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- Herausgeber: John Wiley & Sons
- Kategorie: Fachliteratur
- Serie: What's Your Diagnosis?
- Sprache: Englisch
Small Animal Dermatology: What's Your Diagnosis? provides practical information in an easy-to-reference, well-illustrated format, so that students and practicing veterinarians can develop their clinical dermatology skills and test their knowledge. It offers current diagnostic and therapeutic information on small animal skin diseases through real-world clinical cases. Organized by presenting complaint, each clinical problem is covered through case material and questions revolving around differential diagnoses, diagnostic tools, and treatment planning. Small Animal Dermatology: What's Your Diagnosis? features actual clinical cases that demonstrate common clinical presentations. It covers both common and uncommon dermatologic problems, such as alopecia, changes in skin pigmentation, causes of itch, and more. Designed to enhance clinical problem solving skills, the book can be approached as a series of mini challenges, making it an excellent primer for new clinicians as well as a resource for seasoned veterinarians. * Provides information on diagnosing and treating small animal skin disease in a clinically relevant, case-based format * Offers questions with detailed answers to enhance knowledge of differential diagnoses, diagnostic tools, and treatment options * Takes a problem-based approach to the subject * Helps practitioners and students to develop diagnostic and therapeutic skills and gain confidence * Discusses dermatologic diseases ranging from common to rare Small Animal Dermatology: What's Your Diagnosis? is a helpful resource for veterinary practitioners and students to develop their skills in diagnosing and treating skin disease in dogs and cats.
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Table of Contents
Cover
Acknowledgements
Abbreviations
Introduction
Further reading
Section A:
Case 1:
History
Diagnosis
Treatment and outcome
Prognosis
Discussion
Further reading
Case 2:
History
Diagnosis
Treatment
Prognosis
Discussion
Further reading
Case 3:
History
Diagnosis
Treatment
Re‐inspections and final outcome
Prognosis
Discussion
Further reading
Case 4:
History
Diagnosis
Treatment
Prognosis
Discussion
Further reading
Case 5:
History
Diagnosis and prognosis
Prognosis
Final outcome
Discussion
Further reading
Case 6:
History
Diagnosis
Treatment
Prognosis
Discussion
Further reading
Case 7:
History
Initial treatment
Diagnosis
Treatment
Prognosis
Discussion
Further reading
Case 8:
History
Diagnosis
Treatment
Prognosis
Final outcome
Discussion
Further reading
Section B:
Case 9:
History
Diagnosis
Treatment
Prognosis
Discussion
Further reading
Case 10:
History
Diagnosis
Treatment and further investigations
Final diagnosis and outcome
Prognosis
Discussion
Further reading
Case 11:
History
Diagnosis
Treatment
Prognosis
Discussion
Further reading
Case 12:
History
Diagnosis
Treatment
Prognosis
Discussion
Further reading
Case 13:
History
Diagnosis
Treatment
Prognosis
Further treatment and outcome
Discussion
Further reading
Case 14:
History
Diagnosis
Treatment
Prognosis
Final outcome
Discussion
Further reading
Section C:
Case 15:
History
Diagnosis
Treatment
Prognosis
Discussion
Further reading
Case 16:
History
Diagnosis
Treatment
Prognosis
Discussion
Further reading
Case 17:
History
Diagnosis
Further diagnostic tests
Treatment
Prognosis
Discussion
Further reading
Case 18:
History
Diagnosis
Treatment
Prognosis
Discussion
Further reading
Case 19:
History
Diagnosis
Treatment
Prognosis
Discussion
Further reading
Case 20:
History
Working diagnosis
Treatment
Further testing and outcome
Final diagnosis
Prognosis
Discussion
Further reading
Section D:
Case 21:
History
Diagnosis
Treatment
Prognosis
Discussion
Further reading
Case 22:
History
Diagnosis
Treatment
Prognosis
Discussion
Further reading
Case 23:
History
Diagnosis
Treatment
Prognosis
Discussion
Further reading
Case 24:
History
Diagnosis
Treatment
Prognosis
Discussion
Further reading
Case 25:
History
Diagnosis
Treatment
Prognosis
Discussion
Further reading
Case 26:
History
Diagnosis
Treatment
Re‐evaluations and final outcome
Prognosis
Discussion
Further reading
Case 27:
History
Diagnosis
Treatment
Re‐evaluations and final outcome
Prognosis
Discussion
Further reading
Section E:
Case 28:
History
Diagnosis
Treatment
Prognosis
Further treatment and outcome
Discussion
Further reading
Case 29:
History
Diagnosis
Treatment
Prognosis
Discussion
Further reading
Case 30:
History
Diagnosis
Treatment
Prognosis
Further treatment and outcome
Discussion
Further reading
Case 31:
History
Diagnosis
Treatment
Prognosis
Final outcome
Discussion
Further reading
Case 32:
History
Diagnosis
Treatment
Further diagnostic tests
Prognosis
Discussion
Further reading
Case 33:
History
Diagnosis
Treatment
Prognosis
Discussion
Further reading
Case 34:
History
Diagnosis
Treatment
Prognosis
Discussion
Further reading
Appendix 1: Diagnosis by Case
Appendix 2: Recommended Reading
Index
End User License Agreement
List of Illustrations
Chapter 1
Figure 1.1
Figure 1.2
Figure 1.3 Shows an ultrasound image of the abdomen. There is a complex mass, o...
Figure 1.4 Shows a colour Doppler image of the same mass. The colour flow signa...
Figure 1.5 Shows the dog in dorsal recumbency, at exploratory laparotomy. A lar...
Figure 1.6 Shows the excised mass, with a section of attached vasculature on th...
Figure 1.7 Shows the dog 5 months after initial presentation. He has a brighter...
Figure 1.8 Shows the dog from behind, 5 months after initial presentation. Ther...
Chapter 2
Figure 2.1
Figure 2.2
Figure 2.3
Figure 2.4
Figure 2.5 Shows the caudal dorsum from above. New hair has regrown to complete...
Figure 2.6 Shows the tail and rump from behind. The new hairs in the brown area...
Chapter 3
Figure 3.1
Figure 3.2
Figure 3.3
Figure 3.4 Shows part of a coat brushing mounted in liquid paraffin under a gla...
Figure 3.5 Shows the cat 2 months after initial presentation. There is full reg...
Chapter 4
Figure 4.1
Figure 4.2
Figure 4.3
Figure 4.4
Figure 4.5 Shows detail from a skin scraping, mounted in liquid paraffin and ex...
Figure 4.6 Shows the dog's head after 2 months of treatment. There is good qual...
Chapter 5
Figure 5.1
Figure 5.2
Figure 5.3
Figure 5.4
Figure 5.5
Chapter 6
Figure 6.1
Figure 6.2
Figure 6.3
Figure 6.4 Shows a plucked hair from the dog. There is abnormal melanin clumpin...
Chapter 7
Figure 7.1
Figure 7.2
Figure 7.3
Figure 7.4
Figure 7.5
Figure 7.6 Shows a Petri dish containing Sabouraud's agar and a colony of the d...
Chapter 8
Figure 8.1
Figure 8.2
Figure 8.3
Figure 8.4
Figure 8.5
Figure 8.6 Shows the dog 4 months after stopping prednisolone. There is good ha...
Chapter 9
Figure 9.1
Figure 9.2 Shows the nose after 12 days of oral medication. The skin underlying...
Figure 9.3 Shows the nose after 25 days of oral medication. There is a signific...
Figure 9.4 Shows the dog after five months of receiving medication. There is a ...
Chapter 10
Figure 10.1
Figure 10.2
Figure 10.3
Figure 10.4 Was taken down the microscope and shows detail from an acetate tape...
Figure 10.5 Was taken down the microscope, and shows detail from a hair pluck m...
Figure 10.6 Shows the dog 1 week after initial presentation. He is under genera...
Figure 10.7 Shows the dog after 5 weeks of treatment. The dog has a brighter de...
Figure 10.8 Shows the ventral neck and chest after 5 weeks of treatment. The no...
Chapter 11
Figure 11.1
Figure 11.2
Figure 11.3
Figure 11.4 Shows a 9 year‐old Siberian Husky with depigmentation of the centra...
Chapter 12
Figure 12.1
Figure 12.2
Figure 12.3
Figure 12.4
Figure 12.5 Shows the ventral abdomen 3 weeks later. There are hypopigmented ma...
Figure 12.6 Shows the medial aspect of the left fore limb and adjacent body wal...
Chapter 13
Figure 13.1
Figure 13.2
Figure 13.3
Figure 13.4
Figure 13.5
Figure 13.6
Chapter 14
Figure 14.1
Figure 14.2
Chapter 15
Figure 15.1
Figure 15.2
Figure 15.3
Figure 15.4
Chapter 16
Figure 16.1
Figure 16.2
Figure 16.3
Figure 16.4
Figure 16.5 Shows a low power microscope image of material collected from a ski...
Chapter 17
Figure 17.1
Figure 17.2
Figure 17.3
Figure 17.4
Chapter 18
Figure 18.1
Figure 18.2
Figure 18.3
Figure 18.4 Shows scarring alopecia and hyperpigmentation on the rostro‐dorsal ...
Chapter 19
Figure 19.1
Figure 19.2
Figure 19.3 Shows the ventral neck with the neck fold held open after 4 weeks o...
Chapter 20
Figure 20.1
Figure 20.2
Figure 20.3
Figure 20.4
Figure 20.5 Shows the dog after controlling secondary infections and after 6 we...
Figure 20.6 Shows the left front foot after 6 weeks of treatment with oral pred...
Chapter 21
Figure 21.1
Figure 21.2
Figure 21.3
Figure 21.4
Chapter 22
Figure 22.1
Figure 22.2
Figure 22.3
Figure 22.4 Shows some hairs plucked from the lateral thigh. The hairs are moun...
Figure 22.5 Shows a trichogram at ×400 magnification. The image is taken throug...
Chapter 23
Figure 23.1
Figure 23.2 Shows an image from a coat brushing, mounted in liquid paraffin and...
Figure 23.3 Shows detail from an acetate tape strip preparation. There is a
Che
...
Figure 23.4 Shows detail from an acetate tape strip preparation, seen in detail...
Figure 23.5 Shows the dog 2 months after the start of treatment. There is no vi...
Chapter 24
Figure 24.1
Figure 24.2
Figure 24.3
Figure 24.4
Figure 24.5 Shows an ultrasound image of the cranial abdomen. The liver has a ‘...
Chapter 25
Figure 25.1
Figure 25.2
Figure 25.3 Shows a section of epidermis stained with periodic acid Schiff (PAS...
Chapter 26
Figure 26.1
Figure 26.2
Figure 26.3
Figure 26.4
Figure 26.5 Shows a photomicrograph of a cytology preparation. The touch prepar...
Figure 26.6 Shows the back of the head after 3 weeks of treatment. There is com...
Figure 26.7 Shows the face after 3 weeks of treatment. There is complete resolu...
Chapter 27
Figure 27.1
Figure 27.2
Figure 27.3
Figure 27.4
Figure 27.5
Figure 27.6
Figure 27.7 Shows a hair pluck, mounted in liquid paraffin and examined at ×40 ...
Figure 27.8 Shows the same hair pluck preparation, examined at ×100 magnificati...
Figure 27.9 Shows the dog 5 months after initial presentation. There is complet...
Figure 27.10 Shows the left lateral torso and groin. There is good new hair reg...
Chapter 28
Figure 28.1
Figure 28.2
Figure 28.3
Figure 28.4
Chapter 29
Figure 29.1
Figure 29.2 Shows the left hind limb after 6 weeks of ciclosporin treatment. Th...
Chapter 30
Figure 30.1
Figure 30.2
Figure 30.3 Shows the perianal area after 1 month of treatment. The dog is not ...
Chapter 31
Figure 31.1
Figure 31.2
Figure 31.3
Figure 31.4 Shows the right axilla after 8 weeks of treatment. The ulcers have ...
Figure 31.5 Shows the skin of the groin after 2 years of treatment. There are s...
Chapter 32
Figure 32.1
Figure 32.2
Figure 32.3
Chapter 33
Figure 33.1
Figure 33.2 Shows the nasal planum after three months of treatment, on the same...
Figure 33.3 Shows the nasal planum after 3 months of treatment. There is a pale...
Chapter 34
Figure 34.1
Figure 34.2
Figure 34.3
Figure 34.4
Figure 34.5 Shows the dog's face after 4 weeks of treatment. There is mild swel...
Figure 34.6 Shows the dog's face after 9 weeks of treatment. There is a large p...
Guide
Cover
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Small Animal Dermatology
What's Your Diagnosis?
Jane Coatesworth, M.A., Vet.M.B., Cert.V.D., MRCVS
Animal Health Trust, Lanwades Park, Kentford, Newmarket, Suffolk, UK
Copyright
This edition first published 2019
© 2019 John Wiley & Sons, Inc.
All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, recording or otherwise, except as permitted by law. Advice on how to obtain permission to reuse material from this title is available at http://www.wiley.com/go/permissions.
The right of Jane Coatesworth to be identified as the author of this work has been asserted in accordance with law.
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Limit of Liability/Disclaimer of Warranty
The contents of this work are intended to further general scientific research, understanding, and discussion only and are not intended and should not be relied upon as recommending or promoting scientific method, diagnosis, or treatment by physicians for any particular patient. In view of ongoing research, equipment modifications, changes in governmental regulations, and the constant flow of information relating to the use of medicines, equipment, and devices, the reader is urged to review and evaluate the information provided in the package insert or instructions for each medicine, equipment, or device for, among other things, any changes in the instructions or indication of usage and for added warnings and precautions. While the publisher and authors have used their best efforts in preparing this work, they make no representations or warranties with respect to the accuracy or completeness of the contents of this work and specifically disclaim all warranties, including without limitation any implied warranties of merchantability or fitness for a particular purpose. No warranty may be created or extended by sales representatives, written sales materials or promotional statements for this work. The fact that an organization, website, or product is referred to in this work as a citation and/or potential source of further information does not mean that the publisher and authors endorse the information or services the organization, website, or product may provide or recommendations it may make. This work is sold with the understanding that the publisher is not engaged in rendering professional services. The advice and strategies contained herein may not be suitable for your situation. You should consult with a specialist where appropriate. Further, readers should be aware that websites listed in this work may have changed or disappeared between when this work was written and when it is read. Neither the publisher nor authors shall be liable for any loss of profit or any other commercial damages, including but not limited to special, incidental, consequential, or other damages.
Library of Congress Cataloging-in-Publication Data
Names: Coatesworth, Jane, 1964‐ author.
Title: Small animal dermatology : what's your diagnosis? / Jane
Coatesworth.
Description: Hoboken, NJ : John Wiley & Sons, Inc., 2019. | Series: What's
your diagnosis? | Includes bibliographical references and index. |
Identifiers: LCCN 2018051416 (print) | LCCN 2018053074 (ebook) | ISBN
9781119311140 (Adobe PDF) | ISBN 9781119311126 (ePub) | ISBN 9781119311119
(paperback)
Subjects: | MESH: Skin Diseases–veterinary | Animals, Domestic | Skin
Diseases–therapy | Differential Diagnosis | Case Reports
Classification: LCC SF992.S55 (ebook) | LCC SF992.S55 (print) | NLM SF 901 |
DDC 636.08965–dc23
LC record available at https://lccn.loc.gov/2018051416
Cover Design: Wiley
Cover Images: Courtesy of Jane Coatesworth
Acknowledgements
My grateful thanks and heartfelt appreciation for the love and counsel of my family and friends, and for the kindness and support of many past and current colleagues at the Animal Health Trust.
Abbreviations
ACTH
adrenocorticotropic hormone
ALP
alkaline phosphatase
ALT
alanine aminotransferase
AN
acanthosis nigricans
APTT
activated partial thromboplastin time
ASIT
allergen specific immunotherapy
BAER
brain auditory evoked response
CAFR
cutaneous adverse food reaction
CDA
colour dilution alopecia
CLE
cutaneous lupus erythematosus
DLE
discoid lupus erythematosus
DMSO
dimethyl sulfoxide
EL
epitheliotropic lymphoma
ELISA
enzyme‐linked immunosorbent assay
GABA
gamma‐aminobutyric acid
GGT
gamma‐glutamyltransferase
H&E
haematoxylin and eosin
HAC
hyperadrenocorticism
HCS
hepatocutaneous syndrome
IBD
inflammatory bowel disease
IgE
immunoglobulin E
IgG
immunoglobulin G
MCP
mucocutaneous pyoderma
PARR
PCR for antigen receptor rearrangements
PAS
periodic acid Schiff
PCR
polymerase chain reaction
PF
pemphigus foliaceus
PT
prothrombin time
SA
sebaceous adenitis
SAM‐e
S‐adenosyl‐L‐methionine
SCT
Sertoli cell tumour
SLE
systemic lupus erythematosus
SLIT
sublingual immunotherapy
TCT
thrombin clot time
TSH
thyroid stimulating hormone
UCCR
urine cortisol: creatinine ratio
UDS
uveodermatologic syndrome
VCLE
vesicular cutaneous lupus erythematosus
Introduction
Dermatology is an interesting area of clinical practice. The skin is the largest organ of the body and is continually renewing itself. The skin is influenced by diet, hormones and systemic disease and colonised by bacteria, yeasts and parasites. Despite this variety of interactions, the skin has limited responses to insult and so many skin diseases present with a similar appearance.
Dermatology cases account for around 30% of the case load of small animal first opinion practice. It is important to aim for a definitive diagnosis at an early stage, otherwise cases can be given a series of reactive symptomatic treatments and remain a source of frustration for both vets and owners. Many cases, such as those with allergic skin disease, are controllable but cannot be cured. A realistic prognosis, owner education, financial estimates, owner motivation and an appropriate treatment plan all follow from a definitive diagnosis.
It is very helpful to maintain the discipline of a systematic approach. A well‐rehearsed systematic approach to history taking and physical examination will ensure that important information is not missed when we are tired, busy or distracted. This is followed by noting down a list of the problems. A problem list is not included in the cases in this book as the section heading gives the main presenting problem such as pruritus, alopecia and so on. The History sections are edited to contain only the pertinent points, in contrast to the usual 20 pages of history that may accompany a skin case. Following the problem list, it is very important to develop a list of differential diagnoses. This is a list of possible diseases that fit the history and clinical signs and the list forms the basis on which diagnostic tests are selected. It is helpful to list the differentials in order of likelihood, as this can save time and money when performing diagnostic tests. A disease that is not on the differential list may not be looked for, so time spent creating a good differential list is very helpful and gives structure and direction to the case work‐up. Readers in different geographical areas will have different differential lists, or the same list in a different order, to reflect local prevalence of disease.
Itch scores are referred to in some of the cases in this book. A score of 1/10 is a normal dog with an occasional scratch or lick at the skin and 10/10 is an animal showing almost continuous pruritic behaviour. Asking owners to allocate an itch score to their pet can be helpful in gauging relative pruritus levels. The score is very subjective, but the same owner scoring over time can add useful information to the overall picture. Inviting owners to point to a visual analogue scale has been shown to be more representative than conjuring a number from their thoughts.
Clinicians are problem‐solving detectives with good abilities to analyse and filter large amounts of information. This book is designed to enhance clinical problem‐solving skills and can be approached as a series of mini challenges. The text details the process of clinical decision making using real cases from first and second opinion practice. The book contains a variety of case material from the UK, from the common to the rare. It is not intended to be a comprehensive textbook, but covers the broad range of dermatology discussed in the 34 cases that have been included.
Further reading
2007 Hill, P.B., Lau, P., and Rybnicek, J. (2007). Development of an owner‐assessed scale to measure the severity of pruritus in dogs. Veterinary Dermatology 18: 301–308.
Section AAlopecia
Alopecia is an obvious clinical sign and is frequently of concern to owners. The hair coat can play an important part in the relationship between owner and pet by affecting the way the animal looks and feels. The presence of hair protects the underlying skin from physical, chemical and ultraviolet damage and plays a role in thermoregulation. There is often a wide range of possible causes of alopecia and identifying the specific cause can be challenging. Alopecia can be the result of congenital or hereditary abnormalities in hair growth, endocrine disease, allergic skin disease, hair follicle death, parasites and fungal or bacterial infections.
The term alopecia refers to an abnormal absence of hair, which can be partial or complete. The term hypotrichosis is used for an abnormal diffuse thinning of the hair coat. A sparse hair coat is a normal feature of some locations, such as between the ear and eye of a cat. Glabrous skin is innately very sparsely haired or devoid of hairs. The extent of glabrous skin is breed dependent but typically occurs at the axillae, ventral abdomen and concave aspects of the pinnae. Certain breeds have extensive genetically determined areas of alopecia that are considered to be normal, examples include the Mexican Hairless dog (Xoloitzcuintli), the Chinese Crested dog and the Sphynx cat.
Alopecic cases can be usefully divided into those with inflammatory skin lesions and pruritus, and those with non‐inflammatory skin lesions and no pruritus. The history and clinical examination can help to place a case in one of these two groups. Examples of inflammatory and pruritic skin conditions include allergic skin disease, ectoparasitic disease with a hypersensitivity component, and surface or superficial bacterial or yeast infections. Conditions with non‐inflammatory primary skin lesions include the endocrine diseases and follicular dysplasias. Clinicians need to be alert for secondary bacterial or yeast infections, which may complicate many of the non‐inflammatory conditions and result in focal inflammation and pruritus.
Figure A.1 Shows the ventral neck of a young Clumber Spaniel. There is marked erythema, and extensive self‐inflicted alopecia from persistent rubbing and scratching. The dog has atopic dermatitis and a secondary Malassezia dermatitis.
Non‐inflammatory alopecia is often associated with abnormalities in the hair growth cycle. Thyroid hormone is important in triggering the active growth phase (anagen), consequently dogs with untreated hypothyroidism have an increasing number of hair follicles arrested in telogen. High levels of glucocorticoids or oestrogens can also cause telogen arrest by delaying the onset of anagen. Telogen hairs are eventually shed from the follicles and there is no new hair growth to replace them.
Figure A.2 Shows a group of plucked hairs from a dog with hypothyroidism. The hair bulbs are all in telogen, the resting phase of the hair growth cycle. Telogen hairs have a characteristic narrow and pointed ‘spear shaped’ root end.
Pattern alopecia is a non‐inflammatory and non‐pruritic condition that has a symmetrical pattern and is seen in certain breeds, most notably the Dachshund. The caudal thighs, convex aspects of the pinnae, ventral abdomen, thorax and chest are the commonly affected areas. The hairs and hair follicles become progressively miniaturised and then stop growing, leaving areas of permanent alopecia. Pattern alopecia is first seen in young adult dogs and has a slowly progressive course. It is a cosmetic condition with no associated pruritus or systemic signs.
Post clipping alopecia is an abnormal delay in hair regrowth after clipping. This can occur in any breed, but is more common in plush coated dogs. Plush coated dogs, such as the Nordic breeds, make a significant investment of resources into growing their dense coat. The hairs grow to a fixed length and are then retained in the resting phase (telogen) over a long period of time before being replaced. Clipping a plush coated dog during the long resting phase can lead to a prolonged period of alopecia before new hair regrows. The reason for the delayed anagen is not understood, but it may take up to 2 years for the alopecia to be replaced with a new hair coat.
The hair follicle has a very high level of metabolic activity at the time of new hair production, and is nourished by a plentiful blood supply. Interruptions to the blood supply can result in local ischaemia and the death of hair follicles. The resulting well‐defined areas of scarring alopecia are usually permanent. Ischaemic dermatopathies, with clinical signs of scarring alopecia, include dermatomyositis and local reactions to rabies vaccination. Dermatomyositis is most often seen in the Shetland Sheepdog and Collie breeds, and is a heritable condition.
Figure A.3 Shows the left face of a young adult Jack Russell Terrier. There is a well demarcated alopecic ring surrounding the left eye. The dog is not pruritic and the lesions do not appear to be inflamed. There are similar lesions around the right eye, on the margins of the ear pinnae and at the tip of the tail. Skin biopsies demonstrate a vasculitis/vasculopathy but the inciting cause is unclear. No further lesions occur, but there is persistent alopecia over a 9‐year period of follow up.
Alopecia can occur after inflammation and damage to the hair follicle; for example, in dermatophytosis, demodicosis or bacterial folliculitis. The damage can also be immune mediated; for example, the attack of hair follicles mediated by cytotoxic lymphocytes in alopecia areata. Hair follicles can be damaged by extremes of temperature; for example, the scarring alopecia associated with thermal burns and hot or freeze branding.
Alopecia in cats is often self‐induced. The abrasive tongue, combined with persistent over‐grooming behaviour, can produce extensive hair loss in a relatively short period of time. It can be more challenging in cats to decide if the alopecia is self‐inflicted, as owners typically spend less time observing a cat in comparison to a dog. Examination of plucked hairs is often helpful to show whether hair shafts have been fractured by self‐trauma.
Figure A.4 Shows the right side of a black cat. There is extensive hypotrichosis over the trunk, the proximal tail and proximal hind limbs. The head, distal limbs and distal tail have a normal dense hair coat. This cat has a bilaterally symmetrical self‐induced hypotrichosis, resulting from the over grooming associated with a flea bite hypersensitivity.
Skin biopsy can be a helpful diagnostic tool for cases presenting with alopecia. Biopsies should be taken from the centre of an alopecic area so that the histopathologist can identify and assess well established changes. The presence of bacterial and Malassezia infections can mask the primary pathology, so it is helpful to control these secondary changes before taking biopsies.
Case 1
History
A 6 year‐old male neutered Airedale Terrier is presented with an 8‐month history of hair loss.
The dog is from a rehoming charity and has lived with the owners for the past 3 years. Hair loss was first noticed 8 months ago, starting over the tail head and extending cranially to the lateral body walls, progressing down the hind limbs and most recently involving the neck. He eats, drinks and urinates a normal amount, but is less keen to exercise than usual. The owners have noticed that other male dogs are attracted to their dog in the park. They try to mount him, or to lick his penis. He tolerates this for a short while and then growls and rebuffs them.
Questions
Describe the abnormalities and pertinent normal features in Figures
1.1
and
1.2
.
What differential diagnoses should be considered for this presentation?
What tests could you perform to make the diagnosis?
Figure 1.1
Figure 1.2
Answers
What the figures show
Figure 1.1 shows the left side of the dog. There is an extensive area of alopecia on the left body wall with intense hyperpigmentation of the skin. This pattern is repeated on the right side of the dog. The remaining hair coat has an abnormally soft, sparse, pale coloured and woolly appearance, except for the paws and head, which retain a more normal type of coat. The prepuce is drooped.
Figure 1.2 shows the dog from behind. There is alopecia and marked hyperpigmentation of the caudal and medial aspects of the proximal hind limbs, ventral tail and perineum. The remaining hair coat, above the hocks, is sparse and soft.
Differential diagnoses
Given the appearance of the skin lesions the following conditions should be considered:
Causes of non‐pruritic, bilaterally symmetrical alopecia
Hypothyroidism
Hyperadrenocorticism
(
HAC
)
Cyclic flank alopecia (Airedale Terrier is a predisposed breed)
Sex hormone alopecia
Demodicosis
Dermatophytosis
Causes of the hair coat alterations
Hypothyroidism
HAC
Sex hormone alopecia
Appropriate diagnostic tests
Physical examination reveals a grade 3–4 systolic cardiac murmur. There is moderate enlargement of the mammary glands.
Hair plucks show no Demodex mites.
Haematology shows a low red blood cell count of 5.22 × 1012 l−1 (5.55–8.5 × 1012 l−1) with a normal mean corpuscular volume (normocytic) and a normal mean corpuscular haemoglobin content (normochromic). This mild non‐regenerative anaemia could be associated with chronic neoplasia and/or inflammation, or with early bone marrow dysfunction. Hyperoestrogenism, associated with some testicular tumours, can cause initial stimulation of the bone marrow. There is an elevated white blood cell count 21.2 × 109 l−1 (6–18 × 109 l−1), elevated bands 1.7 × 109 l−1 (0–0.5 × 109 l−1) and an elevated segmented neutrophil count 13.99 × 109 l−1 (4–12 × 109 l−1). The leukocytosis, neutrophilia and a regenerative left shift are indicative of persistent function of the myeloid lineage in the bone marrow and are commonly associated with acute infection, tissue damage or inflammation. Chronic exposure to elevated oestrogen levels can result in significant bone marrow damage and manifest as anaemia, neutropenia and/or thrombocytopenia.
Serum biochemistry shows hypercholesterolaemia 11.2 mmol l−1 (3.6–7 mmol l−1). Total T4 and thyroid stimulating hormone (TSH) assays are not tested at this time as, despite the dog being middle aged, lethargic and hypercholesterolaemic, there is a higher index of suspicion of a sex hormone imbalance. Moreover, this dog has chronic disease, which can lead to thyroid panel results being outside of the normal range despite the thyroid gland having a normal capacity.
Urine cortisol: creatinine ratio (UCCR). This test has a high sensitivity and a low specificity for HAC. It is ideal for ruling out HAC when, as in this case, there is a low index of suspicion for the disease. A UCCR within the normal range confidently rules out HAC (here 17.5 × 106, a normal ratio is below 30 × 106). An elevated ratio would need to be further investigated with a low dose dexamethasone suppression test, or an adrenocorticotropic hormone (ACTH) stimulation test, as it may indicate HAC or other non‐adrenal related illness.
Abdominal ultrasonography, performed conscious, shows a greater than 10 cm diameter complex mass in the mid‐abdomen. The mass is well vascularised and contains multiple cystic structures. The medial iliac lymph nodes are enlarged, slightly heterogeneous and measure around 1 cm in diameter. This may represent local metastasis or reactive local lymphadenopathy. No abnormalities are seen in the liver or spleen. The prostate is mildly enlarged but retains a normal bi‐lobed shape. The mass is presumed to be a retained testicle, but a second testicle could not be identified during the ultrasound examination. Atrophy of the contralateral normal testicle is a common occurrence.
Figure 1.3 Shows an ultrasound image of the abdomen. There is a complex mass, of more than 10 cm diameter, in the mid‐abdomen. The mass contains multiple anechoic areas.
Figure 1.4 Shows a colour Doppler image of the same mass. The colour flow signal indicates that the mass has a well‐developed vascular system.
Diagnosis
Probable hyperoestrogenism, associated with a retained testicle that has undergone neoplastic transformation.
Treatment and outcome
Exploratory laparotomy reveals a large and highly vascular mass. The mass is presumed to be a retained testicle and is removed from the mid‐abdomen with careful ligation of the substantial blood supply. The second testicle is not found. One local lymph node is excised.
Figure 1.5 Shows the dog in dorsal recumbency, at exploratory laparotomy. A large soft tissue mass, found in the mid‐abdomen, is exteriorised but is still attached. The mass is multi‐lobulated, and highly vascular.
Figure 1.6 Shows the excised mass, with a section of attached vasculature on the right. The 20 ml syringe in the foreground gives an impression of scale.
Histopathological examination of the excised mass shows it to be a retained testicle, containing both a mixed Sertoli cell tumour (SCT) and a seminoma. More than one type of primary tumour in a single testicle is not uncommon. The local lymph node shows reactive change, with no evidence of tumour metastasis. Metastasis is uncommon in SCTs and rare in seminomas and interstitial cell tumours.
The dog recovers well after surgery, and gradually becomes more active and playful. There is progressive hair regrowth at the previously alopecic areas. The new hair is dense, lustrous, darker in colour and has a more robust texture than the previous hair coat.
Figure 1.7 Shows the dog 5 months after initial presentation. He has a brighter demeanour and extensive hair regrowth of a normal Airedale‐type hair coat. There are marked changes in the colour, density and texture of the hair coat.
Figure 1.8 Shows the dog from behind, 5 months after initial presentation. There is complete hair regrowth at the previously alopecic areas.
Prognosis
The prognosis is good if the primary tumour is completely excised and no tumour metastasis has occurred. The dog had no apparent oestrogen‐induced myelotoxicity.
There is a risk that the other testicle will undergo neoplastic transformation. Up to 50% of dogs have bilateral tumours. The other testicle is presumably also retained, but could not be located for removal during the exploratory laparotomy.
Discussion
This dog has a feminisation syndrome caused by hyperoestrogenism. A male dog may overproduce oestrogen from a neoplastic testicle, or from excessive adrenal gland activity. A female dog may show hyperoestrogenism associated with cystic ovaries, or by over medication with oestrogen. Oestrogen supplementation is most commonly dispensed for urinary incontinence.
General clinical signs associated with hyperoestrogenism are gynaecomastia, a pendulous prepuce, prostatic enlargement, being attractive to male dogs and vulval swelling. Bone marrow suppression is potentially life threatening.
Dermatological signs associated with hyperoestrogenism include bilaterally symmetrical alopecia. This classically starts caudally, especially involving the perineum, and progresses cranially and ventrally. The alopecic areas, as in this case, are hyperpigmented and there is no primary pruritus. A pathognomic dermatological sign, present in this case but not photographed, is a line of erythema and hyperpigmentation between the prepuce and the perineum. So‐called linear preputial erythema is uniquely associated with the presence of a testicular tumour and is a useful dermatological marker of internal disease.
Testicles initially develop near the kidney. They usually move through the inguinal ring and are often palpable in the normal scrotal position by 3 months of age. Testicles can be retained at any stage of this journey. The tendency to be cryptorchid is inherited as an autosomal recessive trait, although the Airedale Terrier is not recognised as a breed predisposed to this condition.
Three main types of tumour can develop within testicles – SCTs, seminomas and interstitial (Leydig) cell tumours. The three types occur with approximately equal frequency, usually in the older dog. There is a higher incidence of SCTs and seminomas in retained testicles, but not of interstitial cell tumours. It is likely, in this case, that oestrogen was being produced by the SCT rather than by the seminoma. About one‐third of SCTs produce sex hormones, while only a small percentage of seminomas and interstitial cell tumours are functional. Functional SCTs and seminomas tend to produce oestrogens, while functional interstitial cell tumours produce androgens.
Tumour development is likely to be appreciated more quickly in an external testicle than in a retained testicle. The size and shape of the affected testicle is often distorted. Palpation ± ultrasound examination, with comparison to the contralateral testicle, is usually helpful in a descended pair. This dog was adopted from a rehoming charity at 3 years of age as an apparently neutered male. It seems that the history of his undescended testicles was lost at some stage.
Anti‐Müllerian hormone (AMH) may be a useful biomarker for cryptorchidism. AMH is produced by the ovaries and by Sertoli cells in the testicles. Correctly neutered animals would be expected to have no measurable hormone. This ELISA test was not employed in this case as there were highly suggestive clinical signs and the abdominal mass was easily found on ultrasound examination.
Further reading
Hayes, H.M. and Pendergrass, T.W. (1996). Canine testicular tumours: epidemiological features of 410 dogs.
International Journal of Cancer
18: 482–487.
Holst, B.S. and Dreimanis, U. (2015). Anti‐Müllerian hormone: a potentially useful biomarker for the diagnosis of canine Sertoli cell tumours.
BMC Veterinary Research
11: 166.
Lawrence, J.A. and Saba, C.F. (2013). Chapter 28: Tumors of the male reproductive system. In:
Withrow and MacEwen's Small Animal Clinical Oncology
, 5e (ed. S.J. Withrow, D.M. Vail and R.L. Page), 557–561. Maryland Heights, MO: Elsevier Saunders.
Weaver, A.D. (1983). Survey with follow up of 67 dogs with testicular Sertoli cell tumours.
Veterinary Record
113: 105–107.
