Untitled

DERMATOLOGICAL DIAGNOSIS IN DOGS
An approach based on clinical patterns

For this English edition:
Dermatological diagnosis in dogs. An approach based on clinical patterns
Copyright © 2018 Grupo Asís Biomedia, S.L.
Plaza Antonio Beltrán Martínez nº 1, planta 8 - letra I
(Centro empresarial El Trovador)
50002 Zaragoza - Spain
First printing: February 2018
This book has been published originally in Spanish under the title:
Diagnóstico dermatológico en perros a partir de patrones clínicos
© 2017 Grupo Asís Biomedia, S.L.
ISBN Spanish edition: 978-84-16818-84-6
Translation:
Owen Howard
Illustrator:
Jacob Gragera Artal
ISBN: 978-84-17225-35-3
eISBN: 978-84-17225-36-0
D.L.: Z 80-2018
Design, layout and printing:

Servet editorial - Grupo Asís Biomedia, S.L.
www.grupoasis.com
info@grupoasis.com
All rights reserved.

Any form of reproduction, distribution, publication or transformation of this book is only permitted with
the authorisation of its copyright holders, apart from the exceptions allowed by law. Contact CEDRO
(Spanish Centre of Reproduction Rights, www.cedro.org ) if you need to photocopy or scan any part of
this book (www.conlicencia.com ; 0034 91 702 19 70/0034 93 272 04 47).
Warning:
Veterinary science is constantly evolving, as are pharmacology and the other sciences. Inevitably, it is
therefore the responsibility of the veterinary surgeon to determine and verify the dosage, the method of
administration, the duration of treatment and any possible contraindications to the treatments given to
each individual patient, based on his or her professional experience. Neither the publisher nor the author
can be held liable for any damage or harm caused to people, animals or properties resulting from the
correct or incorrect application of the information contained in this book.
To my parents, Félix and Anuncia,
who taught me the importance of effort and have educated me
in human values since before I could write.
To my husband Emilio and my children Emilio and Pablo,

for their unconditional love and constant forgiveness for the
amount of hours I dedicate to the veterinary profession.
To all my former students now working in the field of

veterinary dermatology:
their enthusiasm has fuelled my dedication to learning and
teaching.
To all members of the GEDA group of AVEPA,

who have driven advances in the field of pet dermatology in
for more than 30 years.
ACKNOWLEDGMENTS
Writing this book was only possible thanks to the large numbers of patients
who have attended the Dermatology Service of the Veterinary Hospital of the
University of Zaragoza, and I am extremely grateful to all the pet owners who
allowed me to photograph the skin lesions of their precious pets.
I would like also to thank all the veterinary surgeons who generously shared
their work and some of their images with me: Amparo Ortúñez (Mallorca),
Anabel Dalmau (Reus, Tarragona), Carlota Sancho (Arrabal, Zaragoza),
Dolors Fondevila (UAB, Barcelona), Eva Varela (Casetas, Zaragoza), Laura
Navarro (UZ, Zaragoza), Laura Ordeix (UAB, Barcelona), Mariví Falceto
(UZ, Zaragoza), Pedro Ginel (UCO, Cordoba), Rosana Saiz (Miralbueno,
Zaragoza), Sara Peña (Fuerteventura), and Sergio Villanueva (UZ,
Zaragoza).
The final version of the book is the result of the combined efforts of the entire
editorial team at Grupo Asís, and I am grateful for the manner in which they
have presented the material I provided. I would like to extend special thanks
to Rut Varea, who collaborated on this project, Gema Yagüe for her revision
of the text, and Jacob Gragera for his illustrations. Only veterinary surgeons
like you could rise to such a technical challenge with such quality and
professionalism.
THE AUTHOR
Maite Verde graduated in Veterinary Medicine from the Faculty of Veterinary

Medicine of the University of Zaragoza. She holds a PhD in Veterinary
Medicine and is a Professor of Animal Medicine and Surgery.
She has served as vice-dean of Clinical Services and dean of the Faculty of
Zaragoza (1995–2003), as well as vice-president and president of AVEPA
(Spanish Association of Small Animal Specialists, 2006–2012). She has
been a member of the council of the European Association of Establishments
for Veterinary Education (EAEVE) (2002–2004), is a current member of the
National Commission on Veterinary Specialties of the Spanish Council of
Veterinary Colleges, and is the director of the Veterinary Hospital of the
University of Zaragoza.
A Professor of Internal Medicine and Dermatology, AVEPA-accredited in

Dermatology and Internal Medicine, she is a member of the European Society
of Dermatology (ESVD) and has participated in the organisation of the 3
European ESVD congresses held in Spain. She has also served as secretary
and president of GEDA, AVEPA’s group of experts in dermatology. She
currently heads the Dermatology Service of the Veterinary Hospital of the
University of Zaragoza.
She has published several works and book chapters on dermatology and
internal veterinary medicine and has spoken at congresses and seminars for
both academia and private industry.
Maite Verde
FOREWORD
Management of skin diseases can be frustrating. Remembering all of the

differential diagnoses for a specific dermatological sign can be a challenging
yet critical skill in the development of an efficient diagnostic plan.
Understanding the pathology that results in abnormal cutaneous function,
processes and patterns helps a clinician refine diagnostic and therapeutic
recommendations. In this book, Dr. Verde skillfully articu- lates a logical,
problem-based approach necessary to diagnose dogs with various
dermatological signs. Her extensive clinical knowledge and teaching
experience results in an easy-to-follow and logical approach for each of the
common dermatological abnormalities. Topics include alopecia, seborrhea,
pruritus, and more.
The first chapter introduces the concept of clinical dermatological pattern, its
integration into a list of differential diagnoses and potential diagnostic tests.
The second chapter specifically defines various cutaneous patterns and
insightfully correlates these with the pathologic process and clinical signs.
The reader may expect several “that makes sense” moments while reading
this chapter.
Many excellent photographs, diagrams and charts further enhance the

information. The result is a book with a refreshing approach aimed at guiding
the reader through an efficient work-up of dermatological signs and
ultimately confirmation of a diagnosis.
Dunbar Gram, DVM, DACVD,

Dermatology Service Chief and Clinical Associate Professor,
College of Veterinary Medicine, University of Florida
PREFACE
Most veterinary surgeons who treat pets are generalists, and deal every day
with cases of all kinds that can involve any organ system. Skin conditions are
extremely common, accounting for between 15 % and 25 % of daily
consultations.
General practitioners working in the field of clinical dermatology thus need

tools that allow them to approach and guide the diagnostic process in a
straightforward way from the moment they see the patient. Therefore, when
designing the structure of this book, we selected a format that would allow
the reader to learn about dermatology as they apply the principals and
protocols explained within.
We believe that the simplest and most logical way to approach a

dermatological clinical case is to observe the patient’s appearance and the
predominant lesions and their distribution, and to link this information to a
clinical pattern. By creating a list of possible causes of the clinical pattern in
question, we can identify the most probable causes based on information in
the patient’s clinical history. If we have also identified the appropriate
diagnostic tests, and the order in which they should be performed, it is highly
likely that a definitive diagnosis of most cutaneous processes can be
established by a veterinary surgeon without in-depth knowledge of
dermatology.
The first 2 chapters provide a general introduction to diagnosis based on

clinical patterns, and describe the general characteristics of the skin’s
response to aggressions in general, its response to aggressions that produce
lesions, and the characteristics of the resulting clinical patterns.
The subsequent 5 chapters are dedicated to the most commonly encountered
patterns: multifocal alopecia; generalised alopecia; scaling/crusting and
seborrhoeic; erosive-ulcerative; and papulopustular and vesicular. The last
chapter deals specifically with the diagnosis of pruritus.
The content is designed to allow readers to learn by following a systematic

approach to resolving canine dermatological problems. The format is that of
a small canine dermatological atlas, with over 300 images accompanying the
text.
My hope is that this book will provide students and veterinary surgeons with
a deeper knowledge of dermatology.
Maite Verde
TABLE OF CONTENTS
01 GENERAL CONSIDERATIONS
FOR DIAGNOSIS BASED ON
CLINICAL PATTERNS
Introduction
Identify and define the dermatological pattern
Collect basic information
Establish the list of possible causes of the pattern
Propose tests in a logical order
02 DEFINING CUTANEOUS
PATTERNS
Introduction
Pathophysiological responses of the epidermis to aggressions of the skin
Hyperkeratosis: alterations in the cornification process
Acanthosis: epidermal hyperplasia
Apoptosis
Necrosis
Atrophy of the epidermis
Alterations in the epidermal fluid equilibrium
Intercellular fluid accumulation
Intracellular fluid accumulation
Acantholysis
Exocytosis
Pathophysiological responses of the dermis to skin aggressions
Pathophysiological responses of skin appendages
Pathophysiological responses of the adipose tissue
Cutaneous clinical patterns
Focal-multifocal alopecia pattern
Symmetrical alopecia pattern (regional or generalised)
Scaling/crusting and seborrhoeic pattern
Erosive-ulcerative pattern
Vesicular papulopustular pattern
Nodular pattern
Distinguishing between inflammatory and neoplastic nodules
Pigmentary alteration pattern

Hypopigmentation
Hyperpigmentation
Pruritus
03 FOCAL OR MULTIFOCAL
ALOPECIA
Introduction
Underlying causes of the pattern
Diagnostic procedure
Analysis of the medical history
General examination
Dermatological examination
Distribution of foci of alopecia
Determining whether alopecia is self-induced or true
Type of hair and presence of lesions
Reversible and irreversible alopecia
Diagnostic protocol
Step 1 Brushing and combing
Step 2 Deep and superficial skin scraping
Step 3 Trichogram
Step 4 Wood’s lamp
Step 5 Mycotic culture
Step 6 Surface and fine-needle puncture cytology
Step 7 Serological tests for leishmaniasis
Step 8 Skin biopsy
04 SYMMETRICAL ALOPECIA
(REGIONAL OR
GENERALISED)
Introduction
Factors involved in hair growth and formation
General examination
Common lesions in generalised asymmetrical alopecia
Diagnostic protocol
Step 1 Analysis of the basic characteristics of the patient
Step 2 Confirm or rule out demodicosis
Step 3 Confirm or rule out dermatophytosis
Step 4 Confirm or rule out bacterial folliculitis
Step 5 Confirm or rule out leishmaniasis
Step 6 Age of onset of alopecia
Step 7 Biopsy
05 SCALING/CRUSTING AND
SEBORRHOEIC PATTERN
Introduction
Primary keratinisation alterations
Secondary keratinisation alterations
General examination
Diagnostic protocol
Step 1 Mites, Malassezia, and bacteria on the surface of the skin
Step 2 Intestinal parasites
Step 3 Presence of dermatophytes
Step 5 Flea control
Step 6 Food hypersensitivity
Step 7 Atopic dermatitis caused by aeroallergens
Step 8 Systemic disorders
Step 9 Skin biopsy
06 EROSIVE-ULCERATIVE
PATTERN
Introduction
General examination
Diagnostic protocol
Step 1 Is it a pruritic process?
Step 2 Does the clinical history analysis or the examination reveal any relevant findings?
Step 3 Cytology
Step 5 Biopsy
Step 6 Bacterial culture and antibiogram
Step 7 Mycological culture
Step 8 Other specific tests
07 PAPULOPUSTULAR AND
VESICULAR PATTERN
Introduction
General examination
Diagnostic protocol
Step 1 Scrapings and trichogram
Step 2 Cytology
Step 3 Confirm or rule out Leishmania
Step 4 Mycological culture
Step 5 Bacterial culture and antibiogram
Step 6 Biopsy
08 WHEN THE CLINICAL

PRESENTATION IS PRURITUS
Introduction
Pathophysiology of pruritus
Causes of pruritic signs
Characteristics of pruritus
Intensity of pruritus on a scale of 0 to 10
Seasonality
Onset and evolution
Location and type of lesions accompanying pruritus
General examination
Diagnostic protocol
Step 1 Confirm or rule out the presence of fleas, lice, and Cheyletiella
Step 2 Confirm or rule out the presence of mites on the surface of the skin (Demodex, Sarcoptes,
Trombicula ) and on the ears (Otodectes )
Step 3 Confirm or rule out dermatophytosis
Step 4 Confirm or rule out intestinal parasites
Step 5 Analysis of microscopic structures on the skin surface
Step 7 Institute an antiparasitic treatment and control program (against fleas and gastrointestinal
parasites)
Step 8 Confirm or rule out food hypersensitivity
Step 9 Determine whether the patient fulfils at least 5 clinical criteria for atopy (Favrot, 2010)
Step 10 Therapeutic trial with oclacitinib
Step 11 Identification of airborne allergens in cases of atopic dermatitis
Step 12 Skin biopsy
Treatment
09 REFERENCES
INTRODUCTION
Analysis of clinical patterns is the simplest way diagnose dermatological
problems, since this approach is based on the natural observation of
cutaneous alterations that a patient presents in the clinic (Figs. 1 –3 ).
When basing the diagnosis on dermatological patterns, it is not necessary to

be familiar with all skin diseases, which are very numerous. It is sufficient to
characterise the type of lesions (Box 1 ) displayed by the patient and then
follow the logical steps of a diagnostic protocol.
Establishing a dermatological diagnosis this way is possible thanks to

significant advances in our understanding of the causes of cutaneous
pathologies in dogs, and the corresponding presentations.
In the early 1970s, when the field of veterinary dermatology was in its
infancy, the information available was scarce, or uncorroborated. Since then,
advances in this field have made it possible to establish simpler diagnostic
frameworks based on proven scientific knowledge.
Now, after 40 years of progress in canine dermatology, establishing a

diagnosis based on clinical patterns is the most practical way to learn
dermatology and to teach it to veterinary students and clinicians in general.
Expertise in dermatology is not required to apply a diagnostic protocol based

on clinical patterns. Obviously, this process will be easier for veterinary
surgeons with more experience, since they will be familiar with the
information and will have applied this systematic approach more frequently in
the past. However, each veterinary surgeon can use this diagnostic approach,
adapting it to their own circumstances.
The key to using this system is knowing where to look, and thus acquiring the
habit of properly identifying skin lesions and their distribution.
It is also necessary to know how to identify crucial information in the medical
history in order to create a list of differential diagnoses and perform the
appropriate diagnostic tests for the clinical presentation in question.
To establish a diagnosis based on clinical patterns, one must know how to

identify primary skin lesions, and to associate them with a predominant
morphological pattern. Here lies the key to success: if we fail to correctly
identify the morphological pattern, we begin based on an erroneous premise,
making it more difficult to reach a correct diagnosis.
The following are the central pillars of diagnosis based on clinical patterns:
Identify and define the dermatological pattern after performing a
dermatological examination and observing the lesions.
Collect basic information on the characteristics of the patient from the
medical history and based on the general and dermatological examination
(Boxes 2 and 3 ).
Create a list of possible causes of the observed pattern.
In a logical order, list the tests necessary to identify the underlying cause of
the clinical picture.
01 Multifocal alopecia pattern.

02 Papulopustular and generalised alopecia pattern.
03 Erosive-ulcerative pattern.
BOX 1
IDENTIFY AND DEFINE THE

DERMATOLOGICAL PATTERN
In most cases, it will be easy to recognise the main types of cutaneous lesions
found in dogs, and to characterise the dermatological pattern. However, in
some cases it is difficult to identify a predominant pattern, as the lesions
observed may correspond to several different patterns. In this situation it is
necessary to identify the predominant pattern. For example, if there are
numerous areas or foci of alopecia across the body, in addition to 3 or 4
papulopustular lesions (Fig. 4 ), the main pattern would be characterised as
multifocal alopecia and the papulonodular lesions would be considered
secondary. Conversely, if the patient has 3 or 4 foci of nodular alopecia in a
body region (Fig. 5 ), the pattern would be considered nodular, and the
alopecia in nodular areas would be considered secondary, or of lesser
importance.
To determine the predominant clinical pattern, it is also necessary to look at

the types of lesions and their location. In each case it is useful to note the
following aspects and to illustrate the information collected in the
examination on a silhouette (Fig. 6 ):
Whether the distribution is symmetric or asymmetric.
The affected area or region: head, neck (dorsal and ventral), trunk (dorsal
and ventral), limbs, and tail.
Affected areas subjected to pressure, rubbing, or friction.
Affected mucocutaneous areas (lips, nostrils, eyelids, foreskin, and vulva),
areas of the muzzle, pinnae, or footpads.
Affected mucosa: oral, conjunctival, anal, and genital.
Types of lesions: colour changes, papules, pustules, vesicles, scaling,
crusts, follicular casts, collarettes, alopecia, nodules, erosions, and
ulcers.
The characteristics of the lesions in terms of shape, regular/irregular
appearance, and pigmentation.
Figure 7a shows a case of multifocal alopecia of the left hindlimb, and Figure
7b shows the corresponding lesions marked on a silhouette.
From the information obtained, we can establish the dermatological pattern:

Easily removable or absent hair:
Focal/multifocal alopecia pattern – distributed in foci or round
patches.
Symmetrical generalised alopecia pattern – homogeneously
distributed and affecting large areas.
Prevalence of scales and/or crusts on the skin surface: scaling/crusting and
seborrhoeic or exfoliative dermatosis pattern – multifocal, regional, or
generalised distribution.
Lack of continuity or integrity in the epithelium with predominance of
erosive-ulcerative lesions: erosive-ulcerative pattern.
Lesions that are raised relative to the skin surface:
Papulopustular and vesicular pattern , with predominance of
papular, pustular, vesicular, or bullous lesions, with fluid content.
Nodular pattern , with predominantly solid, raised lesions, consisting
mainly of nodules, plaques, or warts.
Changes in the colour of the skin or hair with no other lesions: pigmentary
alteration pattern.
04 Papulopustular lesions in a case of multifocal alopecia.

05 Papulonodular alopecia.
06 Silhouettes on which lesion location and distribution is indicated. Silhouettes of the right and
left side, as well as dorsal and ventral views, should be used.
07 (a) Focal erythematous alopecia on the hindlimb produced by Microsporum canis. (b)
Silhouette indicating the corresponding lesions observed in the patient in 7a.
COLLECT BASIC INFORMATION

Data on the dog’s age, breed, and sex, as well as information extracted from
the medical history (Box 2 ) and obtained in the general and dermatological
examinations (Box 3 ) will help in reaching a diagnosis. A detailed clinical
history is the simplest and most important element required to establish a
diagnosis in dermatology. The duration of the problem, the age of onset, the
evolution of the disease, the seasonality of the condition, information on
littermates or other siblings, the nature and distribution of the clinical signs,
and the dog’s response to medical treatment should all be discussed with the
owner.
It is also important to consider the presence of other pets, the patient’s diet,
whether the patient lives indoors or outdoors, bed type, deworming and
vaccination programs, and any previous treatments and their effects.
Any observations or concerns mentioned by the owner should also be noted in

chronological order.
BOX 2
BOX 3
ESTABLISH THE LIST OF POSSIBLE
CAUSES OF THE PATTERN
Regardless of whether the clinician can identify a cause for a given pattern,
this book provides the relevant information on the different causes of
cutaneous pathologies and lists the aetiologies associated with each clinical
pattern.
PROPOSE TESTS IN A LOGICAL ORDER

Once the list of differential diagnoses has been drawn up, it is necessary to
consider the tests required to confirm or rule out possible causes in order to
ultimately identify the cause of the clinical pattern. To this end, we begin by
establishing the order of precedence of the causes based on the information
obtained from the medical history and the examination.
Each of the chapters of this book describes the diagnostic procedures

recommended for each dermatological pattern, as well as the order in which
tests should be conducted to reach a definitive diagnosis.
INTRODUCTION
The skin responds to the many aggressions to which it is exposed (Fig. 1 ) by
modifying its physiological mechanisms. This results in microscopic
alterations, as well as observable clinical signs (skin lesions).
Cutaneous tissue can respond to aggressions in a limited number of ways,

which, combined with the distribution of different types of inflammatory cells
that converge in the affected areas, give rise to clinical and histological
patterns, from which we can:
Propose possible causes for the lesions in question.
Suggest categories of disease with similar lesions and common pathogenic
mechanisms.
This way, it is possible to define clinical responses and histopathological

patterns that facilitate the differential diagnosis of cutaneous diseases.
The pathophysiological alterations that occur in the skin in response to

various agents can affect epidermal differentiation and growth, the balance of
dermal and epidermal fluids, the cellular adhesion of keratinocytes,
pigmentation mechanisms, hair and gland formation, the hair growth cycle, the
endothelial structures of the blood and lymph vessels of the cutaneous
plexuses, and receptors and nerve endings. Depending on the affected
structures, different lesions and clinical signs will appear.
01 Schematic showing internal and external aggressions that can affect the skin (based on
Hargis and Ginn, 2012).
PATHOPHYSIOLOGICAL RESPONSES OF
THE EPIDERMIS TO AGGRESSIONS OF
THE SKIN
The pathophysiological changes that occur in the epidermis manifest as
alterations in epidermal differentiation and growth, the balance of epidermal
fluids, cell adhesion, and pigmentation.
In the normal epidermis (Fig. 2 a) there is a balance between the rate of

proliferation of the cells of the stratum basale or basal layer (germ cells) and
the rate of loss of differentiated surface cells (squamous epithelial cells).
Epidermal cell keratinisation (proliferation, differentiation, and cornification)
is regulated by cytokines (including epidermal growth factors, interleukins,
and tumour necrosis factor), various hormones (e.g. cortisol), and nutritional
factors such as proteins, zinc, copper, fatty acids, and vitamins A, B, and D.
Cytokines that regulate the growth and differentiation of keratinocytes are

produced by different types of skin cells, including endothelial cells,
leukocytes, fibroblasts, and keratinocytes themselves. Keratinocytes therefore
exert autocrine control over their own growth and differentiation.
Inflammatory cells can also influence the growth and differentiation of
keratinocytes.
HYPERKERATOSIS: ALTERATIONS IN THE

CORNIFICATION PROCESS
Alterations in the cornification process result in changes in the formation of
the stratum corneum (horny layer) and can be of primary origin, as occurs in
primary (genetically programmed) seborrhoea, or can be secondary to a
variety of processes including inflammation, trauma, and metabolic or
nutritional disorders.
Cornification and keratinisation are terms that are often used interchangeably,
but describe distinct processes. Cornification disorders involve abnormal
production of keratin, lipids, and other components of the stratum corneum,
whereas keratinisation disorders refer primarily to the abnormal production
of the proteins that make up keratin.
Alterations in cornification are known as hyperkeratosis (Figs. 2b and 2c ),

and can be either orthokeratotic or parakeratotic in nature. Both forms of this
process involve the (clinically observable) detachment of large numbers of
scales.
The desquamated epithelial cells are anucleate in the orthokeratotic form, but
possess nuclei in the parakeratotic form. Both orthokeratotic and parakeratotic
hyperkeratosis are considered either nonspecific responses of the skin to
chronic stimuli such as superficial disorders, inflammation, or sun exposure,
or specific responses to primary genetic disorders.
Diagnosis can be confirmed by histological analysis of skin biopsies.

Orthokeratotic hyperkeratosis is accompanied by an increase in the thickness
of the stratum granulosum or granular layer (hypergranulosis), whereas
parakeratotic hyperkeratosis is usually accompanied by a decrease in the
thickness of the granular layer (hypogranulosis).
For reasons unknown, orthokeratotic hyperkeratosis is the predominant

response in the exfoliative processes characteristic of primary seborrhoea of
Cocker Spaniels, ichthyosis, and dermatosis due to vitamin A deficiency.
However, the response to zinc deficiency and hepatocutaneous syndrome is a
parakeratotic form of hyperkeratosis.
Box 1 details the characteristics of these 2 types of hyperkeratosis.
02 Schematic showing the epidermal layers and corresponding microscopic pathophysiological

alterations. (a) Physiological situation (arrows indicate the movement of cells up to the point
of detachment). (b) Orthokeratotic hyperkeratosis, with significant increase in the anucleate
stratum corneum. (c) Parakeratotic hyperkeratosis, with a significant increase in the
nucleated stratum corneum.
BOX 1
ACANTHOSIS: EPIDERMAL HYPERPLASIA

Epidermal hyperplasia (acanthosis) is an alteration in epidermal growth and
differentiation characterised by an increase in the number of cells in this
layer, mainly at the level of the stratum spinosum or spinous layer (thickening
of the stratum spinosum).
Epidermal hyperplasia is a secondary disorder very frequently associated

with chronic inflammation and superficial trauma such as acral lick dermatitis
and chronic allergic dermatitis, and is often seen on the edges of persistent
ulcers.
Acanthosis is a common response to a wide variety of stimuli and has several

histologically distinct forms: regular, irregular, papillary (in papillomas and
calluses), pseudocarcinomatous (in cases of chronic aggression with
granulomatous inflammation and persistent ulcers that fail to heal), and
psoriasiform (psoriasiform lichenoid dermatitis of Springer Spaniels).
APOPTOSIS
Epidermal apoptosis is the programmed cell death of keratinocytes, and is
characterised by eosinophilic cytoplasm and condensation of cytoplasmic
structures and nuclei (Fig. 3 ). Apoptotic keratinocytes, which have a
dyskeratotic appearance, are phagocytosed by adjacent keratinocytes.
Phagocytosis occurs before cells are destroyed and their cellular components
released into the medium, thereby preventing the development of an acute
inflammatory response. Therefore, the process of apoptosis is very different
to that of necrosis, which involves cell lysis, the release of the cell contents
into the extracellular space, and a consequent inflammatory response.
Apoptosis is part of the response mechanism in processes such as erythema
multiforme and lupus erythematosus.
The types of lesions associated with apoptosis are erosions or ulcers, the
severity of which depends on the prevalence and location of apoptotic cells in
the epidermal layers. When apoptosis affects the keratinocytes of the deeper
layers, this results in the formation of ulcerous lesions and crusts secondary to
ulcers caused by the release of inflammatory mediators, leading to the
accumulation of cellular fluid and exudate, which in turn covers and dries the
ulcerated surface.
Apoptosis of keratinocytes is observed in the following processes:

Squamous cell carcinoma.
Vaccine-induced ischaemidermatitis.
Dermatomyositis.
Erythema multiforme.
Chronic cutaneous lupus erythematosus.
Discoid lupus erythematosus.
Systemic lupus erythematosus.
Vesicular lupus erythematosus.
Hair follicle involution during changes in the follicular cycle.
Actinic burns.
Adverse drug reactions.
Vasculitis.
03 Apoptosis of keratinocytes in all epidermal layers. Image courtesy of Dolors Fondevila.
NECROSIS
Necrosis is sudden cell death characterised by nuclear pyknosis (shrunken
and dense nuclei), karyorrhexis (rupture of the nuclear membrane with
fragmentation and release of the contents), karyolysis (complete dissolution of
the nucleus with loss of chromatin), swelling of cytoplasmic structures,
rupture of the plasma membrane, and the release of cytoplasmic elements into
the extracellular space, accompanied by a marked acute inflammatory
response (Fig. 4 ).
Necrosis of the epidermis can give rise to erosions with loss of the
superficial part of the epidermis, or to ulcers with complete loss of the
epidermis and part of the dermis.
Epidermal necrosis can be caused by the following:

Physical injuries caused by laceration, thermal burns, chemical burns, or
freezing.
Lesions resulting from ischaemia or infarction such as vasculitis,
thrombosis due to cryoalbumin disorders, proliferative thrombovascular
necrosis of the pinnae, or infarction caused by septic or sterile
thrombosis.
Poisonous stings or bites (spiders, snakes, or other agents).
04 Diffuse coagulative necrosis in the epidermis, with intensely eosinophilic material and marked
cellular exudate. Image courtesy of Dolors Fondevila.
ATROPHY OF THE EPIDERMIS

Atrophy of the epidermis involves a decrease in keratinocyte number and size
and can occur in response to hormonal imbalances (hyperadrenocorticism
[HAC] or topical corticosteroids), partial ischaemia, or severe malnutrition.
Usually it is accompanied by atrophy of the dermis, which results in very fine
skin, through which vascular structures are visible (Fig. 5 ).
05 Atrophic skin through which the subcutaneous vascularisation is visible.
ALTERATIONS IN THE EPIDERMAL FLUID

EQUILIBRIUM
Intercellular or intracellular accumulation of fluids can result in alterations in
the epidermal fluid equilibrium.
Intercellular fluid accumulation
Intercellular fluid accumulation in the space between cells is known as
epidermal oedema or spongiosis . Severe intercellular oedema is
characterised by the formation of spongiotic vesicles delimited or bordered
by the intercellular bridges (desmosomes) of keratinocytes. This type of tissue
reaction is frequent in cases of epidermal inflammation caused by
staphylococci and Malassezia .
Intracellular fluid accumulation

Intracellular fluid accumulation results in swelling of the cytoplasm of the
keratinocytes. In severe cases, swollen keratinocytes may explode, producing
microvesicles that are delimited by the walls of the fragmented cells
themselves.
Accumulation of intracellular fluid in the keratinocytes of the basal layer

results in the formation of vesicles, a process known as hydropic or vacuolar
degeneration , which is usually sufficiently severe to disrupt the homeostasis
of basal keratinocytes. Hydropic or vacuolar degeneration causes weakening
of the dermoepidermal junction, resulting in the formation of vesicles,
erosions, ulcers, and crusts due to the release of inflammatory mediators
together with fluid and cellular exudate, which dry on the surface and form
crusts. Erythema, depigmentation, and erosions may also be observed.
Examples of processes induced by this mechanism include lupus
erythematosus, dermatomyositis, and certain drug reactions.
The accumulation of intracellular fluid in the keratinocytes of the upper

layers, such as the stratum spinosum, gives rise to globular degeneration .
Affected cells acquire a swollen, balloon-like appearance, lose their
intercellular junctions, and form liquid-filled vesicles. This type of reaction
occurs in some viral processes, such as poxvirus infection, which infects
keratinocytes, causing lysis of cytoplasmic keratin and inducing the formation
and accumulation of large amounts of fluid in the cytoplasmic interior.
ACANTHOLYSIS
Acantholysis is a reaction associated with the destruction of the desmosomes
that bind keratinocytes (Fig. 6 ). It is usually a consequence of immune-
mediated aggressions (e.g. pemphigus) or neutrophilic enzymatic destruction
(as occurs in superficial pyoderma caused by staphylococci or, less
frequently, by Trichophyton spp.).
Depending on the cell layer in which the affected keratinocytes lie, the
following may be observed:
Acantholysis in the subcorneal epidermis, resulting in the formation of
pustules and subcorneal vesicles in which keratinocytes float (pemphigus
foliaceus).
Acantholysis in keratinocytes located above the basal stratum, which
separate the basal layer from the upper layers, as occurs in pemphigus
vulgaris. Fluid accumulation between the disconnected epidermal layers,
resulting in the formation of vesicles/bullae of varying sizes.
06 Acantholysis in different layers of the epidermis. Acantholysis in the (a) stratum granulosum
(subcorneal acantholysis), (b) stratum spinosum (subcorneal acantholysis), and (c) stratum
basale.
EXOCYTOSIS
Exocytosis describes the infiltration and accumulation in the epidermis of
leukocytes or erythrocytes from the dermis.
These inflammatory cells reach the epidermis when there is an inflammatory

focus in the dermis. Leukocyte migration from the superficial vessels to the
epidermis occurs via keratinocytes.
Leukocyte exocytosis is common in inflammatory processes. Typically,

neutrophils form pustules in the interior of the epidermis or the stratum
corneum, although other types of inflammatory cells can also be found,
depending on the type of cytokines involved in the development of the
cutaneous pathology. Identification of the types of leukocytes present can be of
great assistance in establishing the diagnosis of a process. Intraepidermal
eosinophils are associated with insect bites, while intraepidermal
lymphocytes can be observed in immune-mediated processes such as lupus
erythematosus and epitheliotropic lymphoma.
Other processes in which leukocyte exocytosis can be observed include

cutaneous infections by bacteria, Malassezia , or dermatophytes;
hypersensitivity reactions (atopic dermatitis or contact dermatitis); and
immune-mediated diseases such as pemphigus foliaceus or erythematosus
pemphigus.
Erythrocytes may also appear in the epidermis, usually resulting from trauma
or circulatory disorders such as vasodilation, vasculitis, or coagulopathies in
general.
THE DERMIS TO SKIN AGGRESSIONS
The dermis can respond to external aggressions via various mechanisms:
dermal atrophy, fibrosis, collagen alterations, and the deposition of amyloid
substances, mucin, or calcium. However, the most common response in dogs
is an inflammatory response, the nature of which can vary considerably.
Acute inflammatory dermatitis begins with hyperaemia (arteriolar

vasodilatation), oedema (due to increased vascular permeability), and
migration of leukocytes from the vessels of the dermis to the perivascular
zone. In this type of reaction, neutrophils predominate during the first 24 hours
and are replaced by macrophages (within 24–48 hours), although depending
on the type of reaction, mast cells (mediated by IgE), eosinophils, basophils,
and lymphocytes may also be observed (Fig. 7 ).
Chronic inflammatory dermatitis involves contact between the irritant agent

and the skin for weeks or months. The predominant inflammatory cells are
macrophages, lymphocytes, and plasma cells (Fig. 7 ). Chronic dermatitis is a
consequence of persistent infections or autoimmune reactions. Infections are
frequently associated with hypersensitivity reactions or the formation of
granulomas due to the presence of foreign materials in the skin, whereas in
autoimmune reactions autoantigens induce inflammatory immune responses
against certain tissues of the organism, as occurs in lupus erythematosus. The
most abundant cells in chronic dermatitis are macrophages which, in addition
to mediating phagocytosis, release abundant mediators that attack the affected
tissues, contributing to the maintenance of chronic inflammation and fibrosis.
When lymphocytes and plasma cells appear at the site of chronic
inflammation, they are interpreted as indicators of an immune response of the
patient.
The process by which acute inflammation of the skin becomes chronic is

highly variable and can be complicated by many factors, including self-
trauma, secondary bacterial infections, insect bites, and modulation of the
immune response by the patient or in response to treatment. Therefore, it is
difficult to reach a histopathological diagnosis based on this information.
However, based on many years observing the types of inflammatory response
associated with inflammatory skin diseases in dogs, the following histological
patterns have been defined, and constitute useful diagnostic support tools:
perivascular dermatitis, dermoepidermal junction dermatitis, nodular-to-
diffuse dermatitis associated with infectious agents, nodular-to-diffuse
dermatitis in the absence of infectious agents, and vasculitis (Fig. 8 ).
07 (a) Inflammatory cells in the dermis (based on Ackerman, 1999). (b) Cytology of
inflammatory cells.
08 Schematic showing the main inflammatory responses of the dermis. (a) Superficial
perivascular dermatitis with migration of lymphocytes from the vessels to the perivascular
dermis; (b) vasculitis in which leukocytes target the vascular walls and induce necrosis,
inflammation, thrombosis, and infarction; (c) dermoepidermal junction dermatitis with the
accumulation of inflammatory cells in the dermoepidermal junction, which may be cell-poor or
cell-rich, accompanied by vascular degeneration and/or apoptosis of cells of the basal layer; and
(d) nodular to diffuse dermatitis with or without evident microorganisms. Based on Hargis and
Ginn, 2012.
SKIN APPENDAGES
The most important pathophysiological response of skin appendages (hair
follicles and glands) is folliculitis or inflammation of the hair follicle. This is
classified based on the affected anatomical region of the hair and the type of
inflammatory cells involved (Fig. 9 ). The following types of folliculitis are
recognised: perifolliculitis, mural folliculitis, luminal folliculitis,
furunculosis, and bulbitis (inflammation of the hair bulb). Inflammation of the
hair follicles begins in the perifollicular blood vessels and proceeds through
the same phases as inflammation of the dermis. Clinically, folliculitis results
in the loss of hair from the affected areas.
Perifolliculitis, luminal folliculitis, and furunculosis usually occur in

sequence: when the inflammatory process that affects the follicle ruptures the
follicular wall, this gives rise to furunculosis, and the release of the follicular
content into the dermis. Next, depending on the characteristics of the content
scattered throughout the dermal tissue (bacteria, dermatophytes, parasites,
hair fragments, keratin, sebum, etc.), suppurative inflammation may develop,
subsequently evolving to chronic pyogranulomatous inflammation and
ultimately scarring.
Sebaceous adenitis is a specific inflammatory reaction that targets the

sebaceous glands. It is initially characterised by the accumulation of
lymphocytes around the ducts of the sebaceous glands. Subsequently, the
inflammation extends to all sebaceous glandular tissue, with the presence of
lymphocytes, neutrophils, and macrophages, in some cases resulting in the
complete disappearance of the glandular tissue. Chronic lesions are
characterised by the loss or atrophy of the sebaceous glands and epidermal
and follicular hyperkeratosis. Inflammation of the sebaceous glands secondary
to other processes such as folliculitis, demodicosis, uveodermatologic
syndrome, and leishmaniasis can also occur.
09 Microscopic inflammatory patterns in skin appendages. (a) Perifolliculitis with leukocyte

migration from vessels near the follicles to the perifollicular dermis. (b) Mural folliculitis, in
which inflammation is localised within the follicular wall. (c) Luminal folliculitis, in which
inflammatory cells invade the follicular lumen, and usually also infiltrate the follicular wall. (d)
Furunculosis due to rupture of the follicular wall and release of the contents into the surrounding
dermis. (e) Bulbitis or inflammation affecting the bulb or lower segment of the hair follicle. (f)
Sebaceous adenitis, in which the inflammatory infiltrate is located around the sebaceous glands.
Based on Hargis and Ginn, 2012.
THE ADIPOSE TISSUE
Panniculitis is the inflammation of the subcutaneous adipose tissue and can be
caused by infectious agents (bacteria and fungi), and immune-mediated
reactions (lupus erythematosus), physical damage (irritant injections, foreign
bodies, etc.), pancreatitis, and other indeterminate causes (Fig. 10 ).
Panniculitis can be primary or secondary (deep bacterial folliculitis). In dogs
with panniculitis palpation reveals the presence of nodules, usually with a
dorsal distribution, that may ulcerate and release oily and serohaemorrhagic
content. Panniculitis is classified based on the type of inflammatory cells
involved and the absence or presence of microorganisms: neutrophilic,
lymphocytic, granulomatous, or pyogranulomatous panniculitis.
10 Panniculitis. Ulcerated nodule releasing oily-looking serohaemorrhagic fluid.
CUTANEOUS CLINICAL PATTERNS

Clinical cutaneous patterns are the result of pathophysiological responses of
the skin to aggressions caused by different agents (Box 2 ). In the previous
section we described the wide variety of physiological mechanisms that can
be altered and the corresponding lesion types. Each type of microscopic
lesion on the skin of a dog is the consequence of one or more microscopic
mechanisms. Based on this knowledge, related lesions can be grouped under a
common denomination to define a clinical pattern.
To define the dermatological pattern corresponding to each case, it is
necessary to recognise the predominant lesion type displayed by the patient.
Thus, depending on the lesions observed, the following major patterns can be
defined:
Focal-multifocal alopecia pattern.
Regional or generalised symmetrical alopecia pattern.
Scaling/crusting and seborrhoeic pattern.
Erosive-ulcerative pattern.
Papulopustular and vesicular pattern.
Papulonodular pattern with fistulous tracts.
Pigmentary alterations.
A given clinical pattern can be the result of multiple causes, and a given cause
can give rise to lesions characteristic of more than one clinical pattern.
Therefore, for each pattern, it is important to prepare an ordered list of
differential diagnoses (see corresponding sections in the chapters on each
pattern type).
The characteristics of the most important clinical patterns are described

below, and are discussed in greater depth in subsequent individual chapters
(with the exception of the nodular pattern and pigmentary alterations).
BOX 2
FOCAL-MULTIFOCAL ALOPECIA PATTERN
The focal-multifocal alopecia pattern is characterised by the presence of foci
of alopecia of variable size, located in a single body zone (Fig. 11 ), or
distributed multifocally (Figs. 12 and 13 ). The appearance of foci of alopecia
indicates that the underlying cause affects the hair follicle or any level of the
hair structure, resulting in hair loss.
Although many agents can produce focal-multifocal alopecia (see Box 1 in
Chapter 3 ), the following are the most common:
Bacteria on the surface of the skin that produce bacterial folliculitis (Fig. 14
).
Overgrowth of Demodex (demodicosis).
Destruction of the cuticular structure of the hair by superficial pathogenic
fungi (dermatophytosis).
Much less frequently, injection site reactions to drugs (e.g. pipettes for flea
control, inoculation of vaccines, corticosteroids, or progesterone).
While in many cases the foci of alopecia may be accompanied by other

lesions, such as erythema, scales, or papulopustular lesions (Fig. 14 ), the
main pattern should be foci of alopecia.
11 Focal alopecia. Single area of alopecia located on the hindlimb.

12 Multifocal alopecia on the posterior third at the level of the pelvic limbs.
13 Multifocal alopecia. Foci of alopecia on the trunk, head, and limbs.

14 Foci of erythematous alopecia with papulopustular lesions.
SYMMETRICAL ALOPECIA PATTERN

(REGIONAL OR GENERALISED)
The most characteristic feature of the symmetrical alopecia pattern (regional
or generalised) is the symmetrical absence of hair in very large areas, both
within a given body region (Figs. 15 and 16 ) and over practically the entire
body of the dog (Fig. 17 ). Generalised alopecia can be the result of:
The continuous progression of focal-multifocal alopecia. Many of the
causes of focal-multifocal patterns can also give rise to generalised
alopecia.
Other alterations in the mechanism of hair formation and alterations in the
hair growth cycle (see Fig. 4 and Box 2 of Chapter 4 ). The main
processes involved in the development of symmetrical regional or
generalised alopecia are follicular dystrophies, endocrinopathies,
follicular arrest, and telogen effluvium and defluxion.
15 Symmetrical regional alopecia in the posteromedial area of the pelvic limbs.

16 Symmetrical regional alopecia in the neck area.
17 Generalised symmetrical alopecia in the dorsolateral area of the trunk.
SCALING/CRUSTING AND SEBORRHOEIC

PATTERN
The scaling/crusting and seborrhoeic pattern is characterised by the presence
of scales of different sizes and colours, and can affect specific body areas or
manifest as a generalised process (Fig. 18 ). This pattern is associated with
causes that affect the process of epidermal keratinisation (see Boxes 1 and 2
in Chapter 5 ). Alterations in this process, which lasts for about 4 weeks in
dogs, manifest as excessive flaking of the stratum corneum.
This pattern is one of the most difficult to classify as it is often complicated

by other types of lesions, such as alopecia, calluses, hyperkeratosis, erythema,
crusts, follicular casts, or oily-looking hair.
Confirmation of this pattern requires the identification of scales, crusts,

follicular casts, comedones, dry and dull hair, or oily skin and hair (Fig. 19 ).
Among the most frequent causes of the scaling/crusting and seborrhoeic
pattern are primary keratinisation defects of genetic origin, such as ichthyosis
or primary seborrhoea of Cocker Spaniels (vitamin A-responsive
dermatosis), autoimmune processes such as exfoliative lupus, internal
parasites such as leishmaniasis, neoplasias such as epitheliotropic cutaneous
lymphoma, and presentations with a pruritic component such as sarcoptic
mange, flea-bite hypersensitivity, atopic dermatitis, lice bites, and
cheyletiellosis.
18 Generalised dry seborrhoeic process in a dog with leishmaniasis.

19 Seborrhoeic dermatitis with an oily haircoat in a dog with atopic dermatitis.
EROSIVE-ULCERATIVE PATTERN
The erosive-ulcerative pattern is characterised by secondary erosions/ulcers,
resulting from a loss of continuity of the skin affecting either the layers of the
epidermis (erosions) or any level of the dermis (ulcers):
Erosions are circumscribed and depressed lesions of the epidermis that do
not penetrate the basement membrane separating this layer from the
dermis, do not bleed, and resolve without scarring (Fig. 20 ).
Ulcers are deep lesions that span the basement membrane and thus affect
both the epidermis and the dermis (Fig. 21 ). These lesions tend to bleed
easily and become encrusted in an initial attempt at resolution. If they do
not penetrate to the deep dermis they can resolve without scarring or
cause only mild scarring. When the ulcer affects the deepest part of the
dermis, the mechanism set in motion to resolve the lesion produces a very
obvious scar known as an eschar (Fig. 22 ).
Although a skin biopsy is required to adequately differentiate between

erosions and ulcers, this distinction is not essential in the clinic, since canine
skin is very thin and erosions easily progress to ulcers.
Erosions and ulcers may appear as a consequence of different internal factors,

such as leishmaniasis, severe inflammation, immunological reactions against
cutaneous structures, and ischaemic processes; or external factors such as
sunlight, chemicals, and thermal burns.
Ulceration can be the consequence of tissue infarction mechanisms in

occluded vessels, or of constriction caused by thrombosis, emboli,
cryoglobulin, or cryoglobulinaemia.
Ulcers can also develop in granulomatous nodules of various types, such as

those associated with deep mycoses, mycobacteria, or parasitic processes
such as leishmaniasis. The presence of nodules adjacent to ulcerated lesions
is usually indicative or suggestive of neoplastic or granulomatous processes.
20 Erosive lesion on the hindlimb caused by licking.

21 Ulcerated lesions in a case of squamous cell carcinoma.
22 Eschar. Depigmented scar.

VESICULAR PAPULOPUSTULAR PATTERN
The vesicular papulopustular pattern is characterised by the presence of
primary lesions consisting of raised papules, pustules, and/or vesicles. These
3 types of lesions can occur separately, in combination, or together with other
developing lesions, depending on the underlying cause.
The papulopustular form is the most common presentation (Fig. 23 ). The

papulovesicular form (Fig. 24 ) is highly labile, and complicates
identification of the primary lesion. To identify this form, it is advisable to
search for crusts within the area in which the vesicles initially developed.
Pustules are commonly observed in cases of bacterial pyoderma,

demodicosis, pemphigus foliaceus, and sterile pustular dermatitis.
Intraepidermal vesicular presentations are mainly observed in cases of

contact dermatitis, pemphigus vulgaris, and some drug reactions. The most
severe vesicular forms are those produced by lesions at the level of the
dermoepidermal junction (Fig. 25 ), as observed in bullous pemphigoid,
bullous epidermolysis, very severe erythema multiforme, and Shar Pei
mucinosis, and those associated with certain types of burns.
23 Papulopustular lesions.
24 Papulovesicular lesions.
25 Broad blistering lesions on the mucocutaneous junction of the lips.
NODULAR PATTERN
The nodular pattern is defined by the presence of nodules, which are raised
lesions on the surface of the skin of over 1 cm in diameter (Fig. 26 ). This
pattern can be caused by tumour processes affecting the skin and subcutaneous
tissue, which are beyond the scope of this book. As such, there is no specific
chapter dedicated to this particular pattern. However, the most relevant
information is summarised below. Box 3 shows the main causes of nodular
patterns.
Nodules are rounded lesions (Fig. 27 ), which can be ellipsoidal or

cauliflower-like (Fig. 28 ), and solid and cyst-like (Fig. 29 ) or oedematous.
Some nodules can be very similar in size to papules. For differential
diagnosis it is necessary to determine the depth of the lesion and whether it
can be easily palpated (a characteristic of nodules but not papules).
Nodules can extend to the epidermis, dermis, subcutaneous tissue, and muscle.
Based on composition and cellular characteristics, nodules are classified in 5
main groups: noninfectious inflammatory, infectious inflammatory, cystic,
neoplastic, and those lacking a cellular component. Of these, the most
important are inflammatory and neoplastic nodules. It is therefore fundamental
that clinicians know how to distinguish these 2 types of nodules based on
cytology.
26 Nodular lesions of varying sizes in a case of nonepitheliotropic cutaneous lymphoma.
BOX 3
Classification of nodular patterns
Sterile or aseptic inflammatory nodules

Septic inflammatory nodules (infectious processes)
Bacterial inflammatory nodules
Mycotic inflammatory nodules
Parasitic inflammatory nodules
Viral inflammatory nodules
Cyst-like nodules
Neoplastic nodules
Other types of nodules
27 Neoplastic nodules in the lateral area of the trunk.

28 Papillomatous nodule.
29 Cyst-like nodules in a Chinese Crested Dog.

Distinguishing between inflammatory and
neoplastic nodules
In inflammatory nodules, inflammatory cells predominate, and tissue cells are
scarce. The predominance of tissue cells is indicative of a neoplastic or
hyperplastic process. Occasionally, complex structures containing a mixture
of both inflammatory and tissue components may be observed. This can be
interpreted as an inflammatory process with secondary tissue activation, or as
a neoplastic process with secondary inflammation.
The following inflammatory cells should be identified in inflammatory

nodules: neutrophils (degenerate or nondegenerate), lymphocytes, plasma
cells, macrophages, giant cells, eosinophils, and mast cells.
In acute inflammatory processes, neutrophils predominate, accounting for

more than 70 % of the inflammatory cells. The presence of degenerate
neutrophils is very common in bacterial infections. The presence of
nondegenerate neutrophils does not mean that bacterial infection can be ruled
out, but can be indicative of other noninfectious inflammatory processes.
In chronic inflammation, neutrophils are accompanied by other cell types

(mainly macrophages, lymphocytes, plasma cells, and multinucleated giant
cells), which account for approximately 15 % of the total inflammatory cell
population. In very chronic processes multinucleated macrophages the size of
giant cells may be observed.
Epithelial and mesenchymal cells may undergo processes of hyperplasia and

activation in response to inflammatory processes, and thus may be confused
with neoplastic cells, which they resemble. To identify these cells, it is
necessary to determine whether the number of inflammatory cells is
significant relative to that of tissue cells (hyperplastic).
Noninfectious or aseptic inflammatory cutaneous nodules

Noninfectious or aseptic inflammatory cutaneous nodules are characterised by
large numbers of inflammatory cells and the absence of microorganisms. The
following types are described:
Foreign body reactions (Fig. 30 ). These are characterised by
pyogranulomatous inflammations with neutrophils, macrophages,
lymphocytes, plasma cells, eosinophils, mast cells, and in some cases, the
presence of hyperplastic tissue cells.
Nodules after vaccine inoculation. These are characterised by the
presence of predominantly mononuclear inflammatory cells, as well as
abundant bright, eosinophilic, and granular material inside or outside the
macrophages.
Sterile inflammation or necrosis of subcutaneous fat (panniculitis).
Panniculitis is characterised by the presence of inflammatory cells around
fat droplets and reactive mesenchymal cells with fusiform morphology. A
large number of cells may contain clear vacuoles in their cytoplasm.
Eosinophilic reactions. Characterised by large numbers of eosinophils
(generally >10 %), among other inflammatory cells. Occur in parasitic
granulomas and in hypersensitivity reactions. In some cases
mastocytomas are accompanied by an eosinophilic reaction.
Immune-mediated reactions (Fig. 31 ) . Nondegenerate neutrophils
predominate, and are accompanied by low numbers of other inflammatory
cell types (lymphocytes and plasma cells). Cytology is usually
insufficiently sensitive to diagnose these processes.
30 Inflammatory nodules caused by the presence of a spike between the digits.

31 Interdigital nodules in a case of allergic dermatosis.
Inflammatory nodules caused by infectious processes

In some cases the identity of the causative agent may be evident, while in
others it may be suspected based on the predominant cell types or the changes
induced in inflammatory cells. The following situations are described:
Common bacterial infections . Characterised by abundant degenerate
neutrophils and the presence of bacteria inside the neutrophils.
Infections with filamentous bacteria (e.g. Nocardia or Actinomyces ).
Associated with neutrophilic or pyogranulomatous reactions.
Mycobacteria. Give rise to granulomatous reactions in which macrophages
predominate. Cannot be stained using common stains, but leave a negative
space inside the macrophage.
Leishmania (Fig. 32 ). Gives rise to inflammatory reactions with a
predominance of mononuclear cells (plasma cells, macrophages,
histiocytes, or lymphocytes). Reactive hyperplasia of connective cells
may be observed, and amastigotes may be evident inside macrophages or
in the extracellular space.
Fungal infections . Granulomatous nodules secondary to fungal infections
are uncommon in Spain, but occur frequently in other geographic areas
(e.g. Brazil). This group includes cryptococcosis, blastomycosis,
histoplasmosis, sporotrichosis, and dermatophytic granuloma (Fig. 33 ).
Viral infections , such as papillomatosis.
32 Papulonodular lesions due to leishmaniasis.

33 Dermatophytic granulomas. Image courtesy of Amparo Ordúñez.
Cyst-like nodules
Cyst-like nodules include the following forms:
Follicular cysts. The cytology of follicular cysts is characterised by the
presence of abundant keratin (basophilic) and desquamated epithelial
cells, with few nucleated cells. Cytology does not allow distinction from
hair-follicle neoplasm.
Haematomas . Characterised by the presence of blood, macrophages, and
erythrophagocytosis. In certain images, haematomas can closely resemble
vascular neoplasms (haemangioma, haemangiosarcoma) in which
exfoliation of neoplastic cells has not occurred.
Seroma. Needle-puncture reveals the presence of a clear paucicellular
liquid, composed of mononuclear cells that resemble mesothelial cells.
Sialocele or salivary mucocele . Contains viscous fluid. Cells are large,
with abundant cytoplasm and many vacuoles (foam cells). Multinucleated
cells are commonly observed. Cytology revealing a combination of foam
cells and neutrophils is considered compatible with sialadenitis.
Hamartomas or nevi (Fig. 34 ) . These are congenital or acquired lesions
of the pilosebaceous unit or the dermis. They can have a collagenous,
vascular, follicular, or sebaceous component.
34 Hamartoma and follicular cysts. Image courtesy of Carlota Sancho.
Neoplastic nodules
Cutaneous neoplastic nodules can consist of:
Cells of different skin structures of epithelial origin (epidermis, hair
follicle, sebaceous glands, sweat glands), or originating from
mesenchymal tissue or melanin-producing cells.
Cells of the immune system of the skin such as histiocytes, macrophages,
lymphocytes, plasma cells, and mast cells.
Metastasis in the skin of noncutaneous neoplasms such as metastatic
mammary carcinoma.
Although histological classification is mainly based on the type of tissue from

which the neoplasm originates (epithelial, mesenchymal, melanocytic, or
unclassifiable), for veterinary surgeons it is much simpler to classify tumours
of the skin and subcutaneous tissue based on the shape of the cells observed in
cytology. Cytopathological classification is established based on cell
morphology as follows: round-cell neoplasms, epithelial-cell neoplasms,
spindle-cell neoplasms, and melanocyte neoplasms. Subsequently, neoplasms
are examined for signs of malignancy. However, cytology is not always
sufficiently sensitive to differentiate between hyperplasia and benign
neoplasia, between a benign neoplasm and a well-differentiated malignant
neoplasm, or between a neoplasm and a cyst. In many cases, histopathology
can be used to resolve these dilemmas. In any case, neoplastic nodules can be
classified based on cytology as follows:
Round-cell tumour nodules (Fig. 35 ) . These exfoliate large amounts of
cells. This group includes lymphosarcoma, histiocytoma, plasmacytoma,
transmissible venereal tumour, and mastocytoma.
Epithelial-cell tumour nodules (Fig. 36 ). The objective of cytology of this
type of nodule is to at least differentiate between glandular and
nonglandular nodules. Glandular epithelial-cell tumour nodules
(adenomas or carcinomas) form bulky groups of cells with vacuolated
cytoplasm. This group includes tumours of the sebaceous glands, perianal
glands, sweat or apocrine glands, and anal sacs. Nonglandular
epithelial-cell tumours include basal cell tumours, epithelial-cell
tumours of the intermediate layers, squamous cell carcinoma, and tumours
of the hair follicle (infundibular acanthoma or keratoacanthoma,
trichilemmoma, pilomatricoma, trichoblastoma, and trichoepithelioma).
Spindle-cell or mesenchymal-cell tumour nodules (Fig. 37 ). These
originate in the blood vessels, lymphatic vessels, nerves, erector muscles
of the hair, and adipocytes. This group includes fibroma, fibrosarcoma,
myxosarcoma, haemangioma, haemangiosarcoma, haemangiopericytoma,
angioleiomyosarcoma, angioleiomyoma, lipoma, liposarcoma, fibrous
histiocytoma, and anaplastic sarcoma.
Melanoma nodules (Fig. 38 ) . These correspond to tumours that originate
in melanocytes and include melanocytoma and melanoma. The most
important are melanomas, which can consist of epithelial cells, spindle
cells, or round cells. Diagnosis is established when melanin granulation
is observed.
35 Fine-needle puncture (FNP) cytology of a round-cell neoplasm (cutaneous mastocytoma).
Image courtesy of Sara Peña.
36 FNP cytology of an epithelial-cell neoplasm (adenocarcinoma of the perianal glands). Image

courtesy of Sara Peña.
37 FNP cytology of a mesenchymal-cell neoplasm (anaplastic sarcoma). Image courtesy of
Sara Peña.
38 FNP cytology of a melanocytic neoplasm (oral melanoma). Image courtesy of Sara Peña.
Other types of nodules

Nodules distinct from those described above include the following:
Accumulations of mineral products as occurs in circumscribed calcinosis or
calcinosis cutis.
Nodules with no cellular component (e.g. collagen masses).
Sebaceous hyperplasias, fibroanexal dysplasias, lipomatosis, nodular
dermatofibrosis, or apocrine cystomatosis.
The nodular pattern can also include carbuncles (Fig. 39 ), which are deep
necrotising forms of folliculitis with the accumulation of purulent material.
Also included in this pattern are abscesses , which are accumulations of
purulent material located at the deepest level of the dermis or subcutaneous
tissue, and are therefore not visible on the skin surface. The purulent content
is not visible from the surface of the skin. Abscesses usually begins as
folliculitis and are a manifestation of a cutaneous infection caused by
streptococci or staphylococci.
Fistulous sinuses or tracts are pathways that link a suppurative cavity in a

deep cutaneous zone with the surface of the skin, although pathways linking
abscess cavities (Fig. 40 ) or those linking cystic formations can also be
considered tracts.
39 Furunculosis and cellulitis.
40 Fistulous tracts in a German Shepherd with perianal fistulas.

PIGMENTARY ALTERATION PATTERN
While pigmentary alterations may appear to be primarily aesthetic in nature,
in some cases these alterations are the result of a genetic disorder that reflects
a systemic disease, an inflammatory reaction, or a genodermatosis. Other
factors that influence pigmentation include hormones, age, temperature and
inflammatory processes.
Hypopigmentation
Hypopigmentation is a decrease in the amount of melanin in the epidermis and
the superficial dermis. It occurs in response to a decrease in the number of
melanin granules in the cytoplasm of keratinocytes or melanocytes.
Hypopigmentation may be congenital or hereditary, and develops due to a lack
of melanocytes, deficient melanin production by melanocytes, or defects in the
transfer of melanin to keratinocytes (Box 4 ).
Hypopigmentation can also be acquired due to the loss of existing melanin or

the loss of melanocytes (depigmentation). Since copper is a component of
tyrosinase, and the production of melanin depends on this mineral, copper
deficiencies can lead to depigmentation.
Hypopigmentation can be observed postinflammation, in postnecrosis, in

cases of lupus erythematosus, epitheliotropic lymphoma, and
uveodermatologic syndrome (Fig. 41 ), and in vitiligo and albinism (Fig. 42 ).
BOX 4
Main causes of hypopigmentation
Congenital/hereditary
Oculocutaneous albinism
Piebaldism
Uveodermatologic syndrome
Vitiligo
Acquired
Nutritional imbalances (deficiencies in copper, zinc, proteins)
Immune-mediated reactions
Pemphigus complex
Allergic dermatitis of various types
Idiopathic (idiopathic hypopigmentation of the muzzle)
Leishmaniasis
Lupus erythematosus
Other forms of dermatitis with an inflammatory component
Trauma (burns, freezing, surgeries)
41 Uveodermatologic syndrome.
42 Albino dog.
Pigment incontinence
Pigment incontinence is a term used to denote the loss of the pigment melanin
from the basal cell layer of the epidermis or from the outer sheath of the root
of the hair bulb. This occurs when the cells of the basal epidermal layer or the
follicle are damaged, resulting in the loss of melanin from the superficial area
of the dermis or the perifollicular area, respectively, and its capture in
macrophages (Fig. 43 ).
Pigment incontinence can be a nonspecific lesion associated with

inflammation, but can also be indicative of a specific pathology damaging the
basal layer of the epidermis or the melanocytes, as occurs in lupus
erythematosus.
Perifollicular pigment incontinence can also be observed in processes in

which inflammation affects the follicular wall (e.g. demodicosis), or in
conditions involving abnormal growth of the follicular structure (e.g.
follicular dysplasia).
43 Microscopic image of pigment incontinence.
Hyperpigmentation
Hyperpigmentation is an increase in the amount of melanin in the epidermis or
the dermis. It is caused by the accumulation of melanin granules in the
cytoplasm of keratinocytes, and within macrophages and melanocytes of the
perivascular dermis. Hyperpigmentation is classified based on the extent of
the increases in the following parameters: the rate of melanosome synthesis,
melanosome size, the rate of melanocyte-to-keratinocyte transfer of
melanosomes, and melanosome survival inside keratinocytes (Box 5 ).
Hyperpigmentation due to an increase in the number of melanocytes occurs in

lentigo and in response to increased melanin production in chronic
inflammatory processes of allergic origin (Fig. 44 ) and endocrinopathies
(Fig. 45 ).
BOX 5
Main causes of hyperpigmentation
Congenital/hereditary
Lentigo
Nevus
Acquired
Cyclic alopecia
Alopecia X
Endocrinopathies
Neoplasms
Inflammatory processes
Demodicosis, dermatophytosis, pyoderma
Malassezia
Ultraviolet rays in alopecic dogs
44 Hyperpigmentation due to an allergic process.

45 Hyperpigmentation due to an endocrinopathy.
PRURITUS
In reality pruritus is not considered a clinical pattern. However, it is the most
common reason for dermatological veterinary consultations and therefore
warrants a chapter of its own. It is a predominant sign that can accompany any
of the aforementioned patterns, to the extent that any given pattern can be
characterised based on the presence of the defining lesions and the presence
or absence of pruritus.
Any clinical cutaneous presentation that has included pruritus since onset
should be considered a pruritic condition, based on which the appropriate
diagnostic protocol should be selected.
For a clinical pattern to be considered predominantly pruritic, it is necessary

to identify in the patient manifestations of pruritus other than mere scratching
(e.g. chewing, sucking, licking, or rubbing of the affected body part against
walls or furniture).
In these circumstances, it should be borne in mind that the most important
processes with which pruritus is associated are external parasitic diseases of
the skin and allergies. Other pathologies may present with pruritus, but it
should be possible to verify, using information from the patient’s medical
record, whether the pruritus developed after the initial appearance of other
lesion types.
In patients with pruritus it is important to note the body areas that the patient
scratches, as well as the intensity of pruritus, as this information is crucial
when determining the appropriate diagnostic protocol. Acute pruritic
presentations are characterised by the presence of erythematous lesions (Fig.
46 ), papules and scaling; while chronic conditions typically involve
lichenification and hyperpigmentation (Fig. 47 ).
46 Acute pruritic presentation of allergic origin with erythematous lesions.

47 Chronic pruritic condition with lichenification and hyperpigmentation.
INTRODUCTION
Focal or multifocal alopecia is a cutaneous condition characterised by the
appearance of hairless spots or coin-shaped areas (Fig. 1 ).
The loss of hair in foci is typically a consequence of an aggression, usually

inflammatory in nature, affecting the pilosebaceous units. Causes of follicular
inflammation leading to focal hair loss include infectious, parasitic, immune,
and traumatic processes. Focal alopecia can also be the result of vascular
problems, nutritional alterations, or neoplasia, although these causes are less
common.
Depending on the underlying pathophysiological mechanism, focal or multifocal

alopecia can be classified as true or false alopecia:
True alopecia: appears in response to an alteration of the hair shaft or loss of
the hair shaft from the follicle, as occurs when an agent directly damages or
attacks hair structures or affects the growth process.
False alopecia: appears when the hair shaft is broken by self-trauma. In this
case the hair is not lost, but the shaft is cut or fractured at the level of the
epidermis, where the follicular infundibulum ends. This occurs in any
pruritic process (Fig. 2 ).
True alopecia is a consequence of the action of agents that directly attack the
follicular unit, including infections, parasites, immune-mediated processes,
neoplasia, burns, trauma, or vascular pathologies. It can also be the result of
processes that cause inadequate or defective hair growth. Many of these causes
can be controlled, after which the hair will grow back normally. When the hair
follicle is not merely damaged, but the base of the follicle is also destroyed, this
gives rise to cicatricial alopecia, which prevents the regrowth of a new follicle
and results in permanent alopecia.
Hair grows in a systematic, orderly cycle, beginning with a growth (or anagen)
phase, followed by an intermediate or transitional (catagen) phase, a regression
or resting (telogen) phase, and finally, the exogen phase, during which hair is
lost (Fig. 3 ).
True alopecia is a consequence of infection, parasites, immune-mediated
processes, neoplasia, burns, trauma, or vascular pathologies.
The hair growth process can be affected by a lack of stimuli during the growth
phase or by prolongation or arrest of the catagen or telogen phases. On the other
hand, defective hair growth can be the result of intrinsic hair abnormalities
caused by defective genetic coding, giving rise to miniature and/or deformed
(dysplastic) hairs that are easily detached. Alterations in these mechanisms lead
to multifocal alopecia in early disease stages that evolves over time to diffuse
or generalised alopecia (see Chapter 4 for types of follicular alterations and the
factors involved in forming and regulating growth of the hair follicle).
01 English Bulldog with characteristic multifocal alopecia pattern induced by bacterial folliculitis.
02 Pruritic multifocal alopecia in a dog with atopic dermatitis.
03 Schematic showing the phases of the hair growth cycle. Any interference with the mechanism
of hair development and growth can give rise to alopecia, either focal, multifocal, or generalised.
The images in Figures 4 and 5 are practically identical How can

we distinguish true from false alopecia?
Simply ask the owner if the dog has pruritus. If the answer is no, this can be
confirmed by analysing the condition of the hair tips in a trichogram: intact
tips (Fig. 4 ) confirm the absence of pruritus and indicate a case of true
alopecia; if the tips are truncated or fractured (Fig. 5 ), it is likely a case of
false alopecia caused by pruritus.
04 Trichogram of a dog with multifocal alopecia in which the tips of the intact hairs are visible.
05 Trichogram of a dog with multifocal alopecia. The tips of the hairs located around the
alopecic areas are fractured.
UNDERLYING CAUSES OF THE PATTERN
Before examining a dog with focal or multifocal alopecia, it is helpful to
prepare a list of possible causes of this clinical pattern (Box 1 and Fig. 6 ).
BOX 1
Main causes of focal or multifocal alopecia patterns
Sebaceous adenitis1
Alopecia areata
Cicatricial alopecia
Cyclic alopecia1
Pattern alopecia
Traction alopecia
Drug-induced alopecia (corticosteroids, progestogens)
Postclipping alopecia
Postvaccinal alopecia
Demodicosis2
Dermatophytosis2
Familial dermatomyositis
Ischaemic dermatopathy
Zinc-responsive dermatosis
Follicular dysplasia/dystrophy1
Bacterial folliculitis2
Tail gland hyperplasia
Leishmaniasis2
Epitheliotropic lymphoma
Cutaneous lupus
Discoid lupus
Follicular arrest1
Pemphigus foliaceus
Pemphigus vulgaris
Vasculitis
1
Multifocal alopecia that can become generalised.
2
Very frequent presentation.
06 Schematic showing a hair follicle, in which the areas affected by some of the main causes of
canine focal and multifocal alopecia are indicated.
DIAGNOSTIC PROCEDURE
Having introduced the concept of the clinical pattern of focal or multifocal
alopecia, we will next consider the procedure to follow to determine the cause,
discussing the factors to be considered at each stage, and the interpretation
thereof.
To establish a definitive diagnosis of the process underlying focal or multifocal
alopecia, it is necessary to analyse the patient’s clinical history, perform general
and dermatological examinations, and finally, to propose a sequence of
diagnostic tests to rule out potential causes.
ANALYSIS OF THE MEDICAL HISTORY

The following are the most important factors to be considered when diagnosing
dogs with focal or multifocal alopecia.
Age. Diseases such as demodicosis (Fig. 7 ) and dermatophytosis (Fig. 8 )
are very common in young dogs (less than 1-year old). However, they can
also occur in geriatric (Fig. 9 a) or young adult dogs (Fig. 9 b) that have
any type of metabolic or infectious alteration, neoplasm, or endocrinopathy,
or have received immunosuppressive treatment for long periods. In most
young dogs, dermatomyositis (Fig. 10 ) is characterised by vascular lesions
and hair loss. Most cases of atopy occur in patients aged between 6 months
and 3 years, and present with bacterial folliculitis (Fig. 11 ).
Epitheliotropic lymphoma, which can be associated with alopecia (Fig. 12
), is observed in older dogs (generally over 7 years of age).
Sex. No differences in alopecic conditions are observed between males and
females.
Breed. Although focal or multifocal alopecia can affect dogs of any breed, as
well as mixed-breed dogs, certain processes have a marked genetic
component and are thus more common in specific breeds. Colour-dilute
follicular dysplasia affects breeds with dilute haircoats, including the
Poodle, Chihuahua, Chow-Chow, Doberman, Italian Greyhound, Great
Dane, Miniature Pinscher, Dachshund, and Yorkshire Terrier (Fig. 13 ).
Follicular dysplasia is also more common in breeds with long, curly
haircoats, such as Spanish and Portuguese Water Dogs (Fig. 14 ).
Other conditions for which a breed disposition is observed include
sebaceous adenitis in the Akita, Poodle (Fig. 15 ), Samoyed, and Viszla;
zinc-responsive dermatosis in the Siberian Husky and Alaskan Malamute;
pattern alopecia in Dachshunds (Fig. 16 ), and dermatomyositis in Long-
Haired Collies (Fig. 17 ), Beaucerons, and Shetland Sheepdogs, although
mongrels and other breeds can also be affected.
Other processes that can affect any dog show a higher incidence in
specific breeds. For example, demodicosis and idiopathic bacterial
folliculitis are more common in short-haired breeds such as the Boxer,
French Bulldog, English Bulldog, Carlino, Dalmatian, and Doberman.
Pruritus. It is important to determine whether the patient currently has
pruritus or has had pruritus at any stage during the evolution of focal or
multifocal alopecia, and if so, to note the severity thereof. Pruritus is not a
feature of true focal alopecia, except in cases involving infectious
processes such as demodicosis or dermatophytosis, in which mild pruritus
may be observed.
The presence of pruritus from the onset of the cutaneous process is
indicative of self-induced (false) alopecia. Severe pruritic presentations
are characterised by pruritus of an intensity of 8 to 10 on a scale of 1 to 10
(see Chapter 8 ), and are mainly caused by ectoparasites and allergies. By
contrast, pruritus in cases of true alopecia rarely exceeds an intensity of 2
to 3.
Diet . Dietary imbalances are practically nonexistent in dogs fed with
specific canine feeds. However, zinc-responsive dermatosis can occur in
dogs fed on inadequate diets rich in cereals, or in dogs receiving calcium
hypersupplementation, which can interfere with the intestinal absorption of
zinc.
It is necessary to check the qualitative composition of the diet of some
patients to determine whether the diet is balanced, and whether any dietary
imbalance may account for the patient’s alopecia.
Food intolerance is usually accompanied by pruritus, localised lesions,
and self-induced hair loss. Affected dogs may have a history of
gastrointestinal disturbances (diarrhoea, vomiting, loose stools, mucoid
faeces, etc.) associated with certain components of their diet.
Lifestyle . Jack Russells, Dachshunds, and other small-to-medium-sized
hunting breeds are predisposed to Trichophyton infections, given the ease
with which these breeds can access burrows and come into contact with
infected hedgehogs and small rodents.
Presence of lesions in other pets or in humans . The presence of lesions
(Fig. 18 ) in humans who have contact with a dog or in other pets with
whom the dog lives or is in contact with should raise suspicions of
dermatophytosis or infestation by ectoparasites such as fleas, Cheyletiella ,
or Sarcoptes .
Seasonality of alopecia. Some processes are characterised by alopecia with
some degree of seasonality, such as cyclic alopecia, which is associated
with changes in the photoperiod (Fig. 19 ). Some dogs display focal areas
of hair loss in the flanks during the winter months, but regrow hair with the
increase in daylight hours from spring to summer. Conversely, an inverse
seasonal trend may be observed in some dogs.
Hypersensitivity reactions. Dogs that are susceptible to hypersensitivity
reactions are predisposed to staphylococcal infections (Fig. 20 ), leading to
focal alopecia with a potential seasonal component, depending on the type
of allergen responsible for the hypersensitivity reaction. Thus, atopic
dermatitis due to seasonal aeroallergens (many types of pollen) and flea-
bite hypersensitivity can follow a course of focal alopecia due to
staphylococcal folliculitis, occurring mainly between March and June or
September (depending on the geographic area). Similarly, in cases of
recurrent pyoderma, relapses may occur during these same periods.
Vaccinations. The rabies vaccine is the vaccine most commonly implicated in
the development of alopecia, appearing between 2 months and 1 year after
vaccine administration (Fig. 21 ). Small and toy breeds, as well as those
with a white haircoat, appear to be more susceptible to alopecia.
The route of administration appears to be irrelevant, with vaccine-
induced alopecia observed regardless of whether the vaccine is inoculated
subcutaneously or intramuscularly. The resulting alopecia can be focal or
multifocal, with scaling, hyperpigmentation, erosions, nodules, crusts, and
cutaneous atrophy. Lesions can also develop far from the site of
inoculation.
Response to therapy. Certain conclusions can be drawn based on the type of
response observed in a patient that has been treated with antibiotics,
antimycotics, or glucocorticoids. Some immune-mediated pathologies such
as sebaceous adenitis or alopecia areata improve with glucocorticoid
treatment. Similarly, hypersensitivity presentations that are not complicated
with infections respond well to corticosteroid therapy. While processes
such as demodicosis, dermatophytosis, and bacterial folliculitis may
initially respond well to corticosteroid therapy, which controls the
inflammatory component of the process, the treatment response rapidly
worsens and the condition is exacerbated by continued treatment.
07 Six-month-old dog with demodicosis.
08 Eight-month-old dog with dermatophyte lesions.

09 Demodicosis in (a) a geriatric dog with hyperadrenocorticism and (b) a patient with
leishmaniasis.
10 Dermatomyositis in a 14-month-old mongrel dog.

11 Multifocal alopecia due to bacterial folliculitis in a Carlino with atopic dermatitis.
Hyperpigmented multifocal alopecia in a Boxer with cutaneous epitheliotropic lymphoma.

12
13 Multifocal alopecia that has become generalised in a case of colour-dilute follicular dysplasia.
14 General appearance of the haircoat of a Portuguese Water Dog with multifocal alopecia due to
follicular dysplasia. (a) General appearance. (b) Alopecia and changes in hair characteristics in
the affected areas (loss of curls and loss of hair) in the same patient.
15 Area of alopecia caused by sebaceous adenitis in a black-haired Poodle.
16 Pattern alopecia on the pinnae and multifocal alopecia on the lateral area of the trunk in a
Dachshund.
17 Alopecic and erythematous lesions in a Collie with dermatomyositis.
18 Foci of erythematous alopecia caused by dermatophytosis on the neck of the owner of a pet
with dermatophytosis.
19 Cyclic alopecia with confluence of multiple foci on the lateral areas of the trunk in a female
English Bulldog of 4 years of age.
20 Patient with a pruritic presentation of allergic origin accompanied by erythematous multifocal
alopecia.
21 Focal alopecia at the site of vaccine inoculation.
GENERAL EXAMINATION
Even in patients with a single focus of alopecia it is necessary to perform a
general physical examination. This is especially important in adult or geriatric
dogs, since focal alopecia in these animals is usually caused by overgrowth of
bacteria, Demodex , or dermatophytes in response to immunosuppression or to
metabolic or endocrine diseases (e.g. if hypothyroidism (HT) is suspected, it is
necessary to demonstrate bradycardia or testicular atrophy).
DERMATOLOGICAL EXAMINATION
Distribution of foci of alopecia

It is necessary to determine whether these foci are isolated or generalised, and
whether they are symmetrically distributed. Follicular dysplasia and follicle
growth arrest may initially present with multifocal alopecia that becomes
generalised over time. A detailed analysis of the haircoat will provide
indications to help distinguish localised alopecia from early manifestations of a
more generalised process.
Follicular dysplasia can develop slowly, with focal alopecia limited to the
flanks, or can rapidly progress to alopecia affecting large areas of the body.
Usually, unaffected areas remain normal, with good quality hair that is not easily
removed. Alopecia of endocrine origin can begin with focal or multifocal
alopecia of the flanks, but with deterioration of the quality of the surrounding
haircoat, which is dry, scaly, and easily plucked.
Alopecia areata causes hair loss in the facial area, as occurs in cases of
Trichophyton mentagrophytes infection (Fig. 22 ). In these processes, alopecia
is generally limited to the affected areas, and does not progress to other body
areas.
Atopic dermatitis and demodicosis can present with alopecia of the face and
digits. In these cases alopecia is induced by continuous rubbing, licking, or
chewing of pruritic areas, whereas in cases of demodicosis alopecia is the
result of follicular damage caused by the mite.
22 Symmetrical facial alopecia caused by Trichophyton mentagrophytes .
Determining whether alopecia is self-induced or true

In cases of false alopecia or self-induced alopecia, examination of affected
areas of skin reveals the presence of hair that looks like it has been poorly
clipped. Hair at the edges of the alopecic areas cannot be easily plucked. In
cases of true alopecia, alopecic areas contain no remnants of hair shafts and
hair in the peripheral areas can be easily plucked.
Type of hair and presence of lesions

Focal and multifocal alopecia are easily identified in short-haired dogs, but less
so in patients with long, dense haircoats. When alopecia is more diffuse, it is
useful to examine the accompanying lesions.
Absence of lesions. In cases of follicular dysplasia, follicular arrest, or
alopecia of endocrine origin, alopecia is not usually accompanied by other
lesions, and the skin is not usually erythematous or inflamed, except in
cases of complication due to secondary infections.
Epidermal collarettes (Fig. 23 ), papules, pustules, or crusts. These lesions
are indicative of bacterial infection, pemphigus foliaceus, or other
papulopustular processes.
Erythema and scaling. The presence of these lesions together with focal or
multifocal alopecia is cause to suspect an inflammatory process.
Pustules are very commonly observed (Fig. 24 ) in cases of autoimmune
pyoderma and dermatosis, but are not seen in all bacterial infections. For
example, the type of folliculitis that typically affects short-haired dogs is
characterised by alopecic foci distributed across the back, and is rarely
accompanied by primary lesions of infectious origin, such as pustules. Hair
in the affected areas is easily plucked (Fig. 25 ) and follicular casts may be
observed, as well as inflammation of the skin of the affected area,
suggesting an aggression of an infectious nature against the hair follicle.
The presence of these follicular casts can be indicative of follicular
bacterial infection, demodicosis, dermatophytosis, sebaceous adenitis, or
alopecia caused by arrest of the follicular cycle.
Comedones. These can be observed in cases of alopecia due to demodicosis
or dermatophytosis (Fig. 26 ), in endocrine processes (such as
hyperadrenocorticism or hypothyroidism), and following prolonged
corticosteroid treatment.
Comedones may be observed in cases of alopecia due to demodicosis or

dermatophytosis, in endocrine processes such as hyperadrenocorticism or
hypothyroidism, and following prolonged corticosteroid treatment.
23 Epidermal collarettes in a case of multifocal alopecia due to bacterial folliculitis.
24 Pustules in a case of pemphigus foliaceus.
25 Focus of alopecia caused by bacterial folliculitis. The hair at the periphery of the lesion is easily
plucked.
26 Comedones in a case of multifocal alopecia due to dermatophytosis. Image courtesy of Anabel
Dalmau.
Reversible and irreversible alopecia

The appearance of hair in the alopecic area will depend on the type of
inflammatory reaction, vasculopathy, or aggression in question, as well as the
extent of the lesions and the chronicity of the process.
Demodicosis. Most cases of alopecia due to demodicosis resolve fully. Mites
penetrate deep into the hair follicle, causing folliculitis. As the process
worsens, the follicular structures rupture, giving rise to furunculosis, with
very deep lesions that affect a large amount of hair. If these lesions progress
to eschars, there will be no possibility of hair regrowth in the affected
areas.
Dermatophytosis. Fungal hyphae fracture the hair shaft, but once the infected
hair enters telogen phase and is lost, the new hair that replaces it is usually
healthy.
Sebaceous adenitis. Destruction of the sebaceous glands induces follicular
hyperkeratosis and partial or total alopecia of the affected area. In
sebaceous adenitis, permanent alopecia can be prevented by quickly
controlling the process.
Alopecia areata . Activated lymphocytes attack the components of the follicle
and the hair bulb, resulting in loss of the hair shaft. This process is
reversible in most cases.
Irreversible alopecia. Irreversible forms of alopecia include congenital
alopecia, follicular dysplasia, colour dilution alopecia, and, in general, any
alopecia of genetic origin. For example, hereditary dermatomyositis of
Collies follows a course of follicular atrophy and perifollicular fibrosis in
many cases, with complete loss of the hair follicles (irreversible alopecia).
Irreversible alopecia can also be caused by deep bacterial pyoderma that
presents with furunculosis; burns; radiotherapy; or ischaemia that gives rise
to necrotising folliculitis with permanent destruction of the follicles and
cicatricial alopecia. Neoplasms that affect the dermis can directly destroy
hair follicles. Epitheliotropic cutaneous lymphoma (mycosis fungoides) can
cause alopecia due to the invasion of the follicular epithelium by neoplastic
lymphocytes.
DIAGNOSTIC PROTOCOL
To establish a definitive diagnosis of focal or multifocal alopecia, several
laboratory tests should be performed, in the following order:
STEP 1 Brushing and combing
Brushing of the patient’s hair can reveal the presence of large parasites, such
as fleas or Trombicula larvae, which can cause mechanical pruritus or
allergic itching accompanied by secondary bacterial folliculitis.
A fine-toothed comb should be used, paying particular attention to the
ventral area of the neck and trunk, as well as the dorsolumbar zone.
STEP 2 Deep and superficial skin scraping
This approach can be used to confirm or rule out the involvement of

microorganisms, particularly those of the genus Demodex (Fig. 27 ), and any
other mites that live on the epidermal surface.
Scraping is performed with a spatula or a scalpel blade that has been coated
in mineral oil to promote adhesion of the material. For superficial scrapings,
samples can be obtained by simply rubbing in the direction of hair growth
over the alopecic area. For deep scrapings, a fold of skin is held between
the index finger and thumb, and the skin squeezed while scraping in the
direction of hair growth until capillary bleeding is observed.
Considerations when performing a skin scraping

In cases of dogs with long hair, first clip the hair in the area to be
scraped.
Avoid scraping in ulcerated areas.
Scrapings should be performed in areas containing primary lesions,
such as papules or pustules.
A drop of mineral oil is placed on the spatula or scalpel blade and the
material obtained is immediately transferred to a slide and then
observed under an optical microscope at low magnification (4× or
10×).
27 Skin scraping samples in which (a) Demodex canis and (b) Trombicula autumnalis mites
are visible. Image (b) courtesy of Amparo Ortúñez.
STEP 3 Trichogram
This allows identification of the current phase of the hair growth cycle by
determining whether anagen or telogen roots predominate. Using this
technique, it is also possible to observe shafts showing structural alterations
or signs of invasion by fungal spores in the medulla and cortex (Fig. 28 ).
Lactophenol blue can be used to better visualise spores; affected hair shafts
are stained blue while healthy shafts remain unstained.
The accumulation of disorganised melanin in the roots and shafts is

indicative of follicular dystrophies associated with different colour
haircoats (Fig. 29 ). Hairs that resemble an exclamation mark are observed
in cases of alopecia areata .
Follicular casts (Figs. 30 and 31 ) are characteristic of a variety of follicular

processes, including demodicosis, dermatophytosis, sebaceous adenitis, and
some endocrine processes.
Tricography allows analysis of the status of the hair, revealing anomalies in

both the roots and the hair shaft, and enables distinction of true from false
alopecia based on examination of the tips.
28 Trichogram. Medulla and cortex of a hair shaft (upper part) that has lost its structure due to
invasion by fungal spores. In the lower part of the shaft the hair structure is normal.
29 Trichogram. Accumulations of melanin in the hair of a dog with hair-colour-associated

follicular dystrophy.
30 Trichogram. Follicular cast on the hair of a dog with follicular dystrophy.
31 Trichogram. Follicular casts in a dog with sebaceous adenitis.

STEP 4 Wood’s lamp
Greenish fluorescence allows visualisation of infestations caused by

Microsporum canis (Fig. 32 ), but not superficial mycoses produced by
other dermatophyte fungi.
32 A Wood’s lamp produces fluorescence of the haircoat of a dog infested with M. canis.
Wood’s lamp
Considerations when interpreting results

Preparation of the lamp. The lamp should be turned on at least 2
minutes before use to allow it to stabilise.
The examination should be conducted in a dark room, holding the lamp
5 to 10 cm from the skin surface.
Positive fluorescence is that which is visible on the shaft of the affected
hair.
False positives : topical products such as Vaseline, which emits violet
fluorescence; salicylic acid, which emits greenish fluorescence;
white clothing (robes, work overalls), which can produce bluish-
white fluorescence; scales, dandruff, or certain bacteria, such as
Pseudomonas aeruginosa and Corynebacterium ; and certain soaps.
False negatives: previous treatments with topical fungicides such as
povidone and captan.
STEP 5 Mycotic culture
Mycotic cultures should be performed using Sabouraud and DTM media

(Fig. 33 ) to accurately determine the dermatophytosis-causing agent,
regardless of the therapy to be applied.
Detection of fluorescence under a Wood’s lamp is insufficient to establish a

definitive diagnosis of dermatophytosis.
33 Mycotic culture in DTM medium in which M. canis growth is observed.

STEP 6 Surface and fine-needle puncture
cytology
The main objective of this technique is to identify bacterial agents and
inflammatory cells such as neutrophils (indicative of bacterial folliculitis).
Acanthocytes and neutrophils can also be observed in pemphigus-type
processes and neoplastic tissue cells in other situations.
STEP 7 Serological tests for leishmaniasis
Serological tests (quantitative ELISA) for the identification of seropositive

dogs with high levels of antibodies indicative of an active infection. These
tests are usually accompanied by serum protein analysis (see Chapter 4, Fig.
38 ).
STEP 8 Skin biopsy
A skin biopsy is performed after analysing the results of the aforementioned

tests, but not before. The biopsy results will complement the information
obtained in the basic analyses of follicular status (Fig. 34 ). A biopsy is
performed in the following circumstances:
When follicular casts are observed but neither Demodex nor
dermatophytes have been detected.
When a large number of telogen roots are observed, but the patient has no
history of effluvium and endocrine function is normal.
When shaft abnormalities, including pigmentary alterations, are observed.
When a neoplastic cause is suspected (e.g. epitheliotropic lymphoma).
When the process does not respond to conventional therapy.
To establish the definitive diagnosis when the proposed treatment is
potentially deleterious or very expensive.
Skin biopsy is performed after conducting the other tests.

34 Skin biopsy. Hyphae at the base of the hair follicle in a dog with dermatophytosis. Image
courtesy of Dolors Fondevila.
INTRODUCTION
Generalised or regional symmetrical alopecia describes a lack of hair or a
significant decrease in hair density in a particular region (trunk, facial area,
limbs, or abdomen) (Fig. 1 ), or across a broad area of the body (Figs. 2 and 3 )
of the dog. Generalised symmetrical alopecia is relatively common in canine
species.
The mechanisms underlying the development of this type of alopecia are

diverse, but almost all involve either alterations in the process of hair follicle
formation (Fig. 4 ), leading to atrophy and follicular dysplasia/dystrophy, or
slowing or arrest of the hair growth cycle (see Fig. 3, Chapter 3 ), which
remains in catagen or telogen phase.
Other biological processes that cause generalised symmetrical alopecia include

inflammation around the skin appendages (demodicosis, dermatophytosis [Fig. 5
], sebaceous adenitis, generalised vasculopathies affecting the entire haircoat,
cutaneous filariasis, and self-trauma [Fig. 6 ]). Self-trauma will not be
discussed in this chapter, as it is included in the diagnostic protocol for pruritus.
01 Symmetrical alopecia in the lateral region of the trunk.
02 Generalised symmetrical alopecia due to vasculopathy.

03 (a) Dog with alopecia areata universalis. (b) Appearance of the facial area. Images courtesy
of Pedro Ginel.
04 Structure of the hair follicle of the dog: (a) longitudinal section; (b) sagittal sections. Based on
Paus and Peker, 2004.
05 Alopecia of the facial region due to infection with the dermatophyte T. mentagrophytes and
vasculopathy.
06 Self-induced symmetrical alopecia caused by Sarcoptex scabiei .
FACTORS INVOLVED IN HAIR GROWTH AND

FORMATION
The hair follicle is a discrete cutaneous unit and the only structure in mammals
that is continuously regenerated in a cycle consisting of phases of growth
(anagen), regression (catagen), rest (telogen), and hair loss (exogen). The
relative duration of each phase of the hair cycle varies depending on breed, age,
sex, and body region. Hair growth of domestic carnivores is asynchronous
(different follicles are in distinct growth phases at a given moment). It has been
proposed that hair grows continuously in certain breeds, such as the Poodle,
Bobtail, and Schnauzer, although this has not been scientifically proven.
This cycle is controlled by an “intracutaneous clock”, which induces changes in

local signalling mediated by intrinsic factors involved in hair cycle regulation.
This cycle is also regulated by systemic regulatory factors specific to the
organism (endocrine, neuronal, nutritional, and vascular factors) whose
activities affect not only the hair but also the skin as a whole (vascularisation,
immunological reactions, cutaneous architecture, and cell proliferation).
External factors, such as changes in ambient temperature, photoperiod, and
nutrition, also influence hair follicle development (Box 1 ).
BOX 1
Factors involved in hair follicle structure and development
Intrafollicular intrinsic factors

These affect the stem cells, the dermal papilla, the fibrin sheath, and the
follicular matrix.
Cytokines
Growth factors
Signal transduction molecules
Adhesion molecules
Proteases and their inhibitors
Receptors
Extrafollicular intrinsic factors
These affect the connective and adipose tissues.
Neurogenic stimuli
Inflammatory reactions
Vascular reactions
External factors
Season
Photoperiod
Nutrition (essential fatty acids, vitamins A and D, zinc)
Circadian rhythm
Room temperature
Systemic factors (specific to the individual)
Affect the immune system, endocrine system, and nervous systems.
General health status
Stress
Hormones:
Androgens
Cortisol
Oestrogens
Growth hormone (GH)
Melatonin
Prolactin
Proopiomelanocortin
Thyroxine
Genetic influences
These include the following factors:

Genetics . The growth period and length of the hair are genetically
predetermined. The texture and length of the haircoat are encoded by a
combination of 3 genes: FGF-5, RSPO2 , and KRT71 . Haircoat colour is
determined by another 3 genes: Mc1r , Agouti , and CBD103 .
Predominance of the Mc1r or Agouti genes results in predominantly black
and yellow haircoats, respectively. Coat colour dilution is an autosomal
recessive trait, characterised by defective melanosome transport, which
produces large pigment aggregates within melanocytes. This defect is a
consequence of a mutation in the melanophilin (MLPH) gene that affects
colouration but does not cause alopecia.
Photoperiod . The hair cycle is controlled mainly by photoperiod,
environmental temperature, nutrition, hormones, health status, and genetic
factors. Follicular activity peaks during the summer (50 % of follicles in
anagen phase), and is at its lowest in winter (10 % of follicles in anagen
phase).
Dogs exposed to artificial light for many hours can shed intensely throughout the
year.
Feeding. Because hair contains a significant amount of protein, nutrition has

an important influence on hair quality, with nutritional defects resulting in
dull, dry, or brittle hair.
Systemic processes . Systemic disease or stress can shorten the anagen phase
and cause a large proportion of follicles to synchronously enter telogen
phase. These processes can give rise to transient alopecia or telogen
defluxion (see Fig. 3, Chapter 3 ).
In general, the factors that control follicular structure differ to those that control
the hair cycle. Alterations in factors that control follicular structure result in
follicular dysplasia or follicular atrophy, while alterations in factors that affect
the follicular cycle lead to endocrine alopecia, follicular arrest, and telogen
effluvium or defluxion.
Alterations of the follicle (that result in shedding of the hair) can be divided into
3 types:
Structural alterations . In the anagen phase, the hair bulb produces hair
shafts from the keratinocytes of the hair matrix (one of the fastest
proliferating populations of cells in mammals). In the precortical hair
matrix, above the dermal papilla, these cells initiate their terminal
differentiation into trichocytes and receive melanosomes from the
melanocytes of the pigment unit of the hair follicle to pigment the hair shaft.
Pigmentary alterations . The melanocyte is the pigmentary unit of the hair
follicle. Melanocytes produce melanin and are located above and around
the proximal third of the follicular dermal papilla; they transfer
eumelanosomes and pheomelanosomes to keratinocytes in the precortical
matrix of differentiating hair follicles, which undergo apoptosis during each
catagen phase.
Alterations in the hair follicle growth cycle. From the morphological point
of view, transformation of the hair follicle involves a repeated sequence of
phenotypic changes of the follicle that follows a genetically encoded
mechanism, consisting of the telogen phase, 6 stages in the anagen phase (I–
VI), and 8 stages in catagen phase (I–VIII).

Box 2 lists the many potential causes that can be included in the list of
differential diagnoses in a case of generalised symmetrical alopecia. However,
this list can be narrowed down significantly based on the breed in question
(Box 3 ) and the patient’s medical history.
BOX 2
Main causes of generalised or regional symmetrical alopecia
ALOPECIA PRESENT AT BIRTH

X-linked canine follicular dysplasia
Congenital hypotrichosis
Ectodermal defects or dysplasias accompanied by dental dysplasia
Ectodermal defects or dysplasias not accompanied by dental dysplasia
Alopecic dog breeds
ALOPECIA OF ENDOCRINE ORIGIN IN ADULTS

Pituitary dwarfism
Hyperadrenocorticism
Hyperoestrogenism in male (Sertoli-cell tumour) and female (ovarian
tumours or cysts) dogs
Oestradiol-induced hyperoestrogenism caused by contact with
transdermal gel for human use
Hypothyroidism
ALOPECIA OF NONENDOCRINE ORIGIN IN ADULTS
Self-induced1
Pruritus of parasitic origin (Cheyletiella , lice, Sarcoptes )
Pruritus of allergic origin
Atopic dermatitis, food hypersensitivity
Insect-bite hypersensitivity
Contact hypersensitivity
Infectious2
Demodicosis
Dermatophytosis
Leishmaniasis
Immune-mediated2
Alopecia areata universalis
Sebaceous adenitis
Dermatomyositis
Nutritional origin
Follicular dysplasia (structural defects in follicle formation)

Follicle destruction: cicatricial alopecia (eschar)
Hair-colour-associated follicular dysplasia
Alopecia due to colour-dilute follicular dysplasia
Alopecia due to dark-hair (black or brown) follicular dysplasia
Alopecia due to follicular dysplasia in black and tan Dobermans
Follicular lipidosis of mahogany-coloured hairs in Rottweilers
Alopecia associated with melanoderma in Yorkshire Terriers
Follicular dysplasia unrelated to hair colour
Alopecia X caused by follicular arrest3
Recurrent alopecia3
Follicular dysplasia associated with specific breeds
Follicle miniaturisation: pattern alopecia
Pattern alopecia of the pinnae
Pattern alopecia of the nasal bridge
Pattern alopecia of the ventral area
Structural defects of the hair shaft

Spiculosis
Twisted hair or pili torti
Trichorrhexis nodosa
Trichoptilosis
Medullary trichomalacia
Abnormalities in the hair growth cycle

Cyclic or recurrent alopecia3
Postclipping alopecia
Alopecia X due to follicular arrest3
Anagen effluvium
Telogen effluvium
Excessive shedding
Alopecia due to mechanisms of vascular origin

Vasculitis
Ischaemic dermatopathies
Familial canine dermatomyositis of Collies
Juvenile-onset ischaemic dermatopathy in other breeds
Ischaemic dermatopathy of adult dogs
Ischaemic dermatopathy secondary to rabies vaccine
Familial cutaneous vascular disease of German Shepherds
1
Self-induced forms of alopecia are treated in cases of pruritic presentations.
2
Inflammatory processes are implicated in the associated pathogenesis.
3
Presentations that include features corresponding to several of the causes listed in this classification.
BOX 3
Clinical presentations and breeds predisposed to generalised
symmetrical alopecia
Clinical presentation Predisposed breeds
Cyclic or recurrent Airedale Terrier, Bearded Collie, Bouvier

alopecia (flanks) de Flandres, Boxer, French Bulldog, English
Bulldog (Fig. 7 ), Dogue de Bordeaux (Fig.
8 ), Golden Retriever, and Labrador
Retriever
Pattern alopecia pattern Boston Terrier, Chihuahua, Greyhound,

with ventral distribution Miniature Pinscher, Dachshund, and
Whippet
Pattern alopecia of the Chihuahua, Greyhound (Fig. 9 ), Pinscher,

ears and Dachshund (Fig. 10 )
Sebaceous adenitis Akita Inu, Poodle, Belgian Shepherd,

Border Collie, Chow-Chow, Springer
Spaniel, German Shepherd, and Samoyed
Alopecia X or follicular Alaskan Malamute (Fig. 11 ), Miniature

arrest Poodle, Chow-Chow, Siberian Husky (Fig.
12 ), Keeshond, Pomerano (Fig. 13 ), and
Samoyed
Colour-dilute follicular Bull Terrier, Poodle, Chihuahua, Chow-

dysplasia Chow, Doberman, Italian Greyhound, Great
Dane, Münsterländer, Bernese Mountain
Dog, Scottish Shepherd Dog, Pinscher (Fig.
14 ), Saluki, Schipperke, Silky Terrier,
Staffordshire Bull Terrier, Dachshund,
Newfoundland Dog, Whippet, and Yorkshire
Terrier (Fig. 15 )
Black-hair dysplasia Basset Hound, Beagle, Bearded Collie,

Border Collie, American Cocker, Jack
Russell Terrier, and Yorkshire Terrier (Fig.
16 )
Follicular dysplasias of Airedale Terrier, Boxer, French Bulldog,

specific breeds English Bulldog, Doberman, Greyhound,
Golden Retriever, Wirehaired Pointing
Griffon, Siberian Husky, Alaskan Malamute,
Manchester Terrier, Portuguese Water Dog
(Fig. 17 ), Irish Water Spaniel, Miniature
Pinscher, Staffordshire Bull Terrier, and
Terrier
Hyperadrenocorticism Most common in small breeds such as

(HAC) Maltese (Fig. 18 ), Poodle, Dachshund, and
Terrier
Hypothyroidism (HT) More common in medium-to-large breeds,

such as the Labrador Retriever (Fig. 19 )
Congenital hypotrichosis Basset Hound, Beagle, Maltese, French

Bulldog, Poodle, Chihuahua and its crosses,
American Cocker Spaniel, Labrador
Retriever, Lhasa Apso, German Shepherd,
Belgian Shepherd, Rottweiler, Whippet, and
Yorkshire Terrier
Follicular lipidosis Rottweiler (mahogany-coloured hairs) and

hairless breeds: Chinese Crested Dog (Fig.
20 ), Mexican Hairless Dog (Fig. 21 ), and
Peruvian Hairless Dog
Based on Paradis, 2012.
07 Cyclic alopecia in an English Bulldog. Hair loss and hyperpigmentation in the dorsal region.
08 Cyclic non-hyperpigmented alopecia in a Dogue de Bordeaux.

09 Pattern alopecia on the ears of a Greyhound.
10 Pattern alopecia on the ears of a Dachshund.

11 Alopecia X and hyperpigmentation in an Alaskan Malamute.
12 Alopecia X and hyperpigmentation in the neck region.

13 Alopecia X in a German Spitz (Pomeranian) of 5 years of age.
Alopecia due to colour-dilute follicular dysplasia in a Pinscher.

14
15 Colour-dilute follicular dysplasia in a Yorkshire Terrier.
16 Alopecia due to black-hair follicular dysplasia of in a Yorkshire Terrier.

17 Follicular dysplasia in a Portuguese Water Dog.
18 Alopecia and hyperpigmentation due to HAC in a Maltese.

19 Generalised symmetrical alopecia due to hypothyroidism (a and b).
20 Chinese Crested Dog. Hairless breed.

21 Mexican Hairless Dog. Hairless breed.
To identify the cause of a case of generalised symmetrical alopecia, we begin
by analysing the characteristics of the patient and the information in their
medical history, and perform a general physical examination as well as a
dermatological examination. This is followed by a series of laboratory tests,
carried out in 8 steps.

In cases of generalised symmetrical alopecia, the following basic
characteristics of the dog should be considered: age, sex, breed, and body
weight and conformation. Next, an anamnesis is performed in which the medical
history is examined in order to answer all of the following questions:
How old was the dog when hair loss began?
Are any of the dog’s siblings or relatives affected?
Are any other animals or humans affected?
Does the dog show signs of pruritus in the alopecic areas?
In what region of the body was hair loss first observed?
To what extent does the alopecia extend?
Does the alopecia advance and then recede, or has it progressed continuously
since the beginning?
Does the severity of the alopecia change with the seasons?
Is any information available about previous diseases or signs of systemic
disease?
Has the dog recently lost blood, undergone surgery, or become pregnant?
Has the dog been recently vaccinated?
What medication is the dog receiving routinely or periodically?
Has the dog received any medication in the last few weeks?
Are the vector diseases in the area well controlled?
The following are the main factors that can influence this dermatological
pattern.
Age . Several pathological processes associated with generalised
symmetrical alopecia are known to have a very characteristic age of onset.
Alopecia that is present from birth or develops within the first few weeks
of life is considered congenital. Follicular dysplasias begin to manifest
around 6 months of age and demodicosis around 1 year of age (Fig. 22 ).
Follicular arrest (alopecia X) and cyclic alopecia appear for the first time
between 2 and 4 years of age, and gradually worsen. Endocrine processes
include hypothyroidism (HT), which can occur from the age of 5,
hyperadrenocorticism (HAC), which can develop from around 8 or 9 years
of age, and gonadal imbalances, which appear from 10 years of age (Fig.
23 ). Vasculitis due to alopecia or ischaemic vasculopathy (Fig. 24 ) can
begin at any age, depending on the underlying cause (immune-mediated
reactions, drugs, vaccines, secondary infections, or blood parasitoses such
as babesiosis). In general, alopecia of endocrine origin appears for the first
time in adult or geriatric dogs (except in cases of pituitary dwarfism or
congenital pathologies), while nonendocrine alopecia usually develops in
dogs of less than 2 to 4 years of age, particularly those of several weeks or
months of age.
Regardless, it is important to clearly identify the age of onset of alopecia and
determine whether this was preceded by any physiological (gestation, lactation)
or pathological event (postsurgical shock), or any changes in management or
treatment.
Breed and hair colour . Breed can significantly aid orientation of the
diagnosis from the very beginning, since there are many processes specific
to certain breeds (Box 3 ), which are predisposed to certain alopecic
conditions due either to the characteristics of their haircoat or the genetic
component involved.
Doberman and Rottweiler. The colour of affected hair, within a
particular breed, is a determining factor. In general, most common
causes of alopecia can affect any type of hair. However, some
processes only affect hair of a particular colour, in specific breeds.
Accordingly, it is important to carefully evaluate hair colour (some
diluted hair colours can be very subtle). Examples include colour-
dilution alopecia of the blue-haired Doberman and black-hair
follicular dysplasia and follicular lipidosis of Rottweilers (which
only affects mahogany hairs).
Nordic breeds or those with haircoats consisting of large amounts of
secondary hairs. The hair growth cycle in these breeds can be longer
than in others, and hair growth can cease or slow down after clipping
(for 6, 12, or even 24 months) due to changes in the vascular perfusion
of the alopecic area in response to alterations in skin temperature
caused by the lack of hair. Similar arrest or slowing of hair growth in
other breeds is reason to suspect HT, HAC, or alopecia X.
Reproductive disorders. Generalised symmetrical alopecia may be
accompanied by sexual alterations. These alterations can be the direct
cause of alopecia, or may constitute clinical signs that suggest a common
cause underlying both manifestations. These include:
Absence of oestrous cycle (prolonged anoestrous) in females: due to
gonadal or endocrine abnormalities, such as HT or HAC.
Signs of feminisation in males (attraction to other males, pendulous
prepuce, or gynecomastia): indicate hyperoestrogenism (HE).
Abnormalities in secondary sexual characteristics: due to a hormonal
imbalance of gonadal (Fig. 25 ), thyroid, or adrenal origin. In patients
of over 10 years of age, an increase in the size of the vulva in the
absence of other clinical signs in females, or an increase in the size of
the foreskin and mammary glands accompanied by the appearance of
an erythematous line along the prepuce in males (Fig. 26 ), are strong
indicators of HE (caused by a Sertoli-cell tumour or ovarian cysts or
tumours). In male HE, the most obvious systemic signs are bone
marrow aplasia and squamous metaplasia of the prostate, both of
which can significantly facilitate diagnosis.
Other systemic disorders . Polyuria-polydipsia and polyphagia orient the
diagnosis towards HAC. On the other hand, apathy, a “sad” facial
expression with puffy features, and bradycardia (Fig. 27 ) may be
indicative of HT.
Stress or anxiogenic situations. This can lead to follicular arrest and abrupt
shedding of all the hair on the body, a process known as telogen effluvium,
which usually occurs after gestation, lactation (Fig. 28 ), serious illness,
febrile systemic disease, postsurgical shock, or any other stressful situation
to which the animal has been exposed in the preceding 1 to 3 months. The
development of compulsive behaviours can lead to self-trauma and
alopecia affecting a specific body region, such as the hindlimbs or
forelimbs.
Lifestyle . Dogs living in rural areas or houses with open gardens, where
they can come into contact with other uncontrolled dogs or cats, are at
greater risk of infection by dermatophytes or via bites of vectors that
transmit diseases such as leishmaniasis (Fig. 29 ), babesiosis, or
rickettsiosis. Dogs living in the Mediterranean basin are also more likely to
contract leishmaniasis, while those living above the 45th parallel north
(e.g. Belgium, the Netherlands, the United Kingdom, Scandinavia, and
Canada) are more predisposed to recurrent or cyclic flank alopecia caused
by the greater variation in photoperiod. Walking dogs in groups can favour
the spread of dermatophytes or external parasites that can give rise to self-
induced alopecia caused by pruritus. Repeated aggression in a given area
ultimately results in inflammatory cicatricial alopecia, as commonly seen in
cases of traction alopecia in the parietal region in Yorkshire Terriers.
Presence of lesions in pets or humans. As in the case of the focal or
multifocal alopecia pattern, the presence of lesions in humans and/or pets
that live with the dog is cause to investigate the presence of dermatophytes.
Areas affected by alopecia . Some forms of alopecia affect well-demarcated
regions, such as the pinnae (pattern alopecia), the face or head (alopecia
areata ), medial/lateral areas of the trunk (cyclic alopecia), or areas of the
haircoat consisting of hair of a certain colour. Endocrine alopecia
predominantly affects the trunk, without affecting the limbs of head.
Nonendocrine alopecia affects both the trunk and limbs, and in some cases
the head.
Pruritus . The presence of pruritus in alopecic presentations requires careful
analysis. Careful questioning of the owner is required to determine as
accurately as possible whether the dog scratches or not, and if so, whether
this behaviour began before or after the onset of alopecia. If the scratching
preceded the alopecia, it is highly likely that the alopecia is pruritic in
nature, and the diagnostic protocol should be oriented towards pruritic
causes (see Chapter 8 ). However, if pruritus developed during the
evolution of the alopecic process (i.e. during or after hair loss), it is
considered the result of inflammatory lesions secondary to alopecia.
Examples include bacterial complications of alopecia due to HT or HAC,
generalised demodicosis, and follicular dysplasias. Pruritus may also be
secondary to hypersensitivity reactions that develop during
dermatophytoses.
Seasonality, remission, and progression. Reappearance of alopecia during
autumn and winter, after spontaneous remission in spring and summer, is
generally indicative of recurrent flank alopecia. Spontaneous remission
also occurs in cases of anagen defluxion, telogen defluxion, and
postclipping alopecia that is not secondary to an endocrinopathy.
Spontaneous regrowth (of white hair) may also be observed in cases of
alopecia in Portuguese Water Dogs and in alopecia areata . Stress-induced
alopecia develops abruptly, and after 2 to 3 months the hair begins to grow
diffusely, returning to normal levels without the need for treatment.
Follicular dysplasias progress gradually. However, after the loss of hairs
affected by the genetic defect in question, the dysplasia resolves and the
alopecia becomes definitively established. Alopecia of endocrine origin
develops and progresses continuously, eventually affecting the entire
haircoat, unless the hormonal imbalance is resolved. Although the clinical
signs associated with HAC may vary in severity, the corresponding
alopecia does not resolve spontaneously. Similarly, alopecia associated
with inflammatory processes tends to be progressive, without intermittent
remission.
Vaccinations. Vaccination in the preceding weeks or months may cause
postvaccinal alopecia due to vasculopathy.
Response to previous treatments. By the time they arrive at the clinic for a
dermatological consolation, many patients with alopecia have already been
treated with systemic antibiotics, corticosteroids, antimycotics, or
antiparasitics. Analysis of the patient’s response to these compounds can
provide information relevant to the diagnosis. For example, excessive
administration of corticosteroids promotes the development of iatrogenic
Cushing’s syndrome (HAC) and favours exacerbation or spreading of the
condition in cases of alopecia caused by demodicosis or dermatophytosis.
Subcutaneous inoculation of corticosteroids or of progestins is usually
responsible for the appearance of iatrogenic alopecia and skin atrophy.
Oestrogens and cytotoxic drugs, such as cyclophosphamide or doxorubicin,
interfere with the hair growth cycle and can give rise to diffuse generalised
alopecia, hypotrichosis, or complete generalised alopecia.
22 Generalised alopecia in a 9-month-old English Bulldog with demodicosis.

23 Bitch with hyperoestrogenism with visible comedones.
24 Generalised symmetrical alopecia due to vasculopathy.
25 Hyperoestrogenism in an 11-year-old female. Note hypertrophy of the vulva and mammary
glands and diffuse hyperpigmentation.
26 Hyperoestrogenismin a 10-year-old male Poodle. Note ventral alopecia and the appearance of
the testicles.
27 Cocker Spaniel with hypothyroidism. Note the involvement of the facial area, which is puffy and
lends the dog a “sad” expression.
28 Telogen effluvium in a lactating female.

29 Generalised symmetrical alopecia in a dog with leishmaniasis.
GENERAL EXAMINATION
We will first look for systemic clinical signs such as polyuria-polydipsia,
pendulous abdomen, puffy facial features, and abnormal genitalia (e.g.
pendulous prepuce, swollen vulva, gynecomastia or larger-than-usual mammary
glands, the presence of an erythematous line on the prepuce, testicular
asymmetry, monorchidism, or cryptorchidism). If these signs are detected,
specific tests should be conducted to detect the presence of an endocrinopathy.
After performing a general examination the alopecic areas should be carefully
examined and their location indicated on a silhouette to provide a clear
overview of the distribution of the alopecia, indicating whether it is
symmetrical, generalised, regional, or diffuse, and whether it is accompanied by
other lesions.
The first aspect to evaluate is skinfold thickness. An increase in this parameter,
together with hyperpigmentation, is indicative of HT, while a decrease,
accompanied by hyperpigmentation, is indicative of HAC and HE. Deposits of
calcium along the dermal collagen fibres (calcinosis cutis) are characteristic of
spontaneous and iatrogenic HAC, and should be noted.
The most common lesions that accompany alopecic conditions include

erythema, papulopustules and collaretes, follicular casts, scales, comedones,
and pigmentary alterations.
Common lesions in generalised asymmetrical alopecia

Erythema. This is the most common sign of allergic dermatitis. In dogs with
this clinical sign, the presence of pruritus should be assessed, since pruritus
would indicate a high probability of an allergic cause. Erythema is also
typical in generalised demodicosis.
Isolated papulopustules and collarettes (Fig. 30 ). These are indicative of
superficial bacterial complications, which occur very frequently in HT,
HAC, and follicular dysplasias.
Follicular casts and scales . These can appear in any case of alopecia
accompanied by a dyskeratotic process (e.g. sebaceous adenitis) (Fig. 31 ).
Comedones (Fig. 32 ). These lesions usually accompany endocrine alopecia
in later disease stages, and can also be associated with demodicosis and
follicular dysplasia.
Changes in skin colour . Hyperpigmentation is usually observed in alopecic
areas in dogs with cyclic alopecia and alopecia X. Hyperpigmentation is
also observed in cases of chronic inflammation of the skin, which can be
accompanied by lichenification (Fig. 33 ), and during the development of
endocrinopathies (Fig. 34 ). Follicular dysplasias are characterised by
diffuse hyperpigmentation that evolves in parallel with alopecia. By
contrast, alopecia that resolves with the formation of an eschar is
associated with depigmentation.
Changes in hair colour and appearance. In specific breeds, alopecia affects
areas of dilute colour hair or black hair (follicular dysplasias, see
Introduction). The regrowth of white hair in an alopecic area in which
pigmented hair previously grew is indicative of alopecia areata . The
presence of fine and miniaturised hairs is indicative of pattern alopecia. A
colour change to brown, especially in white-haired dogs, is indicative of
licking of the area.
30 (a) Papulopustular dermatophytic lesion on the owner of an affected dog. (b) Collarettes in a
dog with hypothyroidism.
31 Sebaceous adenitis in a Golden Retriever. Symmetrical alopecia in the dorsal region of the trunk.
Abundant comedones in a dog with hyperoestrogenism.

32
33 Lichenification and hyperpigmentation in a chronic allergic inflammatory process.
34 Alopecia and diffuse hyperpigmentation in the ventral thoracic and abdominal region in a dog
with hypothyroidism.
DIAGNOSTIC PROTOCOL
A large number of causes can give rise to generalised alopecia (Box 2 ). To
identify the cause it is necessary to carefully consider all the information
gathered in the analysis of the clinical history, together with the findings of
the general physical and dermatological examinations. The diagnostic
protocol in cases of a clinical pattern of generalised symmetrical alopecia
consists of the following steps:
STEP 1 Analysis of the basic characteristics of the

patient
First, based on the patient’s characteristics, we can confirm or rule out
certain very obvious causes of alopecia (e.g. congenital alopecia, pituitary
dwarfism, testicular neoplasia, cyclic alopecia, malnutrition).
STEP 2 Confirm or rule out demodicosis
The second step, regardless of the dog’s age, is to rule out or confirm the
existence of demodicosis by deep skin scrapings and/or trichography of at
least 5 areas affected by alopecia. Trichography should be a routine
examination in all cases of alopecia (Fig. 35 ).
While the trichogram can be used to diagnose (or rule out) the presence of
Demodex , it also allows examination of the structure of the hair follicles
from root to tip, and the identification of any abnormalities linked to other
follicular dysplastic processes (Fig. 35 c–l and subsequent steps).
The exclusive presence of telogen hairs (golf-club-shaped bulbs) may be

indicative of endocrinopathy. It is also important to look for structural
abnormalities in hair shafts (twisted, sinuous hairs), which are characteristic
of follicular dysplasia and pigmentary abnormalities (large accumulations of
melanin in the shaft, dysplastic hairs in colour-dilution alopecia, or black-
hair follicular dysplasia). Finally, broken tips are indicative of pruritic or
behavioural dermatoses.
35 Trichograms showing hair follicles in different types of generalised symmetrical alopecia.

(a) Presence of Demodex in generalised demodicosis. (b) Hair stem that has been invaded
by dermatophytic spores. (c) Demodicosis and dysplasia of dilute hairs. (d) Telogen root
with accumulated melanosomes. (e) Telogen root in a case of colour-dilute dysplasia. (f)
Follicular cast in a case of sebaceous adenitis. (g) Hair shaft in a case of hair-colour-
associated follicular dystrophy. (h) Hair shaft resembling an exclamation mark in a case of
alopecia areata . (i) Fragile shaft in a case of tricorhexis nodosa. (j) Dystrophic secondary
hairs in a case of follicular alopecia. (k) Hair roots in a case of telogen effluvium. (l) Hair tips
in a case of self-induced symmetrical alopecia.
STEP 3 Confirm or rule out dermatophytosis
The third step is to confirm or rule out dermatophytes as the underlying

cause. Once demodicosis has been ruled out, the aforementioned trichogram
should be analysed for signs of invasion of the cortex and the medulla by
dermatophytic spores and filaments (Fig. 35 b) and a culture in DTM and/or
Saboureau media should be performed (Fig. 36 a). This allows isolation and
identification of the genus and species of the agent involved (Fig. 36 b). In
dogs, the Wood’s lamp is rarely used owing to its poor sensitivity and
specificity.
It is particularly important to investigate the presence of dermatophytes in

cases of trunk alopecia in Yorkshire Terriers.
36 (a) Macroconidia of M. canis stained with Cotton Blue and (b) DTM culture showing
positive growth.
STEP 4 Confirm or rule out bacterial folliculitis
In all cases of alopecia it is important to determine whether or not the patient

has bacterial folliculitis, which can constitute either a complication or the
primary cause of the alopecia.
To confirm or rule out bacterial folliculitis, skin-surface cytology is
performed with adhesive tape stained using the Diff-Quik method (Fig. 37 ).
37 Surface cytology in which abundant desquamated cells, neutrophils, and bacteria are
evident.
STEP 5 Confirm or rule out leishmaniasis
After ruling out the main inflammatory causes of alopecia (demodicosis,

dermatophytosis, and bacterial folliculitis), it is advisable to rule out
leishmaniasis, especially if the dog lives in endemic areas and has
nonpruritic squamous lesions. Our preferred method is serology by
quantitative ELISA accompanied by a proteinogram (Fig. 38 ). Based on our
experience, real-time PCR does not provide clear information about the
patient’s clinical situation.
38 Images of (a) an ELISA plate and several proteinograms showing (b) a normal situation,
(c) oligoclonal gammopathy, and (d) polyclonal gammopathy in 2 patients positive for
Leishmania infantum. Image courtesy of Sergio Villanueva.
STEP 6 Age of onset of alopecia
At this point in the diagnostic procedure it is necessary to consider whether

we are dealing with a dog whose alopecia began at a geriatric age (high
likelihood of an endocrine problem) or one whose alopecia began before 2
to 4 years of age (nonendocrine alopecia) (Box 4 ).
The first signs of nonendocrine alopecia present at early ages in specific

breeds, and can initially have a multifocal distribution, likely indicating
alterations that affect follicle development. By contrast, endocrine alopecia
affects dogs of over 6 or 7 years of age, mainly affects the trunk, and is
usually accompanied by clinical signs in other systems.
BOX 4
Differences between endocrine and nonendocrine forms of
alopecia
Signs Endocrine Nonendocrine
Age of onset >5–6 y Puppies <5 years

(most cases)
Pruritus Initially absent Initially mild
Initial appearance Diffuse alopecia of the Multifocal

trunk alopecia
Hyperpigmentation With progression From onset
Localisation Trunk Trunk, head, and

limbs
Course Progressive Variable
Age 5 years or more

If the age of onset is over 5 years, diagnosis should be oriented towards an
endocrine cause. In older dogs in which the likelihood of an endocrine cause
is high, urinalysis and biochemical and haematological analyses should be
performed. Parameters including alkaline phosphatase and glucose (elevated
in HAC) or cholesterol (elevated in many hypothyroid animals) should be
analysed. Thyroid hormones (cTSH, tT4, fT4) and cortisol levels pre- and
post-ACTH administration can also be measured, or an ultrasound
performed to examine the adrenal glands and gonads. If the suspected cause
is an ovarian tumour or ovarian cyst (HE), it is not advisable to measure
levels of 17-β-oestradiol. Instead, vaginal cytology (which has a much
greater diagnostic value) should be performed, and the patient’s hormonal
status should be evaluated based on the percentage of squamous epithelial
cells (Fig. 39 ). In the case of males, HE caused by a Sertoli-cell tumour
should be analysed by prepuce cytology.
Neither quantification of oestradiol nor basal progesterone (in males or
females) are of any diagnostic value in cases of hyperoestrogenism.
In alopecia X, the determination of progesterone or 17-hydroxyprogesterone

levels, before or after stimulation with ACTH, is of no diagnostic use.
Diagnosis should be based on medical history, breed, and biopsy findings.
Age less than 5 years
In cases involving alopecia in young or young adult dogs with no systemic

signs, with gradual evolution, sometimes beginning with a multifocal
presentation, the trichogram should be analysed for signs of pigmentary
alterations of the roots and shafts that may be indicative of follicular
dystrophy. Skin biopsies should also be performed, since the majority of
causes (once demodicosis, dermatophytosis, and leishmaniasis are ruled
out), require biopsy for confirmation.
39 Types of cells observed in vaginal cytology of a dog. (a) Illustration and (b) microscopic
image of vaginal cytology in a case of hyperoestrogenism, in which cornified superficial
epithelial cells, many of which are anucleate, predominate. Image courtesy of Mariví
Falceto.
STEP 7 Biopsy
Cyclic alopecia, pattern alopecia, hair colour-associated follicular
dysplasia, and follicular dysplasias typical of certain breeds can be
diagnosed based on the information obtained from the clinical history and the
signs observed during the examination. However, in these and other cases,
biopsy will provide histopathological findings (Fig. 40 ) that will allow
establishment of a definitive diagnosis.
Skin biopsy allows classification of alopecia by assessing the activity of

hair follicles (anagen, telogen, and exogen phases) in states of
effluvium/defluxion, their morphological appearance (anomalous dysplastic
forms) in follicular dysplasias, the status of the pigmentary system
(anomalous accumulations of melanin in the hair bulb and anomalous
melanin distribution) in hair-colour-associated follicular dysplasias, and
alterations in follicular keratinisation (trichilemmal keratinisation in cases of
alopecia X and orthokeratotic keratinisation of primary and secondary
follicles in cases of recurrent flank alopecia). Biopsy also allows analysis
of the distribution and type of dermal infiltrate, allowing orientation of the
diagnosis towards various dermatoses such as epitheliotropic lymphoma,
alopecia areata universalis, postvaccinal alopecia, dermatomyositis,
vasculopathies, or granulomatous sebaceous adenitis.
40 (a) Histological image of a cutaneous biopsy showing dystrophic follicles with excess of
trichilemmal keratin in a dog with alopecia X. (b) Histological image of dystrophic follicular
bulbs with abnormal deposits of macromelanosomes in a dog with hair-colour-associated
follicular dystrophy.
INTRODUCTION
The scaling/crusting and seborrhoeic pattern is characterised by the presence of
scales of varying sizes and colouration can have a generalised distribution (Fig.
1 ) or may be limited to a specific area (Fig. 2 ).
The types of lesions associated with this pattern, in addition to scales, are
crusts, comedones, and follicular casts. Excessive lipid secretion may also be
observed, resulting in a greasy-looking/smelling haircoat.
Scaling processes, which correspond to this pattern, are commonly referred to

as seborrhoea. The term seborrhoea is often used in veterinary medicine to
describe different types of alterations in keratinisation. These include the
following:
Dry seborrhoea, which involves the excessive shedding of scales with a dry
and dull haircoat (Fig. 3 ).
Oily seborrhoea, characterised by small scales and greasy skin and haircoat
(Fig. 4 ).
Seborrhoeic dermatitis, characterised by fine scales, a greasy haircoat, and a
cutaneous reaction with inflammatory lesions (Fig. 5 ).
Squamous patterns or seborrhoeic presentations are the consequence of

alterations that can affect any phase of the keratinisation process.
The keratinisation process consists of a series of morphological modifications

and metabolic mechanisms that are genetically programmed and tightly
regulated by many internal and external factors (see Chapter 2 ).
One of the main characteristics of the skin is that it consists of a stratified and
keratinised epidermis, which, like the other epithelia, is in a continuous state of
renewal or turnover. In dogs this process normally takes 22 to 28 days,
beginning with stem cells in the basal layer and ending with the cornification of
these same cells in the stratum corneum (see Chapter 2 ). Although frequently
renewed, the epidermis maintains its thickness in normal conditions by
continuously shedding dead cells, although this is not evident.
Most of the cells that make up the epidermis are keratinocytes, which are
organised into 5 strata or layers, named according to their position and the
structural characteristics of their corresponding keratinocytes:
Stratum basale: consists of proliferative basal cells (germ cells), which are
the only cells to undergo mitosis. These cells are attached to the epidermal
basement membrane, from where they migrate to the upper layers of the skin
surface.
Stratum spinosum : in which the cells of the basal layer transform into spiny
cells. These contain numerous desmosomal glycoproteins on their plasma
membranes that act as anchoring points for neighbouring keratinocytes.
These cells play an important role in keratin formation.
Stratum granulosum: in which the keratinisation process begins. The cells in
this layer contain intensely stained granules filled with keratohyaline for the
production of keratin, and have high concentrations of lysosomal enzymes.
Stratum lucidum : very thin, only present in certain skin areas, such as
footpads. The cells in this layer are anucleate, and their cytoplasm contains
a lipoprotein-rich substance (eleidin), a key role of which is to prevent the
entry and exit of water.
Stratum corneum: consisting of the outermost or terminal cells, which are
fully keratinised, flat, thin cells, or squamous cells known as corneocytes,
whose cytoplasm is practically keratin.
The transformation of the keratinocytes of the stratum granulosum and the

stratum lucidum into corneocytes is the last step of the keratinisation process.
Corneocytes resemble hexagonal sheets, in which the plasma membrane has
been replaced by a dense protein envelope attached to longitudinally arranged
lipid molecules. In addition, their cytoplasm is a hydrophobic mass consisting
of filaggrin (a type of protein) and keratin fibres joined by disulphide bridges
that aggregate to form an impermeable keratinised envelope. The cornification
process thus involves the formation of an intercellular lipid-rich matrix that
performs several important functions, acting as an impermeable barrier,
regulating desquamation, and exerting antimicrobial activity. This structure is
responsible for the maintenance of epidermal hydration, which is altered in
seborrhoeic processes.
01 Generalised scaling presentation.
02 Localised scaling lesions.
03 Dry, dull hair with scales. Dry seborrhoea.
04 Greasy hair. Oily seborrhoea.
05 Seborrhoeic dermatitis.
When the keratinisation process is altered, the number of cells in the stratum
corneum increases, resulting in the presence of scales on the skin surface.
Scaling and seborrhoeic presentations are characterised by abnormal
accumulations of corneocytes that have transformed into scales, which can vary
in size.
Generally, scales are composed of the remains of anucleate cells, but if

keratinocyte transformation occurs at a faster rate, corneocytes can retain their
nucleus, resulting in a type of scaling known as parakeratosis (see Fig. 6 in
Chapter 2 ). Parakeratotic cells accumulate and contribute to the formation of
large scales. Given their resemblance to fish scales, these types of scaling
processes are known as ichthyosiform.
Alterations in the following physiological mechanisms of keratinisation can

lead to the formation of scaling dermatoses with a scaling/crusting and
seborrhoeic pattern:
Alterations in the mechanisms of desquamation.
Alterations in structures that mediate cell cohesion.
Infiltrative processes that alter the epidermis.
Increased keratinocyte proliferation.
Alterations in keratinocyte differentiation.
Alterations of the composition of the lipid film of the stratum corneum.
Defects of keratinisation can be congenital or acquired.
PRIMARY KERATINISATION ALTERATIONS

Primary alterations in keratinisation (Box 1 ), also known as primary
seborrhoea, are characterised by the following features:
Hereditary pathologies, associated with certain breeds. Most are inherited as
autosomal recessive traits (i.e. phenotypically normal parents).
Early appearance of clinical signs, in the first months of life (or before 1 year
of age) (Fig. 6 ).
Disease course characterised by excessive shedding and excessive secretion
of oily material.
Arise as a consequence of a defect in the process of keratinisation or
cornification, or due to abnormal activity of the sebaceous glands.
No alternative causes identified after applying the dermatological diagnostic
protocol.
BOX 1
Main primary (congenital) causes of scaling/crusting and
seborrhoeic presentations in predisposed breeds
Process Predisposed breeds1
Canine acne Boxer, English Bulldog, Doberman, Great

Dane, German Shorthaired Pointer, Mastiff,
Weimaraner
Acrodermatitis Bull Terrier
Sebaceous adenitis Akita-Inu, Beagle, Boxer, Hungarian

Wirehaired Vizsla, Poodle, Chow-Chow,
Collie, Lhasa Apso, German Shepherd,
Miniature Pinscher, Old English Sheepdog,
Samoyed, Dachshund
Psoriasiform lichenoid English Springer Spaniel

dermatitis
Vitamin A-responsive Cocker Spaniel, Labrador Retriever,

dermatosis Miniature Schnauzer
Sebaceous gland dysplasia Beagle, Border Terrier, Poodle, Cocker,

Miniature Schnauzer, Dachshund
Familial footpad Dogue de Bordeaux, Golden Retriever,

Kerry Blue Terrier, Labrador Retriever,
hyperkeratosis Irish Terrier
Nasodigital hyperkeratosis Basset Hound, Beagle, Boston Terrier,

Cocker Spaniel
Epidermolytic ichthyosis Labrador, Norfolk Terrier, Rhodesian

Ridgeback
Nonepidermolytic Boston Terrier, Cairn Terrier, Collie,

ichthyosis Doberman, Golden Retriever, Jack Russell
Terrier, Labrador Retriever, Pit Bull
Terrier, Irish Setter, West Highland White
Terrier (WHWT), Yorkshire Terrier
Exfoliative cutaneous German Shorthaired Pointer

lupus erythematosus
Congenital follicular Siberian Husky, Labrador, Rottweiler

parakeratosis
Nasal parakeratosis Labrador Retriever
Dry keratoconjunctivitis Cavalier King Charles

and ichthyosiform
dermatosis
Seborrhoea of the margins Basset Hound, Beagle, Dachshund, and

of the pinnae other breeds with drooping ears
Primary idiopathic Basset Hound, Cavalier King Charles,

seborrhoea Cocker Spaniel, Doberman, Labrador,
German Shepherd, Irish Setter, Miniature
Schnauzer, Chinese Shar Pei, Springer
Spaniel, WHWT
Schnauzer comedone Miniature schnauzer

syndrome
Type I zinc-responsive Siberian Husky, Alaskan Malamute,

dermatosis syndrome Samoyed
Type II zinc-responsive Puppies of fast growing, large breeds

dermatosis syndrome
Based on Campbell, 2012.
1
Most forms are inherited as autosomal recessive traits from phenotypically normal parents. In many cases
genetic tests can be performed.
06 Ventral scaling in a 4-month-old Golden Retriever with ichthyosis.
SECONDARY KERATINISATION ALTERATIONS

Secondary seborrhoea occurs as a consequence of external or internal
aggressions that alter the proliferation, differentiation, or desquamation of the
epithelium of the skin surface or of the hair follicles. However, the mechanisms
that give rise to the seborrhoea remain unclear.
By contrast, most scaling/crusting or seborrhoeic processes observed in the
clinic are acquired or are associated with other skin diseases (Box 2 ). It is
important to consider nutritional, endocrine, inflammatory, and environmental
factors.
Nutritional factors . An adequate nutritional equilibrium is required for the

maintenance of keratinocyte proliferation and differentiation, since
deficiencies, excesses, or imbalances in carbohydrates, proteins, essential
fatty acids, vitamins, and minerals can lead to seborrhoeic presentations.
Since dog food provides a nutritional balance, seborrhoea due to nutrient
deficiencies is generally observed in dogs with malabsorption,
maldigestion, or metabolic disorders.
Endocrine factors . Hormones can influence cell proliferation and cutaneous
lipid profiles, leading to secondary seborrhoeic presentations. The most
commonly implicated endocrinopathies are hypothyroidism (HT) and
hyperadrenocorticism (HAC), both spontaneous and iatrogenic.
Inflammation . Inflammatory processes of the skin are characterised by
epidermal hyperplasia, accompanied by the production and release of
cytokines, histamine, eicosanoids, leukotrienes, or prostaglandins, which
increase DNA synthesis in the basal stratum, thereby promoting epidermal
proliferation. When the inflammatory process is mild, the associated
seborrhoeic signs are not usually accompanied by pruritus. However,
intense pruritus may be observed in some cases, as occurs in cases of
inflammatory processes induced by atopic dermatitis with or without a food
component, allergic contact dermatitis, dermatophytosis, demodicosis,
cheyletiellosis, lice infestations, and, occasionally, epitheliotropic
lymphoma.
Level of hydration . Alterations in keratinisation imply a loss of the
equilibrium between water that is lost through the epidermis and the level
of hydration of the dog’s skin. Epidermal damage or a decrease in the
barrier’s efficacy in preventing water loss results in imbalance of the
water-holding to water-loss ratio; water-holding capacity (WHC) /
transepidermal water loss (TEWL). Thus, TEWL is increased and
hydration is reduced. A significant increase in TEWL results in the
appearance of scales on the skin. Predisposing factors include low
humidity, excessive bathing with aggressive products, and fatty acid
deficiencies. On the other hand, dryness of the skin (xerosis) is indicative
of a decrease in the water content of the skin, which should be greater than
10 %. Intercellular lipids (sphingolipids, free steroids, and free fatty acids)
of the stratum corneum and the lamellar bodies that trap and prevent excess
water loss also contribute significantly to preventing water loss from the
skin.
Calluses are the most common manifestation of secondary keratinisation

alterations (Fig. 7 ). In dogs, it is relatively common to see presentations in
which excessive desquamation predominates, with a dry and dull looking
haircoat and the presence of follicular casts (Fig. 8 ). In some patients, certain
areas of the skin may acquire a greasy appearance and a bad odour (Fig. 9 ).
Other clinical manifestations associated with altered keratinisation include
acne, hyperkeratosis of the footpads (Fig. 10 ), dermatosis of the margins of the
pinnae (Fig. 11 ), otitis externa (Fig. 12 ), and tail gland hyperplasia (Fig. 13 ).
Dogs with oily seborrhoea or seborrhoeic dermatitis should be carefully

examined for bacterial and yeast overgrowth, since the lipolytic characteristics
of these microorganisms further exacerbate the affected skin.
Yeasts of the genus Malassezia increase the rate of proliferation of

keratinocytes, creating a vicious circle. It is therefore essential to control the
overgrowth of these agents in order to stop the seborrhoeic process.
BOX 2
Main secondary causes of scaling/crusting and seborrhoeic
presentations
Diseases
Flea-allergy dermatitis (FAD)
Atopic dermatitis
Food hypersensitivity
Metabolic disorders
Superficial necrolytic dermatitis
Hepatic diseases
Malabsorption and/or maldigestion
Nutritional imbalances
Essential fatty-acid deficiencies
Protein deficiency
Zinc deficiency
Unbalanced diet
Endocrinopathies
Sex hormone imbalance
Diabetes mellitus
Hypothyroidism
Infectious
Bacteria
Dermatophytes
Leishmania
Malassezia
Viruses (canine distemper)
Environmental
Low relative humidity
Degreasing shampoos
Contact irritants
Neoplasms
Paraneoplastic syndromes
External parasites
Cheyletiellosis
Demodicosis
Pediculosis
Pulicosis
Otodectic mange
Sarcoptic mange
Autoimmune and immune-mediated processes

Sebaceous adenitis
Discoid lupus erythematosus
Systemic lupus erythematosus
Pemphigus foliaceus
Cutaneous drug reaction
Other
Calluses
Tail gland hyperplasia
07 Calloused lesion in the elbow area.
08 (a) Follicular casts in a case of seborrhoeic dermatitis due to food hypersensitivity. (b) Crusted
lesions in a dog with atopic dermatitis.
09 Generalised oily-looking seborrhoea caused by atopic dermatitis.
10 Footpad hyperkeratosis.
11 Scaling dermatosis of the margins of the pinnae.
12 Allergy-associated ceruminous otitis externa with hyperpigmentation and lichenification of the

concave areas of the pinnae.
13 Tail gland hyperplasia.
To establish a definitive diagnosis of a scaling/crusting and seborrhoeic
process, it is necessary to analyse the patient’s clinical history and to perform
general and dermatological examinations. From the beginning of the protocol, it
is important to distinguish between primary and secondary scaling/crusting and
seborrhoeic processes.

The clinical signs and the severity and distribution of the process will depend
on the aetiology and response of the patient. Systemic causes (endocrinopathies,
metabolic, hepatic, or gastrointestinal alterations, or nutritional imbalances)
usually present with generalised signs that are not accompanied by pruritus, but
become pruritic as the disease worsens or is complicated by the overgrowth of
yeast or superficial bacteria. Seborrhoeic signs are usually more severe in
facial and podal areas (especially in intertriginous and interdigital areas), and
in the perineum. Aspects of the medical history that should be analysed in more
detail are detailed below.
Age. It is important to know whether the scaling/crusting and seborrhoeic
presentation appeared before or after 1 year of age. Primary seborrhoea
and diseases associated with a secondary scaling/crusting and seborrhoeic
pattern, such as juvenile-onset generalised demodicosis or dermatophytosis
(Fig. 14 ), can appear before or around 1 year of age. Signs of atopic
dermatitis, which include scaling conditions (Fig. 15 ), appear between 1
and 3 years of age. Finally, HT and other endocrinopathies, which may
present with scaling lesions, appear from 6 to 8 years of age (Fig. 16 ).
Breed. Certain breeds are predisposed to primary keratinisation alterations
(Box 1 ). A breed predisposition is also observed for other diseases that
may be associated with secondary scaling (and hence a scaling/crusting and
seborrhoeic pattern), such as juvenile demodicosis (Fig. 17 ) and atopic
dermatitis.
Pruritus. Pruritus is observed from the outset in the great majority of
secondary seborrhoeic processes (Fig. 18 ). In cases such as these, the
diagnosis should be oriented towards pruritic rather than nonpruritic
processes. However, it is often difficult to determine whether pruritus has
been present since the onset of a presentation, or whether it constitutes a
complication of other lesions of other aetiologies, such as complicated
primary seborrhoea or other processes such as dermatophytosis or
demodicosis. In these situations, the pruritus tends to be of a lesser intensity
than that seen in cases of allergies and external parasitosis. The clinical
signs and the severity and distribution of the process will depend on the
aetiology and response of the patient. Endocrinopathies, metabolic, hepatic,
or gastrointestinal alterations, and nutritional imbalances are not initially
accompanied by pruritus, but can become pruritic if the presentation is
complicated by the overgrowth of superficial microorganisms (bacteria or
yeasts). Allergic dermatitis is accompanied by mild to severe itching from
the outset.
Seasonality. While primary keratinisation defects are not seasonal, secondary
defects may produce seasonal clinical signs, as occurs in cases of atopic
dermatitis due to pollen sensitivity and flea-bite hypersensitivity.
Allergic reactions. The presence of recurrent otitis or episodes of otitis,
conjunctivitis, a history of gastrointestinal problems, and various signs of
pruritus (scratching, licking, or chewing of the legs or other body areas)
may be indicative of an allergic process with a secondary scaling/crusting
and seborrhoeic pattern.
14 Dermatophytosis with scaling.
15 (a) Scaling pattern due to atopic dermatitis of the face. (b) Generalised scales and crusts.
16 Scaling/crusting and seborrhoeic pattern in a dog with hyperadrenocorticism.
17 Scaling/crusting pattern in a dog with demodicosis.

18 Pruritic dermatitis of allergic origin with scaling, lichenification, and hyperpigmentation.
GENERAL EXAMINATION
Polyuria, polydipsia, or polyphagia and searching for cool places to lie down
can be indicative of HAC. HAC should also be suspected in patients with
muscle weakness, hepatomegaly, and pendulous abdomen. If the patient presents
with vomiting or diarrhoea, or is apathetic, it may be indicative of metabolic or
endocrine causes (such as HT) or of liver disease, enteropathy, or
hepatocutaneous syndrome (Fig. 19 ). Bradycardia, enteropathy, and
constipation are suggestive of HT. Endocrinopathy or kidney disease should be
considered if biochemical alterations are observed (e.g. elevated alkaline
phosphatase, low albumin, anaemia, eosinopaenia, low urine density, etc.).
Eosinophilia may be indicative of parasitosis or an allergic condition.
19 Superficial necrolytic dermatosis. Hepatocutaneous syndrome.
Lesions related to abnormal keratinisation (dry scales, greasy-looking hair and
scales, follicular casts, hyperkeratotic or lichenified skin surface, oily odour, or
crusts) should be carefully examined and their location and distribution noted.
These data can then be contrasted with the characteristics of each of the
processes associated with seborrhoeic presentations. The presence of follicular
casts (Fig. 20 ) suggests sebaceous adenitis (Fig. 21 ), vitamin A-responsive
dermatitis, or primary seborrhoea as possible causes, but can also be associated
with other follicular inflammatory processes such as demodicosis.
When analysing the location and distribution of the lesions, the following should
be taken into account:
Acne affects the lower submandibular and perilabial area.
Sarcoptic mange affects the margins of the pinnae (Fig. 22 ), elbows, hocks,
and the ventral thorax.
Nasodigital hyperkeratosis affects the muzzle area (Fig. 23 ) and footpads
(Fig. 24 ).
Clinical signs in cheyletiellosis, demodicosis, and dermatophytosis are
generally focal or multifocal, but in some cases are generalised.
Nasal parakeratosis affects the nasal plane.
In Schnauzer comedone syndrome, lesions develop along the dorsal midline.
Zinc-responsive dermatosis lesions are located in mucocutaneous areas, but
can also be generalised (Fig. 25 ).
Flea-bite allergic dermatitis is characterised by scaly and crusted lesions in
the lumbar zone, tail area, and on the posterior aspect of the hindlimbs (Fig.
26 ); ichthyosis in Golden Retrievers affects the lateral and ventral areas of
the thorax and abdomen (Fig. 27 ).
Allergic dermatitis, although a systemic processes, usually manifests as a
regional seborrhoeic process, although in some cases can be generalised.
Sebaceous adenitis usually begins as a regional process limited to the facial
area and the dorsal or lateral regions of the trunk, after which it can become
generalised.
Systemic causes (endocrinopathies, metabolic, hepatic, or gastrointestinal
alterations, or nutritional imbalances) are associated with generalised
clinical signs.
External agents such as low ambient humidity or inappropriate topical
treatments are also associated with generalised skin signs.
20 Follicular casts evident following brushing of a dog with a scaling process.
21 Generalised scaling process in a Labrador with sebaceous adenitis.

22 Scaling lesions on the margins of the pinnae in a dog with sarcoptic mange.
23 Hyperkeratosis of the muzzle.

24 Footpad hyperkeratosis.
25 Generalised scaling in a case of zinc-responsive dermatosis. Image courtesy of Amparo

Ortúñez.
26 Seborrhoeic dermatitis in the dorsolumbar area in a dog with flea-allergy dermatitis.
27 Lateral aspect of the thorax of a Golden Retriever with generalised scaling due to ichthyosis.
DIAGNOSTIC PROTOCOL
Before beginning diagnostic tests, depending on the clinical history and the
characteristics of the patient’s clinical presentation, it is possible to
determine whether the process is primary or secondary, and whether external
factors (such as inadequate feeding) may be implicated in the scaling
condition.
If analysis of the data suggests a hereditary or genetic keratinisation disease,

a skin biopsy should be performed to determine whether diagnosis can be
established based on the histological pattern observed (Fig. 28 ). Once
diagnosed, it is necessary to properly inform the owner about the genetic
origin of the disease.
If, on the other hand, analysis of the clinical history strongly suggests a
nutritional deficiency, the owner should be informed so that they can resolve
the deficiency and the corresponding pattern.
In other situations, given the abundance of conditions that present with a

scaling/crusting and seborrhoeic pattern and abnormal keratinisation
secondary to other processes, it is crucial to follow the relevant diagnostic
protocol to rule out secondary causes.
28 Histological lesions characterised by orthokeratotic laminar hyperkeratosis with
hypereosinophilia of the stratum corneum, and no histological alterations in the dermis.
Ichthyosis in a Golden Retriever. Image courtesy of Laura Ordeix.
The following are the steps required to confirm or rule out causes of
scaling/crusting and seborrhoeic presentations.
STEP 1 Mites, Malassezia, and bacteria on the

surface of the skin
The objective of the first step is to confirm or rule out the presence of
pruritic agents that may be found on the surface of the skin: Sarcoptes ,
Demodex , Otodectes , lice, Cheyletiella , Malassezia , and bacteria (Fig.
29 ). To do this the following tests should be conducted:
Scraping of the affected areas to detect the presence of mites or lice.
Observation of the ear canal with an otoscope to analyse the
characteristics of the epithelium, the type of secretion and, in some
cases, to detect the presence of ear mites.
Next, an ear swab is obtained and spread on a slide to confirm or rule out
the presence of Otodectes .
Skin-surface cytology using adhesive tape, to detect overgrowth of yeasts
and/or bacteria.
Finally, to confirm that mites are not the cause of the observed pattern,
antiparasitic treatment can be administered to remove all parasites of
the skin surface common to the patient’s geographical area. Treatment
should continue for a minimum of 1 month, regardless of whether the
results of the previous tests are negative.
If overgrowth of yeasts or bacteria is observed, this should be controlled

before proceeding, as the inflammation produced by these agents exacerbates
the seborrhoea and can mask the histological signs of the underlying diseases
in biopsies obtained subsequently.
29 Skin-surface agents that can cause scaling/crusting and seborrhoeic processes.

STEP 2 Intestinal parasites
It is advisable to perform a faecal examination to determine the presence or

absence of intestinal parasites, and to confirm or rule out maldigestion or
intestinal malabsorption processes.
STEP 3 Presence of dermatophytes
The objective of the third step is to confirm or rule out the presence of
pathogenic fungi on the skin surface. Dermatophytes can induce scaling
dermatological presentations more often than expected.
It should be noted that the use of a Wood’s lamp as the sole means of
confirming or ruling out dermatophytes can lead to false negatives, since the
emitted fluorescence is a consequence of the metabolite generated by the
dermatophyte that is attacking the keratin of the cornified structures. As such,
a Wood’s lamp can be used to detect M. canis , but is not reliable for the
detection of other dermatophytes such as T. mentagrophytes .
To confirm or definitively rule out a dermatophytosis, the following

laboratory tests are required:
A trichogram, to examine the status of the hair shafts. Invasion of the
follicular structures confirms the presence of dermatophytes (Fig. 30 ),
If the trichogram is negative, culture in specialised dermatophyte medium
(DTM) and a subsequent microscopic analysis of the macroconidia that
grow in the medium (Fig. 31 ).
30 Trichogram in which invasion of the hair shafts by dermatophytic spores is evident.
31 Macroconidia of M. canis in a positive DTM culture.

The fourth step is to confirm or rule out the presence of Leishmania
infantum in geographical areas in which it is commonly found, as this
parasite can be a primary cause of scaling dermatoses (Fig. 32 ) or can
promote the development of demodicosis, which can also present with
scaling. Several laboratory techniques can be used for this purpose. In our
clinic, the technique of choice is serology using the quantitative ELISA
method, accompanied by a proteinogram (see Fig. 38 in Chapter 4 ).
32 Scaling lesions (a) on the margins of the pinnae and (b) the elbows in a dog with
leishmaniasis.
STEP 5 Flea control
The fifth step involves external parasitic control of the patient with the
seborrhoeic presentation. It is very important to ensure that the flea control
program is adapted to the characteristics of the patient, taking the following
considerations into account:
The environment in which the patient lives and the institution of an
environmental control program that targets adult forms, eggs, and flea
larvae.
The presence of other cats/dogs or other species (cohabitation, visits,
sporadic or regular stays) that may serve as reservoirs or routes of entry
of fleas into the patient’s home.
The products used for flea control, the manner in which they are applied
by the owner, the body areas treated, the frequency of administration,
and whether they are administered by the owner themselves or by
others, etc.
If there is any doubt as to how flea control is being carried out, the owner
should be reminded of the importance of proper control, administered
systematically using the appropriate products and targeting all individuals
and the patient’s surrounding environment. The antiparasitic drugs deemed to
be most effective should be administered for at least 3 consecutive months,
and the effects on the evolution of the scaling dermatosis assessed.
STEP 6 Food hypersensitivity
We proceed to the sixth step when parasitic and infectious agents, as well as
leishmaniasis, have been ruled out as causes of the scaling pattern. Next, it is
necessary to determine whether food hypersensitivity may be the cause of the
seborrhoeic dermatitis.
While food hypersensitivity is rarely the sole cause, atopic dermatitis in

which part of the problem is due to food allergy is not uncommon. Therefore,
it is necessary to determine whether the lesions characteristic of the
seborrhoeic scaling presentation improve when the patient is placed on a
controlled monoprotein or hydrolysed hypoallergenic diet for a minimum of
4 weeks. If improvement is observed, even if the dermatosis is not
completely controlled, the patient’s diet should be corrected accordingly,
maintaining a hypoallergenic diet adapted to the patient until the diagnostic
protocol has been completed.
STEP 7 Atopic dermatitis caused by aeroallergens
The aim of the seventh step is to demonstrate the presence of atopic

dermatitis (Fig. 33 ), once food and flea-bite hypersensitivity have been
ruled out. To this end, Favrot’s diagnostic criteria for atopic dermatitis
should be applied:
Onset at less than 3 years of age.
Patient predominantly lives indoors.
Presence of pruritus that responds to corticosteroids.
Chronic or recurrent yeast infections.
Hindlimb involvement.
Involvement of the pinnae.
Margins of the pinnae are unaffected.
Dorsolumbar area not affected.
If the dog fulfils 5 or more of the above criteria, the patient is considered to
have atopic dermatitis caused by environmental allergens (sensitivity, ~85.5
%; specificity, ~79 %).
33 Atopic dermatitis caused by environmental allergens resulting in a pruritic erythematous

presentation with scaling and crusting.
STEP 8 Systemic disorders
If the scaling process began when the dog was over 6 years of age and all
other tests have been negative, a general assessment should be performed
that includes biochemical (cholesterol, alkaline phosphatase, and glucose),
haematological, and urinary parameters, as well as abdominal ultrasound
and relevant endocrine tests (see Chapter 4 ) to confirm or rule out the
presence of liver disease, kidney disease, diabetes, HT, or HAC.
In cases in which clinical signs appeared in geriatric patients, endocrine,
metabolic, and immunological defects or neoplasms should be considered as
potential causes of the scaling/crusting seborrhoeic pattern. Systemic
disorders can also predispose individuals to other pathologies such as
dermatophytosis, demodicosis, or leishmaniasis, which in turn can
exacerbate scaling processes.
STEP 9 Skin biopsy
Biopsies should be obtained from several areas to confirm primary

keratinisation alterations, and in some cases to identify causes of secondary
seborrhoea, such as superficial necrolytic dermatitis, epitheliotropic
lymphoma, zinc absorption deficiencies, sebaceous adenitis (Fig. 34 ),
pemphigus complex, or lupus.
The cutaneous patterns associated with allergic processes (Fig. 35 ) and

cutaneous parasitosis, and those observed in different endocrine diseases,
can be very similar. As such, histological analysis may not always result in a
definitive diagnosis.
Biopsy samples should be obtained from several areas, including normal

skin and areas both with abundant scales and with less severe scaling.
Before collecting biopsy samples it is important to ensure that any bacterial

or yeast overgrowth on the skin surface has been controlled, as this can
hinder diagnosis of the underlying cause.
34 Sebaceous adenitis. Multinodular granulomatous inflammatory infiltrate around the hair
follicles, in the area of the isthmus, and absence of sebaceous glands. Marked
orthokeratotic hyperkeratosis. Image courtesy of Dolors Fondevila.
35 Histological image showing marked follicular hyperkeratosis in a case of atopic dermatitis in

a West Highland White Terrier.
INTRODUCTION
The erosive-ulcerative (EU) pattern is characterised by the presence of
erosions, ulcers, or a combination of both, although inflammatory lesions such
as erythema, oedema, crusts, depigmentation, or alopecia may be observed in
the surrounding areas.
Erosions are circumscribed lesions characterised by a loss of continuity of the

cutaneous surface (Fig. 1 ), but do not affect the basement membrane. Ulcers are
characterised by a loss of continuity of the cutaneous tissue and depression of
the skin (Fig. 2 ), but with additional destruction of the dermoepidermal
junction.
Erosions and ulcers are considered secondary lesions, since they are derived
from the separation of closely adhered scales and crusts, or are the result of the
evolution of plaques, nodules, or vesiculobullous processes. Erosive-ulcerative
processes can also be the result of self-trauma in cases in which the underlying
causes are associated with pain or itching (Fig. 3 ) or are neurogenic in nature.
Clinically, it is not possible to determine whether a lesion that causes a loss of

skin continuity is an erosion or an ulcer. A skin biopsy is required to establish
the difference.
Erosions can easily evolve into ulcers as a result of various processes,

including infections, exacerbation of self-trauma, or scratching of the affected
area. Therefore, it is more important to determine the cause of the pattern than to
differentiate between these 2 lesion types.
The following are the main pathophysiological mechanisms that can result in the
destruction of cutaneous tissue and give rise to erosive-ulcerative presentations:
Trauma (self-induced or not). Pruritic dermatopathies are frequently
associated with erosive-ulcerative lesions induced by scratching (Fig. 4 ).
The distribution and appearance of the lesions in these cases reflects the
nature of the aggression.
Ischaemic. Loss of blood supply to the skin due to vasculitis or
vasculopathies can also cause erosive-ulcerative lesions (Fig. 5 ).
Obstruction of a large dermal vessel will cause necrosis of the area of skin
irrigated by that vessel, and may result in the development of a perforated
circular ulcer (Fig. 6 ), the appearance of which is typical of lesions of
vascular origin. When smaller capillaries are blocked, an appreciable ulcer
may not develop, but an erosive lesion may form.
Other causes of these types of lesions include infectious (bacteria, fungi),
immunological (immune-mediated diseases [Figs. 7 and 8 ]), neoplastic
(Fig. 9 ), and idiopathic processes.
01 Erosive lesions.
02 Ulcerative lesions. Deep ulcerative lesion (b).
03 Erosive-ulcerative lesions caused by self-induced trauma in response to pruritus and/or pain.
04 Scratching-induced erosive-ulcerative lesions on the neck in a dog with allergic dermatitis.

05 Erosive-ulcerative lesion caused by vascular disease.
06 Perforated ulcer in a case of idiopathic vasculitis.

07 (a) Erosive-ulcerative lesions due to pyoderma in a German Shepherd. (b) Detail of the ulcer.
08 Erosive-ulcerative lesions in a case of pemphigus foliaceus.

09 Erosive-ulcerative lesions caused by a neoplastic process (granulomatous ulceration).

Several factors, both internal and external (Box 1 ), can result in damage of the
cutaneous tissue, affecting the epidermis, dermis, and even subcutaneous tissue.
Similarly, several different processes can result in the appearance of an
erosive-ulcerative pattern (Box 2 ).
One of the main consequences of erosive-ulcerative lesions is that the function

of the skin barrier is impaired, leading to loss of fluids, proteins, and
electrolytes, as well as a greater susceptibility to bacterial colonisation of the
skin. Consequently, when the ulcerated areas are extensive and deep, the
patient’s life may be at risk, as they can develop dehydration, hypoproteinaemia,
and septicaemia (Fig. 10 ), or general discomfort, fever, and apathy (Fig. 11 ).
Therefore, in these situations it is important to institute symptomatic treatment
from the beginning to avoid these complications while investigating the causes
of the erosive-ulcerative process.
BOX 1
Main factors responsible for the erosive-ulcerative pattern
Internal factors
Absence or destruction of specific structures and adhesion molecules
Detachment of epidermal layers by maceration
Transcutaneous elimination of minerals
Widening of the gap between fissures
Evolution of pustular and/or vesicular lesions
Neoplastic infiltration
Severe inflammation
Interruption of blood flow in the area
Necrosis or apoptosis of keratinocytes
Degenerative processes
Vesicular or bullous processes
External factors
Self-trauma due to pruritic processes (very common)
Physical factors:
Actinic (sunlight)
Electrical
Thermal
Chemical factors
Toxic factors
Mechanical trauma
Combination of internal and external factors
External pressure combined with ischaemia, which induces decubitus
ulcers, especially on skin covering bony prominences
Based on Saridomichelakis, 2012.

BOX 2
Main causes of erosive-ulcerative pattern
Allergic
Canine eosinophilic furunculosis
Insect and flea-bite hypersensitivity
Autoimmune and immune-mediated

Juvenile cellulitis
Erythema multiforme complex or Stevens-Johnson syndrome, toxic
epidermal necrolysis (TEN)
Lupus erythematosus complex (systemic and cutaneous)
Pemphigus complex (foliaceous, erythematosus, vulgaris, and
paraneoplastic)
Subepidermal bullous dermatosis
Perianal fistulas
Sterile panniculitis
Adverse drug reactions
Canine uveodermatologic syndrome
Vasculopathies (immune complex vasculitis)
Bacterial
Actinomycosis
Mycobacteriosis
Nocardiosis
Superficial pyoderma (mucocutaneous pyoderma and disseminated
superficial pyoderma)
Superficial pyoderma (pyotraumatic dermatitis and intertrigo)
Deep pyoderma (furunculosis, cellulitis, German Shepherd pyoderma)
Congenital and hereditary

Bull Terrier acrodermatitis
Canine dermatomyositis
Epidermolysis bullosa
Ehlers-Danlos syndrome
Metabolic / endocrine
Calcinosis cutis and calcinosis circumscripta
Superficial necrolytic dermatitis (hepatocutaneous syndrome)
Mycotic
Dermatophytosis (superficial pustular dermatophytosis, kerion,
pseudomycetoma)
Systemic mycoses (blastomycosis, cryptococcosis, sporotrichosis,
histoplasmosis)
Subcutaneous mycoses (pytiosis, sporotrichosis, aspergillosis)
Neoplastic
Squamous cell carcinoma in situ (Bowen disease)
Basal cell carcinoma
Reactive histiocytosis
Cutaneous/epitheliotropic lymphoma
Mastocytoma
Cutaneous metastasis of pulmonary carcinoma
Nutritional
Zinc-responsive dermatosis
Canine dermatosis due to inadequate feeding
Parasitic
Myiasis
Cutaneous microfilariasis
Sarcoptic mange
Protozoa (leishmaniasis)
Various
Canine acne
Acral lick dermatitis (neurodermatitis)
Environmental
Freezing
Foreign bodies
Irritant contact dermatitis
Actinic dermatoses
Snake bites
Bites of various insects
Burns (chemical, electrical, thermal)
Trauma, pressure
10 Stevens-Johnson syndrome. Golden Retriever with very generalised erosive-ulcerative lesions
and septic shock.
11 Generalised idiopathic vasculopathy. (a) General appearance of the patient. Details of lesions in
the (b) dorsal area, (c) medial forelimb, (d) medial hindlimb, (e) axilla, and (f) ventral pectoral
girdle.
The protocol begins with the analysis of the patient’s characteristics and
clinical history, followed by a general physical examination and a
dermatological examination. Finally, a list of possible causes is created and a
diagnostic protocol, which should ultimately enable identification of the cause
of the erosive-ulcerative process, is proposed.
Although pruritic processes associated with this pattern are described in this
chapter, it should be noted that the pruritic pattern predominates over other
lesions, and should be approached using the specific diagnostic protocol
described in Chapter 8 .

Age. In terms of age of onset, congenital and hereditary erosive-ulcerative
processes, as well as juvenile cellulitis (Fig. 12 ), present in puppies,
while deep pyoderma of German Shepherds (Fig. 13 ) and perianal fistulas
(Fig. 14 ) appear for the first time in young or middle-aged dogs.
Neoplasms and metabolic processes more typically affect older dogs.
Sex. Although there are no published data on sex-related susceptibility to this
pattern, some authors have proposed that male dogs are more likely to
develop deep pyoderma, such as German Shepherd pyoderma (Fig. 13 ),
and subcutaneous mycosis.
Breed. Small breeds (e.g. Maltese, Poodle, Lhasa Apso, Pekingese,
Pomeranian, Yorkshire Terrier) are predisposed to erosive-ulcerative
processes around the injection site following administration of vaccines, in
particular the rabies vaccine (Fig. 15 ). On the other hand, mycotic
processes such as actinomycosis or nocardiosis are more common in large
breeds, while in white-haired breeds actinic dermatitis (Fig. 16 ) and
squamous cell carcinoma of the muzzle (Fig. 17 ) are more common.
Generalised vasculitis (Fig. 18 a) accompanied by glomerulopathy is
typically more frequent in greyhounds (Fig. 18 b).
Lifestyle. Dogs that live outdoors are more likely to receive insect or snake
bites, and to experience foreign body reactions (Fig. 19 ), trauma, and
freezing. Sun exposure can cause erosive-ulcerative lesions, as observed in
actinic dermatoses, pemphigus erythematosus, cutaneous lupus
erythematosus (Fig. 20 ), and dermatomyositis (Fig. 21 ). Outdoor-living
dogs are also more likely to develop fungal (e.g. T. mentagrophytes
dermatophytosis [Fig. 22 ], sporotrichosis, or cryptococcosis), bacterial
(e.g. botryomycosis), and parasitic (e.g. leishmaniasis [Fig. 23 ])
infections. Indoor-dwelling dogs, especially those that spend time in
kitchens, are more likely to suffer burns from spilled hot liquids.
Travel. It is important to be aware of any areas that dogs may have travelled
to so that vector diseases or diseases specific to the geographical areas in
question, such as systemic mycoses, leishmaniasis, or cutaneous
microfilariae, can be included in the differential diagnosis.
Rate of onset. Depending on the speed with which the erosive-ulcerative
process has developed, it can be classified from gradual to hyperacute.
Skin reactions to spider and insect bites, reactions to certain drugs
(including vaccines), trauma, fractures, freezing due to exposure to extreme
cold, or burns from electric blankets (Fig. 24 ), among others, have an acute
onset.
Drug reactions. By studying the drugs recently administered to the patient
(within the previous 2 months), specific reactions to certain drugs can be
identified. These include pemphigus-type reactions, lupus erythematosus,
vasculitis, Stevens-Johnson syndrome, toxic epidermal necrolysis (NET),
and panniculitis (Fig. 25 ) associated with antibiotics (e.g. penicillins,
ampicillins, cephalosporins, trimethoprim-sulfamethoxazole,
metronidazole), antifungals (e.g. itraconazole), or phenobarbital. Erosive-
ulcerative lesions can also develop in response to the administration of
anti-inflammatory and immunosuppressive compounds that promote
colonisation and infection of the skin by rapidly growing yeasts, bacteria,
cryptococci, or mycobacteria.
12 Erosive-ulcerative lesions in a case of juvenile cellulitis. Image courtesy of Amparo Ortuñez.

13 Erosive-ulcerative lesions in a German Shepherd with deep pyoderma. (a) General appearance.
(b) Detail of an ulcerative lesion in the ventral area of the thorax.
14 Ulceration of perianal fistulas in a German Shepherd.
15 Erosive-ulcerative lesions around the site of vaccine inoculation. Reaction to (a) the rabies
vaccine and (b) the leishmaniasis vaccine (image courtesy of Eva Varela).
16 Actinic dermatitis. Lesions on (a) the abdomen and hindlimbs and (b) an erosive-ulcerative
lesion around the nipple. Images courtesy of Amparo Ortúñez.
17 Squamous cell carcinoma in a Mastiff.

18 Erosive-ulcerative lesions due to vasculitis. (a) General appearance and (b) detail from Spanish
Greyhound.
19 Erosive-ulcerative lesions in an inflammatory nodule caused by a spike embedded in the
interdigital space.
20 Erosive lesions in a dog with cutaneous lupus erythematosus. Image courtesy of Amparo
Ortúñez.
21 Erosive-ulcerative lesions in a case of cutaneous dermatomyositis.
22 Erosive-ulcerative lesions due to dermatophytosis and vasculopathy.
23 Ulcerative lesions on the bony prominences of a dog with leishmaniasis. (a) Caudal and (b)
rostral areas.
24 Ulcerative lesions caused by a third degree burn from an electric blanket. Image courtesy of
Laura Navarro .
25 Ulcerative panniculitis caused by a drug reaction.

GENERAL EXAMINATION
Dogs with extensive erosive-ulcerative lesions usually show systemic signs,
such as elevated temperature, depression, anorexia, anaemia and weakness,
peripheral lymphadenomegaly, dehydration, electrolyte imbalances, and
proteinuria.
When erosive-ulcerative lesions affect the extremities, lameness may be

observed. Sometimes this clinical pattern is a consequence of systemic
processes with cutaneous manifestations, such as liver disease, hepatocutaneous
syndrome, glomerulopathies (vasculitis with proteinuria, which is more frequent
in greyhounds), hyperadrenocorticism (which can cause calcinosis cutis with
lesions that may ulcerate) (Fig. 26 ), splenomegaly or lymphadenopathy (caused
by leishmaniasis), vasculopathies induced by bacterial septicaemia, systemic
inflammatory infectious diseases, tick-borne diseases, and neoplastic processes
such as cutaneous carcinomatous metastasis of mammary gland neoplasm.
26 Erosive-ulcerative process in an area of papulopustular/vesicular inflammation. This dog has

hyperadrenocorticism, which caused calcinosis cutis, which in turn became ulcerated. Image
courtesy of Amparo Ortúñez.
Dermatological examinations of open skin lesions should always be performed
while wearing gloves, as some of the agents responsible (e.g. mycobacteria and
Sporothrix schenckii , which causes sporotrichosis) have zoonotic potential.
To adequately describe the erosive-ulcerative processes, it is necessary to

characterise different aspects of the lesion, such as the appearance of the
margins and the base, the shape of the lesion, whether it is well defined, its
location or distribution on the body surface (head, trunk, limbs, mucocutaneous
areas), and the appearance of the skin bordering the ulcer. In cases involving
discharge, the appearance and colour should be noted.
Appearance of borders. Pressing with a finger on the skin adjacent to the
lesion can provide an indication of the degree of cohesion between the
epidermal cells. This in turn provides information on the mechanism that
has resulted in the loss of skin continuity. Detachment of the skin is
indicative of failure of the intraepidermal or dermoepidermal junctions
caused by alterations in the desmosomes and/or hemidesmosomes, usually
due to autoimmune processes. The shape of ulcers depends on the
pathophysiological mechanisms involved in their formation. In cases of
ulcers caused by an interruption in blood flow, the skin will have a
perforated appearance. Lesions that form over an area in which a papular,
pustular, vesicular, or bullous lesion has ruptured will be circular and well
defined (Fig. 27 ). Those caused by necrotic cutaneous processes will be
poorly defined.
Discharge. The fluids that emerge from ulcers can be serohaemorrhagic,
haemorrhagic, or purulent, and form crusts upon drying (Fig. 28 ).
A significant number of erosive-ulcerative processes result from constant

licking, due either to itching in the affected area or due to pain (e.g. in the
projection areas of the affected joints) (Fig. 29 ).
Distribution and location. The distribution of erosive-ulcerative lesions can

significantly facilitate diagnosis, since many of the associated processes
have very characteristic patterns of distribution. This information can be
combined with information on the involvement (or noninvolvement) of
specific body areas (Box 1 ), which can also be characteristic of certain
processes. These areas are the mucocutaneous junctions (lips [Fig. 30 ],
orifices of the nostrils and nasal plane [Fig. 31 ], eyelids [Fig. 32 ],
foreskin, vulva, or anus), mucous membranes, pinnae (Fig. 33 ), the scrotal
skin (Fig. 34 ), and the footpads (Fig. 35 ).
27 Ulcerative lesions of the footpads in a German Shorthaired Pointer with epidermolysis bullosa.
28 Crusts on eroded areas.
29 Erosive-ulcerative lesions caused by constant licking of the bony prominence of the carpus.
30 Erosive-ulcerative lesions covered by crusts in a case of mucocutaneous pyoderma of the lips.
31 Erosive-ulcerative lesions on the nasal mucocutaneous junction.

32 Erosive-ulcerative lesions on the mucocutaneous junction of the eyelid.
33 Erosive-ulcerative lesions on the pinna in a case of vasculitis. Image courtesy of Amparo
Ortúñez.
34 Erosive-ulcerative lesions on the scrotum caused by a drug reaction.
35 Erosive-ulcerative lesions on the footpad of a dog with leishmaniasis.
BOX 1
Based on Saridomichelakis, 2012.
DIAGNOSTIC PROTOCOL
Beginning with a list of possible causes of the patient’s erosive-ulcerative

presentation, the series of steps described below should be followed.
STEP 1 Is it a pruritic process?
If the patient presents with a pruritic process in which the observed lesions
are self-induced as a result of scratching, the diagnostic protocol for pruritus
(see Chapter 8 ) should be followed. In cases of a non-self-induced erosive-
ulcerative process, proceed to the second step.
STEP 2 Does the clinical history analysis or the

examination reveal any relevant findings?
Some erosive-ulcerative processes have clinical features that are highly
characteristic of certain pathologies, such as erosive oedematous
inflammation of the facial area in puppies (juvenile cellulitis), erosive-
ulcerative and fistulous lesions in the perianal area of German Shepherds
(perianal fistulas), and erythema, erosions, and uveitis in specific
predisposed breeds such as the Akita Inu (uveodermatologic syndrome).
Physical or chemical burns may also be recorded in the clinical history of
some patients with erosive-ulcerative processes. In these situations, in
which the clinical history and dermatological examination provide evidence
of a specific pathology, specific confirmatory tests should be proposed.
STEP 3 Cytology
Samples are obtained by direct imprinting of the lesions or by lifting the
crusts and obtaining an imprint from underneath using a slide. In cases in
which erosive-ulcerative lesions appear on the surface of nodules, the area
can be compressed or squeezed to release exudate from the open lesion,
which is then imprinted on a slide.
While the samples obtained can be dyed with any dye, Diff-Quik provides
rapid, good quality staining.
Diff-Quik staining allows visualisation of bacteria, fungi, Leishmania

amastigotes, inflammatory cells (Fig. 36 ), acantholytic keratinocytes,
hyperplastic or dysplastic cells, and neoplastic cells.
The inflammatory cells most commonly observed in erosive-ulcerative

processes are neutrophils, which can be either normal or degenerate. The
base of an ulcer commonly contains an inflammatory infiltrate in which
neutrophils predominate, although macrophages, eosinophils, lymphocytes,
plasma cells, and mast cells may appear as the process becomes chronic.
When the proportion of degenerate neutrophils is very high (constituting
over 85 % of the inflammatory cells observed), a septic bacterial
process should be suspected. The presence of phagocytic bacteria will
help confirm the diagnosis. A high proportion of nondegenerate
neutrophils is cause to suspect an immune-mediated process, sterile
irritants, or neoplastic lesions with a significant inflammatory
component.
When histiocytic cells, macrophages, or multinucleated cells are
observed, foreign bodies, or fungal or bacterial infections caused by
Actinomyces, Mycobacterium, or Nocardia should be suspected.
Cytology revealing a mixture of neutrophils and macrophages, or
neutrophils and macrophages together with lymphocytes and plasma
cells, may be indicative of lymphocytic granulomas, foreign body
reaction, or fungal or bacterial infection.
If the percentage of eosinophils exceeds 15–20 %, hypersensitivity
reactions, parasitic processes, mosquito bites, eosinophilic
furunculosis, certain fungal infections, or a neoplastic process
(mastocytoma) should be suspected.
The predominance of lymphocytes and/or plasma cells is cause to suspect
antigenic or immunogenic stimuli in the early stages of viral infections
or chronic inflammatory processes. Lymphoma should be suspected if
the cell population is very homogeneous and other inflammatory cells
are absent.
If dysplastic epithelial cells (not to be confused with neoplastic cells) are
identified, the patient’s presentation can be considered secondary to
inflammation or irritation.
If only bacteria are observed, in the absence of inflammatory cells on the

skin surface, a surface pyoderma should not necessarily be suspected, since
erosive-ulcerative lesions are often contaminated with opportunistic
microorganisms that thrive in the same medium. Licking can result in the
presence of bacteria of the genus Simonsiella spp., which are found in the
oral cavity and are of no diagnostic value.
The presence of phagocytic cocci or bacilli is indicative of potential

bacterial infection of the lesions. In such cases topical or systemic treatment
with adequate antiseptics or antibacterials is recommended. In cases in
which individual bacterial agents such as mycobacteria, Actinomyces spp.,
or Nocardia spp. are suspected, the reference laboratory should be consulted
to request special cultures and stains for these agents.
When acantholytic keratinocytes , either loose or clustered, are observed

floating amongst nondegenerate neutrophils, pemphigus complex should be
suspected (Fig. 37 ).
When noninflammatory cells predominate, it is important to attempt to

identify tissue cells associated with specific neoplastic processes (see
Chapter 2 ). However, it is not always easy to locate neoplastic tissue cells
in imprint cytology of ulcerated nodules. In these situations, fine-needle
puncture (with or without aspiration) provides a more representative
sample. This technique gives better results than imprinting when performing
cytological analysis of the borders or base of ulcers. The neoplastic cells
identified may correspond to epithelial neoplastic processes (large cells,
round cells, or polygonal cells clumped in groups), mesenchymal neoplastic
processes or sarcomas (normally isolated oval, spindle, or star-shaped
cells), and round-cell neoplasia (abundant, isolated round cells).
36 Types of inflammatory cells that can be identified by cytology in erosive-ulcerative lesions.
37 Cytological image of pemphigus in which acantholytic keratinocytes are visible between

nondegenerate neutrophils.

Leishmaniasis is a very common disease in certain European regions, such
as the Mediterranean basin, and can manifest clinically as an erosive-
ulcerative presentation. For this reason, it is useful to confirm or rule out
leishmaniasis in the patient through serology and a proteinogram (see
Chapter 4 ) before proceeding with other tests (leishmaniasis may also have
been detected in the third step) (Fig. 38 ).
38 Cytology of an erosive-ulcerative lesion confirming leishmaniasis. Amastigotes in the

interior of macrophages.
STEP 5 Biopsy
After cytological characterisation, skin biopsy can be used to establish a

probable or presumptive diagnosis or to rule out other processes.
Biopsy provides important diagnostic information on erosive-ulcerative

patterns.
A biopsy is necessary to confirm specific diagnosis of autoimmune or
immune-mediated processes, eosinophilic furunculosis, panniculitis,
vasculopathies, and congenital, hereditary, and neoplastic processes. It is
also a useful diagnostic tool when analysed using special stains such as PAS
(periodic acid Schiff ), which can identify dermatophytes that mimic
autoimmune diseases.
Therefore, it is of utmost importance that the pathological anatomy

laboratory receives samples of skin (ideally 3 samples) properly collected
from strategic zones and, where possible, from all lesion types observed on
the patient.
In cases in which mucocutaneous pyoderma is suspected, or where cytology

indicates the presence of abundant phagocytosed bacteria, it is advisable to
institute antibiotic treatment for 3 to 4 weeks before performing a biopsy:
Mucocutaneous pyoderma and certain autoimmune processes can share

common clinical, and in some cases histopathological, patterns. A
response to treatment is indicative of pyoderma.
If no clinical response to treatment is observed, the pathologist should be

provided with a biopsy sample free from bacterial complication, the
analysis of which will allow establishment of a more accurate
diagnosis, since secondary bacterial infections can mask
histopathological lesions characteristic of other primary dermatopathies.
It is important to consider the particular stage of progression of the

process. Early-stage biopsy specimens are preferred, since chronic lesions
can considerably complicate diagnostic interpretation. This is especially
important in cases of suspected causes that affect the dermoepidermal
junction, mucocutaneous diseases, or processes with systemic clinical signs.
The selection of areas for biopsy is key. Standard procedure is to select

portions of primary lesions whenever possible, even if the pattern being
analysed is characterised by erosive-ulcerative lesions.
Biopsies of erosive-ulcerative presentations should be collected in such a
way that the sample contains sufficient tissue to allow analysis of the
peripheral skin at the borders of the lesion, as well as the borders and base
of the lesion itself.
It is important to provide the laboratory with several pieces , collected from

different areas and of differing appearances, stored separately in properly
labelled vials.
STEP 6 Bacterial culture and antibiogram
The next step is performed when bacterial culture and an antibiogram are
deemed necessary. Thus, in all cases of erosive-ulcerative dermatitis in
which cytology has revealed a bacterial infection (step 3), samples should
be collected for bacterial culture and a corresponding antibiogram. This step
is especially necessary when mycobacteriosis, nocardiosis, or
actinomycosis are suspected, but also in cases of secondary pyoderma of any
type. Samples should be collected in aseptic conditions, after first cleaning
the skin surface. The type of bacteria suspected should be considered, since
some microorganisms require special culture media that are only available
in certain laboratories. Therefore, it is necessary to contact the laboratory to
find out how to collect and transport the sample, and to ensure that the
laboratory can perform the requested identification technique.
STEP 7 Mycological culture
Mycological cultures are indicated in cases of suspected pseudomycetoma

or kerion. A trichogram and Wood’s lamp are of little diagnostic help in
these cases: no fluorescence is detected in erosive-ulcerative lesions, which
is why M. canis infections usually produce false negatives.
If dermatophytosis is suspected, samples should be cultured in media

specific for dermatophytes (DTM and/or Sabouraud agar) to confirm the
process (see Chapter 3 ).
In some cases of kerion or pseudomycetoma, several biopsy samples are
required to perform both the culture and the histopathological analyses. In
cases of subcutaneous or systemic mycoses, which are unique presentations,
the laboratory should be contacted and informed of the suspected process.
Special care must be taken if deep mycoses such as blastomycosis,
histoplasmosis, cryptococcosis, or sporotrichosis are suspected (Fig. 39 ),
given the risk to laboratory technicians, who should be given adequate
notice.
39 Lesions suggestive of deep mycosis. These should be handled with gloves and the
reference laboratory should be contacted to report the suspicion and to request instructions
on how to collect samples for culture and identification.
STEP 8 Other specific tests
In some cases it will be necessary to perform immunohistochemical

techniques, immunofluorescence, ELISA or IFI serology, special staining, or
PCR to establish a definitive diagnosis. In cases of suspected systemic lupus
erythematosus, it may be useful to analyse antinuclear antibodies (ANA).
INTRODUCTION
In this chapter, we discuss the diagnosis of dermatoses with a clinical pattern
characterised by the presence of papular, pustular, and vesicular (PPV)
lesions. The PPV pattern includes both papulopustular (Fig. 1 ) and
papulovesicular processes (Fig. 2 ), since it is difficult to clinically
distinguish one from the other, and both frequently occur in tandem.
Moreover, other secondary lesions such as epidermal collarettes, crusted

pustules, target lesions, scales, and pigmentary alterations may accompany the
primary lesions that define this pattern, and are common to all processes that
begin with papulopustules or vesicles (Fig. 3 ).
Each of the primary and secondary lesions included in this pattern has
defining characteristics, as well as specific underlying mechanisms that
influence their appearance and clinical interpretation.
In dogs isolated papular, pustular, or vesicular lesions may develop,

However, they usually appear as part of a chronological spectrum, beginning
with papules and progressing to pustules or vesicles, with or without crusts,
or attached scales, erythema, epidermal collarettes, alopecia, and
hyperpigmentation (Figs. 4 and 5 ).
Papules are lesions consisting of small elevations of the skin of less than 1
cm in diameter (Fig. 6 ). They are raised above the skin surface and can be
palpated. Papules are usually erythematous and appear as a result of the
accumulation of inflammatory cells in the dermis due to oedema
(intraepidermal or superficial dermal), or as a result of epidermal
hypertrophy. Papules may also appear in certain neoplastic processes, in
cases of calcinosis cutis (deposition of calcium on the dermis), or in
inflammatory reactions in papular forms of leishmaniasis. Papules may or may
not be associated with a hair follicle (follicular or non-follicular papules).
Papules can evolve to develop a crust (Fig. 7 ) composed of serum, blood,

and purulent material that dry on the surface of the skin. Crust formation can
be the result of scratching in pruritic processes or can simply constitute the
natural evolution of the papule. Erythematous papules can be observed in
cases of superficial bacterial folliculitis, flea-bite hypersensitivity, and
sarcoptic mange.
Pustules are small elevations of less than 1 cm in diameter that are similar to
papules but contain purulent content (Fig. 8 ). Pustules can be considered
small abscesses (Fig. 9 ). Sometimes they begin as papules that transform into
pustules as a result of the rupture of the cells of the epidermis and the
accumulation of inflammatory cells in the upper portion (Fig. 10 ).
Depending on their location, pustules may be intraepidermal, subepidermal,

or follicular. Due to the fragility of pustules, they rupture very easily to form
epidermal crusts and collarettes, which form extensive crusted rings or
yellowish crusts that adhere to the skin.
They usually appear as a result of an infectious process and contain

neutrophils and microorganisms. In some pustules bacteria may be absent and
eosinophils may predominate, usually indicating a parasitic or allergic
processes. Sterile pustules can be found in follicular pemphigus, subcorneal
pustular dermatitis, and sterile eosinophilic pustulosis (also known as sterile
eosinophilic pustular dermatitis).
In terms of colour, pustules can be white, yellowish, greenish, or reddish. Size

can also vary considerably, with large pustules observed in certain
conditions. Information on pustule colour and size can be diagnostically
useful. Large, whitish-yellowish and flaccid pustules can be indicative of
impetigo (Fig. 11 ), demodicosis, spontaneous hyperadrenocorticism (HAC),
iatrogenic HAC, immunosuppression, or pemphigus foliaceus. Large,
greenish-coloured pustules (Fig. 12 ) indicate infection by Gram-negative
bacteria and can be associated with bullous impetigo, immunosuppression,
and pemphigus foliaceus.
Vesicles and bullae are very well defined lesions that are raised above the
surface of the epidermis and filled with very light coloured fluid (Fig. 13 ).
Vesicles are similar in size to papules and pustules, whereas bullae (Fig. 14 )
have a diameter of over 1 cm. Because the epidermal “dome” that defines the
vesicle and covers its upper part is very thin, vesicles rupture very easily and
are difficult to identify. It is thus easier to identify other cutaneous lesions
(e.g. collarettes or crusts) that have evolved from vesicles and/or bullae.
Vesicles can be located between the strata of the epidermis (intraepidermal

vesicles) or below the basal stratum (subepidermal vesicles). They form as a
consequence of several mechanisms that involve rupture of the adhesive
bonds between epidermal cells due to physical separation (oedema),
inflammatory reactions, autoimmune aggressions (pemphigus complex), or
epidermolytic toxins of bacterial origin, as occurs in cases of pyoderma or
certain forms of dermatophytosis.
The main processes associated with vesicular or bullous lesions are

pyoderma, insect bites, autoimmune dermatoses, and irritative forms of
dermatitis.
Crusts are lesions formed by the evolution of papules, pustules, or vesicles

that are characteristic of the PPV pattern, and are considered secondary
lesions in this pattern. They are formed when the scales, cells, blood, pus,
serum or any other type of exudate dries and adheres to the surface of the skin
(Fig. 15 ). Crusts can be observed in pyoderma and superficial bacterial
folliculitis, pemphigus foliaceus, furunculosis, vasculitis, sarcoptic mange,
and necrolytic migratory erythema.
Folliculitis is the inflammation of the hair follicle. Papules, pustules, and

crusts can be observed around the base of the hair shaft. The inflammatory
cells that induce inflammation of the hair follicle come from the perifollicular
blood vessels and follow the same haemodynamic pattern as seen in cases of
dermal inflammation, inducing leukocytic changes. Folliculitis is observed in
cases of bacterial infections that affect the hair follicles (Fig. 16 ), and in
dermatophytosis and demodicosis.
01 Papulopustular lesions on the skin surface of the lateral thorax.
02 Papulovesicular lesions in the concave area of the inner pinna in a case of pemphigus
foliaceus.
03 Papulopustules, crusts, and collarettes in a case of generalised juvenile demodicosis.
04 Erythema, papules, and pustules in a case of superficial pyoderma of allergic origin.

05 Papulopustules (periphery of image) and epidermal collarettes (centre) in a case of
superficial pyoderma.
06 Papules caused by trombiculiasis in the medial area of the hindlimb.

07 Papules, pustules, and crusts in a case of generalised pyoderma.
08 Pustules on the abdomen and the medial hindlimbs of a puppy with impetigo.
09 Papules in a case of pemphigus foliaceus.
10 Papules, pustules, and collarettes in a case of pemphigus foliaceus.

11 Whitish-yellow pustules on a dog with demodicosis.
12 Large yellow pustules on a dog with hyperadrenocorticism.

13 Vesicles in the concave area of the pinna.
14 Vesicles and bullae on a Shar Pei dog with cutaneous mucinosis.

15 (a) Circular crusts that have evolved from localised papulopustules. (b) Crusts in a
generalised papulopustular presentation.
16 (a) Bacterial folliculitis in the abdominal area of a dog with semi-long hair and (b) folliculitis
on the dorsal area of the trunk in a short-haired dog, resulting in a moth-eaten appearance.
UNDERLYING CAUSES OF THE

PATTERN
The causes of the PPV pattern are shown in Box 1 . Among the most
commonly implicated processes are bacterial pyoderma, autoimmune
diseases, and other immune-mediated processes. The PPV pattern may also be
observed in less common pathologies, with variable degrees of pruritus,
including sterile eosinophilic pustular dermatitis, subcorneal pustular
dermatitis, and rare forms of canine leishmaniasis (Fig. 17 ).
17 Papules on (a) the eyelid and (b) the posteromedial area of the hindlimbs in a dog with
leishmaniasis.
BOX 1
Main causes of papulopustular and vesicular patterns in dogs
Allergic
Atopic dermatitis
Flea-bite hypersensitivity
Autoimmune
Pemphigus foliaceus
Pemphigus erythematosus
Bullous pemphigoid
Systemic lupus erythematosus
Ectoparasites
Demodex
Pelodera
Fleas
Sarcoptes
Trombicula
Endoparasites
Leishmania
Dirofilaria
Superficial mycosis
Dermatophytes1
Dermatitis due to Malassezia
Superficial bacterial pyoderma

Acne
Folliculitis1
Impetigo
Neoplasia
Mastocytoma
Various
Calcinosis cutis
Juvenile cellulitis
Sterile eosinophilic pustular dermatitis
Subcorneal pustular dermatitis
Idiopathic linear acantholytic pustular dermatosis
Contact irritation
Drug reaction
1
Follicular lesions.
A complete review of the patient’s clinical history, as well as general and
dermatological examinations are fundamental starting points in the diagnostic
approach to the PPV pattern.
In all cases involving a PPV pattern with crusts, collarettes, and diffuse
pigmentation, pyoderma should first be considered. However, pyoderma is
almost always secondary to any other disease and is recurrent, unless the
underlying cause is identified (Box 2 ). Therefore, the following processes
should also be considered:
Hypersensitivity reactions, which are very common, are very often
accompanied by secondary bacterial infections.
Endocrine and metabolic pathologies, such as hypothyroidism (HT), can
present with papulopustular lesions due to associated immune defects.
Autoimmune diseases of the pemphigus complex are characterised by the
development of papulopustular and vesicular patterns with crusts, which
are characteristic of these pathologies.
BOX 2
Main causes of recurrent pyoderma
Pruritic causes
Allergic origin
Contact allergy
Atopy
Flea-bite hypersensitivity
Parasitic origin
Hookworms
Cheyletiellosis
Demodicosis
Insect bites
Ant-like insect bites
Sarcoptic mange
Nonpruritic causes
Endocrine
Hypothyroidism
Sex hormone imbalance
Keratinisation defects
Primary seborrhoea of Cocker Spaniels
Parasitic
Demodicosis
Various
Next, any aspects of the medical history that may provide information of
interest relating to this pattern should be analysed.
Pruritus. This is the first component that should be investigated in cases
involving the PPV pattern. If pruritus exists, it is essential to determine
when it began, and to define its characteristics and intensity.
Moment of onset. It is necessary to know whether pruritus appeared
before or at the same time as the lesions, or whether it constitutes a
complication of the pathological process. In parasitic and allergic
processes, pruritus is the main sign from the beginning. Papules and
pustules can be characteristic of pruritic processes, such as allergies
and ectoparasite infestations.
Characteristics and intensity. Sarcoptic mange is characterised by
papular lesions associated with intense pruritus, and responds
poorly to corticosteroids and oclacitinib. Other parasitic causes
include pulicosis and cheyletiellosis, which are less pruritic than
Sarcoptes infestation, but can also be contagious and produce
lesions in contact areas in humans. However, neither Demodex nor
lice, which are species-specific, are contagious. Bacterial infections
may or may not be pruritic, depending on the agent involved and the
sensitivity of the individual. Some dogs with superficial pyoderma
develop intense pruritus, while others do not.
Autoimmune diseases are considered nonpruritic processes. However, some

dogs with these processes present with pruritus, possibly caused by
inflammatory mediators or secondary infections.
Previous treatments. In some cases patients may have received prior

medical treatment, which should be recorded in the medical history.
Analysis of the response to these treatments can provide important
information.
Oclacitinib or corticosteroids. If the patient has been treated with
oclacitinib or corticosteroids prior to the consultation and the owner
reports an improvement, atopic dermatitis, food hypersensitivity,
flea-bite hypersensitivity, and contact allergy should be considered
as potential causes of the PPV pattern. By contrast, if the patient’s
condition worsened following treatment, the following potential
causes should be considered:
Food hypersensitivity, since oclacitinib and corticosteroids can
initially improve pruritus, after which the response worsens.
The same effect described for food hypersensitivity can also be
observed in cases of sarcoptic mange.
Autoimmune diseases require high doses of corticosteroids.
Accordingly, low doses of anti-inflammatories will result in a
poor response.
Other processes that can manifest with pruritus and a PPV pattern
are demodicosis and dermatophytosis, which worsen in
response to corticosteroid treatment.
Antiparasitics. Administration of appropriate antiparasitic agents
should result in resolution of papulopustular presentations caused by
parasites such as fleas, lice, and Cheyletiella , and skin mites such
as Sarcoptes , Otodectes , and Trombicula larvae. These
considerations should be taken this into account when analysing
prior treatments administered to the patient.
Response to antibiotics. If the patient has been previously treated
with antibiotics, information on the reaction to treatment and
subsequent evolution of the process can greatly aid the diagnostic
process:
A good response indicates the presence of pyoderma.
A partial response is suggestive of immune-mediated processes or
antibiotic resistance.
If bacterial cultures and an antibiogram were performed, a
negative culture in a patient with papulopustular lesions that
responded poorly to antibiotics can provide valuable
information, suggesting a possible autoimmune pathology.
Drug reactions . Many processes that produce a PPV pattern are
induced by drugs or chemicals, which can be difficult to identify.
Therefore, it is important to determine whether there is a
relationship between the administration of a given treatment and the
appearance of papulopustular or vesicular lesions. It should be
borne in mind that clinical manifestations of drug reactions can vary
widely, and can mimic other processes (Fig. 18 ). Many drugs can
induce immunological reactions associated with a PPV pattern, in
some cases also involving pruritus, giving rise to a process that
resembles pemphigus foliaceus.
Disease course . In cases involving acute or hyperacute pruritic lesions of
the face or feet (Figs. 19 and 20 ), the most common causes are
eosinophilic folliculitis or furunculosis caused by insect bites (ants,
wasps, and mosquitoes). Papular lesions in these same areas, but of
slower onset, may be cause to suspect leishmaniasis. It is therefore
necessary to know whether the dog has travelled to areas of risk, whether
the owner applies adequate ectoparasite control measures, and whether
the area in which the dog habitually lives is an area of risk for vector
diseases. It should also be noted whether the process is characterised by
the cyclical appearance of lesions (i.e. lesions that appear and disappear,
or improve and worsen), and whether the patient has a fever or is
depressed prior to or during development of the lesions. The appearance
of lesions in waves is typical of autoimmune diseases, but can also occur
in cases of vasculitis and recurrent deep pyoderma (Fig. 21 ), depending
on the underlying cause.
Seasonality . Diagnosis can also be facilitated by determining whether
lesions appear only during certain periods of the year.
18 Presentation similar to pyoderma of the chin or cellulitis in a case of drug reaction caused by
amoxicillin and clavulanic acid.
19 Furunculosis of the chin.
20 Furunculosis of the paw.

21 Lesions caused by deep recurrent pyoderma.
GENERAL EXAMINATION
In the general physical examination, we will establish whether the patient has
an underlying systemic metabolic, endocrine, renal or hepatic disease. If so,
the PPV pattern is likely a consequence of these systemic anomalies. Dogs
with autoimmune processes or generalised vasculitis may also show systemic
signs such as discomfort, weight loss, fever, inappetence, and
lymphadenopathy.
In general, analytical tests (blood tests, biochemical profiles, and urinalysis)

do not provide much information in skin diseases, but may be of interest in
geriatric patients that have developed skin problems for the first time
(bacterial pyoderma, demodicosis, or dermatophytosis) as a consequence of
endocrine (hypercholesterolaemia, elevated alkaline phosphatase levels) or
metabolic (hypercalcaemia, elevated levels of liver enzymes) processes.
The aim of this examination is to identify the primary lesions of the pattern
(papules, pustules, vesicles), as well as any secondary lesions that have
evolved from primary lesions (e.g. collarettes, target lesions, crusts, or
inflammatory hyperpigmentation), and to determine the lesion distribution,
which in the case of the PPV pattern can significantly facilitate diagnosis:
Elbows, hocks, ventral region, and margins of the pinnae in cases of
sarcoptic mange, with only papular lesions (no collarettes, pustules, or
target lesions).
Facial area, axillae, inguinal area, feet, and/or ventral region of the
abdomen in cases of atopic dermatitis and food hypersensitivity. The
sudden appearance of pustules and/or crusts in the facial area should
increase the suspicion of an autoimmune dermatosis (Fig. 22 ).
Non-follicular papulopustules located only in the abdominal region in
cases of impetigo.
Generalised papulopustules that exclusively affect areas with hair in
cases of bacterial folliculitis and generalised pemphigus.
Pustules and/or crusts in the facial area, inner aspects of the pinnae,
nail bed, and footpad in cases of pemphigus. The exclusive presence of
large, greenish, papulopustular lesions enveloping multiple hair follicles
on the face, pinnae, and/or feet is strongly suggestive of pemphigus or
drug-induced pemphigus. In pemphigus foliaceus, lesions tend to initially
appear on the face and pinnae. Subsequently, during periods of eruption,
the lesions progress in waves, and all lesions progress though similar
evolutionary stages.
Erythematous papulopustular eruptions, crusts, and collarettes that
cover the entire trunk in cases of pyoderma caused by bacterial
folliculitis. Thus, pyoderma should be suspected if dermatological
examination of a patient with a PPV pattern reveals the entire lesion
sequence of the “pustular cycle” (papules, pustules, collarettes, crusts,
follicular casts, adhered scales), predominantly affecting the trunk. It is
very rare for bacterial pyoderma to only affect the facial area, except in
very chronic cases.
Comedones, pustules, and furunculosis in cases of acne, demodicosis,
dermatophytosis, juvenile cellulitis, and infectious and sterile
granulomas.
22 Papulopustular lesions that have evolved from an excoriation on the nasal bridge in a case of
pemphigus foliaceus.
Pyoderma versus pemphigus

In many cases it is necessary to differentiate between these 2 groups of
diseases, since the initial stages of pemphigus complex and pyoderma can
both involve the appearance of papulopustular lesions.
Clinical finding Bacterial pyoderma Pemphigus

Presence of This presentation of Highly compatible
papulopustular bacterial pyoderma is with pemphigus
lesions only very rare
A large number of Not indicative of bacterial Indicative of

papulopustules pyoderma pemphigus
that encompass
multiple hair
follicles
Cytological Abundant degenerate Presence of

examination of neutrophils, in some cases nondegenerate
pustules accompanied by loose neutrophils and
(not accumulated) evident
acantholytic cells accumulations of
acantholytic cells
Response to Pyoderma usually Pemphigus does

antibiotic therapy responds well to not usually
antibiotic treatment respond well to
antibiotic therapy
DIAGNOSTIC PROTOCOL
By consulting Box 1 , which lists the processes associated with the PPV
pattern, the diagnostic tests required to reach a definitive diagnosis, and
the order in which they should be performed, can be established.
STEP 1 Scrapings and trichogram

Deep skin scrapings and a trichogram should be performed, especially if
the PPV pattern is pruritic, as this suggests that either demodicosis (Fig. 23
) or sarcoptic mange may underlie the presentation. However, it is not
always easy to confirm demodicosis based on a skin scraping, particularly
in cases involving a papulopustular presentation in specific locations such
as the limbs, or in certain dogs with a very thick dermis. Therefore, in
certain situations other techniques, such as a trichogram or biopsy, will be
required.
In cases of pododermatitis (Fig. 24 ) in which bleeding caused by
inflammation hinders the collection of a clean sample (Fig. 25 ), it is
advisable to confirm or rule out Demodex using a trichogram.
In cases involving Shar Peis or other breeds with thick skin, which
complicates the removal of Demodex by deep scraping, a biopsy may
be required.
23 Papulopustules in a Shar Pei with demodicosis.

24 Pododermatitis with papulopustules and interdigital vesicles in a case of recurrent
pyoderma. Deep skin scraping causes significant pain.
25 Pododermatitis with erythematous eroded papulopustules in a dog with atopic dermatitis

and demodicosis.
STEP 2 Cytology
Cytology allows analysis of the contents of papules, pustules, and vesicles.

This technique allows identification of inflammatory cells, acantholytic
cells, eosinophils (where the underlying cause is an allergic disease or
pemphigus foliaceus), and microbial agents. It can also be used to
determine whether the bacteria are intracellular or extracellular, in order
to differentiate between overgrowth, bacterial colonisation, and infection.
Acantholytic cells are not found only in pemphigus, but can also appear in
other pathologies, such as certain severe bacterial infections, pustular
dermatophytosis, and contact allergies. Therefore, the presence of
acantholytic cells is not sufficient reason to establish a definitive diagnosis
of pemphigus.
Cytology (by fine-needle puncture) can also be used to determine the

presence of Leishmania amastigotes in papular presentations (Fig. 26 ).
26 (a) Papules caused by phlebotomine bites and (b) Leishmania amastigotes in a cytology
sample obtained from the papules.
STEP 3 Confirm or rule out Leishmania
Papulopustular presentations caused by leishmaniasis are usually

diagnosed by fine-needle puncture cytology. However, in suspicious cases
in which cytology produces a negative result, quantitative serological tests
and a proteinogram (see Chapter 4 ) will be necessary.
STEP 4 Mycological culture
Cultures should be considered for the isolation of dermatophytes,

especially in young dogs (Fig. 27 ) and in adult dogs with papulopustular
lesions, since dermatophytosis can present with a PPV pattern in
immunodeficient geriatric patients.
27 Papulopustules in a 5-month-old dog with dermatophytosis.
STEP 5 Bacterial culture and antibiogram
Papulopustular presentations caused by superficial pyoderma are very

common in clinical practice, and the prescription of antibiotics for 1 month
is common in cases involving the PPV pattern. However, given the
increasing prevalence of antibiotic resistance and the importance of
responsible antibiotic use, it is recommended to first perform a culture and
antibiogram to identify an effective treatment to resolve the pathology in
question.
To collect an adequate sample for bacterial culture, it is necessary to

locate and rupture an intact pustule, from which the contents should be
collected using a sterile swab. If intact pustules cannot be located, a
biopsy sample will be required for an adequate bacterial culture.
Antibiotics and pyoderma

Treatment varies depending on the diagnosis, as described above. Here,
we describe the protocol for the treatment of pyoderma, given the
complexity of treatment and the fact that it is one of the main causes of the
PPV pattern.
Once an antibiotic has been selected based on the results of the

antibiogram, it is administered for a minimum of 3 to 4 weeks and the
evolution of the condition is evaluated in terms of improvements in lesions
and pruritus. The following results can be expected:
Complete disappearance of lesions and pruritus at follow-up visit.
Antibiotic therapy should be prolonged for 1 week from the date of the
total disappearance of clinical signs.
Absence of lesions and pruritus at follow-up visit, but the pyoderma
recurs within weeks of completing the course of antibiotics. In these
cases endocrine and metabolic causes, alterations in cornification, and
drug reactions should be investigated.
Disappearance of the lesions but residual pruritus persists, and
pyoderma recurs some time after completing the course of antibiotics.
This is suggestive of recurrent pyoderma, and indicates that underlying
pruritic causes should be investigated (see Chapter 8 ).
Lesions improve but do not disappear, and new cytology reveals the
presence of bacteria. This is cause to suspect persistent bacterial
folliculitis. Treatment should be continued for 2 weeks after complete
resolution of the process, with the disappearance of all clinical signs.
In addition, the patient should be carefully monitored to ensure that no
relapses occur and that the infection is completely controlled.
Otherwise bacterial resistance may develop. Administration of
antibiotics for short periods can result in relapses and the
development of antibiotic resistance.
No lesion improvement is observed, but cytology reveals an absence of
bacteria. Other causes should be considered (Sarcoptes , food
hypersensitivity, contact allergy, autoimmune disease, epitheliotropic
lymphoma, or calcinosis cutis).
No lesion improvement is observed and cytology reveals the persistence
of bacteria. Antibiotic treatment should be discontinued for 1 week
and cytology repeated. The approach taken will depend on the results
of the cytology. The persistence of bacteria indicates a probable case
of bacterial resistance.
STEP 6 Biopsy
For many processes that manifest with a PPV pattern, a biopsy is required
to confirm the diagnosis. These include diseases of the pemphigus
complex, lupus erythematosus, dermatomyositis, bullous dermatitis,
superficial necrolytic dermatitis, subcorneal pustular dermatosis, and
sterile eosinophilic pustular dermatitis. In all these cases, it is advisable to
first control the infection with antibiotics (if cytology has indicated the
presence of bacteria), and to avoid administering glucocorticoids during
the preceding 2 weeks in order to obtain the best possible sample on
which to base the diagnosis.
Calcinosis cutis is also diagnosed based on analysis of a biopsy sample.

This condition is characterised by the formation of highly pruritic papules
with a hard white core of deposited calcium. It should be included in the
differential diagnosis of any lesions that worsen in response to systemic
corticosteroid administration.
The location of the papules, pustules, and vesicles in the skin layers
provides diagnostically useful information (Box 3 ).
BOX 3
Differential diagnosis of papules, vesicles, and pustules
based on histological localisation
Histological Processes that should be included in the
localisation differential diagnosis
Subcorneal Superficial suppurative necrolytic dermatitis

(Schnauzers)
Subcorneal pustular dermatosis
Bacterial infection
Impetigo
Leishmaniasis
Pemphigus foliaceus
Pemphigus erythematosus
Sterile eosinophilic pustulosis
Stratum Pemphigus erythematosus

granulosum Pemphigus foliaceus
Stratum spinosum Superficial necrolytic dermatosis

Viral dermatoses
Pemphigus vegetans
Sterile eosinophilic pustulosis
Suprabasilar Pemphigus vulgaris
Stratum basale Dermatomyositis

Erythema multiforme
Lupus erythematosus
Exfoliative lupus erythematosus
Vesicular lupus erythematosus
Toxic epidermal necrolysis
Paraneoplastic pemphigus
Subepidermal Dermatitis herpetiformis

Linear IgA dermatosis
Epidermolysis bullosa
Erythema multiforme
Lupus erythematosus
Bullous pemphigoid
Mucomembranous pemphigoid
Based on Miller et al., 2013.
INTRODUCTION
Pruritus is an irritating sensation that creates discomfort in the affected
individual (Fig. 1 ). In humans it is defined as an unpleasant sensation that
induces scratching. While we cannot determine exactly what dogs feel when
they exhibit licking, sucking, scratching, rubbing, or chewing behaviours, these
signs are interpreted as manifestations of pruritus.
Acute pruritus serves a protective function, acting as a warning sign of potential

tissue damage caused by a certain aggression, such as that elicited by a parasite.
Scratching reflects an attempt to suppress the itching sensation, but can
sometime damage the skin.
Dogs, trying to alleviate the discomfort, scratch, chew, lick, suck, and/or rub
affected areas against walls, furniture, or even their owners. These responses to
the itching sensation give rise to self-trauma, resulting in hair loss and the
formation of erosions, ulcers, crusts, or scales. In addition to lesions caused by
loss of skin continuity, skin that is exposed to aggression becomes more
susceptible to secondary infections and the formation of papules and pustules,
or may respond with hyperkeratosis, squamous lesions, crusts, and follicular
casts.
If the veterinary surgeon can clearly establish early on whether pruritus

constitutes the primary clinical sign, or the first sign to appear, and can
categorise the pruritus, this can significantly aid the diagnostic process.
Pruritus should be investigated before any other cutaneous signs of

dermatological disease, and it should be established whether the patient has a
pruritic or nonpruritic presentation. Next, within the category of nonpruritic
processes, different patterns of cutaneous lesions can be identified.
01 Schnauzer with flea-bite hypersensitivity chewing its dorsolumbar area. Examination reveals
intense pruritus.
PATHOPHYSIOLOGY OF PRURITUS
The skin is the most extensive organ of the body, and contains free nerve
endings that can capture a wide range stimuli corresponding to pain, touch, and
itching (Fig. 2 a). Many substances have been identified that can transduce the
sensation of pruritus (e.g. histamines, proteases, prostaglandins, interleukins)
(Box 1 ). These chemical mediators activate nerve endings and generate an
electrical impulse that will follows a long trajectory, passing through multiple
synapses, to reach the central nervous system (CNS), where the sensation of
pruritus is integrated and recognised (Fig. 2 b).
The electrical impulses carry information relating to the pruritic stimulus to the
cortex, following a pathway that begins at the receptors in the skin and continues
along the dorsal root ganglion of the spinal cord, the lateral spinothalamic tract,
and the thalamus (Fig. 2 b). When the electrical impulses reach the cerebral
cortex, the patient perceives the pruritic sensation. The dorsal root of the spinal
cord receives impulses from both the skin and the brain. Brain impulses assist
in controlling the severity of pruritus, and may inhibit or stimulate afferent
impulses from the skin. Therefore, situations such as stress or anxiety can
amplify the perception of pruritus (as has been demonstrated in humans) through
the release of chemical mediators such as opioids.
BOX 1
Chemical mediators of pruritus
Pruritus mediators are substances that induce pruritus, acting at different

levels of the transmission system. They have been identified in many species,
and include:
Certain types of cytokines, such as IL-2 and nerve growth factor (NGF).
LI-31.
Histamine (H1, H2, H3, and H4 receptors).
Lipid mediators (leukotriene B4).
Neuropeptides (substance P or neurotransmitter peptide released from mast
cells).
Opioids (act at the level of the spinal cord: μ-opioids exacerbate pruritus
and κ-opioids attenuate it).
Vasoactive intestinal peptide.
Proteases (tryptase, kallikrein).
Prostaglandin E2.
Serotonin.
Thromboxane A2.
02 (a) Skin sensory receptors and (b) pathways via which the pruritic sensation is transmitted.
Pruritus and pain

Both pruritus and pain serve to warn the animal of the existence of a
potentially dangerous stimulus and associate it with a protective motor
response. However, these 2 states differ significantly. The stimulus induced
by pruritus promotes scratching or chewing to eliminate the stimulus, and this
response in turn produces a pleasant sensation. By contrast, painful stimuli
cause the animal to avoid touching the affected body area and induce an
aggressive motor response. Both pruritus and pain begin at the surface of the
skin and mucous membranes.
The pruritic stimulus is received by the nonspecialised, demyelinated, free

nerve endings located very close to the dermoepidermal junctions. If the
epidermis is removed, the ability to perceive pruritus is lost. Therefore, pruritus
is presumably generated by the activation of subpopulations of sensory fibres
located in the upper layers of the skin. Pruritus originates in the skin in 2 ways:
directly, through the release from keratinocytes of mediators such as
neuropeptides, interleukins, proteases, and cytokines that bind directly to
pruritus receptors;
indirectly, whereby keratinocytes activate other cells, which in turn release
mediators such as nerve growth factor, neurotrophin-4, leukotriene B4 ,
thromboxane-A2 , endothelin-1, endogenous cannabinoids, and β-endorphin.
These substances, in turn, stimulate mast cells to release histamine,
leukotriene B4 , prostaglandins, proteases, and IL-2. This also results in the
release of nerve growth factor from eosinophils.
In both cases, mediators of pruritus bind to pruritic receptors and thus activate
the spinal neurons of the dorsal horn of the spinal cord.
Many mediators of pruritus have been identified. Among the best known are
histamine, for which 4 receptors (H1–H4) are described:
H1 receptors are expressed in sensory nerve fibres and in the endothelium of
blood vessels. When injected intradermally, histamine causes a
vasodilatory reaction with pruritus, erythema, and the formation of papules
(i.e. the triple response of Lewis or neurogenic inflammation).
H2 receptors are also found in the cutaneous sensory nerve fibres, and their
blockade attenuates the sensation of pruritus.
The H3 receptor is predominantly expressed in the CNS and mediates self-
regulation of histamine production.
The H4 receptor is found in inflammatory cells such as mast cells,
eosinophils and lymphocytes, and, when stimulated, increases levels of IL-
31, the most recently described mediator of pruritus in dogs.
Interleukins (IL-2, IL-6, and IL-8) constitute a very important group of
mediators of pruritus. IL-31 is currently considered one of the most important
interleukins in the pruritic process in canine species, and triggers pruritus when
it binds to its receptors and activates janus kinase (JAK) enzymes.
Damage to the skin barrier facilitates penetration by irritant and pruritic agents,
and thus any such imbalance can trigger pruritus. Similarly, a decrease in
hydration of 10 % or more triggers pruritus and scratching. Furthermore, it has
been demonstrated in humans that acute and chronic psychological stress can
contribute to the onset of pruritus. In over 75 % of atopic individuals, clinical
signs worsen in conditions of emotional stress due to interactions between
glucocorticoids, catecholamines, neuropeptides, and other stressors with the
psychoneuroendocrine system.
CAUSES OF PRURITIC SIGNS

Before examining a dog with a pruritic condition, a list of possible causes
should be drawn up. Box 2 shows a list of these causes, among which the most
important are external parasites and allergies.
BOX 2
Causes of pruritus
Type of cause Name of process Distribution
Allergic 1 Allergic contact dermatitis Hairless areas,

footpads, belly,
muzzle
Atopic dermatitis Flexor surfaces,

axillae, groin,
periocular area,
perioral area, ear
canal, generalised
Flea-bite hypersensitivity Caudodorsal area,

generalised
Food hypersensitivity Flexor areas,

axillae, groin,
periocular area,
perioral area, ear
canal, generalised
Insect bites Facial area, pinnae
Infectious Dermatophytosis Facial area,

extremities,
generalised
Dermatitis due to Flexor surfaces,

Malassezia axillae, groin,
footpads, nail fold,
neck, perioral area
Superficial pyoderma Any area with hair
Parasitic 1 Cheyletiellosis Dorsal trunk area
Demodicosis Focal or
generalised
Otitis caused by Otodectes Ears, facial area
Pediculosis Dorsal area,

generalised
Sarcoptic mange Pinnae, elbows,

flanks
Trombiculosis Facial area, feet,

ventral area
Autoimmune or Subcorneal pustular Head and trunk

immune-mediated dermatosis
Systemic lupus Facial area,

erythematosus extremities, trunk,
mucocutaneous
areas, generalised
Pemphigus foliaceus Head, pinnae,

footpads,
generalised
Sterile eosinophilic Multifocal areas on

pustulosis the trunk
Drug reaction Multiple forms
Neoplastic Epitheliotropic lymphoma Generalised
Mastocytoma Variable
Others Calcinosis cutis Variable
Acral lick dermatitis Forelimbs and

hindlimbs, tail
Irritant contact dermatitis Contact zones
Zinc-responsive dermatitis Periocular area,

perilabial area,
weight-bearing
areas of limbs
Seborrhoea Regional or
generalised
1
The most important causes of pruritus are external parasites and hypersensitivity to fleas and
aeroallergens.
It is extremely important to carry out a detailed analysis of the patient’s medical
history, followed by in-depth physical and dermatological examinations. If these
examinations are conducted comprehensively and systematically, it should be
relatively easy to establish a definitive diagnosis.
It should be borne in mind that when the pruritus is chronic in nature, patients
will develop very similar secondary lesions. Regardless of the underlying cause
of the pruritus, all aspects relating to the patient and their clinical history should
be recorded in an orderly and systematic manner.

Age. The age of the dog at the initial onset of pruritus is one of the most
important factors to take into account when prioritising potential causes. In
puppies or dogs of less than 6 months of age, the most common causes of
pruritus are ear mites, Demodex (Fig. 3 ), Chey- letiella (Fig. 4 ), and lice.
In dogs of 6 months to 3 years of age pruritic signs may be indicative of
atopic dermatitis (Fig. 5 ). Food hypersensitivity, like environmental atopic
dermatitis, is also common in dogs of this age range, but can occur at any
age.
Breed. The following breeds are predisposed to allergic dermatitis and to
atopic dermatitis in particular: Boxer, French (Fig. 6 ) and English (Fig. 7 )
Bulldog, Dalmatian, Golden Retriever, Labrador-type breeds (Fig. 8 ), Jack
Russell Terrier, Shar Pei, and West Highland White Terrier (Fig. 9 ). Dogs
with pronounced skin folds, such as the Shar Pei or Bulldog, can easily
develop intertrignous pruritus or skinfold pyoderma. Breeds predisposed to
overgrowth of Malassezia (Basset Hound and West Highland White
Terrier) (Figs. 10 and 11 ) can develop intense pruritus. Breeds
predisposed to demodicosis include the Boxer, English and French
Bulldog, Doberman, Rottweiler, and Shar Pei.
Characteristics of the living area. The characteristics of the dog’s living
area (wooden interiors, carpets, terrazzo flooring, outdoors) should be
carefully analysed, as this will allow us to address any suspicions of
contact allergy or possible flea infestation in protected garden or patio
areas. Dogs that spend many hours in the sun may develop actinic keratosis
(Fig. 12 ) or pruritic squamous cell carcinomas.
Characteristics of the environment, contagiousness. Dogs that live in the
countryside, in areas close to pig farms, or in communities, can contract
(through wildlife) dermatophytosis (via contact with small rodents or their
burrows), sarcoptic mange (via contact with foxes in infested areas), or
Aujeszky’s disease (via ingestion of remnants of infected pigmeat). It is
necessary to know whether the patient shares a home with or receives
regular visits from other pets, as this can result in a persistently high
parasitic load in the environment and can hinder flea control measures.
Furthermore, the presence of other affected animals in the environment
could be indicative of contagious processes such as dermatophytosis,
otocariosis, or cheyletiellosis. The presence of lesions on humans who live
with the dog should be cause to suspect dermatophytosis, fleas,
Cheyletiella , Sarcoptes , or Otodectes. It is important to determine
whether the pruritus began after the patient spent time in a residence or
nursery, or in the house of relatives or friends with other pets, as this can
provide important clues as to the potential existence of a contagious
process. The most common pruritic processes in collectives (nurseries,
breeding facilities, hunting packs, etc.) are caused by flea
infestations/hypersensitivity, Sarcoptes, Cheyletiella, dermatophytes, and
Otodectes.
Diet. It is necessary to investigate any relationships between the patient’s diet
and the onset of pruritus, potentially caused by food hypersensitivity.
Cleaning products used for floors, hair softeners, perfume, and detangling
products can cause pruritic contact dermatitis.
Previous treatments. Antibiotics, corticosteroids, and oclacitinib have rapid
and distinct effects on pruritus, which should be evaluated.
Characteristics of pruritus. The intensity of pruritus, the manner in which it
appeared, its evolution over time, and any seasonal component are very
important factors to take into account in when analysing the patient’s
medical history. Given their importance and significant variability, these
characteristics are explained in the following section.
03 Demodicosis in a puppy.
04 Cheyletiellosis in a puppy.
05 Environmental atopic dermatitis with typical distribution: face, feet, inguinal area, and axillae.
06 French Bulldog with atopic dermatitis with a food component.

07 English Bulldog with atopic dermatitis.
08 Labrador with atopic dermatitis.

09 West Highland White Terrier with atopic dermatitis.
10 Basset Hound with atopic dermatitis and Malassezia overgrowth.

11 West Highland White Terrier with chronic atopic dermatitis with hyperpigmentation,
lichenification, oily seborrhoea, and overgrowth of Malassezia .
12 Pruritus caused by actinic keratitis in the ventral area of a white-coated dog. Image courtesy of
Amparo Ortuñez.
CHARACTERISTICS OF PRURITUS
The first characteristics that should be analysed are intensity, the manner in
which the pruritus appeared, its evolution over time, and seasonality.
Intensity of pruritus on a scale of 0 to 10

The owner should be asked about the frequency and intensity of the dog’s
scratching, and a score applied as follows:
No scratching: 0–10.
Mild pruritus: 2–4.
Moderate pruritus: 5–7. For example, environmental atopic dermatitis and
contact allergy are generally associated with moderate pruritus, scored
between 5 and 7.
Intense pruritus: 8–10. Highly pruritic processes include flea-bite
hypersensitivity, food hypersensitivity, yeast overgrowth, and sarcoptic
mange.
The assessment is conducted using a visual analogue scale, whereby the

severity of pruritus is scored on a scale of 0 to 10. This scale consists of a
vertical line from 0 to 10, on which the owners indicate the point they believe
corresponds to the severity of their dog’s pruritus (Box 3 ). The owner is
instructed to read the descriptions of pruritus severity written next to the
unnumbered vertical line, and then to mark with a dash the point that they
believe corresponds to their dog’s pruritus. Next, a transparency on which the
numbered scale is printed (shown in Box 3 ) is superimposed upon this vertical
line to determine the numeric value corresponding to the owners rating.
BOX 3
Seasonality
Typical seasonal processes include atopic dermatitis caused by pollen allergens
during specific seasons, flea-bite hypersensitivity in certain latitudes, and
infestations caused by Trombicula or lice. Sarcoptic mange is not a seasonal
process, but occurs more frequently in winter (Fig. 13 ).
13 Dog with sarcoptic mange.
Onset and evolution

All information relating to the onset and evolution of the process is important;
establishing a correct diagnosis depends in large part on the accuracy of the
information provided by the owner.
Pruritus is the first sign , followed subsequently by other clinical signs and
lesions. When the owner is certain that pruritus was the most important and
initial sign observed, this is a clear indication of a primary pruritic condition
such as external parasitosis (Sarcoptes, Otodectes, Cheyletiella ) or an allergic
process (flea-bite hypersensitivity or atopic dermatitis). These are pruritic
presentations of rapid onset characterised by intense pruritus from the outset.
However, other processes, including environmental dermatitis and demodicosis,
begin with mild-to-moderate pruritus that becomes progressively more severe
as lesions worsen.
In cases in which it is clear that the patient first developed lesions (papules,
pustules, scales, collarettes, or crusts), which were then followed by pruritus,
as occurs in dermatophytosis, pemphigus, and cutaneous lymphoma, the pruritus
is considered secondary.
Pruritus improves when the patient moves to an environment other than
their usual environment . This can be suggestive of atopic dermatitis caused by
pollen found in a given area (when the new environment is geographically
distinct from the usual one) or contact dermatitis.
Pruritus worsens indoors or outdoors . If the pruritus worsens when the dog
stays indoors, it may be linked to hypersensitivity to dust mites. If it is more
intense when the dog stays outdoors, it is likely related to a reaction to plants,
pollen, or other environmental allergens.
Location and type of lesions accompanying pruritus

Determining the body area affected by pruritus can provide diagnostically useful
information. Flea-bite hypersensitivity produces pruritus of the dorsolumbar
(Fig. 14 ) and inguinal areas, and of the ventral area of the neck (Fig. 15 ),
while atopic dermatitis is associated with pruritus of the face (Fig. 16 ), paws,
inguinal area, axillae, and ventral abdomen (Fig. 6 and Box 2 ). Lesions such as
erythema, scales, and papulopustules located on the face, paws, and inguinal
areas are cause to suspect atopic dermatitis (Fig. 17 ).
By contrast, the appearance of scales and crusts may indicate:

Sarcoptic mange if the lesions are located on the margins of the pinnae, hocks,
and elbows.
Flea-bite hypersensitivity if they are also accompanied by comedones and
alopecia and affect the dorsolumbar and inguinal areas, tail, and ventral
aspect of the neck.
Cheyletiellosis, if scaling is observed in the dorsal area of the trunk.
Given the importance of accurately and systematically collecting all this

information, the veterinary surgeon should note all the owner’s responses on a
dedicated record sheet (Box 4 ).
14 Atopic dermatitis caused by flea bites.
15 A pruritic erythematous presentation, affecting the ventral aspect of the neck, caused by flea-
bite hypersensitivity.
16 Atopic environmental dermatitis affecting the face and ears of a Dachshund.
17 Erythematous lesions on the foot of a dog with atopic dermatitis.

BOX 4
GENERAL EXAMINATION
Most pruritic processes are characterised by the absence of systemic signs, but
some hepatic pathologies, hepatocutaneous syndrome, some renal processes,
and certain endocrinopathies, such as diabetes mellitus, may manifest with
pruritus, in addition to the corresponding general clinical signs and blood test
abnormalities. Involvement of the auditory canal (external otitis) and pinnae
(Fig. 18 ), conjunctivitis, blepharitis, cheilitis (Fig. 19 ), perianal erythema,
anal sac impaction (Fig. 20 ), and perivulvar and preputial erythema are
common in cases of food hypersensitivity and allergies caused by aeroallergens.
In addition, otitis and conjunctivitis are common in cases of atopic dermatitis,
and even flea-bite hypersensitivity. Digestive alterations may be observed in
cases of food hypersensitivity, and rhinitis in cases of aeroallergen allergies. A
history of urticaria or angioedema may precede the development of atopic
dermatitis.
18 Chronic otitis externa in a West Highland White Terrier with atopic dermatitis.
19 Conjunctivitis, blepharitis, and cheilitis in a dog with atopic dermatitis.

20 Perianal erythema and anal sac impaction in a dog with atopic dermatitis.
The patient should be thoroughly examined from the tip of the muzzle to the tip
of the tail, including the face, limbs, and trunk.
The external auditory canal should be examined with an otoscope, and the
pinnae and ear margins should be carefully examined for lesions induced by
parasites and allergies. Pruritus affecting the ears and the flexor surfaces of the
limbs is characteristic of atopic dermatitis and contact dermatitis.
The examination should include the mucocutaneous junctions (Fig. 21 ), mucous

membranes, interdigital areas, nails, footpads, axillae and groin, all of which
are commonly affected in many allergic processes.
Excoriations, broken hairs, and brown discolouration of hair due to constant
licking (caused by saliva) (Fig. 22 ) are typical signs of pruritus.
Alopecia is very common in pruritic conditions due to scratching and chewing

behaviours, and should be distinguished from spontaneous alopecia, which is a
nonpruritic, follicular problem. The localisation of alopecic areas should be
taken into account: self-induced forms of alopecia occur in areas that the dog
can easily chew, lick, or scratch.
The following are the main lesions observed in dermatological examinations of

animals with pruritic conditions:
Erythematous lesions, excoriations, lichenification, and alopecia (Figs. 23
and 24 ) secondary to pruritus. These are common in skin subjected to
chronic self-trauma.
Papules, pustules, and collarettes, which are compatible with superficial
pyoderma.
Comedones and alopecia, which may be indicative of demodicosis.
21 Mucocutaneous pyoderma in a dog with atopic dermatitis.

22 Brown discolouration caused by saliva as a result of pruritus-induced chewing.
23 Erythema, lichenification, hyperpigmentation, and generalised alopecia in a dog with chronic

atopic dermatitis.
24 Alopecia and lichenification in a West Highland White Terrier with food hypersensitivity.
DIAGNOSTIC PROTOCOL
The list of differential diagnoses should include the most probable causes
(Box 2 ), based on the information gathered from the medical history and the
examination.
The order in which subsequent tests are performed should be determined

based on prior confirmation or exclusion of the most frequent processes.
However, since this chapter describes the general diagnostic procedure, the
order of the tests described is based on the general principle of using simple
inexpensive tests that allow us to rule out pruritic causes, beginning with
larger agents (fleas, lice, or Cheyletiella ), followed by intermediate-sized
(mites such as Sarcoptes and Demodex ) and finally microscopic (yeast,
bacteria, dermatophytes) agents. If these causes are ruled out, we can next
focus on allergies, and subsequently move on to less common causes, or
those in which pruritus is not the primary clinical sign, but rather a
complication of the primary process. This procedure involves 12 steps, as
described below.
To improve the sensitivity of the tests, before performing the first and second
steps it may be useful to spray the dog with permethrin- or fipronil-based
external antiparasitics, followed by combing and skin scraping.
STEP 1 Confirm or rule out the presence of fleas,

lice, and Cheyletiella
The first step is to confirm or rule out the presence of external parasites.
These can be observed on the skin surface through a magnifying glass, and
can be collected by passing a fine-toothed comb over the body and
examining the comb for the presence of fleas, ticks, lice, or Cheyletiella
(Fig. 25 ).
25 Larger external parasites that can cause pruritus and can be identified by skin scraping or
trichogram.
STEP 2 Confirm or rule out the presence of mites
on the surface of the skin (Demodex, Sarcoptes,
Trombicula ) and on the ears (Otodectes )
The aim of this second step is to confirm or rule out the presence of mites on
the surface of the skin (Demodex, Sarcoptes or Trombicula ) (Fig. 26 ).
Deep skin scrapings of areas affected by pruritus or erythema should be
performed. These agents can also be visualised in a trichogram. A special
case is the diagnosis of demodicosis in dogs with thick skin, such as the Shar
Pei (see step 12 ).
To detect Otodectes , otoendoscopy is performed to check for the presence

of mites in the ears. Fresh ear swabs can also be examined under a
microscope to check for the presence of mites.
26 Mites that can cause pruritus.
STEP 3 Confirm or rule out dermatophytosis
Next, the presence of pathogenic fungi on the surface of the skin

(dermatophytes) should be confirmed or ruled out (Fig. 27 ). Analysis of the
trichogram can provide an indication of whether the hair shafts have been
invaded by dermatophytic spores. However, to establish a definitive
diagnosis it is necessary to perform a culture in a specific medium for
dermatophytes (DTM) and to subsequently identify macroconidia by staining
with lactophenol Cotton Blue.
While pruritus is not commonly observed in dermatophytic conditions, it has
been observed in conditions caused by both M. canis and T.
mentagrophytes. It is thus important to confirm or rule out these
possibilities. Yorkshire Terriers are particularly predisposed to
dermatophytic conditions that present with pruritus, as well as clinical
pictures that resemble allergic conditions (Fig. 28 ).
27 (a) Trichogram showing pruritus-causing fungi and (b) identification of macroconidia in

positive cultures.
28 Yorkshire Terrier with generalised pruritic dermatophytosis, which presents with a clinical
picture similar to that associated with allergy.
STEP 4 Confirm or rule out intestinal parasites
Faecal parasitological examinations are important since in some patients

infestations with intestinal parasites (hookworms) can induce generalised
and nonspecific pruritus (Fig. 29 a).
In addition, the faeces can also be analysed for Dipylidium, the presence of
which indicates that the patient has come into contact with fleas (Fig. 29 b).
29 (a)Ancylostoma eggs, which can cause nonspecific pruritus and (b) Dipylidium eggs,
indicating that the patient has had, or still has, contact with fleas.
STEP 5 Analysis of microscopic structures on the

skin surface
Microscopic structures (e.g. yeast, bacteria, inflammatory cells) can be
examined by cytology of the skin surface and skin lesions. Samples are
obtained by direct imprinting on a slide or transparent adhesive tape, or by
using a 25-G needle in cases involving papulopustular, vesicular, or nodular
(embossed lesions) lesions. Samples are stained using Diff-Quik solution.
This technique can reveal the presence of Malassezia, cocci, bacilli, and
inflammatory cells (neutrophils, eosinophils, or lymphocytes), and can be
used to examine the appearance of keratinocytes (Fig. 30 ).
30 Microscopic agents that can be identified by Diff-Quik staining.
In endemic areas, leishmaniasis can mimic many other conditions. Although

not usually accompanied by pruritus, dermatological lesions can become
complicated, giving rise to pruritus (Fig. 31 a). Based on our experience, the
laboratory test that provides the most accurate diagnosis is ELISA serology
to quantify levels of circulating antibodies against Leishmania, accompanied
by serum protein analysis. In some cases in which only skin lesions appear,
biopsy and immunohistochemistry are required for a definitive diagnosis
(Fig. 31 b).
31 (a) Erythema, inflammation, and pruritus of the pinna of a dog with leishmaniasis. (b)
Immunohistochemistry positive for Leishmania .
STEP 7 Institute an antiparasitic treatment and

control program (against fleas and gastrointestinal
parasites)
If all the aforementioned tests have been carried out and a diagnosis has not
yet been established, external parasite treatment appropriate to the
circumstances of the patient should be instituted to control fleas and their
larval forms, both in the environment and in all pets that live in the same
house as the patient. Antiparasitic treatments for gastrointestinal parasites
should also be administered.
STEP 8 Confirm or rule out food hypersensitivity
Food hypersensitivity should be considered in cases of dogs of around 1

year of age that present with pruritus. Currently, there are no laboratory tests
of sufficient sensitivity and specificity to diagnose food hypersensitivity.
Therefore, the test of choice is the institution of a hypoallergenic diet.
Ideally, this should be a homemade diet consisting of protein that the patient
has not previously consumed. However, this is not always feasible, and in
most cases specific prepared diets are used. Other alternatives include
hydrolysed and ultrahydrolysed diets, as well as diets consisting exclusively
of amino acids.
If the patient’s diet is the main cause of the pruritus, an evident improvement
will be observed within 2 weeks of beginning the hypoallergenic diet.
Nonetheless, the diet should be maintained for a minimum of 4 weeks. If the
skin condition improves significantly, a provocation diet is instituted. This
involves returning the patient to their former diet to determine whether this
induces relapse (signs will appear within 7 days), thereby confirming the
diagnosis.
While several laboratories offer services to quantify food allergy antibodies,

in our experience the results do not reach the levels required for diagnostic
certainty, and we therefore do not usually include this type of analysis in our
protocol.
STEP 9 Determine whether the patient fulfils at

least 5 clinical criteria for atopy (Favrot, 2010)
The Favrot diagnostic criteria can be used to determine the probability that
the pruritus is caused by hypersensitivity to environmental allergens. Box 5
shows the typical clinical signs of atopic dermatitis, as defined based on
statistical analyses of a large number of diagnosed patients.
Based on currently available epidemiological information, if a dog presents

with a pruritic condition and all causes of pruritus have been ruled out using
the aforementioned steps 1 through 9, and in addition the dog fulfils 5 of the
clinical criteria on this list, the patient can be diagnosed with canine atopic
(inhalant) dermatitis with a sensitivity of 77 % and a specificity of 83 %.
Favrot’s clinical criteria should not be used as the sole diagnostic method
for atopic dermatitis, but rather to rule out other causes of pruritus with
similar clinical signs.
BOX 5
Favrot’s diagnostic criteria
These criteria can be used to evaluate the probability that a dog has atopic
dermatitis.
The age of onset of pruritis is less than 3 years.
The dog spends most of its time indoors.
Pruritus and lesions affect the paws (digits) of the hindlimbs.
Presence of a yeast infection (chronic or recurrent).
The pinnae are affected.
The ear margins are not affected.
The dorsolumbar zone is not affected.
STEP 10 Therapeutic trial with oclacitinib
Oclacitinib exerts both antipruritic and anti-inflammatory effects by

preventing the activation of the JAK system by IL-31. Thanks to the
discovery of this molecule, pruritus can be controlled while the diagnostic
tests are being conducted, since oclacitinib does not interfere with the results
or alter the outcomes of analyses to quantify levels of anti-allergen
antibodies, at least when administered for periods of less than 8 weeks.
Oclacitinib is indicated both in allergic processes and pathologies of other
aetiologies that involve inflammation and pruritus.
In our experience, oclacitinib controls pruritus and inflammation in about 85

% of dogs with atopic dermatitis.
Other fast-acting molecules that can also be used include short-acting

corticosteroids (prednisone, prednisolone, and methylprednisolone).
However, their effects can alter the results of allergy tests. Conducting
therapeutic tests with molecules such as those mentioned above allows us to
determine whether they are effective in the patient and to identify potential
symptomatic treatments in case hyposensitisation cannot be achieved or does
not provide the expected results.
STEP 11 Identification of airborne allergens in

cases of atopic dermatitis
This test is only performed to identify aeroallergens implicated in atopic
dermatitis, always with a view to instituting corresponding hyposensitisation
or desensitisation (immunotherapy) treatment.
Two types of tests are used to identify allergens: direct in vivo tests
(intradermal tests) and indirect in vitro tests (serological tests to quantify
levels of specific antibodies against aeroallergens).
In our view, both procedures provide similar diagnostic and therapeutic

information.
When positive results are obtained, they should be cross-checked with the
patient’s clinical history. In cases of concordance, the appropriate
hyposensitisation therapy should be instituted based on the allergens
identified. In some cases it is possible to modify the immune response of
the dog and to achieve a state of tolerance to the allergens involved.
This response is evaluated 6 months after commencing immunotherapy.
In cases in which no significant improvement is observed, symptomatic
therapy, which will usually have been tested in the previous step, is
instituted.
If allergen testing does not provide positive results, the patient is
considered to have a particular form of atopic dermatitis known as
intrinsic atopic dermatitis or atopic dermatitis-like syndrome, which
presents all the characteristics of atopic dermatitis but for which no
antigens can be detected. In this situation, the only option is symptomatic
antipruritic and anti-inflammatory therapy.
STEP 12 Skin biopsy
The biopsy is an interesting test because it provides information about the

microscopic features of the skin that can sometimes help establish a
definitive diagnosis.
Like clinical patterns, histological patterns can have many causes, and
therefore biopsy will not always help us to discern the cause of pruritus. For
example, in cases of pruritic conditions that have become chronic, resulting
in the appearance of secondary lesions, biopsy is not usually diagnostically
useful. It is also not useful in cases of allergies, even in recently developed
conditions with primary lesions, since these tend to involve very similar
histopathological lesions, which often resemble those caused by some
external parasitoses (e.g. sarcoptic mange).
However, biopsy is essential for the definitive diagnosis of pruritic

epithelial lymphoma in geriatric patients and the diagnosis of pathologies
such as primary seborrhoea, vitamin A-responsive dermatitis, and zinc-
responsive dermatoses, all of which have a pruritic component.
TREATMENT
Antipruritic therapy is based on establishing a definitive diagnosis and applying
a specific treatment, regardless of whether the cause is parasitic, fungal, or
infectious.
However, in the case of allergies it is not always easy to identify the cause, and
even when the causative allergen is detected it is not always possible to avoid
contact between the patient and the allergen. Therefore, symptomatic therapies
that alleviate the patient’s discomfort are required. It is important to bear in
mind that in dogs with atopic dermatitis, structural alterations in the epidermis
favour the penetration of allergens, which exacerbate the pruritus. Certain
factors must also be controlled to avoid exacerbation of pruritus, e.g. flea bites,
certain foods that worsen pruritus, and overgrowth of yeast or bacteria on the
skin surface. The administration of antibiotics is indicated in the latter case
(bacterial overgrowth or superficial pyoderma), but not for other pruritic
conditions, in which antibiotics do not improve clinical signs.
Clinical signs can be alleviated using moisturising/restructuring agents, topical

essential fatty acids, antiparasitics, fatty-acid-rich diets, and, more specifically,
oclacitinib (enzyme inhibitor) and lokivetmab (canine monoclonal antibody).
Oclacitinib and lokivetmab are the 2 most recently discovered molecules for the
symptomatic treatment of atopic dermatitis, and act selectively: oclacitinib
prevents activation of the JAK system enzymes and lokivetmab specifically
blocks IL-31. Both molecules prevent transmission of the pruritic sensation at
the level of the basal ganglia, thereby preventing the associated nerve signal
from reaching the CNS.
Other drugs available for the symptomatic treatment of atopic dermatitis include
corticosteroids, antihistamines, and ciclosporin.
CHAPTER 1. GENERAL
CONSIDERATIONS FOR DIAGNOSIS
BASED ON CLINICAL PATTERNS
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CHAPTER 2. DEFINING CUTANEOUS

PATTERNS
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in general medicine . 5th ed. McGraw-Hill 1999, Vol. 1:41-49.
CHAPTER 3. FOCAL OR MULTIFOCAL

ALOPECIA
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HILL P. Clinical approach to alopecia in dogs-will the hair grow back. Proceedings TNAVC. Small
animal dermatology . 2005; pp. 263-268.
HILLIER A. Differentiating endocrine from non-endocrine alopecia. In: Proceedings 7th World
Veterinary Dermatology Congress. Vancouver. 2012; pp.133-139.
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P ATERSON S. An approach to focal alopecia in the dog. In: Foster A, Foil C, eds. Small animal
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REES C. An approach to canine focal alopecia and multifocal alopecia. In: Jackson H, R Marsella eds.
Small animal dermatology . BSAVA 3rd ed. 2012; pp. 86-90.
RIOS AM. Alopecias focales y multifocales inflamatorias en el perro. In Diagnóstico de la alopecia en
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SPANO F, DONOVAN JC. Alopecia areata: part 2: treatment. Can Fam Physician . 2015; 61(9):757-761.
CHAPTER 4. SYMMETRICAL ALOPECIA

(REGIONAL OR GENERALISED)
BERGER DJ, LEWIS TP, SCHICK AE, MILLER RI, LOEFFLER DG. Canine alopecia secondary to human
topical hormone replacement therapy in six dogs. J Am Anm Hosp Assoc . 2015; 51(2):136-142.
CARLOTTI ND. Overview of non-endocrine alopecias. In: Proceedings 7th World Veterinary
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CERUNDOLO R, REST J. Nonpruritic hair loss. In: Advances in veterinary dermatol . Proceedings 7th
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FERRER LL. Non-Endocrine symmetric alopecia in dogs: clinical management. Proceedings NAVC .
2005; pp. 241-243.
FRANCK L. Canine alopecic dermatoses. Clinician’s brief . 2008 June:64- 68.
HILL P. Clinical approach to alopecia in dogs-will the hair grow back. Proceedings TNAVC. Small
animal dermatology . 2005; pp. 263-268.
HILLIER A. Differentiating endocrine from non-endocrine alopecia. In: Proceedings 7th World
Veterinary Dermatology Congress. Vancouver. 2012; pp. 133-139.
MILLER W H, GRIFFIN CE, CAM PBELL KL. Endocrine and metabolic diseases. In: Muller & Kirk’s
small animal dermatology . Saunders-Elsevier, St Louis, 7th ed. 2013; p. 503.
MILLER WH, GRIFFIN CE, CAM PBELL KL. Miscellaneous alopecias. In: Muller & Kirk’s small animal
dermatology. Saunders-Elsevier, St Louis, 7th ed. 2013; pp. 554-572; pp. 568-569.
MILLER WH, GRIFFIN CE , CAM PBELL KL. Miscellaneous skin diseases. In: Muller & Kirk’s small
animal dermatology , Saunders-Elsevier, St Louis 7th ed. 2013; p. 714.
MÜNTENER T, SCHUEPBACH -REGULAR G, FRANK L, RÜFENACHT S, WELLE MM. Canine
noninflammatory alopecia: a comprehensive evaluation of common and distinguishing histological
characteristics. Vet Dermatol. 2012; 23:206-222.
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OUTERBRIDGE CA, WHITE SD, AFFOLTER VK. Alopecia universalis in a dog with testicular neoplasia.
Vet Dermatol. 2016; 27: 513- 519.
P ARADIS M, CERUNDOLO R. An approach to symmetrical alopecia in the dog. In: Foster A, Foil C, eds.
Small animal dermatology . BSAVA 2nd ed. 2003; pp. 83-93.
P ARADIS M. An approach to symmetrical alopecia in dogs. In: Jackson H, Marsella R, eds. Small
P AUS R, P EKER S. Biología del pelo y de las uñas In: Bolognia, Jorizzo, Rapini eds. Dermatology .
Elsevier-Mosby. 2004; pp. 1007-1030.
RIOS AM. Alopecias generalizadas no inflamatorias en el perro. In: Diagnóstico de la alopecia en el
perro y en el gato . Ed. Servet. 2015; pp. 91-123.
SALO E, FRAILE C, RIOS A, SANCHO PJ. Problemas dermatológicos. AVEPA Formación Continuada
Dermatología . 2013; pp. 1-26.
VARJONEN K, REST J, BOND R. Alopecia in a black Labrador Retriever associated with focal sub-
follicular panniculitis and sebaceous adenitis. Vet Dermatol. 2010; 21:415-419.
WIENER DJ, RÜFENACHT S, KOCH HK, MAULDIN EA, MAYER U, WELLE MM. Estradiol-induced
alopecia in five dogs after contact with a transdermal gel used for the treatment of postmenopausal
symptoms in women. Vet Dermatol . 2015; 26(5): 393-396.
ZUR G, WHITE SD. Hyperadrenocorticism in 10 dogs with skin lesions as the only presenting clinical
signs. JAAHA. 2011; 47:419-427.
CHAPTER 5. SCALING/CRUSTING AND

SEBORRHOEIC PATTERN
BLOOM P. Situación clínica en dermatología. Costras no pruriginosas en el plano nasal. Consulta de
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CAM PBELL KL. An approach to keratinization disorders. In: Jackson H, Marsella R, eds. Small animal
dermatology . BSAVA 3rd ed. 2012; pp. 46-52.
CANNON AG. Hereditary disorders of keratinization. Proceedings Companion Animal Programme
Voorjaarsdagen . 2007; pp. 273-274.
CREDILLE KM. Primary cornification defects. In: Guaguère Eric., editor. A practical guide to canine
dermatology . Pascal Prélaud; Merial: 2008.
DE BOER DJ. Skin scraping for external parasites. Clinician’s brief . 2016 April:43-47.
DEDOLA C, RESSEL L, HILL PB, et al. Idiopathic generalized sebaceous gland hyperplasia of the Border
Terrier: a morphometric study. Vet Dermatol. 2010; 21:494–502.
ELIAS PM, WILLIAM S ML, CRUM RINE D, SCHM UTH M. Ichthyoses; clinical, biochemical and
diagnostic assessment. Series: Current problems in dermatology, 39. Ed. Karger; 2010; pp. 1–29.
LATKOWSKI JAM, FREEDBERG IM. Epidermal cell kinetics, epidermal differentiation, and keratiniztion.
In: Fizpatrick’s dermatology in general medicine . 5th ed. McGraw-Hill 1999; Vol. 1:133-143.
LEE FF, BRADLEY CW, CAIN CL, et al. Localized parakeratotic hyperkeratosis in sixteen Boston terrier
dogs. Vet Dermatol. 2016; 27: 384-e96.
MAULDIN EA. Canine ichthyosis and related disorders of cornification in small animals. Vet Clin North
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MAULDIN EA, CREDILLE KM, DUNSTAN RW, CASAL ML. The clinical and morphologic features of
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MILLER WH, GRIFFIN CE, CAM PBELL KL. Keratinization defects. In: Muller & Kirk’s small animal
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NISHIFUJI K, YOON JS. The stratum corneum: the rampart of the mammalian body. In: Advances in
veterinary dermatology . Ed. Wiley-Blackwell. 2012; Vol 7:65-77.
ORDEIX L, BARDAGÍ M, SCARAM PELLA F, FERRER L, FONDATI A. Demodex injai infestation and dorsal
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P ETERS -KENNEDY J, SCOTT DW, LOFT KE, MILLER WH. Scaling dermatosis in three dogs associated
with abnormal sebaceous gland differentiation. Vet Dermatol. 2014; 25: 23-e8.
REES C. Scaling or keratinization disorders in dogs. Proceedings NAVC . 2011 Jan.
ROSTAHER A. Keratinization disorders. Conference. University of Zurich Division of Dermatology.
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SHIM ADA K, YOON J, YOSHIHARA T, IWASAKI T, NISHIFUJI KOJI . Increased transepidermal water loss
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CHAPTER 6. EROSIVE-ULCERATIVE
PATTERN
Dermatology Congress. Vancouver . 2012; pp. 257-263.
FOSER AP. Blistering and erosive immune-mediated skin diseases. In: Foster A, Foil C, eds. Small
animal dermatology . BSAVA 2nd ed. 2003; pp. 197-205.
GROSS TL, IHRKE PJ, WALDER EJ, AND AFFOLTER VK. Skin diseases of the dog and cat. Clinical
histopathologic diagnosis . 2nd ed. Blackwell Publishing 2005.
JACKSON HA. Autoimmune and immunemediated skin diseases. In: Jackson H, Marsella R, eds. Small
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MILLER WH, GRIFFIN CE, CAM PBELL KL. Autoimmune and immunemediated dermatoses. In: Muller
& Kirk’s small animal dermatology , Saunders-Elsevier, St Louis, 7th ed. 2013; pp. 432-500.
MILLER WH, GRIFFIN CE, CAM PBELL KL. Miscellaneous skin diseases. In: Muller & Kirk’s small
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MOREILLO K. Dermatology update: a new look at ulcerative dermatosis of Shetland sheepdogs and
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CHAPTER 7. PAPULOPUSTULAR AND

VESICULAR PATTERN
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JACKSON HA. Autoimmune and immunemediated skin diseases. In: Jackson H, Marsella R, eds. Small
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CHAPTER 8. WHEN THE CLINICAL

PRESENTATION IS PRURITUS
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DERMATOLOGICAL DIAGNOSIS IN DOGS

An approach based on clinical patterns

First printing: February 2018

Design, layout and printing:

All rights reserved.

To my husband Emilio and my children Emilio and Pablo,

To all my former students now working in the field of

To all members of the GEDA group of AVEPA,

Maite Verde graduated in Veterinary Medicine from the Faculty of Veterinary

A Professor of Internal Medicine and Dermatology, AVEPA-accredited in

Management of skin diseases can be frustrating. Remembering all of the

Many excellent photographs, diagrams and charts further enhance the

Dunbar Gram, DVM, DACVD,

General practitioners working in the field of clinical dermatology thus need

We believe that the simplest and most logical way to approach a

The first 2 chapters provide a general introduction to diagnosis based on

The content is designed to allow readers to learn by following a systematic

Pigmentary alteration pattern

08 WHEN THE CLINICAL

When basing the diagnosis on dermatological patterns, it is not necessary to

Establishing a dermatological diagnosis this way is possible thanks to

Now, after 40 years of progress in canine dermatology, establishing a

Expertise in dermatology is not required to apply a diagnostic protocol based

To establish a diagnosis based on clinical patterns, one must know how to

01 Multifocal alopecia pattern.

IDENTIFY AND DEFINE THE

To determine the predominant clinical pattern, it is also necessary to look at

From the information obtained, we can establish the dermatological pattern:

04 Papulopustular lesions in a case of multifocal alopecia.

COLLECT BASIC INFORMATION

Any observations or concerns mentioned by the owner should also be noted in

PROPOSE TESTS IN A LOGICAL ORDER

Each of the chapters of this book describes the diagnostic procedures

Cutaneous tissue can respond to aggressions in a limited number of ways,

This way, it is possible to define clinical responses and histopathological

The pathophysiological alterations that occur in the skin in response to

In the normal epidermis (Fig. 2 a) there is a balance between the rate of

Cytokines that regulate the growth and differentiation of keratinocytes are

HYPERKERATOSIS: ALTERATIONS IN THE

Alterations in cornification are known as hyperkeratosis (Figs. 2b and 2c ),

Diagnosis can be confirmed by histological analysis of skin biopsies.

For reasons unknown, orthokeratotic hyperkeratosis is the predominant

Box 1 details the characteristics of these 2 types of hyperkeratosis.

02 Schematic showing the epidermal layers and corresponding microscopic pathophysiological

ACANTHOSIS: EPIDERMAL HYPERPLASIA

Epidermal hyperplasia is a secondary disorder very frequently associated

Acanthosis is a common response to a wide variety of stimuli and has several

Apoptosis of keratinocytes is observed in the following processes:

03 Apoptosis of keratinocytes in all epidermal layers. Image courtesy of Dolors Fondevila.

Epidermal necrosis can be caused by the following:

ATROPHY OF THE EPIDERMIS

05 Atrophic skin through which the subcutaneous vascularisation is visible.

ALTERATIONS IN THE EPIDERMAL FLUID

Intracellular fluid accumulation

Accumulation of intracellular fluid in the keratinocytes of the basal layer

The accumulation of intracellular fluid in the keratinocytes of the upper

These inflammatory cells reach the epidermis when there is an inflammatory

Leukocyte exocytosis is common in inflammatory processes. Typically,

Other processes in which leukocyte exocytosis can be observed include

Acute inflammatory dermatitis begins with hyperaemia (arteriolar

Chronic inflammatory dermatitis involves contact between the irritant agent

The process by which acute inflammation of the skin becomes chronic is

Perifolliculitis, luminal folliculitis, and furunculosis usually occur in

Sebaceous adenitis is a specific inflammatory reaction that targets the