Medical, Genetic and Behavioral Risk Factors of Purebred Dogs: Volume 3

By Ross D. Clark DVM

There is no available information at this time. Author will provide once available.

• Language: English
• Publisher: Xlibris US
• Release date: May 23, 2019
• ISBN: 9781796013757

Ross D. Clark DVM

Ross D. Clark, DVM is the founder of Woodland PetCare Centers and a cofounder of National PetCare Centers. He received his doctor of veterinary medicine degree in 1963 from Kansas State University. He is practice management editor for Veterinary Economics Magazine and served as president of the Tulsa County Veterinary Medical Association, the Oklahoma Veterinary Medical Association, and also as president of the Western Veterinary Conference—the world’s largest continuing education conference for veterinarians. American Animal Hospital Association named him Outstanding Practitioner for the Western Region in 1987 and National Merit Award Winner in Toronto, Ontario, Canada, in 1991. Veterinary Partners Incorporated, an organization of veterinarians, lawyers, and accountants that do practice management consulting, recognized Dr. Clark with their prestigious Pioneer Award at the Western Veterinary Conference in 2004. He served two terms as president of Kansas State University Veterinary Medical Alumni Association from 1990 to 1992, and Kansas State University named him an alumni fellow in February of 2003. Over the past forty-five years, Dr. Clark and his partners have cared for show dogs from most states in the United States of America, plus show dogs from Canada, Mexico, and Spain. He is the author of eight books, including Medical, Genetic, and Behavioral Aspects of Purebred Cats and the coauthor of the first and second edition of Medical and Genetic Aspects of Purebred Dogs. He is also author of four management books: first, a practice management manual; second, The Best of Ross Clark; third, Mastering the Marketplace—Taking Your Practice to the Top; and his latest book, Open Book Management for Veterinary Hospital Teams. He has toured throughout the world as a practice management lecturer and consultant. In addition, Dr. Clark has been a Veterinary Economics “Hospital of the Year” judge for over twenty-eight years. Dr. Clark is currently owner and managing partner of four small animal practices and three pet resorts in Oklahoma. Dr. Clark and his team have been doing veterinary practice management consultation, seminars, and appraisals since 1981. Ross is married to Linda Clark, and they have two children, twins Kent and Kimberly Clark.

Book preview

MEDICAL, GENETIC

AND BEHAVIORAL RISK

FACTORS OF

PUREBRED DOGS

V O L   3

TERRIER AND TOY BREEDS

ROSS D. CLARK, DVM

Copyright © 2019 by Veterinary Management Concepts. 791852

ISBN:   Softcover     978-1-7960-1376-4

             Hardcover   978-1-7960-1377-1

             EBook         978-1-7960-1375-7

Library of Congress Control Number: 2019901941

All rights reserved. No part of this book may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or by any information storage and retrieval system, without permission in writing from the copyright owner.

Rev. date: 05/22/2019

Xlibris

1-888-795-4274

www.Xlibris.com

MEDICAL, GENETIC

AND BEHAVIORAL RISK

FACTORS OF

PUREBRED DOGS

BY: ROSS D. CLARK, DVM

H. DAVID HAYNES, DVM – LEAD RESEARCH

AND EDITORIAL ASSISTANT

ART J. QUINN, DVM, DACVO – PROFESSOR EMERITUS,

OKLAHOMA STATE UNIVERSITY CENTER

FOR VETERINARY HEALTH SCIENCES

BRAD HOWARD, DVM – RESEARCH ASSISTANT

PAUL SCHMITZ, DVM – TECHNICAL ASSISTANT

JAN COODY, MBA – TECHNICAL ASSISTANT

NITA RITSCHEL – EXECUTIVE ASSISTANT

GERI HIBBLEN JACKSON – PHOTO ACQUISITIONS

LINDA A. CLARK, RVT, AKC JUDGE – PHOTO ACQUISITIONS

CONTENTS

KERRY BLUE TERRIER

LAKELAND TERRIER

MANCHESTER TERRIER

MINIATURE BULL TERRIER

MINIATURE SCHNAUZER

NORFOLK AND NORWICH TERRIERS

PARSON RUSSELL TERRIER (JACK RUSSELL TERRIER)

RAT TERRIER

RUSSELL TERRIER

SCOTTISH TERRIER

SEALYHAM TERRIER

SKYE TERRIER

FOX TERRIER – SMOOTH AND WIRE

SOFT COATED WHEATEN TERRIER

STAFFORDSHIRE BULL TERRIER

WELSH TERRIER

WEST HIGHLAND WHITE TERRIER

PREFACE

This book provides you with a through description and positive attributes of these breeds including origin, purpose, history, normal heights and weights, acceptable colors and behavioral traits. Our books differ from most books on dog breeds because this book also provides you with a comprehensive and authoritative source of all the known predisposed hereditary health syndromes for the breed. You will find extensive references for each problem described. We also provide the breed club address for this breed and a list of laboratories and organizations that can provide professional help and information.

As a small animal veterinarian, I have always been intrigued by the way dogs have been bred to fill a purpose in life and further impressed that they also tend to love performing that service. Greyhounds and other sight hounds are built for speed with aerodynamic bodies consisting of small head, deep chest, narrow waist and large leg muscles. On the other hand Dachshunds take their name from German words meaning badger dog and they use their long nose, long body and short legs to both track, enter and dig into badger dens.

After developing a practice that catered to clients with show dogs, my interest in each breed continued to grow as I studied and observed more and more about the unique predisposition and incidence of health problems in each breed. Breeders of purebred dogs for show were a challenge and inspirational for me to research and help them with their unique health problems. Historically references to hereditary problems are scattered throughout various Veterinary medical texts and journals such as ophthalmology, neurology, gastroenterology, cardiovascular and dermatology. This book, as well as the other books and articles I have written, is researched and compiled with the intention to provide both veterinarians and dog owners with comprehensive and authoritative predisposition information under the breed name.

At the date of this publication, The American Kennel Club Canine Health Foundation and the The Kennel Club of England reports over 400 known hereditary health syndromes throughout the dog kingdom. At the writing of my first book in 1983, less than 50 hereditary issues are able to be predicted and or diagnosed. Sequencing of the canine genome, DNA tests, metabolic testing including blood tests and urine testing; plus, phenotypic examinations such as radiographs, ultrasound, and CERF or OFA eye registry exams by a Board Certified Veterinary Ophthalmologist have advanced the science of breed related health and behavioral problems.

This book will provide veterinarians, researchers, pet owners and breeders with a comprehensive guide to all the known problems veterinarians and dog owners should consider during pet selection and throughout each life stage of our canine friends.

NOTE

The fact that a breed shows many disorders may be more an indication of the extensive research done on that breed than on its comparative soundness of the breed.

Many genetic disorders are common to several breeds. We do not intend to convey severity of incidence by the length of text within a particular breed chapter. One breed may have forty percent incidence and another breed only four percent. If a thorough study has been done to indicate the percentage of incidence, we make note of it; however, please keep in mind the incidence is only an indicator of the dogs tested. A breed for instance may show eighteen percent incidence of hip dysplasia as indicated by OFA, although breeders and veterinarians may not elect to submit radiographs of hips so severely dysplastic that the owners and their veterinarians know that there is zero chance to be rated as OFA normal.

Please be aware that we have included and identified anecdotal information, defined by Merriam Webster’s dictionary as unscientific observation; however, the observations of breeders and veterinarians with a special interest in the breed will hopefully be converted to scientific research, often underwritten by breed clubs, to confirm or rule out predisposition to breed problems.

You will note that each chapter is thoroughly referenced to help with the reader’s research as well as to credit and appreciate the researchers, writers, and breeders that have helped the animal world and mankind by their work with these genetic disorders.

Ross D. Clark, D.V.M.

KERRY BLUE TERRIER

ORIGIN AND HISTORY

shutterstock_152595914.tif

Kerry Blue Terrier

The Kerry was developed in County Kerry, Ireland. It is probably a cross between a now-extinct herding dog and the Irish wolfhound. It has been recognized as a pure breed for over 100 years. The breed was developed as hunting dogs used to hunt birds and small game silently avoiding the watchful eye of the Irish Wolfhound used by the nobility to guard the royal lands. These dogs are robust trailers and have been put to many uses, including retrieving, cattle herding and police work.

DESCRIPTION

Never suggest a Kerry to anyone who lets their animals run loose. They are fighters and do not get along well with other dogs. The breed has been used successfully for hunting and retrieving small game from land and water. His coat is described as soft, dense and wavy, and it does not shed and can be tolerated by many people with pet allergies.

THE SHOW RING

shutterstock_55477057.tif

Kerry Blue Terrier

The Kerry should be upstanding and balanced. He should have a well-developed and muscular body with definite terrier style and character. A low-slung Kerry is not typical. The ideal Kerry dog should be 18 ½ inches tall at the withers and the average bitch should slightly less. A height of 18-19/1/2 inches for dogs and 17 ½ to 19 for a bitches is preferable. In no case should a dog over 20 inches or under 17 ½ inches or to a bitch over 19 ½ inches or under 17 inches be considered. A fully developed Kerry should weigh between 33 and 40 pounds with bitches proportionately smaller. A black dog over 18 months of age is to be disqualified. Darker (black) areas on the muzzle, face, ears feet and tail are permissible.

BREEDING AND WHELPING

shutterstock_104413346.tif

Kerry Blue Terrier puppies. Note that they are black at birth

All puppies should be born black. They may have some white on the chest, feet, and a few white hairs on the belly. If there is too much white on the chest, it may not grow out. If very small it will disappear or at least will not show after the pup changes color (black to blue). There may be a slight brown cast to its coat at birth.

Whelping problems are not common in this breed. Pups weigh from 8 to 12 ounces. If a dewclaw appears it must be removed, Tails should be docked at three days if puppies are strong and healthy. Tails should be left fairly long (1/2 to 2/3) so the puppy is in balance when mature. The tail should be even with the top of the head at maturity. If the tail is short and thick, more should remain than if it is long and skinny.

A publication of the Kerry Blue Terrier Club of America gives explicit instructions for setting Kerry ears. Instructions have also been provided at the end of this chapter.

RECOGNIZED RISK FACTORS IN KERRY BLUE TERRIERS

CARDIOVASCULAR-HEMATOLOGICAL-RESPIRATORY

Factor IX deficiency (Hemophilia B) has been listed as occurring in the breed. The severity of the disease is based on the level of factor activity in the blood. Affected dogs may die or be lame due to bleeding into muscles and joints. There is an X-linked recessive is mode of inheritance with males being affected and females being carriers. The condition is present at birth. ¹⁰

Factor XI deficiency is known as plasma thromboplastin antecedent deficiency. A missing component in the blood causes prolonged bleeding after trauma or surgery and can cause death, but usually doesn’t. There is an incomplete dominance for mode of genetic inheritance. The age of onset is less than 3 months of age. ⁵, ⁶, ¹⁰, ¹² PennGen and VetGen offer a DNA test for Factor XI deficiency in Kerry Blue Terriers.

VonWillebrands disease (VWD) is caused by reduced levels of vonWillebrand’s factor (VWF), a large glycoprotein that when complexed to Factor VIII, is responsible for platelet adhesion. Affected dogs show prolonged bleeding time after surgery or trauma. VetGen offers a DNA test for VWD in the Kerry Blue. ¹⁴

Patent ductus arteriosus is the failure of the fetal vessel between the aorta and the pulmonary artery to close around the time of birth, causing blood to be shunted from the aorta to the pulmonary artery over perfusing the lungs and under perfusing the rest of the body. A machinery murmur is detected high in the left axillary region. Surgical correction in those dogs with evidence of heart failure should be performed before the dog is 5 months of age to prevent permanent heart damage. There is a polygenic mode of inheritance and the condition is present at birth. ⁶, ¹¹

The Kerry Blue Terrier is at increased risk for autoimmune hemolytic anemia. ⁵, ¹⁰ There is a severe regenerative anemia caused by an immune mediated attack on the dog’s own red blood cells.

DERMATOLOGICAL

Atopic dermatitis (Atopy) is characterized by roughened, itchy, oozing skin caused by immune reactions to various allergens, such as fleas or pollen ¹⁰ The Kerry Blue, like many terriers is believed to be at increased risk for allergies.

Dermoid sinus (dermoid cyst) has been reported in Kerry Blues. A tract forms between the skin and spinal canal. There can be a high frequency of infection extending from the cyst to the spinal cord, meningitis and myelitis may be present. The mode of genetic inheritance is recessive with onset under 3 months of age. ⁶, ¹⁰, ¹²

Familial footpad hyperkeratosis is found in the breed causing severe hyperkeratosis with fissuring and secondary infection involving the entire surface of the pad and all pads on all feet. There is an undefined mode of genetic inheritance. Onset can be by 6 months of age. ⁵, ⁶, ⁸, ¹⁰

Spiculosis is a condition limited to intact male Kerry Blue Terriers between the ages of 6 to 12 months. Spicules are the result of fusion of the primary and secondary hair follicles and are thickened, brittle nodules that are most seen over the lateral hock region. Dogs tend to chew or lick them. The condition usually occurs by 8 months of age.², ⁶, ⁸, ⁹, ¹⁰, ¹²

Vascular nevi have been reported in Kerry Blue Terriers. Nevus is a circumscribed defect of one or more components of the skin. Vascular nevi are seen on the scrotum of middle aged and older Kerry Blue Terriers. Periodic bleeding may occur from these lesions. ⁸

The breed is reported to be at increased risk for basal cell tumors. ⁶

Pilomatrixoma are hair follicle tumors that are rarely invasive or metastatic. There is a breed predilection for these tumors. The tumors are usually solitary and found on the neck, shoulder, lateral thorax and back. The age of onset is over 5 years. ¹, ⁶.⁸, ⁹

There is a possible breed predisposition for cutaneous papillomas (Warts).⁶, ⁸ Single or multiple warts occur in older dogs, more often in males but are uncommon. Papillomavirus is found in the lesions.

ENDOCRINE-EXOCRINE-ENZYMATIC

Hypothyroidism (Autoimmune thyroiditis) is caused by the destruction of the thyroid gland due to an attack from the animal’s own immune system. Clinical signs include weight gain, lethargy and dermatological signs (bilateral symmetric alopecia, thickened skin and hyperpigmentation). ⁵, ¹⁰, ¹² 1.1% of the Thyroid panels submitted to the Orthopedic Foundation for Animals (OFA) Thyroid registry were confirmed abnormal and 8.5% were considered equivocal. ¹³

GASTROINTESTINAL

Chronic active hepatitis in Kerry Blues starts as mild intermittent clinical signs that generally progress and present severe signs of liver disease. There may be anorexia, vomiting, weight loss, ascites, bleeding tendencies and hepatic encephalopathy. Copper commonly accumulates in the liver. Cirrhosis may occur. The disease usually presents at less than 5 years of age. ¹⁰

DENTITION

Oligodontia (Missing teeth): has been reported anecdotally in the breed. ¹¹

MUSCULOSKELETAL

Hip dysplasia is the malformation of the acetabulum resulting in joint laxity that is inherited as a polygenic trait. The OFA ranks the Kerry Blue 141st in its Hip registry with 5.5% of the evaluations being abnormal. ⁵, ¹², ¹³

skeleton1.tif

Normal Hips in a Kerry Blue Terrier

skeleton2.tif

Moderate Hip Dysplasia Source:OFA

Eosinophilic myositis is characterized by inflammatory lesions in the muscle in various parts of the body. These are generally firm to the touch and painful. Depending on the location, there may be lameness. ¹⁰

Craniomandibular osteopathy (CMO) has been reported in the breed. The disease is a non inflammatory, noncancerous proliferative disease involving the mandible, the tympanic bullae and occasionally other bones of the head. Dogs may have pain and difficulty opening their mouths and have difficulty swallowing. The condition may regress when the dog reaches maturity. There is a recessive mode of inheritance with the onset by 6 months of age. ¹⁰, ¹²(1096)

Elbow dysplasia has been documented in the breed. The disease is inherited as a polygenic trait and can appear in three forms that can occur singly or together. These abnormalities are pathology of the medial coronoid process of the ulna, ununited anconeal process of the ulna or osteochondritis of the medial humeral condyle. 4.6% of the elbow evaluations for the Kerry Blue submitted to the OFA were abnormal. ¹³

Patellar luxation has been reported anecdotally in the breed.⁵, ¹² Abnormal development of the structures of the knee allow the patella (kneecap) to slip from its normal location. The patella usually dislocates to the middle (medial) in small breeds and to the outside (laterally) in large breeds.

NEUROLIGIC

Cerebellar abiotrophy (Progressive Neuronal Abiotrophy-PNA, Canine Multiple System Degeneration-CMSD) was first reported in Kerry Blue Terriers in 1968. The condition is a progressive degenerative disease in Kerry Blue Terriers that begins as pelvic limb stiffness and mild head tremor at 9 to 16 weeks of age. Dogs later become hypermetric and may not be able to stand by 12 to 18 months of age and be totally incapacitated by the age of two. There is degeneration of Purkinje cells in the cerebellar cortex as well as extrapyramidal tracts, substantia nigra and olivary nuclei. There is no treatment. Mode of genetic inheritance is autosomal recessive. In March 2013 the mutation for CMSD in the Kerry Blue and the Chinese Crested was discovered and a DNA test is now available through the OFA. ³, ⁶, ⁷, ⁹, ¹⁰, ¹², ¹⁶

Degenerative myelopathy (DM) has been reported in Kerry Blue Terriers. This slowly progressive disease involves the long tracts of the thoracolumbar spinal cord and begins with rear limb ataxia and knuckling of the paws, which progresses to rear limb paresis. Lesions found during post mortem examination implicate an immune mediated attack on spinal tissue. A missense mutation in the SOD1 gene appears to put the homozygous dog at risk for DM. The SOD1 is responsible for the conversion of superperoxide radicals to hydrogen peroxide and molecular oxygen. A DNA test for the mutation that predisposes the dog for degenerative myelopathy is available through the Orthopedic Foundation for Animals. Based on Kerrys tested at time of writing, 11% are at risk (carrying two copies of the mutation) and 40% are carriers with only one copy.⁷, ⁹, ¹⁰, ¹²(¹⁸⁷), ¹³

OPHTHALMIC

The following ocular disorders have been documented or reported in Kerry Blue Terriers.

Blepharophimosis (Narrow Palpebral Fissure): Small palpebral fissure in the absence of microphthalmia (small globe) is observed bilaterally. This can be corrected by surgery at the lateral canthus. ⁴, ¹⁰

Macropalpebral fissure (Macroblepharon, diamond eye): Excessively large palpebral fissure, resulting in the exposure of the sclera and cornea. There is an undefined mode of inheritance. ¹⁰

00000004_Superior_Distichiasis.tif

Distichiasis; Note the presence of eyelashes directed toward the cornea

Distichiasis: Presence of an additional row of eyelashes on the lid margin that sometimes cause irritation. There is an undefined mode of genetic inheritance. The condition may occur at any age. ⁴, ¹⁰, ¹¹

Trichiasis: Normally placed hair or cilia abnormally directed toward the eye ¹⁰

Ectropion: Turning out of the eyelids, causing excessive exposure of the eyeball. ¹⁰

Entropion: Turning in of the eyelids, causing the eyelashes to rub the eyeball. The lateral canthus is most often involved in the Kerry Blue. Both entropion and ectropion are inherited as polygenic traits, meaning a number of factors determine their presence. These factors include the amount and weight of skin on the face, the contents of the orbit and the shape of the skull. ⁴, ⁶, ¹¹ ¹²

Keratoconjunctivitis sicca (KCS, Dry eye): Inadequate production of the aqueous portion of the tears causing irritation of the conjunctiva and the cornea. The most common cause is autoimmune destruction of the lacrimal glands. There is an undefined mode of inheritance. ⁴, ¹⁰, ¹²

00000017%20Corneal%20Dystrophy.tif

Corneal Dystrophy (epithelial/stromal)

Corneal dystrophy (epithelial/stromal): A non inflammatory grayish white opacity in one or more corneal layers. The lesions are usually bilateral and probably inherited. ¹¹

00000011%20Persistent%20Pupillary%20Membranes.tif

Persistent Pupillary Membranes-PPM

Persistent pupillary membranes (PPM) are vascular remnants existing in the anterior chamber of the eye that have failed to regress during the neonatal period. These strands may bridge from the iris to the iris, the iris to the lens or cornea or form sheets of tissue in the anterior chamber. In the Kerry, they bridge from one part of the iris to another. ¹¹

Cataracts: Any lens opacity that obscures vision and may cause blindness is considered a cataract. Cataracts under 2 years of age have been recognized in the breed. ⁶, ¹⁰, ¹¹, ¹²

P19.tif

Cataract

Vitreous degeneration: Liquefaction of the vitreous gel that may predispose for retinal detachment or glaucoma. ¹¹

Progressive retinal atrophy (PRA): Degeneration of the retinal vision cells, which progresses to blindness. Late onset PRA (5-6 years) has been reported in Kerry Blue Terriers. The mode of inheritance is usually recessive. ⁶, ¹⁰, ¹²

UROGENITAL

Cryptorchidism is the absence of testicles due to retention in the abdomen or inguinal region. It may be unilateral or bilateral and the testicles may slide in and out of the scrotum. Mode of inheritance is most likely an undefined recessive trait involving more than one gene. If the testicles are not in the scrotum by 4 months of age, they most likely will not appear. ⁵, ⁹, ¹⁰

A true hermaphrodite (XX sex reversal) is defined as the presence of gonadal tissue for both sexes (ovotestis) and external female genitalia, due to a full compliment of both male and female chromosomes. ⁶, ¹⁰, ¹¹

In the pseudohermaphrodite (XX male, XY female) the male has male organs with some female characteristics and the female has female organs with some male characteristics. The age of onset is birth. ⁵, ¹⁰, ¹¹

BEHAVIOR

The Kerry is an affectionate and gentle companion. He is intelligent and exuberant. He is readily trainable, but can be stubborn. He can be quarrelsome with other dogs. Excessively aggressive dogs are extremely assertive or forceful with other dogs. There is an undefined mode of inheritance. The condition occurs around 3 years of age. ¹⁰

OLD AGE

Kerry Blue Terriers live to be 11 to 15 years of age. Cancer and kidney/liver failure were the most commonly reported causes of death in a breeder’s survey. Older Kerrys are more prone to sebaceous cysts than other breeds.

MISCELLANEOUS FACTS AND RESOURCES

This is a list of Genetic tests available for Kerry Blue Terriers to identify inherited medical problems that may be recommended by your Veterinarian.

GENETIC TESTS AVAILABLE FOR THE KERRY BLUE TERRIER

Condition Laboratory

For information about the laboratories performing these tests and sample submission contact: www.offa.org/dna_labs.html

Additional health screening tests recommended for the Kerry Blue Terrier by the Canine Health Information Center (CHIC)

Here is how CHIC works to help dog fanciers improve their breeds

CHIC works with national breed clubs, the AKC Canine Health Foundation and the Orthopedic Foundation for Animals (OFA) to create a list of health screening procedures designed to eliminate inherited health problems from dogs used for breeding. The procedures vary from breed to breed and may change if new problems are identified or new tests become available. A dog must have completed all the required health screening procedures in order to receive a CHIC number. For more information contact: www.caninehealthinfo.org/

CHIC REQUIREMENTS FOR THE KERRY BLUE TERRIER

Hip Dysplasia: OFA or PennHIP Evaluation

Eye Exam by a boarded ACVO Ophthalmologist: Results registered with CERF or OFA

VonWillebrand’s Disease (Optional): VetGen DNA test with results registered with the OFA. First generation offspring of tested dogs are eligible for Clear by Parentage.

Degenerative Myelopathy (Optional): OFA/University of Missouri DNA test. First generation offspring of tested dogs are eligible for Clear by Parentage.

Factor XI Deficiency (Optional): PennGen Factor XI DNA test. First generation offspring of tested dogs are eligible for Clear by Parentage. ¹⁵

NATIONAL BREED CLUB

The National Breed Club is a good place to discover all the things you can do with your Kerry Blue Terrier and to contact other Kerry owners.

UNITED STATES KERRY BLUE TERRIER CLUB, INC.

www.uskbtc.com

REFERENCES

1. Kirk, R.W. & Bistner, S.I. Handbook of Veterinary Procedures and Emergency Treatment: Hereditary Defects in Dogs. 1975; Table 124, p. 661

2. Martin, T.C. DVM Personal Communication 1993. Adair Gardens Pet Hospital, Belleville, IL

3. Delahunta, A. & Averill, D.R. Jr. Hereditary Cerebellar Cortical and Extra-Pyramidal Nuclear Abiotrophy in Kerry Blue Terriers. JAVMA 1681: 1119-1123; 1976

4. Magrane, W.C. Canine Ophthalmology Lea & Febiger, Philadelphia 1977 3rd Ed.

5. Kellogg, Scott DVM "The Kerry Blue Terrier and Health" Kerry Blue Terrier Club Handbook

6. Gough, A & Thomas, A. "Breed Predispositions to Disease in Dogs and Cats, 2nd ed." Blackwell Publishing UK, 2010

7. Lorenz, M DVM & Kornegay, J DVM, PhD. "Handbook of Vet Neurology" Saunders St. Louis 2004 4th Ed.

8. Scott, D.W. DVM & Miller, W.H. Jr. VMD & Griffin, C.E. DVM Muller & Kirk’s Small Animal Dermatology Saunders, Philadelphia 2001 6th Ed.

9. Tilley, L.P. DVM & Smith, FWK Jr. DVM "The 5-Minute Veterinary Consult- Canine and Feline" Lippencott, Williams & Wilkins Philadelphia 2004 3rd Ed.

10. Padgett, G. A. DVM Control of Canine Genetic Diseases Howell Book House New York 1998

11. ACVO Ocular Disorders Presumed To Be Inherited in Purebred Dogs 6th ed. 2013

12. Ackerman, Lowell, The Genetic Connection: A Guide to Health Problems in Purebred Dogs. Lakewood, AAHA Press 1999

13. Orthopedic Foundation for Animals website: www.offa.org

14. VetGen website: www.vetrgen.com

15. Breed requirements; Kerry Blue Terriers, Canine Health Information Center: www.caninehealthinfo.org

16. PNA? Canine Multiple System Degeneration? Canine Genetic Disease Network: www.caninegeneticdiseases.net/PNA/index.htm

LAKELAND TERRIER

ORIGIN AND HISTORY

shutterstock_37722382.tif

Lakeland Terrier head

The Lakeland Terrier was originally known as the Patterdale Terrier derived from the old Black and Tan Terrier, it is one of the oldest working terriers recognized today. Originating in Cumberland County in England’s Lake District, it was bred by farmers to hunt fox and otter.

In 1871, a Lakeland Terrier is said to have crawled 25 feet under rock in pursuit of an otter. To free the entombed dog required three days of blasting.

DESCRIPTION

Lakeland Terriers are calmer and less excitable than the other long-legged terriers of the British Isles. Some are hyperactive, however, when not in familiar surroundings. If a dog has behavior problems, obedience training and restructuring of the environment are advised. Its heritage of hunting quarry often larger than itself has made the Lakeland relatively insensitive to pain when excited; thus physical punishment is seldom very effective.

The Lakeland Terrier is in the same class of terriers as the Welsh and the Wire Fox. The Lakeland is smaller than the Welsh and shorter than the Wire Fox but is heavier boned than the latter. The Lakeland is more social and fun loving than the Welsh but not as active as the Wire Fox. ¹⁴

This breed is affectionate and sensitive to their owner’s wishes. The breed will tolerate children who are respectful and will accept poking and prodding to a certain limit.

THE SHOW RING

shutterstock_16645078.tif

Lakeland Terriers

The ideal height for these dogs is 14 l/2 inches from withers to ground, with l/2 inch deviation in either direction permissible. The ideal height for a bitch is about one inch less. The weight of the well-balanced male in hard show condition is 17 pounds. The dog is squarely built and the bitch may be slightly longer. Balance and proportion are of primary importance.

The Lakie comes in a variety of colors: blue, black, liver, red and wheaten. The saddle may be blue, black, liver or varying shades of grizzle.

Disqualifications are: overshot or undershot bites.

shutterstock_164521028.tif

BREEDING AND WHELPING

Lakeland Terrier bitches exhibit normal estrus. Highest rates of conception can be obtained by breeding every other day for standing heat. The interval between seasons varies. Intervals of 12 to 15 months are not uncommon.

Onset of the first estrus as late as 20 to 24 months of age should not be considered abnormal.

The average litter is three or four puppies. Provided the bitch is not allowed to gain too much weight, whelping is usually easy. There is no evidence of predilection for breeding problems or problems in rearing puppies.

Lakeland Terrier puppies vary in weight according to the size of the bitch and the number of whelps. By 3 months of age, size at maturity can be predicted. Dogs should weigh 7 ton 8 pounds at 3 months, and bitches should weigh 6 to 7 l/2 pounds.

GROWTH

The whelps are almost solid black at birth. If a puppy has tan points, the mature color will be black and tan, black or red grizzle and tan, or blue and tan. Red puppies are born self-colored. Liver and tan dogs are rare. In saddled specimens, the color begins to break at 2 to 8 weeks.

Generally, the earlier the black color begins to recede, the more restricted the saddle will be. The color may continue to grizzle until the 2nd or 3rd year. White markings on the throat, feet, belly and back of the neck may occur and are sometimes extensive. Elongated markings on the midline tend to disappear, as do markings on the toes.

Dewclaws should be removed, and tails should be docked so that they will be level with the top of the skull when the dog matures (leave about 2/3). However, there is no formula for docking that is agreed upon by everyone.

Some puppies born with short tails (Brachury) ⁶ will need only about l/2 inch removed.

RECOGNIZED RISK FACTORS IN LAKELAND TERRIERS

CARDIOVASCULAR-HEMATOLOGICAL-RESPIRATORY

VonWillebrands disease (VWD) has been reported in Lakeland Terrier. ⁴, ⁵(485), ⁶ VWD is a defect in the synthesis of vonWillebrand’s factor (VWF) a large glycoprotein that when complexed to Factor VIII is responsible for platelet adhesion. The severity of the condition is dependent on the level of VWF present but the disease usually results in prolonged bleeding after surgery or trauma. It is believed to be inherited as an incomplete dominant trait with variable expressivity.

The Lakeland Terrier is predisposed to ventricular septal defects resulting in a left to right shunt. ⁷, ⁸

Interruption of the aortic arch was reported in a 4 month old female Lakeland Terrier. ⁹ There was complete interruption of the aortic arch between the brachiocephalic trunk and the subclavian artery. Collateral circulation including a patent ductus arteriosus maintained life. A small ventricular septal defect was also present.

DERMATOLOGICAL

The Lakeland Terrier is at increased risk for dermatomyositis, a hereditary inflammatory condition of the skin and muscles that occurs in young dogs ⁸, ¹⁰ Clinical signs include alopecia, erythema, scaling and crusting. The ears, lips, periocular region, feet and tip of the tail are most often affected. Ulceration will occur in severe cases. Myositis occurs months after the skin lesions. The extent of the myositis varies from case to case. The masseter and temporalis muscles may atrophy and the dog will have difficulty swallowing. Megaesophagus may also occur. Topical therapy and high doses of glucocorticoids are indicated.

ENDOCRINE-EXOCRINE-ENZYMATIC

Hypothyroidism has been listed as occurring in the breed. ⁶ There is destruction of the thyroid gland due to an attack from the animal’s own immune system. Clinical signs include, weight gain, lethargy and dermatological signs (bilateral, symmetric alopecia, brittle hair coat, thickened skin and hyperpigmentation).

DENTITION

Prognathism (Under shot jaw) is a recognized problem in the Lakeland Terrier. ⁵(278), ⁶ Brachygnathism (Over shot jaw) has also been listed as occurring in the breed. ⁶

The Lakeland Terrier is reported to be the only breed affected by a condition known as fused teeth. ⁶ Two separate teeth are fused together by the enamel.

MUSCULOSKELETAL

The Lakeland Terrier is one of the breeds at greatest risk for Legg-Calve’ Perthes’ disease (LP) ³, ⁵(153), ⁶, ⁸ Ischemia of the hip joint results in lameness due to aseptic necrosis of the femoral head and neck. Clinical signs usually appear between 4 and 12 months of age with only one leg being affected. Conservative management including use of a non weight bearing sling have had limited success and surgical removal of the femoral head and neck is usually necessary.

Elbow dysplasia (Ununited anconeal process) ¹, ⁶ and hip dysplasia ⁶ has both been reported in the breed; however, no abnormal evaluations for either condition have been submitted to the Orthopedic Foundation for Animals (OFA). ¹¹

bones.tif

Elbow Dysplasia, Ununited Anocneal Process, grade 2 Source: OFA

NEUROLIGIC

Intervertebral disc disease has been listed as occurring in Lakeland Terriers.⁶ Rupture of the disc capsule sends material from the nucleus pulposa into the spinal canal putting pressure on the cord. This results in back pain and progressive paresis or paralysis.

OPHTHALMIC

Microphthalmia is an abnormally small eye ball that is often associated with other ocular abnormalities. In the Lakeland Terrier, microphthalmia is inherited as an autosomal recessive trait and is associated with persistent papillary membranes. ⁵(903), ⁶, ⁷ It may also be seen with cataract formation and retinal detachment.

eye1.tif

Lens Luxation (Displaced lens) with secondary Glaucoma

Narrow angle glaucoma in dogs under 9 years of age and glaucoma of undetermined cause in dogs under 3 years of age have been reported in Lakeland Terriers. ⁵, ⁶, ⁷ Glaucoma is elevation of intraocular pressure caused by the inability of the intraocular fluid to leave through the iridocorneal angle.

00000004_Superior_Distichiasis.tif

Distichiasis; Note the presence of eyelashes directed toward the cornea

Distichiasis is the abnormal location of eyelashes along the lid margin. It occurs in the Lakeland Terrier and may cause corneal irritation. ², ⁶

The Lakeland Terrier has a possible breed predisposition primary lens luxation (PLL). ², ⁵, ⁶, ⁷ The luxation may be a partial or complete dislocation from its normal position behind the pupil and cause a secondary glaucoma. The condition is caused by a splice donor mutation on the ADAMTS17 gene. The OFA and Optigen offer a test for primary lens luxation. ¹¹, ¹³

00000005%20Cataract.tif

Cataract

Cataracts, inherited as an autosomal recessive trait have been documented in the Lakeland Terrier. ⁵(903), ⁶, ⁷ A cataract is defined as a complete or partial opacity of the lens and/or its capsule that when complete, will cause blindness in the affected eye. The cataract is located on the posterior subcapsular cortex and progresses slowly beginning at 1-3 years of age.

00000011%20Persistent%20Pupillary%20Membranes.tif

Persistent Pupillary Membranes

Persistent pupillary membranes (PPM) have been recognized in Lakeland Terriers. ⁶, ¹² PPM are vascular remnants that have failed to regress existing in the anterior chamber of the eye. They may bridge from the iris to the iris, the iris to the lens or cornea or form sheets in the anterior chamber. The number and location determine vision impairment. All forms of PPM can occur in the Lakeland.

UROGENITAL

Cryptorchidism is prevalent in the breed. ⁵, ⁶ Cryptorchidism is the absence of testicles due to retention in the abdomen or inguinal region. It may be unilateral or bilateral and the testicles may slide in and out of the scrotum. Mode of inheritance is most likely an undefined recessive trait involving more than one gene. If the testicles are not in the scrotum by 4 months of age, they most likely will not appear.

The Lakeland Terrier is one of the breeds listed as being at risk for ectopic ureters.⁶ One or both ureters attach on a location other than the craniolateral aspect of the trigone of the bladder. This may result in urinary incontinence, hydronephrosis and recurrent urinary tract infections.

BEHAVIOR

The Lakey is a lively, friendly companion dog. His acute hearing makes him an excellent watch dog. Excessive aggressiveness toward dogs and people has been listed as occurring in the breed. ⁶

OLD AGE

The Lakeland Terrier remains vigorous into old age, living for 15 years or longer.

MISCELLANEOUS FACTS AND RESOURCES

This is a list of Genetic tests available for the Lakeland Terrier to identify inherited medical problems that may be recommended by your Veterinarian.

GENETIC TESTS AVAILABLE FOR LAKELAND TERRIERS

Condition                                               Laboratory

Primary Lens Luxation                        OFA, Optigen

For information about the laboratories performing these tests and sample submission contact: www.offa.org/dna_labs.html

NATIONAL BREED CLUB

The National Breed Club is a good place to discover all the things you can do with your Lakeland Terrier and to contact other Lakeland owners.

UNITED STATES LAKELAND TERRIER CLUB

http://uslakelandterrier.org

REFERENCES

1. Foley, C.W., Osweiler, G., Lasley, J.F. Abnormalities of Companion Animals: Analysis of Heritability. Iowa State Press 1975: 104

2. Quinn, A.J. Personal Communication.

3. Lee, R. and Fry, P.D. ‘Some Observations on the Occurrence of ECP in the Dog," J. Sm. Anim. Prac. 10: 309-317; 1696.

4. Dodds, W. Jean, Personal Communication.

5. Ackerman, Lowell, the Genetic Connection: A Guide to Health Problems in Purebred Dogs. Lakewood, AAHA Press. 1999

6. Padgett, George A. Control of Canine Genetic Diseases. New York, Howell Book House. 1998

7. Gough, Alex, Thomas, Alison, Breed Predisposition to Disease in Dogs and Cats, 2nd ed. Ames, Blackwell Publishing. 2010

8. Tilley, Lawrence P., smith, Francis W.K. Jr. the 5 Minute Veterinary Consult; Canine and Feline, 3rd ed. Baltimore, Lippincott Williams and Wilkins. 2004

9. Scott, Danny W., Miller, William H. Jr., Griffin, Craig E. Muller and Kirk’s Small animal Dermatology-6th ed. Philadelphia, W. B. Saunders co. 2001

10. Orthopedic Foundation for Animals website: www.offa.org

11. Genetics Committee of the American College of Veterinary Ophthalmologists, Ocular Disorders Presumed to be Inherited in Purebred Dogs, 5th ed. 2009

12. Farias, F.H., Johnson, G.S., Taylor, J.F. An ADAMTS17 splice donor site mutation in dogs with primary lens luxation. Invest Ophthalmol Vis Sci 2010 Sep; 51(9):4716-21

13. Peterka, S."