydroisoxazol-3-yl)3’-H-spiro(azetidine-3,1’-(2)benzofuran)-1-yl)-2-(methylsulfonyl)ethanone. SIMPARICA contains the S-enantiomer of sarolaner.

The chemical structure of the S-enantiomer of sarolaner is: Indications: SIMPARICA kills adult fleas, and is indicated for the treatment and prevention of flea infestations (Ctenocephalides felis), and the treatment and control of tick infestations [Amblyomma americanum (Lone Star tick), Amblyomma maculatum (Gulf Coast tick), Dermacentor variabilis (American dog tick), and Rhipicephalus sanguineus (brown dog tick)] for one month in dogs 6 months of age or older and weighing 2.8 pounds or more.

Dosage and Administration: SIMPARICA is given orally once a month at the recommended minimum dosage of 0.91 mg/lb (2 mg/kg).

Dosage Schedule: F

F

F

O

N

O

CI

F

CI

N

O

O

S

O

Body Weight 2.8 to 5.5 lbs 5.6 to 11.0 lbs 11.1 to 22.0 lbs 22.1 to 44.0 lbs 44.1 to 88.0 lbs 88.1 to 132.0 lbs >132.1 lbs

SAROLANER per Tablet (mg) Number of Tablets Administered 5 One 10 One 20 One 40 One 80 One 120 One Administer the appropriate combination of tablets

SIMPARICA can be offered by hand, in the food, or administered like other tablet medications.

Care should be taken that the dog consumes the complete dose, and treated animals should be observed for a few minutes to ensure that part of the dose is not lost or refused.

If a dose is missed, administer SIMPARICA and resume a monthly dosing schedule.

SIMPARICA should be administered at monthly intervals.

Flea Treatment and Prevention: Treatment with SIMPARICA may begin at any time of the year. In areas where fleas are common year-round, monthly treatment with SIMPARICA can continue the entire year without interruption.

To minimize the likelihood of flea re-infestation, it is important to treat all dogs and cats within a household with an approved flea control product.

Tick Treatment and Control: Treatment with SIMPARICA can begin at any time of the year (see Effectiveness).

Contraindications: There are no known contraindications for the use of SIMPARICA. Warnings: Not for use in humans. Keep this and all drugs out of reach of children and pets. For use in dogs only. Do not use SIMPARICA in cats.

SIMPARICA should not be used in dogs less than 6 months of age (see Animal Safety).

Precautions: SIMPARICA may cause abnormal neurologic signs such as tremors, decreased conscious proprioception, ataxia, decreased or absent menace, and/or seizures (see Animal Safety).

The safe use of SIMPARICA has not been evaluated in breeding, pregnant, or lactating dogs.

Adverse Reactions: SIMPARICA was administered in a well-controlled US field study, which included a total of 479 dogs (315 dogs treated with SIMPARICA and 164 dogs treated with active control once monthly for three treatments).

Over the 90-day study period, all observations of potential adverse reactions were recorded.

Table 1. Dogs with adverse reactions Adverse reaction

sarolaner N

Vomiting Diarrhea Lethargy Inappetence

3 2 1 0

sarolaner % (n = 315) 0.95% 0.63% 0.32% 0%

active control N 9 2 2 3

active control % (n =164) 5.50% 1.20% 1.20% 1.80%

Additionally, one female dog aged 8.6 years exhibited lethargy, ataxia while posturing to eliminate, elevated third eyelids, and inappetence one day after receiving SIMPARICA concurrently with a heartworm preventative (ivermectin/pyrantel pamoate). The signs resolved one day later. After the day 14 visit, the owner elected to withdraw the dog from the study.

TVP-2017-0102_FEATURE_CE_IRIS-CKD.indd 51 1 ZOSI15_052_SINGLE_PI_8.125x10.875_MECH.indd

For a copy of the Safety Data Sheet (SDS) or to report adverse reactions call Zoetis Inc. at 1-888-963-8471. Additional information can be found at www.SIMPARICA.com. For additional information about adverse drug experience reporting for animal drugs, contact FDA at 1-888-FDA-VETS or http://www.fda.gov/AnimalVeterinary/SafetyHealth.

Clinical Pharmacology: Sarolaner is rapidly and well absorbed following oral administration of SIMPARICA. In a study of 12 Beagle dogs the mean maximum plasma concentration (Cmax) was 1100 ng/mL and the mean time to maximum concentration (Tmax) occurred at 3 hours following a single oral dose of 2 mg/kg to fasted animals. The mean oral bioavailability was 86% and 107% in fasted and fed dogs, respectively. The mean oral T1/2 values for fasted and fed animals was 10 and 12 days respectively.

Sarolaner is distributed widely; the mean volume of distribution (Vdss) was 2.81 L/kg bodyweight following a 2 mg/kg intravenous dose of sarolaner. Sarolaner is highly bound (≥99.9%) to plasma proteins. The metabolism of sarolaner appears to be minimal in the dog. The primary route of sarolaner elimination from dogs is biliary excretion with elimination via the feces.

Following repeat administration of SIMPARICA once every 28 days for 10 doses to Beagle dogs at 1X, 3X, and 5X the maximum intended clinical dose of 4 mg/kg, steady-state plasma concentrations were reached after the 6th dose. Following treatment at 1X, 3X, and 5X the maximum intended clinical dose of 4 mg/kg, sarolaner systemic exposure was dose proportional over the range 1X to 5X. Mode of Action: The active substance of SIMPARICA, sarolaner, is an acaricide and insecticide belonging to the isoxazoline group. Sarolaner inhibits the function of the neurotransmitter gamma aminobutyric acid (GABA) receptor and glutamate receptor, and works at the neuromuscular junction in insects. This results in uncontrolled neuromuscular activity leading to death in insects or acarines.

Effectiveness: In a well-controlled laboratory study, SIMPARICA began to kill fleas 3 hours after initial administration and reduced the number of live fleas by ≥96.2% within 8 hours after flea infestation through Day 35.

In a separate well-controlled laboratory study, SIMPARICA demonstrated 100% effectiveness against adult fleas within 24 hours following treatment and maintained 100% effectiveness against weekly re-infestations for 35 days.

In a study to explore flea egg production and viability, SIMPARICA killed fleas before they could lay eggs for 35 days. In a study to simulate a flea-infested home environment, with flea infestations established prior to the start of treatment and re-infestations on Days 7, 37 and 67, SIMPARICA administered monthly for three months demonstrated >95.6% reduction in adult fleas within 14 days after treatment and reached 100% on Day 60.

In well-controlled laboratory studies, SIMPARICA demonstrated ≥99% effectiveness against an initial infestation of Amblyomma americanum, Amblyomma maculatum, Dermacentor variabilis, and Rhipicephalus sanguineus 48 hours post-administration and maintained >96% effectiveness 48 hours post re-infestation for 30 days.

In a well-controlled 90-day US field study conducted in households with existing flea infestations of varying severity, the effectiveness of SIMPARICA against fleas on Day 30, 60 and 90 visits compared to baseline was 99.4%, 99.8%, and 100%, respectively. Dogs with signs of flea allergy dermatitis showed improvement in erythema, papules, scaling, alopecia, dermatitis/pyodermatitis and pruritus as a direct result of eliminating fleas.

Animal Safety: In a margin of safety study, SIMPARICA was administered orally to 8-week-old Beagle puppies at doses of 0, 1X, 3X, and 5X the maximum recommended dose (4 mg/kg) at 28-day intervals for 10 doses (8 dogs per group). The control group received placebo tablets. No neurologic signs were observed in the 1X group. In the 3X group, one male dog exhibited tremors and ataxia post-dose on Day 0; one female dog exhibited tremors on Days 1, 2, 3, and 5; and one female dog exhibited tremors on Day 1. In the 5X group, one female dog had a seizure on Day 61 (5 days after third dose); one female dog had tremors post-dose on Day 0 and abnormal head coordination after dosing on Day 140; and one female dog exhibited seizures associated with the second and fourth doses and tremors associated with the second and third doses. All dogs recovered without treatment. Except for the observation of abnormal head coordination in one dog in the 5X group two hours after dosing on Day 140 (dose 6). There were no treatment-related neurological signs observed once the dogs reached the age of 6 months.

In a separate exploratory pharmacokinetic study, one female dog dosed at 12 mg/kg (3X the maximum recommended dose) exhibited lethargy, anorexia, and multiple neurological signs including ataxia, tremors, disorientation, hypersalivation, diminished proprioception, and absent menace, approximately 2 days after a third monthly dose. The dog was not treated, and was ultimately euthanized. The first two doses resulted in plasma concentrations that were consistent with those of the other dogs in the treatment group. Starting at 7 hours after the third dose, there was a rapid 2.5 fold increase in plasma concentrations within 41 hours, resulting in a Cmax more than 7-fold higher than the mean Cmax at the maximum recommended use dose. No cause for the sudden increase in sarolaner plasma concentrations was identified.

Storage Information: Store at or below 30°C (86°F) with excursions permitted up to 40°C (104°F).

How Supplied: SIMPARICA (sarolaner) Chewables are available in six flavored tablet sizes: 5, 10, 20, 40, 80, and 120 mg. Each tablet size is available in color-coded packages of one, three, or six tablets.

NADA #141-452, Approved by FDA

Distributed by: Zoetis Inc. Kalamazoo, MI 49007 Made in Switzerland December 2015

30491300A&P

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PEER REVIEWED

Treatment Guidelines for Chronic Kidney Disease in Dogs & Cats LEARNING OBJECTIVES

After reading this article, participants will be able to identify the IRIS stages of CKD and understand how staging guides further diagnostics and treatment.

OVERVIEW

This article illustrates appropriate diagnostic and therapeutic management of dogs and cats with CKD based on differentiation of the patientâ&#x20AC;&#x2122;s stage of CKD.

1. In Stage 1 and early stage 2 CKD, the primary treatment strategy is: a. Reducing patient clinical signs and improving quality of life b. Renoprotective therapies to slow progression of kidney disease c. Identification and correction of primary or complicating diseases d. Correction of anemia e. Correction of acidosis

5. Which of the following is not compatible with a diagnosis of Stage 1 CKD? a. Primary polydipsia b. Renal palpation or imaging abnormalities c. Persistent renal proteinuria d. Persistent increases in SDMA in a nonazotemic patient e. Increase in serum creatinine > 0.3 mg/dL within the reference interval that is not associated with changes in muscle mass or hydration

2. In mid Stage 2 and Stage 3 CKD, the primary treatment strategy is: a. Reducing patient clinical signs and improving quality of life b. Renoprotective therapies to slow progression of kidney disease c. Identification and correction of primary or complicating diseases d. Correction of anorexia/calorie malnutrition e. Correction of potassium depletion

6. The IRIS CKD staging system should be used as a guide to diagnose CKD in dogs and cats. a. True b. False

3. In late Stage 3 and Stage 4 CKD, the primary treatment strategy is: a. Reducing patient clinical signs and improving quality of life b. Renoprotective therapies to slow progression of kidney disease c. Identification and correction of primary or complicating diseases d. Reduction of serum SDMA concentrations e. Gradual transition to a renal diet 4. Serum creatinine concentrations can be influenced by: a. Prerenal dehydration b. Postrenal urethral obstruction c. Patient muscle mass d. Breed characteristics e. All of the above

NOTE

Questions online may differ from those here; answers are available once CE test is taken at vetmedteam.com/tvp.aspx.

Tests are valid for 2 years from date of approval.

52

This article is RACEapproved for 1 hour of continuing education credit.

To receive credit, take the approved test online at vetmedteam.com/tvp.aspx (CE fee of $5/article).

7. Renal proteinuria is: a. Always associated with a UPC > 1 b. Intermittent and often transient c. Frequently associated with an active urine sediment d. Either of glomerular or tubular origin e. Of no prognostic significance in CKD 8. Which of the following is not thought to contribute to renal disease progression? a. Soft tissue mineralization b. Intraglomerular hypertension c. Proteinuria d. Anorexia/calorie malnutrition e. Glomerulosclerosis 9. Dogs and cats with Stage 1 CKD will invariably progress to Stage 2 CKD. a. True b. False 10. Which of the following is most important in the management of anorexia/calorie malnutrition? a. Correction of dehydration b. Use of appetite stimulants c. Use of gastric acid blocking drugs d. Use of antiemetics e. Providing dietary variety

CHRONIC KIDNEY DISEASE IN DOGS & CATS

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CONTINUING EDUCATION CHRONIC KIDNEY DISEASE IN DOGS & CATS continued from page 50

8. Syme HM, Markwell PJ, Pfeiffer D, Elliott J. Survival of cats with naturally occurring chronic renal failure is related to severity of proteinuria. J Vet Intern Med 2006; 20(3):528-535.

9. Polzin DJ, Osborne CA, Ross S, Jacob F. Dietary management of feline chronic renal failure: Where are we now? In what direction are we headed? J Feline Med Surg 2000; 2(2):75-82.

10. Jacob F, Polzin DJ, Osborne CA, et al. Clinical evaluation of dietary modification for treatment of spontaneous renal failure in dogs.

JAVMA 2002; 220(8):1163-1170.

11. Grauer GF, Greco DS, Getzy DM, et al. Effects of enalapril versus placebo as a treatment for canine idiopathic glomerulonephritis. J Vet Intern Med 2000; 14(5):526-533.

12. King JN, Gunn-Moore DA, Tasker S, et al. Tolerability and efficacy of benazepril in cats with chronic kidney disease. J Vet Intern Med 2006; 20(5):1054-1064.

13. Jenkins TL, Coleman AE, Schmiedt CW, Brown SA. Attenuation of the pressor response to exogenous angiotensin by angiotensin receptor blockers and benazepril hydrochloride in clinically normal cats. Am J Vet Res 2015; 76(9):807-813.

14. Sent U, Gossl R, Elliott J, et al. Comparison of efficacy of long-term oral treatment with telmisartan and benazepril in cats with chronic kidney disease. J Vet Intern Med 2015; 29:1479-1487.

15. Atkins CE, Rausch WP, Gardner SY, et al. The effect of amlodipine and the combination of amlodipine and enalapril on the reninangiotensin-aldosterone system in the dog. J Vet Pharmacol Ther 2007; 30(5):394-400.

16. Jepsen RE, Syme HM, Elliott J. Plasma renin activity and aldosterone concentrations in hypertensive cats with and without azotemia and in response to amlodipine besylate. J Vet Intern Med 2014; 28(1):144-153.

17. Polzin D, Ross S, Osborne C, et al. Clinical benefit of calcitriol in canine chronic kidney disease (abstract). J Vet Intern Med 2005; 19:433.

18. Lippi I, Guidi G, Marchetti V, et al. Prognostic role of the product of serum calcium and phosphorus concentrations in dogs with chronic kidney disease: 31 cases (2008-2010). JAVMA 2014; 245(10):11351140.

19. Parkinson S, Tolbert K, Messenger K, et al. Evaluation of the effect of orally administered acid suppressants on intragastic pH in cats. J Vet Intern Med 2015; 29(1):104-112.

20. Quimby JM, Brock WT, Moses K, et al. Chronic use of maropitant for the management of vomiting and inappetence in cats with chronic kidney disease: A blinded, placebo-controlled clinical trial. J Fel Med Surg 2015; 17(8):692-697.

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Don’t miss out on the veterinary profession’s premier internal medicine continuing education event.

Register by April 30, 2017 to get 15% off full general registration using code 2017VMA. www.ACVIMForum.org

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Interpretation of Dental Radiographs in Dogs & Cats Part 1: Principles & Normal Findings Santiago Peralta, DVM, DAVDC, and Nadine Fiani, BVSc, DAVDC, Cornell University

Dental radiography is considered part of the standard of care for dogs and cats undergoing dental intervention.1,2 Radiographs are essential for identifying and documenting the nature and severity of dental disorders and conditions.3-5 Dental radiographs often reveal relevant clinical information that would be missed based solely on an oral examination (ie, visual examination and periodontal probing), underscoring the critical role of radiographs as part of a systematic diagnostic approach.4,5

QUALITY OF RADIOGRAPHS The diagnostic quality and potential utility of dental radiographs are influenced by many factors, including:6,7

• Patient positioning • Radiographic projections • Radiographic exposure time • Quality of processing.

All of these purely technical aspects of radiography can be optimized by following standard procedures, as have been described elsewhere.7,8 Diagnostic-

quality radiographs can be achieved with relative ease via proper training, practice, and experience.

Specialized equipment is also required, including a dental X-ray generator and an analog or computerized dental radiograph processing system.9

DIAGNOSTIC POTENTIAL From a purely medical perspective, it is the clinician’s ability to identify lesions of potential clinical interest and interpret them in the context of the individual patient’s signalment, history, and clinical findings, which ultimately leads to an accurate diagnosis and adequate treatment planning.

Normal radiographic findings are defined as those consistent with what is considered typical, average, or expected and are free of any indicators of disease.

Normal variations are defined as radiographic findings that deviate from what is considered typical, average, or expected but that would not otherwise indicate any preventive or therapeutic medical or surgical intervention, monitoring, or maintenance recommendations.

Abnormal radiographic findings are any findings considered pathologic.

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Proper dental radiographic interpretation requires knowledge of normal anatomic structures and a solid understanding of the pathogenic mechanisms involved with dental diseases, disorders, and conditions that affect dogs and cats. This article describes the most basic skills and knowledge required for radiographic interpretation, as well as the radiographic characteristics of teeth and surrounding tissues and structures during health and disease.

Interpretation of Dental Radiographs in Dogs & Cats Part 1 of this article series: •D escribes appropriate mounting and display of radiographic films/plates for reviewing purposes •E xplains a recommended workflow to review radiographs and record findings •P resents radiographic examples of normal relevant structures.

Part 2 focuses on common normal radiographic variations, as well as abnormal findings, including explanations of the underlying disease processes when pertinent, comments on the diagnostic limitations of dental radiography, and current imaging alternatives.

The articles in this series assume the reader is familiar with basic dental radiographic acquisition techniques, concepts, and skills.

ORIENTING & MOUNTING DENTAL RADIOGRAPHS Dental radiographic interpretation starts with the correct display and mounting of the

A

B

FIGURE 1. Intraoral radiograph (A) of the right maxillary premolar and molar teeth in a 5-year-old cat; extraoral radiograph (B) showing the same teeth in 3-year-old cat. The dotted lines show the trajectory of the zygomatic arches on both radiographs, illustrating how more superimposition with structures of interest occurs in the intraoral view than in the extraoral view.

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images. Radiographs are typically obtained intraorally, although some clinicians prefer an extraoral view when imaging the maxillary premolar/molar region in cats (Figure 1).

Display Whether using films or plates, ensure that the radiograph is displayed on the correct side.

With film, a raised dot (or bubble) can be observed or felt with the fingers at one of its corners. Except when using extraoral technique, this dot marks the plate’s exposed side; it should be on the top side when viewing the film.

With computerized systems, the image usually is displayed automatically on the computer screen in the way it was exposed. However, care must be taken not to accidentally invert the radiograph (most software programs have this function) because the mirror image created may be confused as a radiograph from the opposite side of the mouth (Figure 2).

Because the dental radiographic software assumes the radiographs are obtained intraorally, the only time a radiograph should be inverted intentionally is when an extraoral projection is used.

Mounting In the majority of patients, a full-mouth study is obtained preoperatively; individual images are usually obtained only under specific circumstances (eg, during/ after surgery, for follow-up studies of individual teeth).

A

B

FIGURE 2. Lateral intraoral radiograph (A) of the right maxillary canine tooth in an 8-year-old dog; the radiograph is oriented properly based on dental radiographic viewing standards. Mirror image (B) of the same tooth that would be confused as the left maxillary canine tooth based on its orientation.

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The total number of radiographs may range from 10 to 20, depending on size of the animal, but the images are always displayed based on labial mounting (Figure 3). Labial mounting consists of organizing images with the:

• Maxillary radiographs shown on the upper half of the study • Mandibular radiographs on the lower half • Radiographs of the patient’s right side on the left • Radiographs of the patient’s left side on the right.

The first step when mounting is to determine whether the radiographs correspond to maxillary or mandibular dentition and rotate them as needed, with the maxillary teeth pointed downward and mandibular teeth pointed upward. Identifying structures unique to the maxilla or mandible assists the process:

• The presence of the palatine fissures and/ or nasal turbinates, or the characteristic shapes, size, and number of roots of the maxillary fourth premolar and molar teeth, identify radiographs of maxillary teeth.

• In contrast, presence of the mandibular symphysis, mandibular canal, mental foramina, or ventral mandibular cortex, or the characteristic shapes, size, and number of roots of the mandibular first, second, and third molar teeth, indicates mandibular dentition.

FIGURE 3. Labially mounted full-mouth radiographic study from a 5-year-old dog. The maxillary (Max) teeth are displayed on the upper half, and the mandibular (Mand) teeth are displayed on the lower half. The letters R and L indicate the right and left sides, respectively.

The next step is to assign radiographs to the left, center, or right of the study. Initially, the two occlusal radiographs (ie, one maxillary, one mandibular) are placed in the center. For all other radiographs, the dentition present is identified in order to place the film/plate on the side in which the mesial teeth are located closer, and the distal teeth farther, to the occlusal radiograph.

RECOMMENDED WORKFLOW Once the full-mouth study is mounted properly, the radiographs are ready for review.

Radiographs usually are reviewed twice.

The first review occurs during the treatment planning stage, usually while the patient is under general anesthesia (Figure 4). The ideal time for review is after dental charting has been completed and the animal is receiving complete periodontal treatment (ie, supra- and subgingival ultrasonic scaling with or without hand scaling) prior to any surgical intervention as indicated by clinical and radiographic findings (eg, extractions, biopsy, periodontal surgery, endodontic therapy).

This initial radiograph review should be performed in the context of the oral examination findings that were recorded in the patient’s chart. This allows the clinician to establish a tooth-by-tooth diagnosis and decide whether disease is present and, if so, which treatment is indicated.

FIGURE 4. The initial dental radiographic review usually occurs in a clinical setting. The clinical findings (dental chart) are compared with the radiographic findings, and a treatment plan is established, usually while the patient is still under general anesthesia.

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A second and more meticulous review is recommended to allow a detailed radiographic report to be written and incorporated into the patient’s medical record.

This can be done after the procedure has ended to avoid unnecessarily prolonging the anesthetic event.

REVIEWING DENTAL RADIOGRAPHS To minimize oversight when reviewing radiographs, establish a routine based on both the order in which the radiographs are examined and certain predetermined categories.

A logical sequence is to examine quadrants in the following order:

• Left maxillary • Left mandibular • Right mandibular.

For each quadrant, review the most mesial tooth first and the most distal tooth last. Assess each quadrant separately based on the following predetermined clinically and radiographically relevant categories.

Anatomic & Developmental Findings Assess the presence, number, and relative size, shape, and direction of the teeth and corresponding roots and identify dental tissues, anatomic areas of interest, and surrounding structures. All findings should be interpreted with consideration of the age, size, and breed of the patient.

B

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Finally, distinguish radiographically deciduous from permanent teeth. Deciduous teeth are relatively smaller and less radiodense than permanent teeth. Under normal circumstances based on average eruption times, the term mixed dentition is applied when permanent and deciduous teeth are present simultaneously in the oral cavity (Figure 6).

C

FIGURE 5. Lateral intraoral radiograph (A) of the left canine tooth in a 6-month-old dog showing a relatively wide pulp cavity (asterisk), relatively thin dentinal walls, and an incompletely formed apex (black arrow). Radiographs (B and C) corresponding to the same projection and tooth in an 11-month-old dog and a 9-year-old dog, respectively. Compare the differences in apex, pulp width, and dentinal wall thickness, as would be expected based on the animals’ ages.

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Dentin deposition begins prior to tooth eruption and, under physiologic conditions, continues throughout the life of each permanent tooth. Any dentin secreted prior to eruption is called primary dentin. Once the tooth erupts, usually with still very thin dentinal walls, all further dentin secretion that occurs under physiologic conditions is called secondary dentin (Figure 5). As the animal ages, more dentin is secreted and the pulp cavity diameter gradually narrows (see Endodontic Findings).

Apex formation (Figure 5) describes eruption of the permanent tooth prior to full formation of the apex. An incompletely formed apex is often referred to as an open apex. Apex formation lasts a few weeks after eruption and is usually complete by the age of 9 months in both cats and dogs.

• Right maxillary

A

Two normal developmental processes are relevant when evaluating radiographs: dentin deposition and apex formation.

FIGURE 6. Mixed dentition in a 6-month-old dog. The full-mouth study shows the simultaneous presence of erupted deciduous and permanent teeth. L = left; Mand = mandibular teeth; Max = maxillary teeth; R = right.

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What You Need to Know To decide whether radiographic findings are normal, the clinician should be familiar with normal: • Tooth and root anatomy • Tooth and root development stages • Deciduous and permanent dentition formulas • N ormal deciduous tooth exfoliation times • N ormal dental and maxillofacial anatomy • Any pertinent variations among specific breeds.

Periodontal Findings The attachment apparatus of teeth (periodontium) consists of the gingiva, periodontal ligament (PDL), cementum, and alveolar bone (Figure 7).

Alveolar bone is mineralized and large enough to be seen directly on radiographs. Normal alveolar bone should provide coverage to the entire root(s), and its margin should be located immediately apical to the cementoenamel junction (CEJ) of the tooth. In multirooted teeth, the area between roots (ie, furcation) should be occupied evenly by cancellous bone.

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The PDL cannot be seen because it is composed mostly of nonmineralized collagen fibers. Under normal circumstances, however, the space occupied by the PDL can be seen as a relatively narrow, regular, lucent area located between the root(s) and surrounding alveolar bone.

On the osseous side of PDL space, a dense opaque line, referred to as lamina dura, can be traced around all roots. Anatomically, the lamina dura corresponds to the compact bone that normally lines the alveolus.

While cementum is partially mineralized, it is too thin to be discernible on radiographs. Conversely, while gingiva is not usually mineralized, it is thick enough to be visible sometimes on radiographs. If visible, normal gingiva should appear as a subtle soft tissue opacity immediately coronal to the alveolar margin that extends just beyond the CEJ without covering larger areas of the crown.

Endodontic Findings The structures of interest when evaluating the endodontic status of teeth are the pulp cavity, apex, and periapical tissues (Figures 7–10). The integrity of each crown and root is also assessed.

Determining What Constitutes Normal Because radiographs are two-dimensional images often representing complex anatomic structures, care must be taken not to under- or overestimate what may constitute normal findings.

FIGURE 7. Normal periodontal and endodontic findings. Lateral intraoral radiograph (A) of the left maxillary tooth in an 8-year-old showing the alveolar margin (black arrowheads) in close proximity to the cementoenamel junction (CEJ; dotted line). The gingiva is visible as a soft tissue opacity (asterisks) along the alveolar margin. The periodontal ligament (PDL) space can be traced around the entire root as a regular and relatively narrow lucent line surrounded by the lamina dura, seen as a thin, opaque line (yellow arrowhead).

The apex and periapical structures (dotted red circle) show a normal PDL space. Intraoral parallel view (B) of the caudal mandible in an 8-year-old dog showing the same normal structures as shown in A; note the presence of cancellous bone occupying the entire furcation areas of the first and second molar teeth (black arrows).

CEJ and canine alveolar margins: In some cases, additional projections of the same tooth may be necessary. A relevant example is the occlusal view of canine teeth. Because the distance between the CEJ and alveolar margin of canine teeth cannot be established easily on an occlusal projection, a lateral radiograph is necessary to document the periodontal status more accurately (Figure 7 and Figure 9).

CEJ and incisor alveolar margins: In contrast, the periodontal status of the mandibular incisors in dogs does not always correlate with clinical findings and can be overestimated easily. Namely, the radiographs of clinically normal incisors (ie, no mobility, increased probing depth, or gingival recession) often reveal an apparently increased distance between the CEJ and alveolar margin (Figure 8).

In all of these cases, always correlate clinical and radiographic findings prior to establishing a diagnosis and/or making any clinical decisions.

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The pulp cavity—the entire area occupied by the pulp—is divided into three distinct areas: pulp chamber, root canal, and pulp horns in multirooted teeth. As noted, the width of the pulp cavity of permanent teeth decreases with age.

Because this process occurs bilaterally at similar rates, no pulp cavity width discrepancies should be noted when comparing endodontically normal teeth with their contralateral counterparts (Figures 8–10).

The apex refers to the most distal third portion of the root and is the location of the apical delta.

The clinician should always scrutinize the radiographs of areas in which teeth are missing to rule out the presence of retained roots. However, the clinician must be aware that endodontically diseased teeth sometimes appear radiographically normal.

Other Findings With regard to teeth, other findings usually include those that do not fit into any of the above categories.

Because these findings typically correspond to either normal variations or pathologic findings, however, representative examples will be presented in Part 2.

The periapical tissues—the PDL space surrounding the apex and the tissues in its immediate vicinity—should be normal. That is, the width of the PDL space in this area should be consistent with the width of the PDL space on the sides of the root, and no evidence of bone lysis affecting the bone periapically should be present.

Several non-dental structures are visible on dental radiographs that could potentially reveal abnormalities or disease. Therefore, the clinician should be familiar with the normal radiographic appearance of these structures.

Finally, root length and appearance of an endodontically normal tooth should be similar to those of its contralateral counterpart.

The nasal cavity is viewed on maxillary occlusal radiographs (Figure 9). Under normal circumstances, the following should be present:

Nasal Cavity

• Well-defined turbinate pattern

FIGURE 8. Occlusal mandibular radiograph in a 7-yearold dog showing a normal mandibular symphysis (arrowheads). Note the symmetric diameter of the pulp cavity at the left and right canine teeth (asterisks).

The clinical examination revealed periodontally sound mandibular incisors; despite this, note that the alveolar margin is located apical to the cementoenamel junction at all mandibular incisors.

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FIGURE 9. Intraoral occlusal maxillary radiograph in a 6-year-old dog illustrating the difficulty in assessing the periodontal status (ie, distance between the alveolar margin and CEJ) at the canine teeth (white arrowheads). Note that the pulp cavities of both canine teeth are of similar diameter, which is expected in endodontically healthy teeth, as well as the normal turbinate pattern present in the nasal cavity.

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• Relatively symmetric separation of right and left cavities by vomer and septum • Palatine fissures clearly visible as two distinct lucent round or oval-shaped structures caudal to the maxillary incisor teeth.

Mandibular Structures

A normal mandibular symphysis appears radiographically as a relatively narrow lucent line that joins the two mandibles at the midline, with the right and left mandibular incisors in symmetric occlusion. The mandibular symphysis can be relatively linear, although in cats it follows more of a zigzag pattern (Figures 8 and 10).

The mandibular bodies should also be assessed.

Despite some degree of variability among dog breeds with regard to shape and relative size, the mandibular canal should be visible as a relatively lucent linear structure occupying the middle and/or ventral third of the mandibular body (Figure 11).

In cats and medium- to large-breed dogs, the roots of the mandibular premolar and molar teeth are located

in the area most dorsal to the canal; in small dogs, the roots of the mandibular fourth premolar and first molar teeth extend into and/or beyond the canal and, in some cases, to the level of the ventral cortex of the mandible.

To avoid misinterpreting them as pathologic findings, note the appearance and typical location of the middle and caudal mental foramina. These structures are usually well defined radiographically and appear as round or oval-shaped lucencies ventral to the first and/or second mandibular premolar teeth and third and/or fourth mandibular premolar teeth, sometimes overlapping with the apex of one of the roots (Figure 12).

A

B

C

D

FIGURE 11. Intraoral parallel radiographs showing the normal appearance of the mandibular canal in the caudal mandibular body area. Note the relative position and size of the associated roots in an 8-year-old small dog (A), 4-year-old large dog (B), 12-year-old cat (C), and 7-year-old medium-sized dog (D).

FIGURE 10. Occlusal mandibular radiograph in a 4-year-old cat showing symmetric diameter in pulp cavity width at both canine teeth (asterisks) and the typical zigzag appearance of the mandibular symphysis (arrowheads).

FIGURE 12. Intraoral radiograph of the rostral mandibular premolar area showing the middle and distal mental foramina (arrows).

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The most caudal areas of the mandibular body and the ramus are not visible on dental radiographs. Other imaging modalities should be considered, if medically indicated.

Temporomandibular Joint

The use of dental films for extraoral imaging of the temporomandibular joint has been described;10 however, examples are not included in this article because the diagnostic yield is poor, especially compared with advanced imaging modalities, and imaging of this structure is beyond what is considered dental radiography.

References 1.

Eisner ER. Standard of care in North American small animal dental service. Vet Clin North Am Small Anim Pract 2013; 43:447-469.

2. Holmstrom SE, Bellows J, Juriga S, et al. 2013 AAHA dental care guidelines for dogs and cats. JAAHA 2013; 49:75-82.

3. Lommer MJ, Verstraete FJ. Radiographic patterns of periodontitis in cats: 147 cases (1998-1999). JAVMA 2001; 218:230-234.

Glossary CEJ cementoenamel junction PDL periodontal ligament

7. Tsugawa AJ, Verstraete FJ. How to obtain and interpret periodontal radiographs in dogs. Clin Tech Small Anim Pract 2000; 15:204-210.

8. Lommer MJ, Verstraete FJ, Terpak CH. Dental radiographic technique in cats. Comp Cont Educ Pract Vet 2000; 22:107-116.

9. Coffman CR, Brigden GM. Oral and dental imaging equipment and techniques for small animals. Vet Clin North Am Small Anim Pract 2013;43:489-506.

10. DuPont GA, DeBowes LJ, (eds). Temporomandibular joint. In Atlas of Dental Radiography in Dogs and Cats. Saint Louis, MO: Saunders Elsevier, 2009, pp 122-133.

11. Lommer MJ, Verstraete FJ, Terpak CH. Dental radiographic technique in cats. Compend Contin Educ Pract Vet 2000; 22:107-116.

12. Floyd MR. The modified Triadan system: Nomenclature for veterinary dentistry. J Vet Dent 1991; 8:18-19.

13. White SC, Pharoah MJ (eds). Oral Radiology: Principles and Interpretation. 6th ed. St. Louis: Mosby/Elsevier, 2009.

4. Verstraete FJ, Kass PH, Terpak CH. Diagnostic value of full-mouth radiography in dogs. Am J Vet Res 1998; 59:686-691.

5. Verstraete FJ, Kass PH, Terpak CH. Diagnostic value of full-mouth radiography in cats. Am J Vet Res 1998; 59:692-695.

6. Lemmons M. Clinical feline dental radiography. Vet Clin North Am Small Anim Pract 2013; 43:533-554.

Santiago Peralta

Santiago Peralta, DVM, DAVDC, is an assistant professor of dentistry and oral surgery at Cornell University College of Veterinary Medicine. His clinical and research interests include the microbial pathogenesis of dental diseases, comparative aspects of maxillofacial birth defects, comparative aspects of maxillofacial imaging, and molecular mechanism of oral tumor formation in dogs and cats. Dr. Peralta received his DVM from Universidad de La Salle in Bogota, Colombia and completed a 3-year residency in dentistry and oral surgery at the University of CaliforniaDavis.

Nadine Fiani

Nadine Fiani, BVSc, DAVDC, is an assistant clinical professor of dentistry and oral surgery at Cornell University College of Veterinary Medicine. She has an interest in education and a clinical interest in endodontics and zoo dentistry. Dr. Fiani received her veterinary degree from the University of Sydney and completed a rotating internship followed by a 3-year residency in dentistry and oral surgery at the University of California Davis. Prior to her current position, Dr. Fiani spent 3 years in private referral practice in Sydney.

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Notes on Images All radiographic images are representative examples that support the explanations presented in the article. They are displayed based on labial mounting and considered to be of diagnostic quality. Some of the images have been cropped, but the structures of interest have not been altered or enhanced in any way.

All images were acquired following standard technique for small animals7,11 using a commercially available dental X-ray unit (Heliodent DS, Sirona, Bensheim, Germany) and a computerized radiographic processor using phosphor plates of size 0, 2, or 4 with corresponding software (CS7600, Carestream, Rochester, NY). Due to space limitations, most radiographs shown are from dogs, but radiographs from cats are included if a feline-specific point needs to be made.

In case some readers are unfamiliar with other accepted systems (ie, modified Triadan), anatomic dental nomenclature is used here.12 For more information, interested readers are encouraged to consult a more specialized source.13

The College of Veterinary Medicine at Cornell University (CVM) owns and retains the copyrights to all images. The CVM grants permission to use the provided images within the context of the articles titled Interpretation of Dental Radiographs in Dogs & Cats - Part 1: Principles & Normal Findings and Interpretation of Dental Radiographs in Dogs & Cats - Part 2: Abnormal Findings.

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Interpretation of Dental Radiographs in Dogs & Cats Part 1: Principles & Normal Findings LEARNING OBJECTIVES

After reading this article, clinicians should: • Recognize the importance of appropriately mounting and displaying dental radiographic films/plates for review and interpretation purposes • Understand how to establish a reproducible workflow to review and record pertinent findings systematically • Be able to describe how normal dental and associated structures appear radiographically.

OVERVIEW

This article is RACE-approved for 1 hour of continuing education credit.

To receive credit, take the approved test online at vetmedteam.com/ tvp.aspx (CE fee of $5/article).

This article, page 55, is the first of two articles that focus on interpretation of dental radiographs in dogs and cats. It includes basic principles of dental radiographic interpretation and describes normal radiographic findings.

1. Choose the most appropriate orientation for the radiograph shown below.

3. Which of the following statements about dental radiography in dogs and cats is TRUE? a. Full-mouth radiographic studies are not recommended. b. Radiographs are not necessary if dental charting was performed. c. Dental radiographs are by definition always obtained intraorally. d. Radiographs and dental charting are both necessary to establish a diagnosis and treatment plan.

4. From what type of animal was the following radiograph most likely obtained?

a. Rotate the image 90 degrees clockwise. b. Rotate the image 180 degrees. c. Rotate the image 90 degrees counterclockwise. d. The image should remain as it is.

2. What structure does the radiograph in Question 1 show? a. Right maxillary canine tooth b. Left maxillary canine tooth c. Left mandibular canine tooth d. Right mandibular canine tooth

NOTE

a. b. c. d.

6-month-old dog 6-year-old dog 12-year-old dog Cannot determine based on the image

Questions online may differ from those here; answers are available once CE test is taken at vetmedteam.com/tvp.aspx.

Tests are valid for 2 years from date of approval.

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5. What type of radiograph is shown in Question 4? a. Standard extraoral view of the rostral maxilla b. Standard occlusal radiograph of the mandible c. Standard occlusal view of the maxilla d. Cannot determine based on the image 6. Assuming both are appropriately displayed (ie, based on labial mounting), which of the following images corresponds to the left mandibular molar/premolar teeth?

7. What structures are part of the periodontium? a. Gingiva, apical delta, cementum, periodontal ligament b. Gingiva, pulp, cementum, periodontal ligament c. Gingiva, alveolar bone, cementum, periodontal ligament d. None of the above 8. What is the area occupied by the dental pulp and surrounded by dentinal walls? a. Root canal b. Pulp cavity c. Pulp canal d. Pulp chamber 9. What are the radiographic areas of interest when evaluating the endodontic status of a tooth? a. Integrity of the crown and root b. Relative pulp cavity width c. Periapical structures d. All of the above

a. b. c. d .

10. Which of the following cannot be assessed using standard dental radiographic technique? a. Mandibular ramus b. Alveolar bone height relative to the cementoenamel junction c. Mandibular body d. Mandibular symphysis

Top image Bottom image Neither Both

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ACVN NUTRITION NOTES

Featuring Fiber: Understanding Types of Fiber & Clinical Uses Deborah E. Linder, DVM, MS, DACVN Cummings School of Veterinary Medicine at Tufts University shutterstock.com/Chutima Chaochaiya

The American College of Veterinary Nutrition (acvn.org) and Today’s Veterinary Practice are delighted to bring you the Nutrition Notes column, which provides the highest-quality, cutting-edge information on companion animal nutrition, written by the ACVN’s foremost nutrition specialists.

The primary objectives of the ACVN are to: • Advance the specialty area of veterinary nutrition • I ncrease the competence of those practicing in this field • Establish requirements for certification in veterinary nutrition ncourage continuing education for both specialists •E and general practitioners

Understanding the different types of fiber— and when to implement fiber in a nutrition plan for dogs and cats—can be challenging and complicated. In addition, some cats and dogs that present with gastrointestinal conditions can be managed with diets or supplements that contain particular levels and types of fiber.

Choosing an ideal diet or supplement may involve a trial-and-error process to determine the exact fiber needs of each individual pet. Ongoing communication with clients during this process plays an integral role in successful management.

• Promote evidence-based research

DEFINING FIBER

•E nhance dissemination of the latest veterinary nutrition knowledge.

The different types of fiber can be defined in 2 ways:

The ACVN achieves these objectives in many ways, including designating specialists in animal nutrition, providing continuing education through several media, supporting veterinary nutrition residency programs, and offering a wide array of resources related to veterinary nutrition, such as this column.

• By fiber solubility • By fiber fermentability.

Solubility describes how fibers are able to disperse in water (Table 1, page 70), while fermentability describes the rate at which fibers produce short-chain fatty acids (SCFAs) through the help of microorganisms.

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TABLE 1 Examples of Fiber Sources in Pet Foods1 Soluble fibers

Guar gum, pectin, carrageen

Insoluble fibers

Cellulose, lignin

Mixed fiber source

Beet pulp, psyllium

These definitions have some crossover as many soluble fibers also tend to be highly fermentable.

In a clinical setting, however, describing fibers by their solubility in water is the most relevant because solubility:

• Directly affects composition of feces • Is easier to measure than fermentability, which makes information on solubility more readily available.

Insoluble Fiber Insoluble fibers, such as cellulose, increase fecal output and, in doing so, stimulate motility in the intestines and increase intestinal transit time. High amounts of insoluble fiber can often be found in veterinary therapeutic diets formulated for canine diabetes, feline hairball control, or weight management.

However, take caution when supplementing with large amounts, as insoluble fiber can mildly alter nutrient digestibility.2-3 Diets formulated by high-quality pet food companies, though, take this change in digestibility into account and alter the nutrient content of diets accordingly.

FIBER SOLUBILITY

Client Communication Tip

Soluble Fiber

What determines whether pet food companies are producing high-quality products?

Soluble fibers, such as pectins and gums, are the types of fiber that best absorb water. These fibers are usually also highly fermentable, which means that bacteria convert the fibers rapidly to SCFAs, the preferred energy source for cells in the colon.

Adding soluble fiber can promote healthy colonic mucosa and immune function in the lower intestine.

However, increasing soluble fiber—whether by supplement or selecting a diet high in soluble fiber—should be done slowly and incrementally to allow adaptation of the intestinal microbiome to the new amount of fermentable material.

Client Communication Tip Insoluble “woody” fibers are more than fillers.

Insoluble fibers, such as lignin or cellulose, are frequently obtained from “woody plants” that are not generally considered food sources.

Rather, these fibers are part of the cell wall that allows plants to maintain their structure. The media sometimes misconstrues this information to mean that wood or cardboard are cheap fillers used in pet food to save money. However, insoluble fibers serve many therapeutic functions and are intentionally used in pet foods to improve gut health and help, not hurt, pets.

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The World Small Animal Veterinary Association (WSAVA) has created guidelines that help pet owners and veterinarians determine whether companies are producing highquality products. For example, does a company employ board-certified veterinary nutritionists and PhDlevel animal nutrition scientists to properly formulate and test foods? A full list of the guidelines is available at wsava.org/nutrition-toolkit. 4

FIBER ON THE LABEL The term “high fiber” can be confusing, as fiber is added and analyzed in pet foods in many different ways. Pet food labels are only required to have the guaranteed analysis—the maximum or minimum percentage of nutrients on an as-fed, or by weight, basis. This means, for example, that a pet food with maximum 12% crude fiber has no more than 12 grams of crude fiber for every 100 grams of total pet food. However, since the amount is a maximum, it could have any amount less than 12%.

Information in this format is not very helpful to veterinarians or pet owners when comparing

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fiber content between diets or estimating the typical amount of fiber in each batch of food.

Furthermore, crude fiber on these labels only accounts for a variable portion of insoluble fibers; it does not provide total content of fiber.

To estimate the overall fiber in diets, obtain the total dietary fiber (TDF), which includes soluble and insoluble fiber, on an energy basis (grams/ Megacalorie [Mcal; 1000 kcal]) from the typical analysis—not guaranteed analysis—of the diet.

This way, fiber content can be compared among diets of differing calorie or moisture content (Table 2). A typical or average nutrient analysis of TDF should be in company product guides or available by contacting the manufacturer.

Owners may be quick to look to the ingredient list to determine soluble or insoluble fiber ingredients, but the total amount of fiber in the diet is not known without the TDF. While TDF is not precise because TABLE 2 Example of Comparing Diet Profiles DIET A NUTRIENT PROFILE

DIET B NUTRIENT PROFILE

Total dietary fiber (g/Mcal)

54.9

25.1

Crude fiber (g/Mcal)

27.9

4.6

11.3

10

Cellulose, psyllium

Beet pulp, psyllium

27.9

4.6

27

22.4

54.9

25.1

TYPICAL ANALYSIS

GUARANTEED ANALYSIS Maximum crude fiber (%) Ingredients ROUGH ESTIMATES Insoluble fiber (g/Mcal) Soluble fiber (g/Mcal) Total fiber (g/Mcal)

Commentary: In this case, because the guaranteed analysis only appears to show a 1% difference in fiber, a pet owner may be led to think these diets are close in fiber content. When the fiber amounts are compared using the rough estimate and typical analysis, however, Diet A has twice the total fiber of Diet B. In addition, while both provide soluble fibers with psyllium ingredients, Diet A has 6× more insoluble fiber. This is an important consideration when comparing diets and deciding which one will benefit the patient based on the types of fiber present. Calling pet food companies to inquire about fiber content and breakdown of types of fiber can ensure accuracy of fiber content and appropriate use.

not all insoluble fibers are measured using crude fiber analysis, a rough estimate of total, insoluble, and soluble fiber can be obtained with the TDF and crude fiber information on an energy basis. However, it is also important to note that individual animals (and their microbes) may respond differently to specific sources of fiber or combinations of specific compounds, so trial and error of diets may still be necessary for personalized care of each cat or dog.

Client Communication Tip Pet food labels are not helpful in comparing dietary fiber.

Let owners know that the pet food label is not helpful in comparing fiber among diets. The best way to compare is to ask companies to provide the TDF on an energy basis to better understand the fiber content of a diet.

CLINICAL INDICATIONS FOR FIBER Obtaining a full medical and dietary history helps guide diet selection and may suggest an underlying cause of gastrointestinal illness.

A medical history may suggest whether the patient has a large intestinal or small intestinal problem, which may help guide the type or level of fiber needed (Table 3, page 72). For example, increased frequency, urgency, and frank blood or mucus in stool suggests a large intestinal problem and trial-and-error management would likely

Client Communication Tip Obtaining a dietary history is a key component of the appointment.

A full dietary history—that includes all previous diets, treats, chews, table scraps, and food used for medication administration—can help rule out dietary indiscretion in gastrointestinal illness. This history can also elucidate any food items at risk of contamination by bacteria (eg, chews, such as bully sticks, or raw food diets). 5,6 Example diet history forms can be found online at wsava.org/nutrition-toolkit.4

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TABLE 3 Conditions for Which Fiber May Assist in Nutritional Management Anal gland or sac disease Dental disease* Diabetes Dietary indiscretion Enteritis Exocrine pancreatic insufficiency Infectious disease/small intestinal bacterial overgrowth Inflammatory bowel disease

HOW TO GET STARTED Which Fiber to Look for in Diets Each pet must be considered individually when considering the amounts of each of types of fibers in the various commercially available diets; not all pets with the same condition respond similarly to nutritional management. For example, low fat, highly digestible diets (ie, low insoluble fiber) are commonly recommended for intestinal disease;1 however, one study in cats demonstrated that dietary fat content did not affect clinical outcome.7

Intestinal neoplasia Megacolon Stress colitis Weight management * Fiber is used in dental diets to create a matrix that mechanically removes plaque from teeth.

start with increased insoluble fiber diets. A fecal scoring chart (Figure) provides a numeric system for accurately and consistently describing stool.

A history of previous diets may guide what ratio of insoluble or soluble fiber will benefit the patient.

A dietary history that includes aspects of the home environment may also guide management; for example, diarrhea that occurs when a family member leaves for business may indicate stress colitis.

A full medical workup, such as diagnostic imaging or a dietary elimination trial, may be necessary for severe or chronic cases in which nutritional management alone cannot alleviate clinical signs.

Client Communication Tip

In general, diseases affecting the large intestine (ie, colitis, anal gland or sac disease) may best be managed by trying diets higher in insoluble fibers, while diseases affecting the small intestine (ie, chronic enteritis, exocrine pancreatic insufficiency) may benefit from the addition of soluble fibers. If it is unclear which type of fiber may be helpful, a moderate mixed fiber diet can be used for an initial trial. In addition, contacting a board-certified veterinary nutritionist (a listing can be found at acvn.org) to formulate a balanced, homecooked diet could also be elected by owners who would like more control over fiber sources and content.

Full Nutrient Profiles Unless the patient has a proven food allergy (diagnosed through a dietary elimination trial), the overall nutrient profile should determine the diet rather than ingredients. For further consideration, diets high in fiber may have a lower caloric density; therefore, energy needs may also need to be taken into account. An underweight diabetic dog, for example, may have difficulty consuming enough low calorie, high fiber food to maintain weight. In this example, consideration of the fat and calorie content, as well as the fiber content, is of importance.

A formulated pet food or therapeutic diet is the preferred source for fiber.

Supplementation

Commercial pet foods or veterinary therapeutic diets are the best way to provide fiber to dogs and cats because they are formulated to provide the appropriate essential nutrients. For example, canned pumpkin is popular with pet owners as a fiber supplement, but the amount needed to be beneficial may unbalance the total diet (ie, the pumpkin would provide significantly more than 10% of a petâ&#x20AC;&#x2122;s total calories).

Fiber can be supplemented outside the diet, but there is limited guidance for standardized dosages.

One study found benefits in dogs with a median dosage of 2 tablespoons per day of a common human psyllium supplement, although there was a range of 0.25 to 6 tablespoons per day.8

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Fecal Scoring Chart SCORE

SPECIMEN EXAMPLE

CHARACTERISTICS

1

• Very hard and dry • Often expelled as individual pellets • Requires much effort to expel from body • Leaves no residue on ground when picked up

2

• Firm, but not hard, pliable • Segmented in appearance • Little or no residue on ground when picked up

3

• Log shaped, moist surface • Little or no segmentation • Leaves residue on ground, but holds form when picked up

4

• Very moist and soggy • Log shaped • Leaves residue on ground and loses form when picked up

5

• Very moist, but has a distinct shape • Present in piles rather than logs • Leaves residue on ground and loses form when picked up

6

• Has texture, but no defined shape • Present as piles or spots • Leaves residue on ground when picked up

7

• Watery • No texture • Present in flat puddles

FIGURE. Fecal scoring chart. Reprinted with permission from Purina (purina.com)

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More Client Communication Tips

Glossary

Clinical Management with Fiber.

Megacalorie (Mcal) 1000 kcal

• When adding insoluble fiber, tell dog owners in advance that the increased fecal bulk may mean that they will need to schedule more walks during the day to avoid accidents.

SCFA short-chain fatty acids TDF total dietary fiber WSAVA World Small Animal Veterinary Association

• For clients that really want to provide treats, they can use a portion of their pets’ daily kibble as treats until stool has reached desired consistency.

• Because gut bacteria take time to adapt during diet changes, encourage clients to transition between diets slowly (7–10 days).

•L et clients know that mild loose stool is expected with any diet change.

• Setting expectations is crucial, and it is helpful to tell clients that dietary management alone may not be successful.

• Home-cooked diets are commonly sought by clients who suspect a gastrointestinal issue in their pets. Recommend a consult with a board-certified veterinary nutritionist (ACVN.org) to ensure the diet is formulated properly without any deficiencies.

If supplemented, fiber should always be given gradually over a few days until the stool reaches the desired composition. Use fecal charts (Figure), which allow clients to objectively chart their pets’ stool production and quality and provide more objective feedback.

Prebiotics and probiotics are also commonly used supplements: Prebiotics are fermentable carbohydrates—also called oligosaccharides— and, because of their ability to foster beneficial (“the good”) bacteria in the intestinal tract, are considered beneficial for pets. There are many

commercially available prebiotic supplements to help cultivate healthy gut bacteria. Meanwhile, probiotics are not actually a source of fiber, but are ingested microorganisms (the “good” bacteria themselves) that are associated with benefits for humans and animals. It is important to note that quality control can vary and only products that are independently tested should be used.9

IN SUMMARY Fiber can be an integral part of nutritional management for many disease conditions in dogs and cats. Understanding the different types of fiber and how to determine the fiber content of commercial diets for cats and dogs can guide optimal diet selection. Because each animal (and their gastrointestinal microbes) may react differently, trial and error is often necessary to determine the exact fiber needs of each individual pet. Ongoing communication with clients during this process plays an integral role in successful management.

References 1.

Cave N. Nutritional management of gastrointestinal disease. In Fascetti AJ, Delaney SJ (eds): Applied Veterinary Clinical Nutrition.

Chichester (UK): Wiley-Blackwell, 2012, pp 175-220.

2. Harmon DL, Walker JA, Silvio JM, et al. Nutrient digestibility in dogs fed fiber-containing diets. Vet Clin Nutr 1999; 6(1):6-10.

3. Prola L, Dobenecker B, Mussa PP, Kienzle E. Influence of cellulose fibre length on faecal quality, mineral excretion and nutrient digestibility in cat. J Anim Phys Anim Nutr 2010; 94:362-367.

Deborah E. Linder

Deborah E. Linder, DVM, MS, DACVN, is a research assistant professor in clinical nutrition at Tufts Cummings School of Veterinary Medicine and head of the Tufts Obesity Clinic for Animals.

Her interests include obesity management and effective client education, and she has focused her research on safe and effective weight loss strategies for pets as well as the effect of obesity on pet and human well-being. Dr. Linder received her DVM from Tufts Cummings School of Veterinary Medicine.

4. Freeman L, Becvarova I, Cave N, et al. WSAVA nutritional assessment guidelines. Compend Contin Educ Vet 2011; 33(8):E1-E9.

5. Weese JS, Rousseau J, Arroyo L. Bacteriological evaluation of commercial canine and feline raw diets. Can Vet J 2005; 46(6):513-516.

6. Freeman LM, Janecko N, Weese JS. Nutritional and microbial analysis of bully sticks and survey of opinions about pet treats. Can Vet J 2013; 54:50-54.

7. Laflamme DP, Xu H, Long GM. Effect of diets differing in fat content on chronic diarrhea in cats. J Vet Intern Med 2011; 25(2): 230-235.

8. Lieb MS. Treatment of chronic idiopathic large-bowel diarrhea in dogs with a highly digestible diet and soluble fiber: A retrospective review of 37 cases. J Vet Intern Med 2000; 14:27-32.

9. Ridgway MD. Probiotics. Clin Brief 2013; 2:21-23.

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1 DOSE: 12 WEEKS OF COMPLIANCE *

VET-RECOMMENDED BRAVECTO TAKES CARE OF KILLING FLEAS AND TICKS FOR 12 WEEKS* WITH JUST 1 CHEW. ®

Nearly 3X longer flea and tick protection than monthly treatments – 12 weeks!1* Fast-acting protection kills 100% of fleas in under 12 hours1,2 Improves client compliance with less frequent dosing1

ORDER PRESCRIPTION-ONLY BRAVECTO® FOR YOUR CLINIC Contact your Merck Animal Health rep or distributor partner.

BRAVECTOVETS.COM *Bravecto kills fleas, prevents flea infestations, and kills ticks (black-legged tick, American dog tick, and brown dog tick) for 12 weeks.

Bravecto also kills lone star ticks for 8 weeks.

IMPORTANT SAFETY INFORMATION: The most common adverse reactions recorded in clinical trials were vomiting, decreased appetite, diarrhea, lethargy, polydipsia, and flatulence. Bravecto has not been shown to be effective for 12-weeks’ duration in puppies less than 6 months of age.

Bravecto is not effective against lone star ticks beyond 8 weeks after dosing.

References: 1. Bravecto [prescribing information]. Madison, NJ: Merck Animal Health; 2014. 2. Taenzler J, et al. Parasites & Vectors. 2014;7:567.

Please see Brief Summary in final pages.

Copyright © 2016 Intervet Inc., d/b/a Merck Animal Health, a subsidiary of Merck & Co., Inc. All rights reserved. US/BRV/1116/0105

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NADA 141-426, Approved by FDA

BRIEF SUMMARY (For full Prescribing Information, see package insert) Caution: Federal (USA) law restricts this drug to use by or on the order of a licensed veterinarian.

Indications: Bravecto kills adult fleas and is indicated for the treatment and prevention of flea infestations (Ctenocephalides felis) and the treatment and control of tick infestations [Ixodes scapularis (black-legged tick), Dermacentor variabilis (American dog tick), and Rhipicephalus sanguineus (brown dog tick)] for 12 weeks in dogs and puppies 6 months of age and older, and weighing 4.4 pounds or greater.

Bravecto is also indicated for the treatment and control of Amblyomma americanum (lone star tick) infestations for 8 weeks in dogs and puppies 6 months of age and older, and weighing 4.4 pounds or greater.

Contraindications: There are no known contraindications for the use of the product.

Warnings: Not for human use. Keep this and all drugs out of the reach of children. Keep the product in the original packaging until use, in order to prevent children from getting direct access to the product. Do not eat, drink or smoke while handling the product. Wash hands thoroughly with soap and water immediately after use of the product.

Precautions: Bravecto has not been shown to be effective for 12-weeks duration in puppies less than 6 months of age. Bravecto is not effective against Amblyomma americanum ticks beyond 8 weeks after dosing.

Adverse Reactions: In a well-controlled U.S. field study, which included 294 dogs (224 dogs were administered Bravecto every 12 weeks and 70 dogs were administered an oral active control every 4 weeks and were provided with a tick collar); there were no serious adverse reactions. All potential adverse reactions were recorded in dogs treated with Bravecto over a 182-day period and in dogs treated with the active control over an 84-day period. The most frequently reported adverse reaction in dogs in the Bravecto and active control groups was vomiting.

Percentage of Dogs with Adverse Reactions in the Field Study Adverse Reaction (AR)

Bravecto Group: Percentage of Dogs with the AR During the 182-Day Study (n=224 dogs)

Active Control Group: Percentage of Dogs with the AR During the 84-Day Study (n=70 dogs)

Vomiting

7.1

14.3

Decreased Appetite

6.7

0.0

Diarrhea

4.9

2.9

Lethargy

5.4

7.1

Polydipsia

1.8

4.3

Flatulence

1.3

0.0

In a well-controlled laboratory dose confirmation study, one dog developed edema and hyperemia of the upper lips within one hour of receiving Bravecto. The edema improved progressively through the day and had resolved without medical intervention by the next morning.

For technical assistance or to report a suspected adverse drug reaction, contact Merck Animal Health at 1-800-224-5318. Additional information can be found at www.bravecto.com. For additional information about adverse drug experience reporting for animal drugs, contact FDA at 1-888-FDA-VETS or online at http://www.fda.gov/AnimalVeterinary/ SafetyHealth.

How Supplied: Bravecto is available in five strengths (112.5, 250, 500, 1000, and 1400 mg fluralaner per chew). Each chew is packaged individually into aluminum foil blister packs sealed with a peelable paper backed foil lid stock. Product may be packaged in 1, 2, or 4 chews per package.

Distributed by: Intervet Inc (d/b/a Merck Animal Health) Madison, NJ 07940 Made in Austria Copyright Š 2014 Intervet Inc, a subsidiary of Merck & Company Inc. All rights reserved 154545R1 Reference: Bravecto [prescribing information] Madison, NJ: Merck Animal Health; 2014 Available by veterinary prescription only.

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DERMATOLOGY DETAILS

Updates on the Management of Canine Demodicosis Sandra N. Koch, DVM, MS, DACVD University of Minnesota

Canine demodicosis is a common inflammatory parasitic skin disease believed to be associated with a genetic or immunologic disorder. This disease allows mites from the normal cutaneous biota to proliferate in the hair follicles and sebaceous glands, leading to alopecia, erythema, scaling, hair casting, pustules, furunculosis, and secondary infections.1-3 The face and forelegs to the entire body surface of the dog may be affected.1-3 Three morphologically different types of Demodex mites exist in dogs:

establish prognosis and provide a successful treatment, it is very important to evaluate the:

• Age of onset • Extent and location of skin lesions • Presence of secondary infections • General health of the dog.1,3,5 Independent of age, it is important to identify and treat any predisposing or contributing factors in order to achieve a successful outcome.1-3

1. Demodex canis: The most common form of Demodex (Figure 1) 2. D cornei: A short-body form, likely a morphological variant of D canis4 (Figure 2, page 78) 3. D injai: A long-body form1-3 (Figure 3, page 78) Published studies indicate similar efficacy of treatment regardless of the type of mite.1,2

THERAPEUTIC APPROACH Effective treatment of generalized demodicosis requires a multimodal approach.1,2 In order to

FIGURE 1. Demodex canis identified on skin scrapings.

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AGE OF ONSET

Adult-Onset

Juvenile-Onset

In dogs older than 18 months of age, demodicosis may occur as a result of immunosuppression due to drugs (eg, glucocorticoids, ciclosporin, oclacitinib maleate, chemotherapy) or systemic disease (eg, hyperadrenocorticism, hypothyroidism, neoplasia, malnutrition, parasitism).1,3 Therefore, dogs with adult-onset demodicosis should have a detailed physical examination and full diagnostic workup (Table 1) performed to identify underlying diseases.

Demodicosis may occur in dogs 18 months of age or younger as a result of an immunocompromised state associated with endoparasitism, malnutrition, or health debilitation. Puppies may also develop demodicosis due to an immature immune system or mite-specific immunoincompetency.1,3 The increased prevalence in certain breeds indicates a hereditary basis for juvenile-onset demodicosis, particularly for the generalized form.3

Evidence has indicated that successful treatment of an underlying disease may contribute to remission of demodicosis.1,3 However, up to 56% of dogs with adult-onset canine demodicosis have been reported to have no detectable underlying disease.2

EXTENT & LOCATION OF LESIONS Localized Form1 • Four skin lesions or fewer • Lesion diameter ≤ 2.5 cm

FIGURE 2. Short-bodied form: Demodex cornei.

Prognosis for localized demodicosis is good, as most lesions resolve spontaneously within 6 to 8 weeks.1,3 Topical therapy with benzoyl peroxide shampoo or gel may be recommended.1,3

Generalized Form1 • More than 4 skin lesions • Lesion diameter > 2.5 cm (Figures 4 and 5) • And/or feet are affected TABLE 1 Demodicosis: Diagnostic Analysis Complete blood count Serum biochemical profile Urinalysis Heartworm and fecal tests Lymph node aspirates Thyroid and adrenal testing Abdominal ultrasound FIGURE 3. Long-bodied form: Demodex injai.

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Overall prognosis for resolution of skin lesions is good (Figure 6), but prognosis depends on the patient’s health status and underlying conditions or presence of immunosuppression.1,3 Spontaneous remission in a subset of young dogs has been reported to be 30% to 50%3; however, the true incidence of spontaneous resolution of generalized demodicosis is unknown.

Relapses of generalized demodicosis are not uncommon.1 Dogs may be euthanized as owners may be unable to afford cost of therapy or commit to the necessary intense management.1-3 In some patients with refractory or noncurable demodicosis, treatment may be lifelong.1,2

PRESENCE OF SECONDARY INFECTIONS Secondary bacterial and yeast skin and ear infections are common problems associated with canine demodicosis, which aggravate the skin disease and cause or contribute to pruritus.1,3 Identifying and treating these secondary infections is very important to the successful treatment of demodicosis.1,3 Topical and/or oral antibiotics may be prescribed according to clinical signs and cytology. Bacterial culture and susceptibility testing should be performed in patients that do not respond to antibiotic therapy or have a history of multiple antibiotic courses, in an attempt to identify and treat resistant bacteria.

FIGURE 4. Generalized demodicosis.

Most dogs benefit from weekly antimicrobial baths with benzoyl peroxide or chlorhexidine shampoos.1,3

MITICIDAL THERAPIES Multiple conventional and newer therapeutic options currently exist for generalized demodicosis (Table 2, page 80);1-3,6 however, most of these therapies are extralabel, can be difficult to administer, and may lead to adverse effects. Miticidal therapy may need to be adjusted according to the dog’s response and tolerance.

FIGURE 5. Generalized demodicosis.

FIGURE 6. Patient from Figures 4 and 5 after treatment for demodicosis.

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TABLE 2 Canine Generalized Demodicosis: Acaricidal Treatment Options DRUG

DOSAGE

ADVERSE EFFECTS

COMMENTS

Hyperglycemia, bradycardia, depression, lethargy, polydipsia, polyuria, vomiting, diarrhea, transitory pruritus, sedation

• • • •

LABELED FOR CANINE DEMODICOSIS Amitraz (Mitaban, zoetisus.com)

0.025%–0.06% topical rinses weekly to every 2 weeks

ood evidence for use G Labeled at 0.125% Q 2 weeks Dogs > 4 months of age Avoid other sedating agents, such as GABA agonists (eg, benzodiazepines), alpha-adrenergic agonists (eg, xylazine), and heterocyclic antidepressants (eg, amitriptyline)

EXTRALABEL USE FOR CANINE DEMODICOSIS IN THE U.S. Afoxolaner (Nexgard, merial.us)

1 tablet PO Q 2–4 weeks

Vomiting, diarrhea, lethargy, dry/flaky skin

•F urther studies needed to establish protocol, efficacy, and safety • Dogs ≥ 8 weeks of age • Use with caution in dogs with history of seizures • Safety has not been evaluated in breeding, pregnant, or lactating dogs

Doramectin (Dectomax, zoetisus.com; Doramec, agrovetmarket.com)

0.6 mg/kg PO or SC weekly or twice weekly

Lethargy; neurologic signs, such as tremors, mydriasis, ataxia, coma, death

•S ome evidence for use • 0.3 mg/kg twice weekly may reduce adverse effects • Do not use in herding breeds and their crosses or dogs with confirmed ABCB1-1Delta (MDR-1) gene mutation

Fluralaner (Bravecto, merck.com)

1 tablet PO Q 12 weeks

Vomiting, diarrhea, anorexia, flatulence, lethargy

•F urther studies needed to establish protocol, efficacy, and safety • Dogs ≥ 6 months of age • Safe for use in breeding, pregnant, and lactating dogs • Safe for use in dogs with ABCB1-1Delta (MDR-1) gene mutation, such as collies

Ivermectin (Ivomec 1%, merial.us; Ivermax 1%, aspenveterinary resources.com)

0.3–0.6 mg/kg PO Q 24 H

Lethargy; vomiting; neurologic signs, such as tremors, mydriasis, ataxia, coma, death

•G ood evidence for use • Do not use in herding breeds and their crosses or dogs with confirmed ABCB1-1Delta (MDR-1) gene mutation • Do not use concurrently with spinosad (Comfortis and Trifexis, elanco.us) due to resulting severe neurologic adverse effects

Milbemycin oxime (Interceptor, elanco.us)

1–2 mg/kg PO Q 24 H

Lethargy; vomiting; neurologic signs, such as tremors and ataxia

ood evidence for use •G • Use with caution in herding breeds and their crosses or dogs with confirmed ABCB1-1Delta (MDR-1) gene mutation

Moxidectin (Cydectin, bi-vetmedica.com)

0.2–0.5 mg/kg PO Q 24 H

Lethargy; neurologic signs, such as tremors, mydriasis, ataxia, lethargy, coma, death

•G ood evidence for use • Do not use in herding breeds and their crosses or dogs with confirmed ABCB1-1Delta (MDR-1) gene mutation

Moxidectin + Imidacloprid (Advantage Multi for Dogs, bayerdvm.com; known as Advocate in Europe)

1 tube/dog topical spot-on weekly

Local cutaneous inflammation or irritation, pruritus, lethargy, reduced appetite, and hyperactivity

•G ood evidence for use • Dogs ≥ 7 weeks of age • Do not use, or use with caution, in herding breeds and their crosses or dogs with confirmed ABCB11Delta (MDR-1) gene mutation

Sarolaner (Simparica, zoetisus.com)

1 tablet PO Q 4 weeks

Vomiting, diarrhea, lethargy; may cause neurologic signs, such as tremors, ataxia, and seizures

•F urther studies needed to establish protocol, efficacy, and safety • Dogs ≥ 6 months of age • Safety has not been evaluated in breeding, pregnant, or lactating dogs

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Amitraz Therapy Amitraz (Mitaban, zoetisus.com) is a monoamine oxidase inhibitor approved by the FDA for treatment of generalized demodicosis in dogs older than 4 months of age.5 There is good evidence to recommend weekly amitraz rinses for the treatment of canine demodicosis.1,5 However, based on published reports, amitraz seems to be less efficacious in adult-onset demodicosis.1 Recommended concentrations range from 0.025% to 0.06% once weekly to every other week,1,3,5,6 but other protocols have been reported (Table 3). Clinical efficacy increases with increased concentration and shorter treatment intervals.1 Dogs should be treated in well-ventilated areas.

For heavily infested dogs, or dogs with medium or long coats, clipping the hair coat is advisable.1,3 Transitory sedation and depression, pruritus, lethargy, hyperglycemia, bradycardia, polydipsia, polyuria, vomiting, and diarrhea may occur.3,6 Marked ataxia and lethargy are rare.3 Amitraz use should be avoided in Chihuahuas and toy breeds as they are reportedly sensitive to amitraz.2

Macrocyclic Lactone Therapy While macrocyclic lactones are not licensed in the United States for treatment of canine demodicosis, they are widely used by veterinarians due to their known efficacy.

Certain precautions should be taken when using macrocyclic lactones:

• Macrocyclic lactones should not be administered to herding breeds and their crosses, including collies, Shetland sheepdogs, Old English sheepdogs, border collies, bearded collies, and Australian shepherds.

• These dogs have a higher risk of depression, ataxia, coma, and death due to their predisposition to the ABCB1-1Δ (MDR-1) gene mutation.3,6 • Prior to prescribing macrocyclic lactones in these breeds, it is recommended that evaluation for the ABCB1-1Δ genotype be performed or alternative treatment pursued.

• A polymerase chain reaction test is available from Washington State University (vcpl.vetmed.wsu.edu).

• In dogs without the ABCB1-1Δ mutation, including puppies, use of lower doses or gradual dose increase of macrocyclic lactones—on a daily or weekly basis—is usually recommended due to possible drug neurotoxicity.1,3,7 • Do not implement macrocyclic lactone therapy in patients without up-to-date negative heartworm tests or in those with heartworm disease.6 Other heartworm preventives should be discontinued during treatment.6 Milbemycin oxime (Interceptor, elanco.us) is licensed in the U.S. as a heartworm and intestinal parasite preventive in dogs older than 4 weeks of age.

There is good evidence to recommend milbemycin (1–2 mg/kg PO Q 24 H) for treatment of canine demodicosis.1,5 Milbemycin is better tolerated by dogs compared with other macrocyclic lactones, and may have a higher margin of safety. However, it should be used carefully in dogs with the ABCB1-1Δ gene mutation due to reports of neurologic side effects in these dogs.1

TABLE 3 Demodicosis: Amitraz Therapy

Mild to moderate cases

0.025% to 0.06% once weekly to every other week; apply with sponge or spray and leave on, allowing dog to air dry3

Severe or unresponsive cases

0.125% solution applied once to twice weekly; apply with sponge or spray and leave on, allowing dog to air dry3

Pododemodicosis

Immersion of feet for at least 10 minutes in footbath of amitraz1

Otodemodicosis

Amitraz ear drops (amitraz concentrate diluted 1:10 with mineral oil)1

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Ivermectin use (0.3–0.6 mg/kg PO Q 24 H) for treatment of canine demodicosis is supported by good evidence.1,3,6 To mask its bitter taste, ivermectin may be mixed with fruit sauce or ice cream. Do not use concurrently with spinosad (ie, Comfortis and Trifexis [elanco.us]) due to a drug interaction, which results in severe neurologic adverse effects.8 Doramectin use (0.6 mg/kg PO or SC weekly or twice weekly) for treatment of canine generalized demodicosis is supported by some evidence.1,3,5-7 A recent retrospective study, which included 232 dogs, demonstrated that weekly SC injections of doramectin was a useful and well tolerated treatment for canine generalized demodicosis; remission was reported in 94.8% of the dogs.9 Moxidectin use (0.2–0.5 mg/kg PO Q 24 H) for treatment of canine demodicosis is supported by good evidence.1,3,5,6 Moxidectin 2.5% + imidacloprid 10% (Advantage Multi, bayerdvm.com) is a spot-on medication approved for prevention of fleas, heartworm, and intestinal parasites in dogs of at least 7 weeks of age. This product:

• Has good evidence supporting its use as a weekly treatment for dogs with juvenile-onset demodicosis or mild forms of the disease, or those that cannot receive or tolerate amitraz or macrocyclic lactones1,3,5,10,11 • Seems to be well tolerated without the potential toxicity associated with other avermectin products, and is safe for dogs with the ABCB1-1Δ mutation1,10,11 • Was shown to have a much higher success rate when administered weekly or every 2 weeks versus monthly in mildly affected, juvenile-onset patients compared with moderately or severely affected dogs.1,10,11 In dogs prone to recurrent demodicosis, I recommend use of Advantage Multi Q 4 weeks to help prevent relapses.

Isoxazoline Therapy The following isoxazolines are flavored, chewable tablets newly available as veterinary prescriptions and labeled for the prevention and treatment of flea and tick infestations in dogs:

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• Fluralaner (Bravecto, merck.com) • Afoxolaner (Nexgard, merial.us) • Sarolaner (Simparica, zoetisus.com).

These medications can be used in young dogs of at least 6 months (fluralaner and sarolaner) and 8 weeks (afoxolaner) of age.

Mechanism of Action. Fluralaner, afoxolaner, and sarolaner have similar mechanisms of action, antagonistically binding primarily to the arthropod gamma-aminobutyric acid and glutamate receptor regulated chloride channel and inhibiting the arthropod nervous system, causing paralysis and death. They possess potent, fast, and long-lasting insecticide and acaricide effects, offering 4 (afoxolaner and sarolaner) and 12 (fluralaner) weeks of protection.

Adverse Effects. These products are generally quite safe. The most frequently reported adverse effects include vomiting, diarrhea, anorexia, lethargy, and flatulence. Specific considerations include:

• Afoxolaner should be used with caution in dogs that have a history of seizures.

• Sarolaner may cause neurologic signs, including tremors, ataxia, and seizures.

• Fluralaner is labeled as safe for use in breeding, pregnant, and lactating dogs, as well as in dogs with the ABCB1-1Δ gene mutation.

Use in Demodicosis. Recently, these medications have been anecdotally suggested as an alternative efficacious treatment for canine demodicosis. To date, 3 studies investigating the use of this new class of parasiticide for the treatment of canine demodicosis have been published.12-14 Note, in the following studies, that Advocate is the European version of Advantage Multi.

One open study12 compared the effect of Bravecto (fluralaner; single dose) with Advocate (moxidectin + imidacloprid; applied Q 28 days) in 16 dogs with generalized demodicosis. Dogs treated with fluralaner had lower mean mite counts after treatment (99.8% on day 28, and 100% on days 56 and 84) compared to those treated with moxidectin/imidacloprid (98% on day 28, 96.5% on day 56, and 94.7% on day 84).

Statistically, on days 56 and 84, significantly fewer

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mites were found on dogs treated with fluralaner compared with those treated with moxidectin/ imidacloprid. Reduction of mite counts was consistent with reduction in clinical signs in both groups.

A similar study13 compared the efficacy of Nexgard (afoxolaner) with Advocate (moxidectin + imidacloprid), both administered biweekly on days 0, 14, 28, and 56, in 8 dogs with generalized demodicosis. Dogs treated with afoxolaner had lower mite counts after treatment (99.2%, 99.9%, and 100% on days 28, 56, and 84, respectively) compared with those treated with moxidectin/ imidacloprid (89.8%, 85.2%, and 86.6% on days 28, , and 84 respectively). On days 28, 56, and 84, mite reductions were significantly higher in dogs treated with afoxolaner; skin condition in these dogs also improved significantly from day 28 to day 84.

Another recent study14 investigated the efficacy of Simparica (sarolaner; doses on days 0, 30, and 60) compared with Advocate (moxidectin + imidacloprid; weekly applications from days 0 to 81) for the treatment of 16 dogs with generalized demodicosis for 91 days. The study demonstrated that dogs treated with sarolaner had significant mite count reduction after the first dose (97.1% and 99.8% at days 14 and 29, respectively), with no live mites detected at 44 days and thereafter. Dogs treated with moxidectin/imidacloprid experience mite count reduction of 84.4% and 95.6% at days 14 and 29, respectively, with no mites detected at 74 days and thereafter. All dogs in both groups showed marked improvement in clinical signs.

The results of these studies are encouraging because this new treatment modality offers the potential to provide effective and safe control of canine demodicosis, with low administration frequency, while helping prevent and control fleas and ticks.

SUPPORTIVE THERAPY It is extremely important to improve nutrition by feeding a balanced, age-appropriate diet and treating intestinal parasites or other stress factors, particularly in puppies, stray or rescued, and sick dogs.1-3 Most dogs with demodicosis are treated on an outpatient basis; however, dogs with severe

Therapies Lacking Evidence of Efficacy According to evidence-based studies, there is currently insufficient evidence to recommend treatment of canine demodicosis with amitraz collars, closantel, deltamethrin, vitamin E, muramyl dipeptide, phoxime, and herbal and homeopathic products.1 There is current evidence against use of weekly pour-on or injectable ivermectin, lufenuron, ronnel, oral selamectin, and levamisole.1

generalized demodicosis, pododermatitis, deep pyoderma, sepsis, pain, fever, dehydration, and complications from underlying diseases may require hospitalization for supportive care. Fluids, systemic antibiotics, and pain medications may be required.

MONITORING & DURATION OF TREATMENT One of the most common reasons for treatment failure is ending therapy too soon.1 Clinical resolution usually occurs 0.5 to 6 months sooner than parasitologic cure.3 Therefore, it is important to rely on length of therapy, rather than clinical appearance, to finalize treatment since clinically improved dogs may still harbor mites.

Dogs Affected by Demodicosis: Therapeutic Precautions Avoid glucocorticoids, progestogens, ciclosporin (Atopica, novartis.com), and oclacitinib maleate (Apoquel, zoetisus.com) due to their immunosuppressive effects.1,3 These agents may inhibit the host immune response, preventing resolution of Demodex infection or inducing relapses. Apoquel is contraindicated in patients with demodicosis or a history of demodicosis.

Avoid use of other P-glycoprotein inhibitors when administering avermectins, such as azole antifungals and ciclosporin, due to potential synergistic toxicosis.1,3 Do not administer macrocyclic lactone medications to herding breeds and their crosses, including collies, Shetland sheepdogs, Old English sheepdogs, border collies, bearded collies, and Australian shepherds, as there is a higher risk of depression, ataxia, coma, and death due to their predisposition to the ABCB1-1Delta gene mutation. 3,5 Relapses may occur at times of stress, such as estrus, pregnancy, lactation, and systemic diseases.1,3

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1. Perform recheck visits and skin scrapings every 4 weeks to monitor response.

2. Continue treatment until 2 consecutive negative skin scrapings are obtained.1,3 A minimum of 4 to 6 skin scraping sites should be negative.3 Usually, at least 3 to 4 months of treatment are needed.

3. If there is no reduction in mite numbers after several skin scrapings, especially if active mite reproduction is seen (eggs, larvae, and nymphs), reinvestigate for the presence of underlying causes or consider an alternative treatment.1,3 4. Monitor patients for 12 months after treatment is discontinued, with rechecks and skin scrapings performed every 3 to 4 months to monitor for relapses.1,3 Relapses were reported in 10% to 45% of patients.3 One study demonstrated that the largest percentage of recurrence of disease occurred within the first few months after treatment discontinuation.4 Interestingly, the same study also demonstrated that older dogs were more sensitive to side effects of therapy but were generally clear of mites more quickly than younger dogs.4 5. Consider life-long therapy in dogs that respond to therapy clinically but do not have negative skin scrapings and in those with frequent relapses despite proper treatment duration.1,3 Based on recently published guidelines for the treatment of demodicosis, Demodex resistance to acaricidal therapy has not been reported.1 Remember, during monitoring, the presence of any live, dead, and/or fragments of Demodex mites on skin scrapings should be considered positive, indicating the need for continued treatment.1,3

CLIENT EDUCATION Client education is extremely important.1,3 Clients should know and understand the following:

• Dogs with adult-onset demodicosis need a complete workup for possible underlying conditions.

• About 10% of dogs with localized demodicosis may progress to generalized form.

• Treatment of generalized demodicosis may be lengthy and costly.

• Clinical signs often improve before parasitologic cure; therefore, frequent rechecks and skin scrapings are important to achieve treatment success.

• There is a possibility of recurrence after treatment discontinuation, especially if therapy is ended prematurely, leading to disease relapse.

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• Some dogs can be controlled but not cured, particularly those treated with immunosuppressive drugs that cannot be discontinued or with unidentified, uncontrolled, or noncurable underlying conditions.

Sandra Koch

Sandra Koch, DVM, MS, DACVD, is an associate professor of veterinary dermatology at University of Minnesota College of Veterinary Medicine. She is primarily involved with clinical service and teaching, and her special interests include allergic and infectious skin diseases, particularly multidrug- and methicillin-resistant Staphylococcus skin and ear infections and dermatologic therapies. She is the primary author of Canine and Feline Dermatology Drug Handbook.

• According to current evidence-based guidelines, dogs with demodicosis requiring parasiticidal therapy should not be bred due to potential heredity.1 In addition, the pros, cons, and contraindications of various treatment options should be explained to clients.

IN SUMMARY In most dogs, demodicosis has a good prognosis for cure as long as underlying diseases are identified and treated properly. Treatment should be monitored monthly with multiple skin scrapings and extended beyond clinical and microscopic cure to minimize recurrences. Canine demodicosis can be a challenge to treat; however, the future is brighter with multiple therapeutic options available and the advancement of new, potentially safer, efficacious, and easier-toadminister therapies, such as the isoxazolines.

10% imidacloprid and 2.5% moxidectin (Advocate, Bayer Healthcare). Vet Dermatol 2009; 20(5-6):441-446.

12. Fourie JJ, Liebenberg JE, Horak IG, et al. Efficacy of orally administered fluralaner (Bravecto) or topically applied imidacloprid/moxidectin (Advocate) against generalized demodicosis in dogs. Parasit Vectors 2015; 8:187-193.

13. Beugnet F, Halos L, Larsen D, de Vos. Efficacy of oral afoxolaner for the treatment of canine generalised demodicosis. Parasite 2016; 23:14 Published. Parasite 2016; 23(14): 1-8.

14. Six RH, Becskei C, Mazaleski MM, et al. Efficacy of sarolaner, a novel oral isoxazoline, against two common mite infestations in dogs: Demodex spp and Otodectes spp. Vet Parasitol 2016 (in press). doi.org/10.1016/j.vetpar.2016.02.027, published. Vet Parasitol 2016; 222: 62-22.

References 1.

Mueller RS, Bensignor E, Ferrer L, et al. Treatment of demodicosis in dogs: 2011 clinical practice guidelines. Vet Dermatol 2012; 23(2):86-96, e20-1.

No One Breeds Knowledge Like We Do

2. Singh SK, Kumar M, Jadhav RK, Saxena SK. An update on therapeutic management of canine demodicosis. Vet World 2011; 4(1):41-44.

3. Miller WH, Griffin CE, Campbell KL. Parasitic skin diseases. Muller & Kirk’s Small Animal Dermatology, 7th ed. St. Louis: Saunders, 2013, pp 310-313.

The Merck Veterinary Manual, 11th Edition Completely updated and expanded

4. Sastra N, Ravera I, Villanueva S, et al. Phylogenetic relationships in three species of canine Demodex mite based on partial sequences of mitochondrial 16S rDNA. Vet Dermatol 2012; 23(6):509-e101.

For sh disco ow u stop b nt Available at all B o oth #2 y bookstores and 006 e-tailers everywhere

5. Arsenovic M, Pezo L, Vasic N, et al. The main factors influencing canine demodicosis treatment outcome and determination of optimal therapy. Parasitol Res 2015; 114(7):2415-2426.

6. Koch SN, Torres SMF, Plumb DC. Canine and Feline Dermatology Drug Handbook. Oxford: Wiley-Blackwell, 2012, pp 73-338.

7. Bissonnette S, Paradis M, Danealu I, et al. The ABCB1-1Δ mutation is not responsible for subchronic neurotoxicity seen in dogs of non-collie breeds following macrocyclic lactones treatment for generalized demodicosis. Vet Dermatol 2009; 20:60-66.

ISBN-13: 978-0-911910-61-2 ISBN-10: 0-911910-61-1

8. Hutt JH, Prior IC, Shipstone MA. Treatment of canine generalized demodicosis using weekly injections of doramectin: 232 cases in the USA (2002-2012). Vet Dermatol 2015; 26(5):345-349.

$65.00

This new edition covers all domesticated species and diseases in veterinary medicine worldwide, and includes:

9. Dunn ST, Hedges L, Sampson KE, et al. Pharmacokinetic interaction of the antiparasitic agents ivermectin and spinosad in dogs. Drug Metab Dispos 2011; 39(5):789-795.

• Hundreds of color images • New chapters on backyard poultry, toxicology workplace hazards • New section on public health and zoonoses • Expanded coverage of fish and aquaculture

10. Paterson TE, Halliwell RE, Fields PJ, et al. Canine generalized demodicosis treated with varying doses of a 2.5% moxidectin + 10% imidacloprid spot-on and oral ivermectin: Parasiticidal effects and long-term treatment outcomes. Vet Parasitol 2014; 205(3-4):687-696.

11. Mueller RS, Meyer D, Bensignor E, et al. Treatment of canine generalized demodicosis with a spot-on formulation containing

Copyright © 2016 Merck Sharp & Dohme Corp., a subsidiary of Merck & Co., Inc. All rights reserved.

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Your 3-in-1 and

DONE recommendation every month

More pet owners recommend Trifexis than any other brand1

Talk to your Elanco sales representative about 3-in-1 protection

Indications

Trifexis is indicated for the prevention of heartworm disease (Dirofilaria immitis). Trifexis kills fleas and is indicated for the prevention and treatment of flea infestations (Ctenocephalides felis), and the treatment and control of adult hookworm (Ancylostoma caninum), adult roundworm (Toxocara canis and Toxascaris leonina) and adult whipworm (Trichuris vulpis) infections in dogs and puppies 8 weeks of age or older and 5 pounds of body weight or greater.

Important Safety Information

Serious adverse reactions have been reported following concomitant extra-label use of ivermectin with spinosad alone, one of the components of Trifexis. Treatment with fewer than three monthly doses aſter the last exposure to mosquitoes may not provide complete heartworm prevention.

Prior to administration of Trifexis, dogs should be tested for existing heartworm infection. Use with caution in breeding females. The safe use of Trifexis in breeding males has not been evaluated. Use with caution in dogs with pre-existing epilepsy.

The most common adverse reactions reported are vomiting, lethargy, pruritus, anorexia and diarrhea. To ensure heartworm prevention, dogs should be observed for one hour aſter administration. If vomiting occurs within one hour, redose. Puppies less than 14 weeks of age may experience a higher rate of vomiting. For product information, including complete safety information, see page XX. 1 Brand Experience Tracker Research, March 2016.

Trifexis®, Elanco™, and the Diagonal Bar™ are trademarks owned by or licensed to Eli Lilly and Company, its subsidiaries or affiliates. © 2017 Eli Lilly and Company, its subsidiaries or affiliates. USCACTFX00947

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AHS HEARTWORM HOTLINE

Heartworm Disease: The Science, the Practice, the Future A Selective Summary of the 15th Triennial Heartworm Symposium Clarke Atkins, DVM, DACVIM (SAIM & Cardiology), North Carolina State University shutterstock.com/juninatt and paulrommer

Key areas of presentation and discussion included: The Heartworm Hotline column is presented in partnership between Today’s Veterinary Practice and the American Heartworm Society (heartwormsociety.org).

The goal of the column is to communicate practical and timely information on prevention, diagnosis, and treatment of heartworm disease, as well as highlight current topics related to heartworm research and findings in veterinary medicine.

• Heartworm diagnosis • Heartworm pathology • Adulticidal therapy in dogs • Lack of efficacy (LOE) and heartworm resistance • Vector epidemiology, climate influences, and mosquito-blocking activity.

HEARTWORM DIAGNOSIS: Heartworm disease (HWD) is one of the most important and complex diseases addressed in veterinary medicine, and its persistence continues to confound veterinarians, researchers, and pharmaceutical companies. During the American Heartworm Society (AHS)’s 15th Triennial Heartworm Symposium, which took place September 11 to 13, 2016, in New Orleans, changes in climate, heartworm vectors, prevention practices, and treatment protocols were all highlighted as important reasons to continue expanding HWD knowledge.

Is heat treatment of serum samples necessary?

Since the 14th Triennial Heartworm Symposium in September 2013, heat treatment of serum samples—a routine practice in the days before point-of-care commercial antigen tests became available—has been a topic of some debate. At issue is the fact that commercial heartworm antigen tests can produce false-negative results when circulating antibodies bind to heartworm antigen, rendering the antigen unavailable for detection.

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Speakers included Drs. Rick Alleman, James Carmichael, Brian DiGangi, Laura Kramer, Norma LaBarthe, Lindsay Starkey, and Luigi Venco, and topics included the pros and cons of heat treatment of serum samples and a comparison of commercial antigen tests.

Heat treatment does not determine presence of live worms or efficacy of therapy. A positive result on a heartworm antigen test performed on a heat-treated sample does not reflect a live worm test, and heat treatment of serum should not be used to determine the success or failure of adulticidal therapies.

While time of testing and stage of infection may each play a role, the importance of these findings is not yet clear. In several presented studies, a small but significant percentage (5%–10%) of negative samples converted to positive with heat treatment.

These data suggested that (1) timing of testing may be important and (2) false-negative results may be more likely in the early stages of infection and after exposure to macrocyclic lactones.

How do current antigen tests hold up when compared with the “gold standard” tests? The commercial heartworm antigen tests available to veterinary practitioners are believed to be highly accurate. However, a study from Auburn University found discrepant results in 6.6% of samples tested with the SNAP Heartworm RT (idexx.com) and Enhanced WITNESS HW (zoetisus.com) tests compared with the enzymelinked immunosorbent assay DiroCHEK heartworm antigen test (zoetisus.com), the accepted “gold standard,” with some minimal differences between the 2 commercial tests (Figure 1).

Not every dog with a negative result on an antigen test should have its serum sample heat treated. Performing this extra step may be beneficial when microfilariae and/or heartworm clinical signs are present in dogs that test negative on a commercial antigen test.

DOG

INITIAL TEST RESULT

DIROCHEK®

WITNESS®

SNAP® RT

1

BL

+

+

-

2

BL

+

+

-

3

BL

+

-

-

4

BL

+

+

-

5

BL

+

+

-

6

BL

+

-

-

7

BL

-

+

-

8

BL

-

+

-

9

BL

-

+

-

10

BL

-

-

+

FIGURE 1. Data are shown Key for 10 of 100 field samples, submitted to Auburn University – False (-) because of borderline (BL) + False (+) results. Samples were retested, using 2 commercial heartworm BL Borderline tests, Snap RT (idexx.com) and WITNESS HW (zoetisus.com), and 10 of the 100 results were discrepant. Those 10 (Table) were compared using DiroCHEK (zoetisus.com) and each tested kit had a small number of false positives and false negatives, but both tests performed well with overall sensitivity/specificity of 91/99% for Snap RT and 97/96% for WITNESS HW.

88

HEARTWORM PATHOLOGY: How do the effects of heartworm infection affect approach to therapy?

Understanding how heartworm infection affects the animal is key to devising treatment strategies that minimize adverse events.

Speakers on this topic included Drs. Ray Dillon, Elena Carretón, Changbaig Hyun, and Randolph Winter. Topics included the cardiopulmonary effects of heartworm byproducts in the circulation of dogs, cats, and rats and the evaluation of inflammatory biomarkers in dogs with HWD both before and after adulticidal treatment.

Future treatment may be based on blocking the effects of byproducts of heartworm death. Undefined byproducts from living and dead heartworms produce harmful consequences. An Auburn University study among dogs, cats, and rats found these byproducts induced systemic hypotension, cardiogenic shock, edema of type 1 pneumocytes, and loss of capillary integrity in dogs. The effects were much milder in cats and almost nonexistent in rats. Finding ways to block the effects of heartworm death in dogs and cats may form the basis of an important disease management strategy in the future.

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Cardiac damage can result from infection and therapy, but can also be reduced by therapy. Levels of cardiac injury, inflammatory, and hemostatic markers are elevated in dogs with heartworm infection. Elevations are especially marked in dogs with severe disease. Studies at the Kangwon National University College of Veterinary Medicine in South Korea and the Research Institute of Biomedical and Health Sciences at the University of Las Palmas de Gran Canaria in Spain found that:

• Dogs with more severe clinical signs of heartworm infection had higher levels of cardiopulmonary and inflammatory biomarkers.

Thus, they were likely at greater risk for adverse events associated with adulticidal therapy.

• Administration of melarsomine caused some biomarkers to rise, then fall, while others remained at elevated levels for some months after treatment.

Researchers postulated that pretreatment with macrocyclic lactones and doxycycline before melarsomine (per the AHS protocol) may reduce myocardial damage and vascular inflammation. On the basis of these results, 2 investigators questioned the necessity of routine administration of steroids to asymptomatic dogs around the time of treatment.

While little work has addressed the utility of evaluating inflammatory biomarkers in cats with HWD, a recent study reported that seropositive cats had significantly higher concentrations of positive acute phase proteins, serum amyloid A, haptoglobin, and ceruloplasmin.

ADULTICIDAL THERAPY IN DOGS: Is there a new alternative in the treatment of heartworm infection?

While adulticidal treatment of heartworm infection using melarsomine is considered the standard of care in the U.S, not every dog is a candidate. Reasons to consider alternative adulticide protocols include limited availability of melarsomine (the drug is completely unavailable in some countries), prohibitive expense for some owners, and the dog’s inability to withstand the potential complications of adulticidal treatment.

Varying opinions on different treatment protocols sparked lively discussion during coverage of studies on nonarsenical heartworm treatment protocols, minocycline versus doxycycline in heartworm treatment protocols, and the susceptibility gap in treatment of canine heartworm infections.

Speakers on this topic included Drs. Marisa Ames, Dwight Bowman, Michael Dzimianski, Claudio Genchi, Changbaig Hyun, Laura Kramer, Mark Papich, and Molly Savadelis.

Adulticidal protocols using moxidectin/imidacloprid and doxycycline are under investigation. “Slow kill” protocols with macrocyclic lactones are considered undesirable because they allow disease progression during this prolonged therapy and potentially add to the risk for resistance. Researchers presented studies from Colorado State University, the University of Parma in Italy, and the University of Georgia on protocols that incorporate the combination of doxycycline and moxidectin/imidacloprid, which is both microfilaricidal and adulticidal. Protocols and success rates varied, but results were overall promising.

Minocycline may be an alternative to doxycycline.

Minocycline, like doxycycline, is a tetracycline that has been considered as an alternative antibiotic choice when doxycycline is not available. While more work is needed to document its efficacy for treating canine HWD and, specifically, its anti-Wolbachia activity, several potential advantages include better absorption with oral administration, better tissue distribution, and better intercellular penetration. When administered to dogs, it should be given before feeding at the same dosage recommended for doxycycline.

The validity of the “susceptibility gap” was questioned. The “susceptibility gap” in dogs with adult heartworms is the period in which heartworms are not susceptible to macrocyclic lactone preventives or the adulticide melarsomine, based on product labels. Because melarsomine has some degree of efficacy against 4-month-old worms, it was postulated that combining melarsomine with macrocyclic lactones at the outset of treating heartworm-positive dogs may eliminate this gap; the author questioned the merits of delaying adulticidal treatment to allow further maturation of tissue-stage larvae.

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The current pre-adulticide delay, advocated by the AHS, is not meant to close the susceptibility gap but to allow the “wolbachiostatic” effects of doxycycline to have a longer period to degrade the adult heartworm, thereby enhancing the protective effects of doxycycline on postadulticidal pulmonary insult.

Furthermore, the use of doxycycline has essentially “closed” the susceptibility gap, eliminating tissuedwelling L3 and L4 larvae and 50% of immature adults during the first 60 to 90 days of infection.

LOE & HEARTWORM RESISTANCE: What is the current status of heartworm resistance?

The topic of heartworm resistance headlined the 14th Triennial Symposium and continues to be an area of high interest and importance. Presentations at this year’s conference focused on trends in LOE reports, the importance of resistance in today’s veterinary practice, genetic profiles of potentially resistant isolates, and practitioner identification of potentially resistant isolates. Speakers on this topic included Drs. Clarke Atkins, Catherine Bourguinat, Dwight Bowman, Timothy Geary, Ray Kaplan, Tom McTier, Andrew Moorhead, Roger Pritchard, and Adrian Wolstenholme.

The majority of LOE claims are not valid.

Approximately 45,000 unsubstantiated macrocyclic lactone LOE claims have been reported to the U.S. Food and Drug Administration Center for Veterinary Medicine, with the largest numbers reported between 2008 and 2010. Most affected animals were age 1.5 to 4 years. The validity of LOE reports has been questioned; most reimbursement claims were invalidated after careful scrutiny of medical records and product purchase history. Of the small percentage of LOE claims that have received an FDA-causality score, just 20%, year-to-year, have been graded as a 6 on a 0-to-6 scale (a score of 6 indicates strong evidence of drug failure). That percentage appears to be falling, with just 10% of claims graded as 6 over the past 4 years.

Heartworm resistance reports are declining.

Frequency of storm activity in the most heavily heartworm-endemic areas (eg, the Mississippi Delta) has recently been low. Storms are postulated

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to have been a factor in past years, when heavy hurricane activity precipitated increases in mosquitoes and mosquito diversity, abandoned dogs, dogs without housing, inadequate heartworm prevention, and, ultimately, HWD incidence. The role of recognized macrocyclic lactone resistance in the heartworm epidemic of 2005 to 2014 (but not the existence of resistance) was questioned.

A new approach to identification or resistance in suspect cases was presented. Practitioners concerned that they may be seeing resistant cases in their practices can use a new clinical decision tree created at the University of Georgia College of Veterinary Medicine. The step-by-step process includes careful review of the case records to verify gaps in prevention. If suspicion persists, practitioners are advised to quantitate microfilariae and then perform a microfilaria suppression test. The test administers ivermectin (50 mg/kg) or milbemycin (1 mg/kg) with retesting 7 days later. If microfilariae are eliminated, the odds of a resistant biotype being involved are extremely low. Meanwhile, when microfilariae are not significantly suppressed (< 75% reduction), the suspicion of resistance increases.

Studies evaluating heartworm resistance are ongoing. Heartworm resistance is a real, but complex, phenomenon that does not follow known patterns of resistance development.

Although specific genetic markers for resistant heartworms remain elusive, studies to understand the genetic factors involved in heartworm resistance are ongoing and may offer future strategies for predicting heartworm resistance or susceptibility to preventives.

VECTOR EPIDEMIOLOGY, CLIMATE INFLUENCES, & MOSQUITO-BLOCKING ACTIVITY: What have we learned about heartworm transmission and prevention?

This session assembled the most diverse group of experts, with presentations on entomology, parasitology, human malarial research, microclimate

AHS HEARTWORM HOTLINE

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P O R T L A N D ,

O R E G O N

AU G U ST 20-23 , 2017 T HE HILTON P O R T L A N D & EX EC U T I V E TOW E R The NAVC is extending its popular educational platform to the great Northwest with an innovative experience unlike any conference you’ve seen before.

NAVC LIVE will feature professional “case theater” veterinarian/client presentations, live-streamed general sessions, short talks, Q&A for remote attendees and clinical content in a non-clinical setting, as well as engaging networking opportunities, key tours and experiences in one of the West Coast’s hottest travel destinations.

Register now at NAVC.com/Live TVP-0102_COLUMN_AHS-Heartworm-Hotline.indd 91

12/15/16 5:54 PM

More from the 15th Triennial Heartworm Symposium

Glossary AHS American Heartworm Society

The AHS’s 15th Triennial Heartworm Symposium was attended by scientists and clinicians from 13 countries and 29 states and had 37 speakers from seven countries. To read a symposium snapshot, visit heartwormsociety.org/ images/2016_AHS_SymposiumCB.pdf..

In addition, the AHS website and YouTube page feature videos of interviews with several symposium speakers and moderators, including Drs. Clarke Atkins, Byron Blagburn, Dwight Bowman, Ray Dillon, Ray Kaplan, Laura Kramer, Tanja McKay, and Matthew Miller. These videos can be viewed at youtube.com/user/americanheartworm.

Scientific papers from the symposium will be published in a future issue of the Journal of Veterinary Parasitology. AHS members can access all past symposium proceedings free of charge. To join the AHS, visit heartwormsociety.org/ membership/join.

data, and the role of mosquito blocking in heartworm prevention. Speakers on this topic included Drs. John McCall, Tanja McKay, Tom Nelson, Audrey Odom, and Michael Povelones.

Our understanding of the dynamics of heartworm transmission by mosquitoes continues to evolve. More than 20 species of mosquitoes in the U.S. today can carry heartworm, and each has a different habitat and behavior—some feed at night and others during the day; some live where they emerge, while others travel; some live in rural areas and outdoors, while others prefer urban areas and indoor habitats. Certain mosquito species that carry heartworm, such as Aedes aegypti and A albopictus (Figure 2), are also known to carry human pathogens, such as the Zika virus.

HW heartworm HWD heartworm disease LOE lack of efficacy

Studies of malaria transmission may suggest avenues of HW research. Studies on the spread of malaria, a human mosquito-borne disease, may offer potential areas of future study of mosquito-borne HWD. Human studies indicate that mosquitoes are more likely to feed on individuals with malaria, based on the presence of terpenes, volatile organic compounds that attract mosquitoes.

CDC’s Response to Zika This finding could lend itself to strategies for ESTIMATED range of Aedes albopictus both disease detection and prevention.

and Aedes aegypti in the United States, 2016*

Aedes aegypti mosquito

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· Exact locations or num mosquitoes living in an Aedes aegypti

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· Risk or likelihood that mosquitoes will spread These maps show

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A multimodal approach to heartworm prevention is recommended. A multimodal heartworm prevention approach, which, in addition to behavioral and housing modification, combines traditional preventives and repellentsinsecticides. This approach is achieved by (1) deploying macrocyclic lactone compounds and (2) blocking both the transmission of microfilariae to mosquitoes and the transmission of the infective stage of Dirofilaria immitis to dogs through the use of the next generation of topical repellent-insecticides.

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* Maps have been updated from a variety of sources. These maps represent CDC’s best estimate of the potential range of Aedes aegypti and Aedes albopictus in the

FIGURE 2. These of for the Centers United States.

Maps aremaps, not meantcourtesy to represent risk spread of disease. for Disease Control, represent the best estimate of the potential range of Aedes aegypti and Aedes albopictus in the United States. Reprinted from the U.S. CS264451-F Department of Health and Human Services, Centers for April 1, 2016 Disease Control and Prevention.

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Clients want to fight fleas and ticks – not their dogs.

Protect dogs with the beefflavored chew they love.1

Data on file at Merial.

1

®NexGard is a registered trademark, and TM FRONTLINE VET LABS is a trademark, of Merial. ©2016 Merial, Inc., Duluth, GA. All rights reserved. NEX16TRADEADS3 (01/17).

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IMPORTANT SAFETY INFORMATION: NexGard® is for use in dogs only. The most frequently reported adverse reactions included pruritus, vomiting, dry/flaky skin, diarrhea, lethargy, and lack of appetite. The safe use of NexGard in pregnant, breeding, or lactating dogs has not been evaluated. Use with caution in dogs with a history of seizures. For more information, see full prescribing information or visit www.NexGardForDogs.com.

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TODAY’S VETERINARY NEWS continued from page 18

CAUTION: Federal (USA) law restricts this drug to use by or on the order of a licensed veterinarian.

Description: NexGard® (afoxolaner) is available in four sizes of beef-flavored, soft chewables for oral administration to dogs and puppies according to their weight. Each chewable is formulated to provide a minimum afoxolaner dosage of 1.14 mg/lb (2.5 mg/ kg). Afoxolaner has the chemical composition 1-Naphthalenecarboxamide, 4-[5- [3-chloro-5-(trifluoromethyl)-phenyl]-4, 5-dihydro-5-(trifluoromethyl)-3-isoxazolyl]-N-[2-oxo-2-[(2,2,2-trifluoroethyl)amino]ethyl.

Indications: NexGard kills adult fleas and is indicated for the treatment and prevention of flea infestations (Ctenocephalides felis), and the treatment and control of Black-legged tick (Ixodes scapularis), American Dog tick (Dermacentor variabilis), Lone Star tick (Amblyomma americanum), and Brown dog tick (Rhipicephalus sanguineus) infestations in dogs and puppies 8 weeks of age and older, weighing 4 pounds of body weight or greater, for one month.

Dosage and Administration: NexGard is given orally once a month, at the minimum dosage of 1.14 mg/lb (2.5 mg/kg).

Dosing Schedule: Body Weight 4.0 to 10.0 lbs.

10.1 to 24.0 lbs.

24.1 to 60.0 lbs.

60.1 to 121.0 lbs.

Over 121.0 lbs.

Afoxolaner Per Chewables Chewable (mg) Administered 11.3 One 28.3 One 68 One 136 One Administer the appropriate combination of chewables

NexGard can be administered with or without food. Care should be taken that the dog consumes the complete dose, and treated animals should be observed for a few minutes to ensure that part of the dose is not lost or refused. If it is suspected that any of the dose has been lost or if vomiting occurs within two hours of administration, redose with another full dose. If a dose is missed, administer NexGard and resume a monthly dosing schedule.

Flea Treatment and Prevention: Treatment with NexGard may begin at any time of the year. In areas where fleas are common year-round, monthly treatment with NexGard should continue the entire year without interruption.

To minimize the likelihood of flea reinfestation, it is important to treat all animals within a household with an approved flea control product.

Tick Treatment and Control: Treatment with NexGard may begin at any time of the year (see Effectiveness).

Contraindications: There are no known contraindications for the use of NexGard.

Warnings: Not for use in humans. Keep this and all drugs out of the reach of children. In case of accidental ingestion, contact a physician immediately.

Precautions: The safe use of NexGard in breeding, pregnant or lactating dogs has not been evaluated. Use with caution in dogs with a history of seizures (see Adverse Reactions).

Adverse Reactions: In a well-controlled US field study, which included a total of 333 households and 615 treated dogs (415 administered afoxolaner; 200 administered active control), no serious adverse reactions were observed with NexGard.

Over the 90-day study period, all observations of potential adverse reactions were recorded. The most frequent reactions reported at an incidence of > 1% within any of the three months of observations are presented in the following table. The most frequently reported adverse reaction was vomiting. The occurrence of vomiting was generally self-limiting and of short duration and tended to decrease with subsequent doses in both groups. Five treated dogs experienced anorexia during the study, and two of those dogs experienced anorexia with the first dose but not subsequent doses.

Table 1: Dogs With Adverse Reactions.

Treatment Group Afoxolaner

Vomiting (with and without blood) Dry/Flaky Skin Diarrhea (with and without blood) Lethargy Anorexia

N1 17 13 13 7 5

% (n=415) 4.1 3.1 3.1 1.7 1.2

Oral active control

N2 25 2 7 4 9

% (n=200) 12.5 1.0 3.5 2.0 4.5

1 Number of dogs in the afoxolaner treatment group with the identified abnormality.

2 Number of dogs in the control group with the identified abnormality.

In the US field study, one dog with a history of seizures experienced a seizure on the same day after receiving the first dose and on the same day after receiving the second dose of NexGard. This dog experienced a third seizure one week after receiving the third dose. The dog remained enrolled and completed the study. Another dog with a history of seizures had a seizure 19 days after the third dose of NexGard. The dog remained enrolled and completed the study. A third dog with a history of seizures received NexGard and experienced no seizures throughout the study.

To report suspected adverse events, for technical assistance or to obtain a copy of the MSDS, contact Merial at 1-888-6374251 or www.merial.com/NexGard. For additional information about adverse drug experience reporting for animal drugs, contact FDA at 1-888-FDA-VETS or online at http://www.fda.gov/AnimalVeterinary/SafetyHealth.

Mode of Action: Afoxolaner is a member of the isoxazoline family, shown to bind at a binding site to inhibit insect and acarine ligand-gated chloride channels, in particular those gated by the neurotransmitter gamma-aminobutyric acid (GABA), thereby blocking preand post-synaptic transfer of chloride ions across cell membranes. Prolonged afoxolaner-induced hyperexcitation results in uncontrolled activity of the central nervous system and death of insects and acarines. The selective toxicity of afoxolaner between insects and acarines and mammals may be inferred by the differential sensitivity of the insects and acarines’ GABA receptors versus mammalian GABA receptors.

Effectiveness: In a well-controlled laboratory study, NexGard began to kill fleas four hours after initial administration and demonstrated >99% effectiveness at eight hours. In a separate well-controlled laboratory study, NexGard demonstrated 100% effectiveness against adult fleas 24 hours post-infestation for 35 days, and was ≥ 93% effective at 12 hours post-infestation through Day 21, and on Day 35. On Day 28, NexGard was 81.1% effective 12 hours post-infestation. Dogs in both the treated and control groups that were infested with fleas on Day -1 generated flea eggs at 12- and 24-hours post-treatment (0-11 eggs and 1-17 eggs in the NexGard treated dogs, and 4-90 eggs and 0-118 eggs in the control dogs, at 12- and 24-hours, respectively). At subsequent evaluations post-infestation, fleas from dogs in the treated group were essentially unable to produce any eggs (0-1 eggs) while fleas from dogs in the control group continued to produce eggs (1-141 eggs).

In a 90-day US field study conducted in households with existing flea infestations of varying severity, the effectiveness of NexGard against fleas on the Day 30, 60 and 90 visits compared with baseline was 98.0%, 99.7%, and 99.9%, respectively.

Collectively, the data from the three studies (two laboratory and one field) demonstrate that NexGard kills fleas before they can lay eggs, thus preventing subsequent flea infestations after the start of treatment of existing flea infestations.

In well-controlled laboratory studies, NexGard demonstrated >97% effectiveness against Dermacentor variabilis, >94% effectiveness against Ixodes scapularis, and >93% effectiveness against Rhipicephalus sanguineus, 48 hours post-infestation for 30 days. At 72 hours post-infestation, NexGard demonstrated >97% effectiveness against Amblyomma americanum for 30 days.

Animal Safety: In a margin of safety study, NexGard was administered orally to 8 to 9-week-old Beagle puppies at 1, 3, and 5 times the maximum exposure dose (6.3 mg/kg) for three treatments every 28 days, followed by three treatments every 14 days, for a total of six treatments. Dogs in the control group were sham-dosed. There were no clinically-relevant effects related to treatment on physical examination, body weight, food consumption, clinical pathology (hematology, clinical chemistries, or coagulation tests), gross pathology, histopathology or organ weights. Vomiting occurred throughout the study, with a similar incidence in the treated and control groups, including one dog in the 5x group that vomited four hours after treatment.

In a well-controlled field study, NexGard was used concomitantly with other medications, such as vaccines, anthelmintics, antibiotics (including topicals), steroids, NSAIDS, anesthetics, and antihistamines. No adverse reactions were observed from the concomitant use of NexGard with other medications.

Storage Information: Store at or below 30°C (86°F) with excursions permitted up to 40°C (104°F).

How Supplied: NexGard is available in four sizes of beef-flavored soft chewables: 11.3, 28.3, 68 or 136 mg afoxolaner. Each chewable size is available in color-coded packages of 1, 3 or 6 beef-flavored chewables.

NADA 141-406, Approved by FDA Marketed by: Frontline Vet Labs™, a Division of Merial, Inc. Duluth, GA 30096-4640 USA Made in Brazil. ®NexGard is a registered trademark, and TMFRONTLINE VET LABS is a trademark, of Merial. ©2015 Merial. All rights reserved.

1050-4493-03 Rev. 1/2015

FIRST USDA-APPROVED IMMUNOMODULATOR FOR CANINE OSTEOARTHRITIS T-Cyte Therapeutics, Inc has announced the launch of Lymphocyte T-Cell Immunomodulator (LTCI) as the first USDA-approved treatment option for canine osteoarthritis (OA), a debilitating condition affecting 16 to 20 million dogs in the United States. The only naturally-occurring treatment aid for OA, LTCI is administered via a subcutaneous injection and is effective in increasing the number and function of precursors of a regulatory T cell population, thereby dampening the immune-mediated process associated with OA. ■ To learn more, please visit tcyte.com.

LAUNCH OF NEW CANCER TREATMENT Torigen Pharmaceuticals, Inc, a biotherapeutic company focused on treating cancer in animals, has announced the commercialization and market launch of their product, VetiVax, which uses the patient’s own tumor cells to create a personalized treatment. VetiVax educates the patient’s immune system to recognize the tumor as foreign and attack the cancer. Developed at the University of Notre Dame, with over 10 years of supporting research, VetiVax is a whole cell tissue immunotherapy that allows for a variety of tumor antigens to be presented to the immune system, and the treatment can be used for multiple tumor types.

■ For more information, visit vetivax.com.

POSTSURGICAL PAIN THERAPEUTIC NOW AVAILABLE Aratana has announced that Nocita (bupivacaine liposome injectable suspension) has been made commercially available to veterinarians in the United States, which is the company’s first launch of an FDA-approved therapeutic. Nocita is a long-acting, local anesthetic that lasts up to 72 hours post surgery by releasing bupivacaine over time from multi-vesicular liposomes deposited in the tissue. The therapeutic is administered as a single dose by tissue infiltration during closure of cranial cruciate ligament surgery in dogs. The U.S. Food and Drug Administration’s Center for Veterinary Medicine (CVM) approved Nocita in August of 2016.

■ Visit nocita.aratana.com to learn more.

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PRACTICAL TOXICOLOGY

The Decontamination Dilemma: Bromethalin Ingestion Renee Tourdot, DVM, ASPCA Animal Poison Control Center

shutterstock.com/Ysbrand Cosijn

Welcome to Practical Toxicology, brought to you in partnership between Today’s Veterinary Practice and the ASPCA Animal Poison Control Center (APCC) (www.aspcapro.org/poison). This column provides practical clinical information about diagnosing and treating pets that have been exposed to potentially harmful substances.

Bromethalin-based rodenticide bait exposures have become increasingly common since the product became available in 1985.1 In 2015, the American Society for the Prevention of Cruelty to Animals Animal Poison Control Center received 2791 calls regarding exposures to bromethalin-based rodenticides.2

The APCC: •P rovides 24-hour diagnostic and treatment recommendations by specially trained veterinary toxicologists •P rotects and improves animal lives through toxicology education, consulting services, and case data review eveloped and maintains AnTox, an animal toxicology •D database system that identifies and characterizes toxic effects of substances in animals •W orks closely with human poison control centers to provide animal poisoning information • Offers extensive veterinary toxicology consulting to organizations in industry, government, and agriculture.

If treating a patient that requires emergency care for poisoning, call the APCC at 888-426-4435.

Exposures to this toxin present a unique challenge to clinicians. Once signs of convulsant syndrome—a neurologic syndrome caused by bromethalin toxicosis—have developed, prognosis for recovery is poor.3,4 Therefore, most clinicians seem aware that prompt and aggressive decontamination measures must be taken. However, if decontamination is too aggressive, iatrogenic hypernatremia can develop, and clinical hypernatremia can be just as life-threatening as a large bromethalin exposure.

To further complicate matters, clinical signs of hypernatremia can appear similar to the neurologic signs caused by bromethalin.5 If clinicians are not aware of, or monitoring for, a significant rise in the patient’s serum sodium level, hypernatremia may be mistaken for bromethalin toxicosis,

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resulting in incorrect treatment being instituted, which can worsen the patient’s prognosis.

This article provides guidance on how to treat patients with bromethalin exposure, while taking these challenges into consideration.

CONSIDER THIS CASE: EVALUATION Dusty, a 6-year-old, 21-kg male castrated hound mix, is presented to an emergency hospital.

History Shortly before presentation, Dusty’s owner found him carrying part of a rodenticide bait block and subsequently discovered a box of bait blocks on the basement floor. The owner believes the box of bait blocks was stored in the basement when she purchased the home 5 years ago, and she knows the box was not on the floor yesterday evening—the last time the owner was in the basement. There are no other pets in the home.

To calculate the dosage ingested, the concentration of bromethalin in the bait needs to be determined.

• It is important to verify the rodenticide product, active ingredient, and concentration.

This information should be taken directly from the packaging whenever possible.

• While most bromethalin-based rodenticides have a concentration of 0.01%, some commercial products have higher concentrations.

• A bromethalin concentration of 0.01% equals 0.1 mg of bromethalin in each gram of bait.

Using a concentration of 0.01%, the potential dosage ingested by Dusty can then be calculated: 1. There are 28.4 grams in 1 ounce; therefore, Dusty may have ingested up to 192 grams of bait.

Learn More The Animal Poison Control Center (APCC) provides 24-hour diagnostic and treatment recommendations by specially trained veterinary toxicologists. If treating a patient that requires emergency care for poisoning, call the APCC at 888-426-4435.

Rodenticide Evaluation Evaluation of the box label suggests that it once held 12 rodenticide bait blocks, each weighing 1 ounce. The box now contains 5 blocks plus the portion of the block the owner recovered from the dog’s mouth, which appears to be no larger than one quarter of a block. The label on the box says the active ingredient is 0.01% bromethalin.

Calculating Rodenticide Dosage After evaluating patient history and the rodenticide itself, the dosage of bromethalin ingested needs to be calculated.

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Based on patient history, it can be determined that Dusty was exposed to up to 6.75 ounces of the rodenticide (12−5.25 = 6.75 blocks). This is the worst-case scenario: the largest amount of bait that Dusty may have ingested is the missing portion of the block he was discovered carrying plus the missing blocks from the box.

6.75 oz × 28.4 g/oz = 192 g 2. If each gram of bait has 0.1 mg of bromethalin, Dusty may have ingested up to 19 mg of bromethalin.

0.1 mg/g × 192 g = 19.2 mg 3. Finally, when 19 mg bromethalin is converted to mg/kg, Dusty may have ingested up to 0.9 mg/kg of bromethalin.

19 mg / 21 kg = 0.9 mg/kg What does this mean? Is this a concerning exposure and, if so, how concerning? How aggressive does decontamination need to be?

To answer these questions, the kinetics and toxicity of bromethalin need to be discussed.

APCC PRACTICAL TOXICOLOGY

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BROMETHALIN TOXICITY Mechanism of Action & Kinetics Bromethalin’s metabolite, desmethyl bromethalin, is primarily responsible for the uncoupling of oxidative phosphorylation in neuronal mitochondria.4 This results in a depletion of adenosine triphosphate from the cell, causing impairment of the sodium potassium pump.

When pump function is poor, sodium and fluid accumulate within the myelin sheaths. This edema accounts for the neurologic signs seen with bromethalin ingestion. Because the edema is within the myelin, this may also explain why traditional medical management of central nervous system edema, such as administration of diuretics and mannitol, has limited success.3 Bromethalin is excreted primarily through the bile, and it is suspected to undergo enterohepatic recycling because experimental studies have shown that multiple doses of activated charcoal are more effective at preventing the neurologic syndrome rather than a single dose.4

Cats demonstrate a similar clinical course to dogs, but are much more sensitive to bromethalin. The LD50 in cats is 0.54 mg/kg.4 Cats may also demonstrate ileus and resultant abdominal distention.1,5

Range of Dosages The dosages cited for dogs and cats are medians, and any individual patient may be more sensitive to the effects of bromethalin.

The APCC has recorded hindlimb weakness occurring, although rarely, at dosages as low as 0.15 mg/kg in dogs, and tremors, depression, anorexia, and death occurring at dosages as low as 0.95 mg/kg, even though the experimental minimum lethal dose is reported to be 2.5 mg/kg.1,2 In cats, signs have occurred at dosages less than 0.24 mg/kg,2 and depression, ataxia, paresis, and death have occurred at dosages as low as 0.45 mg/kg.3

Clinical Presentation

It also appears that dogs younger than 1 year of age may be more susceptible to the effects of bromethalin, which may be due to the immature blood–brain barrier in juveniles.

The clinical presentation of bromethalin toxicosis is dose dependent.

MANAGEMENT OF BROMETHALIN EXPOSURES

At lower exposure dosages (below the 50% lethal dose [LD50] of 3.65 mg/kg for dogs), a paralytic syndrome can develop, typically within 24 to 86 hours after exposure. This syndrome can cause hindlimb paresis and ataxia, and patients may recover from these signs over a period of weeks to months.

Based on the kinetics and toxicity of bromethalin, clinicians must take a conservative approach when deciding at what dosage to begin decontamination efforts and how aggressively to decontaminate. In addition, the time that has elapsed between exposure and decontamination must be taken into account (Table, page 98).

The signs of paralytic syndrome may progress, with development of absent deep pain sensation, upper motor neuron bladder paralysis, central nervous system depression, tremors, hyperesthesia, seizures, and death.1,4 This convulsant syndrome is usually, but not always, associated with larger exposures to bromethalin (above the LD50), and signs typically develop within 4 to 36 hours after ingestion.1,6,7

ADMINISTRATION OF ACTIVATED CHARCOAL Prior to decontamination with activated charcoal, consider administering an antiemetic. This may help reduce the risk for aspiration secondary to vomiting, as well as treat any nausea, which may encourage the patient to drink water.

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Alternative decontamination measures have been proposed and tried, yet no published evidence supports a recommendation for their clinical use at this time. The following measures are not recommended as the standard of care for bromethalin exposures.

The first dose of activated charcoal should be the largest dose (1 to 2 g/kg)2 and, ideally, contain a cathartic agent, such as sorbitol, unless the patient already has diarrhea. Subsequent doses should be half the original dose, with no cathartic included. If there is no evidence of charcoal in the rectum within 8 hours after the first dose, consider administering a warm water enema.6

Intralipid Emulsion Bromethalin is very lipophilic; therefore, in theory, intralipid emulsion therapy has the potential to reduce bromethalin concentrations in the body.9 If this therapy is to benefit the patient at all, it would likely be within the first several hours after an exposure because bromethalin is rapidly absorbed (peak plasma concentrations occur in 4 hours in rats).1,4 Reversal of the neurologic syndrome by intralipid emulsion is unlikely once the neurons are damaged. There is no solid evidence to support the routine use of intralipid therapy for bromethalin exposures at this time.

The potential for activated charcoal to cause potentially lethal hypernatremia should not be underestimated. The mechanism for this effect is not definitively understood but is thought to result from the osmotic effect of the activated charcoal pulling water into the gastrointestinal tract.8 When administering activated charcoal (especially in repeated doses):

Decontamination Measures: Not Recommended

Cholestyramine Cholestyramine is an indigestible ion exchange resin that has been successfully used for decontamination with other agents that undergo extensive enterohepatic recirculation, such as cholecalciferol and certain nonsteroidal anti-inflammatory drugs.10-13 Cholestyramine binds with bile acids in the intestine, preventing their reabsorption and producing an insoluble complex that is excreted in the feces.14 It is unknown at this time whether cholestyramine can be used successfully for bromethalin decontamination.

• It is vital to closely monitor the patient for hypernatremia: obtain a baseline serum sodium level prior to administering activated charcoal and recheck it before administering the next dose.

• Maintain the patient on intravenous balanced crystalloid fluids—such as lactated Ringer’s solution, Normosol R (hospira.com), or Plasma-Lyte (baxterhealthcare.com)—and provide unlimited access to oral water to help prevent hypernatremia.

TABLE Decontamination Recommendations for Bromethalin Ingestion DOSE INGESTED (MG/KG)

TIME SINCE EXPOSURE

ACTION

DOGS 0.1–0.49

0.5–0.75

> 0.75

<4H

Emesis or 1 dose activated charcoal

>4H

1 dose activated charcoal

<4H

Emesis + activated charcoal Q 8 H for 24 H (3 doses total)

>4H

Activated charcoal Q 8 H for 24 H (3 doses total)

<4H

Emesis + activated charcoal Q 8 H for 48 H (6 doses total)

>4H

Activated charcoal Q 8 H for 48 H (6 doses total)

<4H

Emesis or 1 dose activated charcoal

>4H

1 dose activated charcoal

<4H

Emesis + activated charcoal Q 8 H for 24 H (3 doses total)

>4H

Activated charcoal Q 8 H for 24 H (3 doses total)

<4H

Emesis + activated charcoal Q 8 H for 48 H (6 doses total)

>4H

Activated charcoal Q 8 H for 48 H (6 doses total)

CATS 0.05–0.09

0.1–0.3

> 0.3

Table information based on ASPCA APCC recommendations for bromethalin ingestion

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• If a patient’s sodium level increases 5 mmol/L or more from baseline, provide free water (oral, enema, or 5% dextrose solution in water) and postpone the following dose until the sodium level has decreased.

Activated Charcoal

Decontamination Method6,7

Dusty then receives 230 mL of 10% activated charcoal with sorbitol. His baseline sodium is 146 mmol/L. Seven hours after this treatment, Dusty’s sodium level is 151 mmol/L (mEq/L); his fluid rate is increased to 2 times the maintenance rate and he is given an enema.

To summarize the information known about Dusty’s exposure, he was exposed to bromethalin while carrying the rodenticide block (< 4 H) and his worst-case-scenario exposure dosage is 0.9 mg/kg bromethalin. The Table recommends:

One hour later, his serum sodium decreases to 148 mmol/L. Dusty is administered 115 mL of 10% activated charcoal without sorbitol. The remaining doses of charcoal are administered without complication.

CONSIDER THIS CASE: THERAPY

• Induction of emesis and • Administration of activated charcoal Q 8 H for 48 H (6 doses total).

Because exposure may have taken place as early as the previous evening, it is important to perform a rectal examination and/or to evaluate the feces. If the feces are the color of the bait, a gentle warm water enema (5–10 mL/kg) to help decontaminate the colon is recommended.

Therapeutic Approach Emesis

Outcome Dusty is discharged from the hospital 54 hours after admission without developing signs of bromethalin toxicosis.

LD50 = 50% lethal dose.

References 1.

Dorman DC, Parker AJ, Buck WB. Bromethalin toxicosis in the dog.

Part I: Clinical effects. JAAHA 1990; 26:589-594.

2. ASPCA Animal Poison Control Center database, unpublished data, 2015.

Dusty is admitted to the hospital, and emesis is induced with apomorphine (0.04 mg/kg IV).

A few small pieces of green material, suspected to be the bait, are seen in the vomitus. He is administered maropitant (1 mg/kg SC) as well as lactated Ringer’s solution IV at 1.5 times the maintenance rate of 60 mL/kg/day.

3. Dorman DC, Parker AJ, Buck WB. Bromethalin toxicosis in the dog.

Part II: Selected treatments for the toxic syndrome. JAAHA 1990; 26:595-598.

4. Dorman DC. Bromethalin. In Peterson ME, Talcott PA (eds): Small Animal Toxicology, 3rd ed. St. Louis: Elsevier Saunders, 2013, pp 471478.

5. Bates MC, Roady P, Lehner AF, et al. Atypical bromethalin intoxication in a dog: Pathologic features and identification of an isomeric breakdown product. BMC Vet Res 2015; 11:244.

6. DeClementi C, Sobczak BR. Common rodenticide toxicoses in small animals. Vet Clin North Am Small Anim Pract 2012; 42:349-360.

7. Dunayer E. Bromethalin: The other rodenticide. Vet Med 2003; 98:732-736.

8. Plumb DC. Plumb’s Veterinary Drug Handbook, 7th ed. Stockholm, WI: PharmaVet Inc, 2011, pp 193-195.

Renee Tourdot

Renee Tourdot, DVM, is a consulting veterinarian in clinical toxicology with the ASPCA Animal Poison Control Center (APCC). Dr. Tourdot received her DVM from University of Wisconsin–Madison and completed an internship in small animal medicine and surgery at Coral Springs Animal Hospital in Coral Springs, Florida. Dr. Tourdot practiced emergency medicine and surgery at Wisconsin Veterinary Referral Center before joining the APCC in 2015.

9. Dorman DC, Simon J, Harlin KA, Buck WB. Diagnosis of bromethalin toxicosis in the dog. J Vet Diagn Invest 1990; 2:123-128.

10. Ferry DG, Grazeley LR, Busby WJ. Enhanced elimination of piroxicam by administration of activated charcoal or cholestyramine. Eur J Clin Pharmacol 1990; 39:599-601.

11. Calvo M, Dominguez-Gil A. Interaction of naproxen with cholestyramine. Biopharmaceut Drug Dispos 1984; 5:33-42.

12. Busch U, Heinzel G, Narjes H. The effect of cholestyramine on the pharmacokinetics of meloxicam, a new non-steroidal antiinflammatory drug (NSAID), in man. Eur J Clin Pharmacol 1995; 48:269-272.

13. Thompson WG, Thompson GR. Effect of cholestyramine on the absorption of vitamin D3 and calcium. Gut 1969; 10:717-722.

14. Questran oral suspension, cholestyramine oral suspension. Spring Valley, NY: Par Pharmaceutical Co, Inc, 2006.

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CLINICAL INSIGHTS

CLINICAL INSIGHTS

A Cancer Diagnosis Is Not a Death Sentence Sue Ettinger, DVM, DACVIM (Oncology) drsuecancervet.com shutterstock.com/Annette Shaff

Welcome to the first in a series of articles by Dr. Susan Ettinger (drsuecancervet.com), head of the Oncology Department at Animal Specialty Center in Yonkers, New York. Dr. Ettinger’s mission is to promote awareness and education about cancer in pets. In the Clinical Insights column, she will combine her expertise in oncology with her experiences in practice to detail how clinicians can better care for cancer patients.

With a low tail wag, Reese slowly walked across my examination room to greet me. I could tell his cancer was taking a toll. Prior to the consultation, I had reviewed his medical record, which told me my patient was a dog with advanced metastatic cancer. While I am often surprised at how well dogs with advanced cancer often appear, Reese was not one of those pets.

Two months earlier, Reese—a 9-year-old male castrated pit bull/mixed breed dog— had been diagnosed with a right-sided anal sac adenocarcinoma by his primary care

veterinarian. Reese was also hypercalcemic, a well-documented negative prognostic predictor.

Two weeks later, Reese was evaluated by a boarded medical oncologist, who performed staging diagnostics to determine the severity of the cancer.

The oncologist found metastasis to the sublumbar lymph nodes and lungs and initiated oral prednisone therapy for the hypercalcemia and chemotherapy.

Reese became my patient when the oncologist moved across the country. Despite 6 weeks of therapy, he had not improved. His owner reported tenesmus from the large anal sac tumor and the markedly enlarged sublumbar lymph node. Reese had a poor appetite and was being hand fed by his family.

Reese’s radiographs were shocking: His chest was filled with wall-to-wall and overlapping pulmonary nodules—often described as a snowstorm or lungs filled with cotton balls. These images explained Reese’s labored breathing and frequent coughing, which occurred throughout the night.

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Sadly, a dog like Reese has a grim prognosis, typically 1 to 2 months to live from diagnosis, and Reese’s cancer had been identified 2 months ago. What would I say to his family?

There were no options. Or were there?

BREAKING BAD NEWS

MOVING BEYOND MISCONCEPTIONS

However, in my opinion, the general practice veterinarian and team have the more difficult job— they have to tell clients that the biopsy or aspirate of the mass is cancerous, or that there is a high suspicion of cancer. They must often say things, such as: I have bad news about the bone x-rays.

Cancer is a scary word that is often equated with death. To many, cancer also equals pain and suffering. People sometimes think there is no hope.

Because I am a cancer specialist, people are frequently surprised to hear that I love my job. They assume it must be depressing and hopeless, and that pets could not possibly handle cancer treatment or benefit from it. Treatment only makes pets more ill, right?

I disagree. Cancer is not a death sentence. While we all want a cure for cancer, I encourage us to consider many cancers as chronic conditions that may require chronic therapy, such as kidney or heart disease.

There are so many myths and misconceptions about cancer in pets, but one important fact is that treatment is often very well-tolerated.

There are treatment options, and a wide range of them, including surgery, radiation, chemotherapy, and palliative and supportive care.

As an oncologist, I recommend treatment when the pet is likely to live longer with it than without it. Thankfully, most pets feel good, if not great, during treatment. My motto is, “Live longer, live well.” My patients need to do both—and they do. That is why I love my job.

Being a cancer specialist often means delivering tough news: The cancer has spread. The cancer has relapsed.

The cancer is no longer responding to treatment.

Speaking of Oprah Like Reese, Oprah—an 8-year-old female spayed Doberman pinscher—also had advanced cancer but, unlike Reese, she was not showing any signs.

She was an affectionate, energetic dog referred to my practice for a large cranial mediastinal mass observed on chest radiographs by her primary care veterinarian.

Computed tomography confirmed 2 large thoracic masses (> 8–10 cm), thought to be metastatic lymph nodes, and cytology of the cranial mass confirmed carcinoma. Two additional smaller masses were noted in the pulmonary parenchyma. Oprah had a history of an intermediate-grade mammary carcinoma, which was resected 10 months earlier.

While it was not clear whether the thoracic nodules were metastatic, the presence of multiple masses precluded Oprah from surgery, and conventional chemotherapy is typically not effective for macroscopic disease. I started to feel anxious at the prospect of breaking the bad news—that Oprah had multiple chest masses—to her owner.

Oprah’s story continues on page 107.

There are frustrating and heartbreaking moments, especially when I lose a patient to cancer after sharing months or years working together with the pet and owners. But, most of the time, treating cancer in pets is about providing quality of life to the pet and more quality time to its owners, as well as hope.

Most of my cancer patients are quite healthy and treatment allows them to lead happy lives. Some even live longer and better than expected (see Speaking of Oprah).

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Talking about cancer is not fun, and it is stressful for clinicians, who carry the burden of responsibility for communicating bad news. When a pet has cancer, the human–animal bond becomes strained and fragile, making communication between the veterinarian and the owner even more challenging than other clinician–client conversations. Yet, this communication is critical to optimal patient care.

Sadly, guidelines and training to help veterinarians broach difficult cancer conversations about diagnosis, prognosis, treatment, and palliative care options are lacking. In addition, training for “cancer communication” in veterinary school varies with regard to content, duration, and methods. There is often a gap between veterinary school curriculum and the acquisition of the skills needed to be successful in practice.

As a result, many veterinarians and specialists feel unprepared for these conversations, and most oncologists learn to “break bad news” by observing more experienced colleagues.

I am constantly improving my skills so that I can convey distressing news gently, and I help other veterinarians do this as well. However, in school and my residency I was taught the “data dump” method—delivery of a monologue of information. While owners told me I had done a good job and answered all their questions, I came to realize that we—the veterinary profession— can do a better job when talking about cancer.

Better cancer communication begins by learning the following 3 words and what they represent: 1. Aware. Be aware of the challenges both you, as the veterinarian, and the client face.

2. Where. Where are you delivering the bad news?

Aim for a private location, such as an examination room, and do it in person, not on the phone.

Make sure you have sufficient time and attention.

3. How. How do you prepare yourself? Ask open-ended questions, be empathetic, use inclusive language, and make it a dialogue—a conversation. Use the “chunks and check” approach: give a chunk of information; then check for understanding.

I have found that these core communication skills save me time and allow more efficient clinician–client interaction. Breaking bad news may not be easy or fun, but we can improve the experience for the veterinary team and the pet owner. Once we break the news, we start to cover the options, such as chemotherapy.

TREATING WITH CHEMOTHERAPY Most pet owners are surprised that dogs and cats do not experience chemotherapeutic side effects. I have watched human friends and family members get extremely sick after chemotherapy, and they are sometimes hospitalized from severe side effects.

Thankfully, that is not how pets respond.

The overall toxicity rate is very low in veterinary chemotherapy patients. In my experience, the majority of pets, approximately 80%, have no side effects. Only 15% to 20% experience mild to moderate side effects that last a few days, and side effects are less common in cats than dogs.

Serious complications, such as severe inappetence, dehydration, vomiting, and diarrhea, occur in less than 5% of chemotherapy patients. These patients may require hospitalization for supportive care to address dehydration, infection, or sepsis.

In my experience, with a dose reduction and prophylactic medications, most of these patients can successfully receive that same drug again.

Owners are also relieved to learn that most pets do not lose their hair. Alopecia (hair loss) occurs because chemotherapeutic agents target all rapidly dividing cells, including hair follicles. In dogs, some potentially affected breeds—poodles, Scottish terriers, and West Highland white terriers— have continuously growing coats. Alopecia is rare in cats, but they may lose their whiskers.

While undergoing chemotherapy, shaved areas on the pet (eg, for limb catheters, abdominal ultrasound) do tend to grow hair back more slowly. The good news is that hair and whiskers regrow once the treatments have completed. Occasionally, hair grows back a different texture or color and, in cats, the hair coat is typically softer and referred to as a chemo coat.

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It is important to remember, and remind clients, that pets do not care about cosmetic side effects, and these effects do not impact quality of life.

However, I do recommend advising pet owners about the potential loss of whiskers and hair coat to avoid any unnecessary surprises.

Cancer treatment is not a binding contract. I always encourage clients who are considering chemotherapy to let me administer 1 to 2 doses and see how the pet reacts. Most clients are so pleased that they continue with treatment and I can adjust the dose and other medications to ensure quality of life during treatment.

I cannot tell you how often clients tell me their pets undergoing chemotherapy have more energy than they did 6 months or a year ago—before they had cancer and before they began receiving chemotherapy. I think it is a testament to how well most pets feel during and after chemotherapy.

LIVING IN THE MOMENT Another important aspect in veterinary oncology is to remember that the patients do not “know” they have cancer. Of course, dogs and cats feel pain and do not enjoy feeling unwell but, unlike humans, pets do not deal with the psychological aspect of cancer. Pets live in the moment, and I think “ignorance is bliss” in these situations.

Just in Case: Preventing Chemotherapy Side Effects While most side effects of chemotherapy are mild and self-limiting, we can improve the quality of life for these patients through proactive client education and a prophylactic approach.

For patients receiving injectable chemotherapy that is likely to cause nausea or vomiting, such as doxorubicin, I administer antiemetics (eg, maropitant) concurrently with the chemotherapy treatment.

All patients receiving chemotherapy are discharged with “just-in-case” medications, including maropitant, metronidazole, and a probiotic, and detailed instruction sheets on when and how to use them. This leaves clients prepared in case the patient has gastrointestinal side effects at home.

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Instead, it’s the pet owners who must absorb all the cancer information—remission rates, survival statistics, treatment options, treatment schedule, and costs. I advise my clients to avoid stressing about their pets’ response to treatment and prognosis because stressing will not change the outcome. And I tell them to let me worry about the disease, treatment, doses, and response.

The client’s role is to give me feedback on how the pet did after treatment and to give the pet its prescribed medications. Clients need to enjoy each day, for each day with a pet is a gift.

NEW THERAPIES ARE ARRIVING It is an exciting time to be an oncologist. New therapies are available and even more are on the horizon.

Newer radiation therapy options, such as stereotactic radiation, can treat some tumors (eg, brain, nasal) in 1 to 3 treatments (rather than 15–20), with fewer anesthesia episodes, side effects, and practice visits. We also now have targeted therapy, such as the tyrosine kinase inhibitor Palladia (toceranib phosphate; zoetisus.com) for canine mast cell tumors and the melanoma vaccine Oncept (merial.com) for canine oral and digit malignant melanoma.

Other new therapeutics are in earlier phases of development and clinical studies and, in some cases, we are waiting for published data on response rates. These include a monoclonal antibody immunotherapy for B-cell lymphoma (aratana.com), a canine lymphoma DNA vaccine (merial.com), and nucleotide prodrug from VetDC for dogs and possibly cats (vet-dc.com).

A canine osteosarcoma vaccine (aratana.com) is being studied at the University of Pennsylvania as an aid to treatment with amputation and chemotherapy. Early results look promising, with an increase in survival times and only mild to moderate adverse effects.

Other supportive medications in the pipeline include Entyce (capromorelin; aratana.com), an appetite stimulant, and Canalevia (crofelemer; jaguaranimalhealth.com), which is for treatment of chemotherapy-induced diarrhea.

It is exciting to know that the near future may hold new tools for our cancer toolbox.

CLINICAL INSIGHTS

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CLINICAL INSIGHTS

CONTINUED: REESE & OPRAH During my residency, I was taught that patients with advanced metastatic disease—dogs like Reese—would likely live 1 to 2 months, so I focused on palliative care and pain management. However, I no longer define cancer treatment success by complete remission.

Partial response or even stable disease is successful if we improve or maintain a good quality of life.

In dogs and cats with advanced metastatic disease in which maximum tolerated dose (MTD) chemotherapy is no longer effective, metronomic chemotherapy may inhibit tumor growth and, thus, stabilize disease. This “pulse” chemotherapy provides uninterrupted low doses of cytotoxic drugs at regular, continuous, and frequent intervals.

Eliminating breaks between dosages reduces or eliminates the ability of the tumor cells to repair damage or alter their microenvironments. Instead of killing cancer cells directly with MTD (highdose) chemotherapy, this therapy targets blood vessels that allow tumors to grow and metastasize.

This therapeutic approach is what I chose for Reese and Oprah, and both of them received off-label oral Palladia for its anti-angiogenic effects, with low-dose (metronomic) oral cyclophosphamide for its effect on regulatory T cells.

Reese Two months later, follow-up chest radiographs showed smaller and less defined nodular opacities. More important, Reese’s appetite had improved and his coughing was decreased, resulting in weight gain and great energy.

Even though Reese presented with advanced metastasis, he lived 10 more months. His protocol was well-tolerated, and Reese’s owners were pleased with the quality of life that resulted from therapy.

Oprah Oprah’s follow-up chest radiographs at 2 months showed stable disease, but I was shocked at her 7-month recheck radiographs—the cranial mass was gone and the caudal one had decreased in size.

Each Patient is an Individual A veterinary professional should educate clients that cancer is one name for many different diseases. Lymphoma is different from hemangiosarcoma, oral melanoma, or osteosarcoma.

Lymphoma in cats is different from that in dogs. A client may know someone whose dog did not tolerate chemotherapy treatment, such as doxorubicin, but that does not mean his or her newly diagnosed pet will not tolerate the same treatment. The other patient may have had advancedstage cancer and preexisting conditions that complicated treatment. Remind clients that each pet is an individual.

Oprah is still my patient today, 2 years and 11 months later. She has had some side effects from the cyclophosphamide, including sterile hemorrhagic cystitis. Most recently she developed idiopathic dilated cardiomyopathy that resulted in heart failure, but monitoring and care by a cardiologist has resulted in improvement.

IN SUMMARY Today, there are options for pets with cancer, even those with advanced metastatic cancer as demonstrated by Reese and Oprah. These options include new therapeutic modalities and a more preventive approach with treatment, complemented by improved communication about cancer. Do not think cancer is a death sentence. Think hope, think options, and think live longer, live well.

Sue Ettinger

Sue Ettinger, DVM, DACVIM (Oncology), is head of the Oncology Department at Animal Specialty & Emergency Center in Wappinger Falls, in the Hudson Valley of New York. Also known as Dr. Sue Cancer Vet, she is the coauthor of the second edition of The Dog Cancer Survival Guide, cohost of the podcast The Pet Cancer Vet (radiopetlady. com), and an international speaker. Dr. Ettinger developed See Something, Do Something, Why Wait? Aspirate—a cancer awareness initiative for skin and superficial tumors in dogs and cats.

She received her DVM from Cornell University and completed a medical oncology residency at The Animal Medical Center in New York City. Dr. Ettinger can be found on Facebook (facebook.com/DrSueCancerVet) and Twitter (@DrSueCancerVet).

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NAVC KEYNOTE COMMENTARY

NAVC KEYNOTE COMMENTARY FOR THE VETERINARY COMMUNITY

A Regulatory Road Map for Telehealth & Pet Health Care Mark Cushing, JD, Animal Policy Group, LLC, Knoxville, Tennessee; Washington, DC; Portland, Oregon

shutterstock.com/Andrei Rahalski

The veterinary profession in the United States decided to take telemedicine seriously in 2016.

The NAVC (navc.com) launched its Veterinary Innovation Council (VIC) a year ago and numerous organizations stepped up to participate in its first project—a telehealth pilot. In April 2017, Texas A&M College of Veterinary Medicine (vetmed.tamu.edu) and the NAVC are collaborating to host the Veterinary Innovation Summit, which will include a robust examination of telemedicine and the VIC pilot results.

Also in 2016, the American Veterinary Medical Association (AVMA, avma.org) convened telemedicine task force meetings, while Banfield Pet Hospital (banfield.com) devoted a session of its September Pet Healthcare Industry Summit to telemedicine.

Most important, the American Association of Veterinary State Boards (AAVSB, aavsb.org) devoted a full afternoon of its 2016 annual meeting to the topic of telemedicine. Under the leadership of new AAVSB Executive Director, Jim Penrod, state veterinary board regulators decided to proactively address telemedicine and explore its implications for veterinary medical care.

Let’s Talk About Telemedicine Telemedicine does not refer to telephone consultations among veterinarians and diagnostic specialists, which have been happening for a long time. Rather, it describes real-time electronic encounters among veterinarians, pet owners, and pets, during which the parties see and talk to each other. Add to this the electronic communication tools of email, texts, and the like, and suddenly pet health care begins to mirror 21st century human health care.

IT’S GOING TO HAPPEN Was there something in the water throughout the country? Or has the intersection of consumerfriendly electronics and human health care advances finally prompted veterinary medicine to “jump into” telemedicine with both feet?

It’s no longer a question of whether veterinarians will embrace telemedicine technologies, but when… and how. The veterinary profession and its animal health partners are eager to get this right, so how do we make it happen, not just at conferences, but every day in practices across the U.S.?

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What veterinary telemedicine needs is a regulatory road map that removes barriers to making telemedicine a reality. Hopefully, this article is a start. It’s written for the veterinary practitioner in any state in this country who asks a simple question: if telemedicine is a good idea for pet health care, then how do we make it happen?

WHAT’S IN A NAME? Telemedicine is more than a telephone call; it describes the use of the internet in veterinary medical practice.

When a veterinary–client–patient relationship (VCPR) exists, the veterinarian may communicate with the client in any way she chooses: in person or by telephone, internet, fax, Skype, carrier pigeon…you name it. All that matters, for regulatory purposes, particularly in the area of prescription medicines, is the veterinarian’s familiarity with the pet through a relatively recent in-person examination.

The Federation of State Medical Boards (FSMB, fsmb.org) defines telemedicine as the practice of medicine using electronic communications, information technology, or other means between a licensee in one location and a patient in another location, with or without an intervening health care provider.

The challenge of telemedicine in this context is one of staffing, pricing, technology, and standard of care requirements spelled out in state veterinary practice acts. Technology can be a key to client engagement, which is important because it drives client satisfaction and nurtures a long-term relationship between the veterinarian and the pet owner.

The American Telemedicine Association (ATA, americantelemed.org) uses a shorter version, defining telemedicine as a tool to facilitate health care delivery… to augment, and not replace, the clinical practice, judgment, and the expertise of the health care provider.

These are important issues, but not the focus of this article. I will leave it to trade associations and technology providers to determine how best to engage practitioners with the array of telemedicine tools for existing clients.

Insert veterinary before the words medicine or health care and you have veterinary telemedicine—a real-time electronic engagement among veterinarians, pet owners, and pets.

DETERMINING THE DIRECTION To design a road map, we need to determine the direction of telemedicine in veterinary medicine.

The 2 broad goals discussed most often are: 1. To provide familiar electronic tools to existing clients, which allows communication between veterinarians and pet owners after visits or in lieu of visits, if the situation warrants.

2. To reach out to pet owners who do not have a veterinarian and provide convenient and familiar tools that introduce them to the path of veterinary care for their pets.

The first category of pet owners presents a different set of challenges than the second: put simply, the telemedicine road map for existing clients does not pose regulatory barriers, but this is not the case with telemedicine for potential clients.

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EXISTING CLIENT CHALLENGES

NON-CLIENTS FACE REGULATORY WALLS Here’s the dilemma for the veterinarian brimming with enthusiasm and ready to reach out to new clients through telemedicine: If this practitioner attends a veterinary conference, he or she is likely to run headlong into a gale force of resistance asserting that a VCPR cannot be created through telemedicine.

Every jurisdiction, except Connecticut, Alaska, and the District of Columbia, spells out the requirements for a VCPR, which includes an in-person physical examination of the pet. But here is the real-world challenge:

• Between 40% to 50% of pet owners—who love their pets—do not seek regular veterinary care.

• While ads, social media, neighbors, friends, the Partners for Healthy Pets initiative, and every known tool of persuasion have implored pet owners to visit veterinary clinics, they consistently vote no. Hence, no VCPR. • As such, these pets receive no medical care, although their owners may access all manner of internetbased information to learn about their pets’ health.

NAVC KEYNOTE COMMENTARY

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NAVC KEYNOTE COMMENTARY

• These pet owners probably use smartphones and other electronic tools to manage much of their lives, including personal medical care. However, 48 states forbid a veterinarian from attempting to engage an owner through electronic tools, or vice versa, without a VCPR in place.

• Once again, the pet’s health care goes unattended since the pet owner already has decided against visiting the clinic.

The result? The VCPR serves as a wall, rather than a door into the world of veterinary health care. Does this make sense?

HUMAN MEDICINE LEADS THE WAY If you’ve read this far, then you’re scratching your head, wondering how many lobbyists or lawyers (favorite professions of this author) are required to fix the problem. However, I’m pleased to say very few, thanks to human medicine.

Lawyers and lobbyists, with doctors, have been busy for 2 decades in human health care arenas, working through the exact issues facing veterinary telemedicine:

• Doctor–client relationship: Can this be formed via telemedicine? Yes, in 47 states.

• Multi-state licensure: Can state boards still require the treating doctor to be licensed where the patient resides? Yes, although some states are more flexible.

• Online prescriptions: Is a doctor–client relationship still a requirement? Yes. • Informed consent: Can state boards require that a client consent to being served through telemedicine? Yes, although some states do not require this.

• Privacy/security: Can state boards require that telemedicine adhere to the same requirements as in-person examinations and treatment? Yes. • Standards of care: Are they the same for telemedicine as for in-person examinations and treatment? Yes. Supplemented by FSMB and ATA resources, the states have learned from each other and, subsequently, all 50 have developed some level of telemedicine laws and regulations. Most important, human health care treats telemedicine as a staple of health care delivery.

IF WE WANT IT, WE CAN HAVE IT All we need to do is follow the lead already set in place by human telemedicine and learn from their lessons. It really is that simple.

State veterinary medical boards can walk across their state capitols and consult sister state medical boards. The AAVSB can reach out to its sister FSMB and the ATA. These organizations have worked through the issues and created templates we can adapt with relatively little effort.

The veterinary profession in each state may partner with its state veterinary board, and nationally with the AAVSB, to initiate task forces and implement appropriate regulations in relatively short order, if we want to. It’s not a matter of complexity, but of interest or willpower.

I can hear skeptics howling that it’s not that easy.

It actually could be—we don’t have to start from scratch—but, of course, there will be work involved (and some need for lawyer/lobbyist services). And the argument we often hear—that veterinary medicine is different because pets cannot speak for themselves—does not hold water since a large share of human health care involves pediatric patients who cannot articulate their conditions or symptoms.

Forty-seven states now allow a human doctor–patient relationship to be created through telemedicine.

You can be assured that virtually every state resisted this when the process started decades ago, but experience, shared learning, and consumer familiarity with electronic technologies and devices changed people’s minds and opened up state medical

State of Telemedicine In human medicine, Texas, Alabama, and Arkansas are the most conservative states, with limited telemedicine privileges. In veterinary medicine, Connecticut, Alaska, and D.C. have no VCPR rules and may be more flexible with regard to telemedicine privileges, but telemedicine is not being actively practiced in any state beyond consultations between veterinarians.

continued on page 116

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Hyperthyroid cats:

The IDEXX SDMA Test is a more reliable indicator of kidney function than creatinine

by Roberta Relford, DVM, MS, PhD, DACVIM, DAVCP SDMA Hyperthyroidism is a disease seen primarily in older cats, in which kidney disease is also common.

Muscle mass

The clinical challenge is that hyperthyroidism can mask the presence of kidney disease,1 and until now, there has not been a reliable routine diagnostic test that can assess kidney function in cats affected by hyperthyroidism.2

Creatinine

Creatinine, being a by-product of muscle, is underproduced in feline hyperthyroidism as a result of muscle loss and becomes a poor indicator of kidney function. Creatinine is also lowered by the hyperfiltration associated with the increased metabolic state.

Healthy cat

The IDEXX SDMA™ Test is not impacted by weight loss and muscle mass and appears to be only slightly blunted by hyperfiltration,3 making it a much more reliable marker of kidney function in hyperthyroid cats.4

Hyperthyroid cat

SDMA is not impacted as muscle mass decreases.

Creatinine decreases as muscle mass decreases.

When 1,959 cats were evaluated, creatinine levels dropped whereas the SDMA concentrations remained relatively unchanged.

Thus SDMA was able to identify significantly more cats with poor kidney function. When provided, the average body weight had significantly declined in this population of cats.3 Hyperthyroid

Grey Zone

RI 2.3 mg/dL

Total T4 (µg/dL)

Creatinine decreases with loss of muscle mass in hyperthyroid cats, making it unreliable in detecting underlying kidney disease.

TVP_COLUMN_Keynote-Commentary.indd 112

Hyperthyroid

Hyperthyroid

SDMA (µg/dL)

Creatinine (mg/dL)

Grey Zone

RI 14 ug/dL

Total T4 (µg/dL)

SDMA* is not impacted by loss of muscle mass in hyperthyroid cats, making it a more reliable indicator of underlying kidney disease.

12/15/16 5:58 PM

Data research findings

Figure 1.

General feline population >5 years old n = 453,126

Percent of all samples

SDMA is a more reliable indicator of kidney function in hyperthyroid cats than creatinine. To demonstrate that SDMA remains relatively stable in the face of both muscle loss and hyperfiltration, a large retrospective data analysis3 was performed comparing creatinine and SDMA results in cats older than 5 years of age. It also compared the number of cats with kidney disease identified by creatinine versus the number of cats identified by SDMA as having kidney disease.

The prevalence of kidney disease was evaluated in a general population of cats and compared to a hyperthyroid feline population.

Figure 2.

more

IDEXX SDMA

Hyperthyroid feline population

Percent of all samples

n = 2,000

In the hyperthyroid feline population: Creatinine results above the reference interval decreased dramatically from 14% to 3.5% in the general population; whereas, the proportion of cats with increased SDMA above the reference interval remained similar to the general population at 20.6% (figure 2).

20.6%

6X

more

3.5% Creatinine

20.6%

This robust retrospective data analysis demonstrated that there is a profound effect on creatinine results in hyperthyroid cats. The decrease in creatinine results are due to loss of muscle mass and appears to only be slightly blunted as a result of hyperfiltration effects.

The IDEXX SDMA™ Test reliably identified 6 times more hyperthyroid cats with kidney disease than creatinine.

Creatinine missed 82%† of hyperthyroid cats that the IDEXX SDMA Test identified as having kidney disease.

2X

14%

Creatinine

In the general feline population: Creatinine was found to be increased above the reference interval in only 14% of the cats; SDMA was increased in 27% (figure 1). These results align with numerous studies that have shown that SDMA can detect kidney disease when creatinine is normal because SDMA is highly correlated to kidney function, not impacted by muscle mass, not impacted by diet or gender and is more sensitive at identifying disease earlier. These findings suggest that by using the IDEXX SDMA Test, veterinarians have the opportunity to diagnose kidney disease 2 times more in feline patients.

Conclusion

27%

IDEXX SDMA

The IDEXX SDMA Test identified more hyperthyroid cats with kidney disease than creatinine

IDEXX SDMA

3.5% Creatinine

Creatinine missed

82%

Find out everything you need to know about the IDEXX SDMA Test.

Learn more at idexx.com/SDMA

*Symmetric dimethylarginine †

Kidney disease was identified in 72 hyperthyroid cats out of the total general feline population (n = 2,000), or 3.5%, using creatinine alone. However, kidney disease

was identified in 412 hyperthyroid cats out of the total general feline population, or 20.6%, by adding the IDEXX SDMA Test. This means that using creatinine alone missed 340 hyperthyroid cats with kidney disease, or 82%.

References 1. Williams T. Chronic kidney disease in cats with hyperthyroidism. Clin Brief. Sept 2015:10–12.

2. Jepson R. Feline hyperthyroidism and chronic kidney disease. In: Proceedings from the BSAVA Congress; April 9–12, 2015; Birmingham, UK. 3. Data on file at IDEXX Laboratories, Inc. Westbrook, Maine USA. 4. Hall JA, Yerramilli M, Obare E, Yerramilli M, Yu S, Jewell DE. Comparison of serum concentrations of symmetric dimethylarginine and creatinine as kidney function biomarkers in healthy geriatric cats fed reduced protein foods enriched with fish oil, L-carnitine, and medium-chain triglycerides. Vet J. 2014;202(3):588–596.

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Lori Thompson, DVM, DACVD Animal Allergy and Dermatology Center of Indiana Indianapolis, Indiana HOW I TREAT

How I Treat…

Otitis Media/Interna AN INTERVIEW WITH DR. LORI THOMPSON

Today’s Veterinary Practice introduces our new column, How I Treat. This column is based on the popular How I Treat sessions presented at the annual NAVC Conference in Orlando, Florida (navc.com/conference).

This column features interviews with leading veterinary specialists on pertinent clinical topics, with the goal of bringing practitioners essential information on therapeutic approaches.

In this How I Treat interview, Lori Thompson, DVM, DACVD, answers our questions about key treatment protocols for otitis media/interna.

Otitis media—inflammation of the middle ear structures, occurs in dogs and cats of all ages and presents unilaterally or bilaterally.1 Untreated otitis media can lead to otitis interna—inflammation of the inner ear structures—or to rupture of an intact tympanic membrane with subsequent otorrhea or otitis externa.1 Q. If a culture is not available to provide guidance on antimicrobial therapy, what is the best antibiotic approach to ensure successful treatment?

cytologic findings. If cocci are the predominant bacteria present, Staphylococcus is most likely.

Whereas, chains of cocci often represent Streptococcus and rod-shaped bacteria are likely Pseudomonas.

When choosing an antibiotic to treat otitis media, select one that is known to penetrate bone; then dose at the higher end of the dosing range (Table 1). Because higher doses of antibiotics are needed, marbofloxacin remains the best fluoroquinolone choice in cats due to the reported risk of retinal damage when enrofloxacin is used at doses higher than 5 mg/kg Q 24 H. Remember that cytology and culture samples from the horizontal ear canal and from the middle ear may vary significantly in the same patient. For this reason, if a culture from the middle ear is not available to provide guidance with regard to antibiotic selection, cytologic evidence demonstrating the type of infection present in the middle ear (cocci only versus mixed infection) is very important to help guide treatment recommendations.

A. If a culture of the middle ear is not available or feasible, the antibiotic choice is best based on TABLE 1 Selected Antibiotic Treatment for Otitis Media Based on Cytology Results CYTOLOGY RESULT

Cocci (likely Staphylococcus)

Mixed infection

ANTIBIOTIC

DOSAGE

Cefpodoxime

10 mg/kg PO Q 24 H

Cephalexin

22–30 mg/kg PO Q 12 H

Clindamycin

10 mg/kg PO Q 12 H

Enrofloxacin

10–20 mg/kg PO Q 24 H

Marbofloxacin

5 mg/kg PO Q 24 H

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Perforated eardrum in 10-year-old West Highland white terrier with a history of chronic otitis externa secondary to atopy.

HOW I TREAT

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HOW I TREAT

Q. How long should antibiotic therapy be continued?

with more obvious signs, such as vocalization, shying away, and avoidance.

A. Antibiotic therapy should be continued for 7 to 10 days past clinical resolution. In patients with otitis media/interna, it is not uncommon to sustain uninterrupted antibiotic therapy for 6 to 12 weeks.

Because it is difficult for antibiotics to reach target organisms within the middle ear, use doses at the higher end of the reference range.

Anti-inflammatories, such as systemic corticosteroids or nonsteroidal anti-inflammatory drugs (NSAIDs), are almost always indicated as well. However, NSAIDs must not be used in combination with systemic corticosteroids due to the potential for side effects.

Given the frequency of mixed infections and the presence of organisms with unpredictable susceptibility patterns, antibiotic selection should be based, whenever possible, on culture and sensitivity results obtained from the middle ear. This is especially important given the longer course of treatment often required, similar to a patient with osteomyelitis.

Q. Are anti-inflammatories and/or analgesics part of your therapeutic strategy?

A. Absolutely! The role of pain management in the treatment of otitis externa/media/interna is extremely undervalued and underutilized. Otitis media/interna, just like cases of osteomyelitis, can be extremely painful. Since our patients are typically stoic, their levels of pain can easily be underestimated.

There are several good choices available to clinicians for pain management; effective choices for the management of otitis media/externa are listed in Table 2. Advise owners to monitor for less obvious indicators of pain, such as decreased interaction, anorexia, and lethargy, in combination

Whenever possible, I favor the use of systemic corticosteroids over NSAIDs in patients with otitis media/interna. Corticosteroids not only decrease the intense inflammation found in middle ear disease, but also have been found to decrease the amount and viscosity of the exudate and mucus produced within the bulla. By decreasing the inflammation present, the amount of free space within the bulla and horizontal ear canals increases, allowing better access for medication and improved epithelial migration.

The 2 most commonly used corticosteroids in the treatment of otitis media/interna are listed in Table 2.

In my experience, triamcinolone appears to be more effective in decreasing the proliferative changes associated with chronic otitis and has fewer adverse side effects (eg, excessive drinking, urination).

Q. Is there a role for topical therapy in treatment of otitis media/interna?

A. There is indeed a role for topical therapy. Usually, the clinician’s best chance for resolution is to create a treatment plan that utilizes a multimodal approach that combines topical therapy and systemic therapy with pain management.

TABLE 2 Selected Analgesic & Antiinflammatory Drugs for Otitis Media/Interna TYPE

DRUG

DOSAGE

Gabapentin

10–12 mg/kg PO Q 12–24 H

Tramadol

2–5 mg/kg PO Q 8 H

Prednisone

1–2 mg/kg PO Q 24 H for 7–14 days; then taper to QOD dosing

Triamcinolone

0.1–0.2 mg/kg PO Q 24 H for 7–14 days; then taper to QOD dosing

Analgesic

Corticosteroid

Acute otitis media in a 2-year-old standard poodle (post myringotomy).

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NAVC KEYNOTE COMMENTARY

HOW I TREAT

NAVC KEYNOTE COMMENTARY continued from page 111

boards to the possibilities of telemedicine. In veterinary terms, these boards turned the VCPR into a doorway for health care, not an impenetrable wall.

Why can’t veterinary medicine do the same thing?

Ruptured tympanum in a cocker spaniel with a history of chronic otitis externa.

It is important to remember that both topical and systemic medications carry the risk of ototoxicity —drugor chemical-related damage to the inner ear that may affect hearing and balance. Therefore, it may be best to use products that can be infused into the tympanic bulla with minimal to no risk of ototoxicity; these include:

• Antibiotics: Enrofloxacin, ticarcillin, and ceftazidime • Antifungals: Clotrimazole, miconazole, and nystatin • Aqueous forms of anti-inflammatories: Dexamethasone and fluocinolone • Ceruminolytics: Cerumene (a squalene) and Tris-EDTA flush.

References

2. Robson DG, Burton G, Bassett R. Correlation between topical antibiotic selection, in vitro bacterial antibiotic sensitivity and clinical response in 16 cases of canine otitis externa complicated by P aeruginosa. Proc North Am Vet Derm Forum, 2010.

Lori Thompson

Lori Thompson, DVM, DACVD, owns Animal Allergy and Dermatology Center of Indiana in Indianapolis. Dr. Thompson is also an active member of the American College of Veterinary Dermatology and American Academy of Veterinary Dermatology, a consultant for VIN, and serves as the chairperson for the AVMA task force on veterinary compounding legislation. After receiving her DVM from Purdue University, Dr. Thompson practiced small animal medicine before completing a 3-year residency in veterinary dermatology.

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CALL TO ACTION So let the discussions begin by studying state medical practice acts and telemedicine precedents.

In a year, we could see state veterinary medical associations and boards working in tandem to offer practice act reforms to state legislatures, opening the door for pet telemedicine.

Just think about the possibilities, as we take advantage of existing models, to make the process simple, streamlined, and practical.

Mark Cushing

1. Kahn CM (ed). Otitis media and interna. The Merck Veterinary Manual, 10 ed.

Whitehouse Station, NJ: Merck & Co, 2010, pp 486 antimicrobial susceptibility of Pseudomonas aeruginosa in biofilm in vitro. Vet Dermatol 2014; 25(2):120-123.

116

Veterinary and human medicine are governed at the state level, but practice acts vary among states. Solutions are readily available­­—no state can say it doesn’t have the resources to tackle telemedicine. Also, the AAVSB has taken the lead to provide valuable resources for the states.

Other veterinary organizations, including AVMA and state veterinary medical associations, can also step up and push for a more modern, flexible view of the VCPR.

Mark Cushing, JD, is the Founding Partner of the Animal Policy Group, LLC, with offices in Knoxville, TN; Portland, OR; and Washington, DC. Mark also serves as University Counsel and VP of Public Affairs at Lincoln Memorial University in Harrogate, TN. A long-time political strategist, lobbyist, corporate executive, and former litigator, Mark now specializes in animal health, animal welfare, veterinary medicine, and veterinary educational issues. He is a frequent speaker at veterinary medicine and other animal policy-related conferences, an adjunct professor at the LMU Duncan School of Law, an adjunct faculty member in animal law at the Lewis & Clark Law School (Portland, OR), and a visiting lecturer at the University of Oregon School of Law. Mark is an honors graduate with distinction from Stanford University and the Willamette University College of Law.

HOW I TREAT

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